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Muscle Glycogen during Prolonged Severe Exercise
Abstract
10 well trained and 10 untrained subjects worked to complete exhaustion on a bicycle ergometer with work loads averaging 77 (76–87) per cent of their individual maximal aerobic power. Determinations of glycogen used by working muscles (biopsy of lateral portion of the quadriceps femoris muscles) and of combusted carbohydrate (Vo2 and RQ) were performed at certain intervals from the start of work to exhaustion. At a combustion rate of about 3 g carbohydrate per minute (RQ around 0.9 or higher) and at average values for glycogen in resting muscle of 1.6 (1.1–2.5)g/100 wet muscle, the effective work time was around 85 min for the untrained and 90 min for the trained subjects. At the end of the exhaustive exercise the glycogen content averaged 0.06 g in the untrained and 0.12 g/100 g wet muscle in the trained subjects. A close relationship between utilized glycogen and combusted carbohydrate was found, and it seems highly probable that at high relative workloads primarily the glycogen stores in the exercising muscles will limit the capacity for prolonged strenuous work.
... It is well established that carbohydrates (CHOs) and lipids are the main fuels oxidised by skeletal muscle during endurance exercise [6,7]. Accordingly, muscle glycogen is a major energy source utilised during endurance exercise, and a direct relationship between fatigue and muscle glycogen levels has been demonstrated [6][7][8], ultimately leading to an impaired performance when glycogen levels become depleted [6][7][8]. The current nutritional recommendations after an exercise bout highlight a high CHO availability with an intake of~1.2 g CHO/kg/hr during the first hours of recovery [4,9]. ...
... It is well established that carbohydrates (CHOs) and lipids are the main fuels oxidised by skeletal muscle during endurance exercise [6,7]. Accordingly, muscle glycogen is a major energy source utilised during endurance exercise, and a direct relationship between fatigue and muscle glycogen levels has been demonstrated [6][7][8], ultimately leading to an impaired performance when glycogen levels become depleted [6][7][8]. The current nutritional recommendations after an exercise bout highlight a high CHO availability with an intake of~1.2 g CHO/kg/hr during the first hours of recovery [4,9]. ...
... This was repeated until the participants were unable to maintain the required power for 1 min. A previous study [8] has demonstrated very low levels of muscle glycogen when cycling in 20 min intervals until exhaustion. Heart rate (HR) was measured during EX1, including at the approximate mid-point of every sprint, as well as during the TTE performance test (heart rate monitor: Polar H10 heart rate sensor). ...
The main purpose of this study was to investigate the effect of a novel alginate-encapsulated carbohydrate–protein (CHO–PRO ratio 2:1) supplement (ALG) on cycling performance. The ALG, designed to control the release of nutrients, was compared to an isocaloric carbohydrate-only control (CON). Alginate encapsulation of CHOs has the potential to reduce the risk of carious lesions. Methods: In a randomised cross-over clinical trial, 14 men completed a preliminary test over 2 experimental days separated by ~6 days. An experimental day consisted of an exercise bout (EX1) of cycling until exhaustion at W~73%, followed by 5 h of recovery and a subsequent time-to-exhaustion (TTE) performance test at W~65%. Subjects ingested either ALG (0.8 g CHO/kg/hr + 0.4 g PRO/kg/hr) or CON (1.2 g CHO/kg/hr) during the first 2 h of recovery. Results: Participants cycled on average 75.2 ± 5.9 min during EX1. Levels of plasma branched-chain amino acids decreased significantly after EX1, and increased significantly with the intake of ALG during the recovery period. During recovery, a significantly higher plasma insulin and glucose response was observed after intake of CON compared to ALG. Intake of ALG increased plasma glucagon, free fatty acids, and glycerol significantly. No differences were found in the TTE between the supplements (p = 0.13) nor in the pH of the subjects’ saliva. Conclusions: During the ALG supplement, plasma amino acids remained elevated during the recovery. Despite the 1/3 less CHO intake with ALG compared to CON, the TTE performance was similar after intake of either supplement.
... Thus, being human, they were naturally biased towards conclusions that would advance the importance of their novel innovation. Their bias in turn made it more likely that, from the moment they applied the muscle biopsy technique, these authors would promote a model of human performance in which muscle glycogen would be the key determinant of performance during prolonged exercise [15,[17][18][19][20][21][22][23][24]. ...
... The popular conclusion from these two iconic studies was that the pre-exercise muscle glycogen content is the pre-eminent determinant of human exercise performance [21,23]; that pre-exercise concentrations can be maximized by a specific diet/exercise regime [22,23]; that this procedure substantially improves human exercise performance because the cause of fatigue and of 'slowing down' (Figure 7) in more prolonged exercise is the near-total depletion of muscle glycogen stores. ...
... Little direct support exists for any of these possibilities ((current author's added emphasis). The strongest evidence linking any of these possibilities to muscle fatigue is a consistent observation that fatigue during endurance exercise is associated with glycogen depletion [17,18,21,36]'. ...
The introduction of the needle muscle biopsy technique in the 1960s allowed muscle tissue to be sampled from exercising humans for the first time. The finding that muscle glycogen content reached low levels at exhaustion suggested that the metabolic cause of fatigue during prolonged exercise had been discovered. A special pre-exercise diet that maximized pre-exercise muscle glycogen storage also increased time to fatigue during prolonged exercise. The logical conclusion was that the athlete’s pre-exercise muscle glycogen content is the single most important acutely modifiable determinant of endurance capacity. Muscle biochemists proposed that skeletal muscle has an obligatory dependence on high rates of muscle glycogen/carbohydrate oxidation, especially during high intensity or prolonged exercise. Without this obligatory carbohydrate oxidation from muscle glycogen, optimum muscle metabolism cannot be sustained; fatigue develops and exercise performance is impaired. As plausible as this explanation may appear, it has never been proven. Here, I propose an alternate explanation. All the original studies overlooked one crucial finding, specifically that not only were muscle glycogen concentrations low at exhaustion in all trials, but hypoglycemia was also always present. Here, I provide the historical and modern evidence showing that the blood glucose concentration—reflecting the liver glycogen rather than the muscle glycogen content—is the homeostatically-regulated (protected) variable that drives the metabolic response to prolonged exercise. If this is so, nutritional interventions that enhance exercise performance, especially during prolonged exercise, will be those that assist the body in its efforts to maintain the blood glucose concentration within the normal range.
... During prolonged exercise at low to moderate intensity, glycogen depletion predominantly occurs in slow-twitch fibers, whereas depletion occurs more rapidly in fast-twitch fibers at high intensities (237,395). It is a general finding that glycogen depletion impairs performance during long-duration exercise and repeated intense exercise (33,51,275,290), as first described by Bergström, Hultman, Hermansen, and Saltin (51)(52)(53)290). Reduction of glycolytic rate and higher cost of work are considered as factors underlying the detrimental effect of glycogen depletion on performance (109,395,396). ...
... During prolonged exercise at low to moderate intensity, glycogen depletion predominantly occurs in slow-twitch fibers, whereas depletion occurs more rapidly in fast-twitch fibers at high intensities (237,395). It is a general finding that glycogen depletion impairs performance during long-duration exercise and repeated intense exercise (33,51,275,290), as first described by Bergström, Hultman, Hermansen, and Saltin (51)(52)(53)290). Reduction of glycolytic rate and higher cost of work are considered as factors underlying the detrimental effect of glycogen depletion on performance (109,395,396). ...
... Changes of plasma and myoplasmic lactateand pH are minor with prolonged exercise (73,478), as is depletion of high-energy phosphates (73), which makes these aspects as unlikely fatigue factors. However, depletion of muscle glycogen to very low levels is frequently described as the main player in fatigue during prolonged submaximal exercise (51,237,290,462,538,540,542) and may contribute to a reduction of Na + /K + -ATPase activity (330) and impairment of Ca 2+ release from the sarcoplasmic reticulum (115,231,540). Indeed, reduced Ca 2+ handing is commonly observed in muscle homogenates after prolonged exercise (73,424,540). ...
Exercise causes major shifts in multiple ions (e.g., K+ , Na+ , H+ , lactate- , Ca2+ , and Cl- ) during muscle activity that contributes to development of muscle fatigue. Sarcolemmal processes can be impaired by the trans-sarcolemmal rundown of ion gradients for K+ , Na+ , and Ca2+ during fatiguing exercise, while changes in gradients for Cl- and Cl- conductance may exert either protective or detrimental effects on fatigue. Myocellular H+ accumulation may also contribute to fatigue development by lowering glycolytic rate and has been shown to act synergistically with inorganic phosphate (Pi) to compromise cross-bridge function. In addition, sarcoplasmic reticulum Ca2+ release function is severely affected by fatiguing exercise. Skeletal muscle has a multitude of ion transport systems that counter exercise-related ionic shifts of which the Na+ /K+ -ATPase is of major importance. Metabolic perturbations occurring during exercise can exacerbate trans-sarcolemmal ionic shifts, in particular for K+ and Cl- , respectively via metabolic regulation of the ATP-sensitive K+ channel (KATP ) and the chloride channel isoform 1 (ClC-1). Ion transport systems are highly adaptable to exercise training resulting in an enhanced ability to counter ionic disturbances to delay fatigue and improve exercise performance. In this article, we discuss (i) the ionic shifts occurring during exercise, (ii) the role of ion transport systems in skeletal muscle for ionic regulation, (iii) how ionic disturbances affect sarcolemmal processes and muscle fatigue, (iv) how metabolic perturbations exacerbate ionic shifts during exercise, and (v) how pharmacological manipulation and exercise training regulate ion transport systems to influence exercise performance in humans. © 2021 American Physiological Society. Compr Physiol 11:1895-1959, 2021.
... Nevertheless, in the literature, to our best knowledge, data regarding the strength decay during sustained maximal muscle contraction are scarce, particularly in OLD persons. The strength decay on the other hand is reasonably described in Y [15][16][17][18][19]. Recently, we published unique data [11] where we compared the forcetime characteristics during the FR test of 100 Y, 100 OLD community-dwelling persons, and 91 HOSP when using a modified Pneu handgrip system, which allowed continuous recording of the strength. ...
... Independent of which handgrip system was used, Y were unable to sustain the maximal handgrip effort as long as MA and OLD (except for FR 100-75 measured with Pneu). As Y were stronger than MA (only men when using Pneu) and OLD for Pneu and Hydr, this finding could partly be assigned to earlier occurrence of hypoxia in Y due to compression of arteries by the contracting stronger forearm muscles during the sustained maximal handgrip effort [18,19]. The last part of the strength decay (FR 75-50 ) was longer in OLD compared to MA when using Pneu. ...
Introduction:
Fatigue resistance (FR) can be assessed as the time during which grip strength (GS) drops to 50% of its maximum during a sustained maximal voluntary contraction. For the first time, we compared force-time characteristics during FR test between two different handgrip systems and investigated age- and clinical-related differences in order to verify if a briefer test protocol (i.e., until 75%) could be sufficiently informative.
Methods:
A cohort of young healthy controls (Y, <30 y, 24 ± 3 y, 54% women), middle-aged (MA, 30-65 y, 47 ± 11 y, 54% women), and older (OLD, >65 y, 77 ± 7 y, 50% women) community-dwelling persons, and hospitalized geriatric patients (HOSP, 84 ± 5 y, 50% women) performed the FR test. For this purpose, an adapted vigorimeter (original rubber bulb of the Martin Vigorimeter connected to a Unik 5000 pressure gauge) here defined as "pneumatic handgrip system" (Pneu) and Dynamometer G200 system (original Jamar Dynamometer handle with an in-build strength gauge) here defined as "hydraulic handgrip system" (Hydr) were used. Force-time curves were analysed from 100% to 75% and from 75% to 50% of the initial maximal GS during the FR test. The area under the curve (GW) was calculated by integrating the actual GS at each time interval (i.e., 1/5,000 s) and corrected for body weight (GW/body weight).
Results:
For both systems, we found fair associations between FR100-50 and FR100-75 (Pneu mean difference = 50.1 s [95% CI: 47.9-52.4], r2 = 0.48; Hydr mean difference = 28.4 s [95% CI: 27.0-29.7], r2 = 0.52, all p < 0.001) and also moderate associations between GW(100-50)/body weight and GW(100-75)/body weight (Pneu mean difference = 32.1 kPa*s/kg [95% CI: 30.6-33.6], r2 = 0.72; Hydr mean difference = 8.1 kg*s/kg [95% CI: 7.7-8.6], r2 = 0.68, all p < 0.001). Between MA and OLD, we found a significant age-related difference in the GW results in the first 25% strength decay for Pneu (10.2 ± 0.6 kPa*s/kg against 7.1 ± 1.2 kPa*s/kg, respectively).
Conclusion:
The brief test protocol is valid. Differences within the first 25% strength decay in GW between OLD and HOSP were identified when using Pneu but not when using Hydr. Therefore, a brief FR test protocol using a continuous registration of the strength decay seems to be sufficiently informative in a clinical setting to appraise muscle fatigability, however, only when using a Pneu system.
... The profound influence of muscle insulin sensitivity on whole-body glucose metabolism and glycemic control is central in physical performance, metabolic health, and daily life for patients with diabetes. For example, exercise endurance is tightly linked to muscle glycogen content (21,22), and the insulin-sensitizing effect following a single bout of exercise secures glucose partitioning toward glycogen in the prior contracted muscles, allowing glycogen levels to become supercompensated if glucose is available (3,11). These adaptations ensure faster recovery and increase endurance during subsequent exercise. ...
... Nevertheless, it can be speculated that the change in set point for glycogen storage level imparts an evolutionary advantage. Muscle glycogen content is a key determinant of exercise endurance (21,22), and augmented glycogen levels would effectively improve the chances of a successful hunt or escape in primeval settings. If true, this hypothesis underlines the need for future therapeutics aiming to restore glucose homeostasis by manipulating muscle glucose uptake via improving insulin sensitivity and enhancing the set point for glycogen. ...
Exercise profoundly influences glycemic control by enhancing muscle insulin sensitivity, thus promoting glucometabolic health. While prior glycogen breakdown so far has been deemed integral for muscle insulin sensitivity to be potentiated by exercise, the mechanisms underlying this phenomenon remain enigmatic. We have combined original data from 13 of our studies that investigated insulin action in skeletal muscle either under rested conditions or following a bout of one-legged knee extensor exercise in healthy young male individuals (n = 106). Insulin-stimulated glucose uptake was potentiated and occurred substantially faster in the prior contracted muscles. In this otherwise homogenous group of individuals, a remarkable biological diversity in the glucometabolic responses to insulin is apparent both in skeletal muscle and at the whole-body level. In contrast to the prevailing concept, our analyses reveal that insulin-stimulated muscle glucose uptake and the potentiation thereof by exercise are not associated with muscle glycogen synthase activity, muscle glycogen content, or degree of glycogen utilization during the preceding exercise bout. Our data further suggest that the phenomenon of improved insulin sensitivity in prior contracted muscle is not regulated in a homeostatic feedback manner from glycogen. Instead, we put forward the idea that this phenomenon is regulated by cellular allostatic mechanisms that elevate the muscle glycogen storage set point and enhance insulin sensitivity to promote the uptake of glucose toward faster glycogen resynthesis without development of glucose overload/toxicity or feedback inhibition.
... glycogen content and the duration of exercise that could be sustained during exercise at high intensity (75% VO 2 max). Many of these studies also reported that the termination of prolonged exercise was associated with near-total muscle glycogen depletion [5,7,11,13]. ...
... This belief originates, at least in part, in a series of iconic Scandinavian studies undertaken in the late 1960s. Adopting the novel percutaneous needle muscle biopsy technique [4], these studies measured the disappearance of glycogen from muscle during both prolonged [5][6][7][8][9][10][11][12] and high intensity [13] exercise. The most frequently cited study [10] reported a linear associational relationship between the pre-exercise muscle High fat diet improves metabolic flexibility during progressive exercise to exhaustion (VO 2 max testing) and during 5 km running time trials exercise intensity. ...
Recently we reported similar performances in both progressive tests to exhaustion (VO2max) and 5km running time trials (5KTT) after consuming low-carbohydrate, high-fat (LCHF) or high-carbohydrate, low-fat (HCLF) diets. Accordingly, we tested the null hypothesis that the metabolic responses during both tests would be similar across diets. In a randomized, counterbalanced, cross-over design, seven male athletes (VO2max: 61.9 ± 6.1 mL/kg/min; age: 35.6 ± 8.4 years; height: 178.7 ± 4.1 cm; mass: 68.6 ± 1.6 kg; body fat: 5.0 ± 1.3%) completed six weeks of LCHF (6/69/25% energy carbohydrate/fat/protein) and HCLF (57/28/15% energy carbohydrate/fat/protein) diets, separated by a two-week washout. Substrate utilization and energy expenditure were measured during VO2max tests and 5KTTs. The LCHF diet markedly increased fat oxidation and reduced carbohydrate oxidation, with no associated impairment in either the VO2max tests or the 5KTTs. Following the LCHF diet, athletes generated 50% or more of their energy requirements from fat at exercise intensities up to 90% VO2max and reached the crossover point for substrate utilization at ~85% VO2max. In contrast, following the HCLF diet, carbohydrate provided more than 50% of the total energy consumption at all exercise intensities. During the 5KTT, ~56% of energy was derived from fat following the LCHF diet whereas more than 93% of the energy came from carbohydrate following the HCLF diet. This study provides evidence of greater metabolic flexibility following LCHF eating and challenges the popular doctrines of “carbohydrate dependence” for high intensity exercise and the role dietary macronutrients play in human performance.
... Glycogen is likely the major energy substrate during most forms of physical exercise, especially during moderate (≥ 50% of maximal oxygen uptake ((VO 2 max)) to heavy activities lasting > 20 s (Hultman and Sjoholm 1983a). It has long been recognized that glycogen availability limits exercise endurance in humans at intensities corresponding to 60-80% of VO 2 max Hermansen et al. 1967), which generally includes activities such as running, cycling, skiing, etc. This observation has led to strategies to increase muscle glycogen levels prior to performance testing/competitions (i.e., glycogen supercompensation/loading). ...
... 2005b; Testoni et al. 2017;Danforth 1964;Xirouchaki et al. 2016), whereas in humans, values generally range from 300 to 600 (Gaitanos et al. 1993;Harris et al. 1974;Hermansen et al. 1967;Yan et al. 1993), and can reach levels of 1000 after glycogen supercompensation (Bergstrom and Hultman 1966b). Thus, human muscle contains ~ 10 times as much glycogen as does mouse muscle, despite similar activities of phosphorylase and GS in the two species as measured under the same assay conditions (Jiao et al. 1999;Katz 1997;Blackwood et al. , 2021Sandstrom et al. 2004;Katz et al. 1991a). ...
Glycogen is a branched, glucose polymer and the storage form of glucose in cells. Glycogen has traditionally been viewed as a key substrate for muscle ATP production during conditions of high energy demand and considered to be limiting for work capacity and force generation under defined conditions. Glycogenolysis is catalyzed by phosphorylase, while glycogenesis is catalyzed by glycogen synthase. For many years, it was believed that a primer was required for de novo glycogen synthesis and the protein considered responsible for this process was ultimately discovered and named glycogenin. However, the subsequent observation of glycogen storage in the absence of functional glycogenin raises questions about the true role of the protein. In resting muscle, phosphorylase is generally considered to be present in two forms: non-phosphorylated and inactive (phosphorylase b ) and phosphorylated and constitutively active (phosphorylase a ). Initially, it was believed that activation of phosphorylase during intense muscle contraction was primarily accounted for by phosphorylation of phosphorylase b (activated by increases in AMP) to a , and that glycogen synthesis during recovery from exercise occurred solely through mechanisms controlled by glucose transport and glycogen synthase. However, it now appears that these views require modifications. Moreover, the traditional roles of glycogen in muscle function have been extended in recent years and in some instances, the original concepts have undergone revision. Thus, despite the extensive amount of knowledge accrued during the past 100 years, several critical questions remain regarding the regulation of glycogen metabolism and its role in living muscle.
... Peripheral fatigue, on the other hand, is characterized by a decrease in the contractile strength of muscle fibers. This is caused by the inhibition of the crossbridge interaction due to the accumulation of inorganic phosphate and hydrogen ions in the sarcolemma (18), lower calcium release (29), and decreases in available metabolic substrates (12). ...
International Journal of Exercise Science 17(2): 648-659, 2024. This study aimed to investigate the effects of chronic β-alanine (βA) plus acute sodium bicarbonate (SB) co-supplementation on neuromuscular fatigue during high-intensity intermittent efforts in swimming. Eleven regional and national competitive-level young swimmers performed a neuromuscular fatigue assessment before and immediately after two 20 × 25-m front crawl maximal efforts every 90 s, performed at pre-and post-4-week co-supplementation. Neuromuscular fatigue was evaluated by percutaneous electrical stimuli through the twitch interpolation technique on the triceps brachii and quadriceps femoris. Performance was defined by the mean time of the 20 efforts and blood samples to lactate concentrations were collected every four efforts. Participants supplemented 3.2-6.4 g•day −1 of chronic βA or placebo (PL) during four weeks, and acute 0.3 g•kg −1 of SB or PL 60 min before the second assessment (allowing βA+SB and PL+PL groups). No statistical changes were found in neuromuscular fatigue of triceps brachii. In the quadriceps femoris, a main effect of time was found in potentiated twitch delta values in pooled groups, showing a statistical increase of 19.01% after four weeks (Δ = 13.05 [0.35-25.75] N; p = 0.044), without time × group interactions. No statistical difference was found in the swimming performance. Blood lactate increased by 25.06% only in the βA+SB group (Δ = 6.40 [4.62-8.18] mM; pBonf < 0.001) after the supplementation period. In conclusion, 4-week βA and SB co-supplementation were not able to reduce neuromuscular fatigue levels and improve performance in high-intensity intermittent efforts, but statistically increased blood lactate levels.
... While this result appears contradictory, it aligns with the slower glycogen degradation rate in Gde5 skKO skeletal muscles. Notably, several studies have demonstrated a strong correlation between glycogen levels and muscle fatigue [54][55][56] . A previous study in humans demonstrated that slower glycogen utilization improves endurance capacity 57 . ...
Glycerophosphocholine (GPC) is an important precursor for intracellular choline supply in phosphatidylcholine (PC) metabolism. GDE5/Gpcpd1 hydrolyzes GPC into choline and glycerol 3-phosphate; this study aimed to elucidate its physiological function in vivo. Heterozygous whole-body GDE5-deficient mice reveal a significant GPC accumulation across tissues, while homozygous whole-body knockout results in embryonic lethality. Skeletal muscle-specific GDE5 deletion (Gde5 skKO) exhibits reduced passive force and improved fatigue resistance in electrically stimulated gastrocnemius muscles in vivo. GDE5 deficiency also results in higher glycolytic metabolites and glycogen levels, and glycerophospholipids alteration, including reduced levels of phospholipids that bind polyunsaturated fatty acids (PUFAs), such as DHA. Interestingly, this PC fatty acid compositional change is similar to that observed in skeletal muscles of denervated and Duchenne muscular dystrophy mouse models. These are accompanied by decrease of GDE5 expression, suggesting a regulatory role of GDE5 activity for glycerophospholipid profiles. Furthermore, a DHA-rich diet enhances contractile force and lowers fatigue resistance, suggesting a functional relationship between PC fatty acid composition and muscle function. Finally, skinned fiber experiments show that GDE5 loss increases the probability of the ryanodine receptor opening and lowers the maximum Ca²⁺-activated force. Collectively, GDE5 activity plays roles in PC and glucose/glycogen metabolism in skeletal muscle.
... This is based on a strong correlation between pre-exercise muscle glycogen content and exercise capacity, 1 as well as an association between low glycogen levels and task failure. 2 The link between glycogen depletion and muscle fatigue is poorly understood, with some studies suggesting a connection to sarcoplasmic reticulum Ca 2+ release 3,4 and muscle excitability, 5,6 but not all. 7,8 This inconsistency may stem from a high fiber-to-fiber variability in glycogen content. ...
During submaximal exercise, there is a heterogeneous recruitment of skeletal muscle fibers, with an ensuing heterogeneous depletion of muscle glycogen both within and between fiber types. Here, we show that the mean (95% CI) mitochondrial volume as a percentage of fiber volume of non‐glycogen‐depleted fibers was 2 (−10:6), 5 (−21:11), and 12 (−21:−2)% lower than all the sampled fibers after continuing exercise for 1, 2 h, and until task failure, respectively. Therefore, a glycogen‐dependent fatigue of individual fibers during submaximal exercise may reduce the muscular oxidative power. These findings suggest a relationship between glycogen and mitochondrial content in individual muscle fibers, which is important for understanding fatigue during prolonged exercise.
... Many of the beneficial effects of exercise have been attributed to adaptations to skeletal muscle (Thyfault & Bergouignan, 2020). Seminal works published in the 1960s were the first to provide mechanistic insights into how training-induced changes to skeletal muscle might contribute to improved health (Bergström et al., 1967;Hermansen et al., 1967). Much of this work has focused on training-induced changes to mitochondria (the powerhouses of the cells). ...
Exercise is a powerful non‐pharmacological intervention for the treatment and prevention of numerous chronic diseases. Contracting skeletal muscles provoke widespread perturbations in numerous cells, tissues and organs, which stimulate multiple integrated adaptations that ultimately contribute to the many health benefits associated with regular exercise. Despite much research, the molecular mechanisms driving such changes are not completely resolved. Technological advancements beginning in the early 1960s have opened new avenues to explore the mechanisms responsible for the many beneficial adaptations to exercise. This has led to increased research into the role of small peptides (<100 amino acids) and mitochondrially derived peptides in metabolism and disease, including those coded within small open reading frames (sORFs; coding sequences that encode small peptides). Recently, it has been hypothesized that sORF‐encoded mitochondrially derived peptides and other small peptides play significant roles as exercise‐sensitive peptides in exercise‐induced physiological adaptation. In this review, we highlight the discovery of mitochondrially derived peptides and newly discovered small peptides involved in metabolism, with a specific emphasis on their functions in exercise‐induced adaptations and the prevention of metabolic diseases. In light of the few studies available, we also present data on how both single exercise sessions and exercise training affect expression of sORF‐encoded mitochondrially derived peptides. Finally, we outline numerous research questions that await investigation regarding the roles of mitochondrially derived peptides in metabolism and prevention of various diseases, in addition to their roles in exercise‐induced physiological adaptations, for future studies. image
... J Physiol 601.24 K + -glycogen interaction as a putative mechanism for fatigue in vivo Exercise performance is traditionally thought to worsen only when whole-muscle glycogen falls severely, such as occurs with prolonged strenuous exercise (Bergström et al., 1967;Hermansen et al., 1967;Ørtenblad et al., 2013;Gejl et al., 2014). In fact, it has been proposed that in human muscle there is a critical threshold glycogen content of 250-300 μmol/g dry wt below which performance declines (Ørtenblad et al., 2011, 2013Vigh-Larsen et al., 2021). ...
A reduced muscle glycogen content and potassium (K⁺) disturbances across muscle membranes occur concomitantly during repeated intense exercise and together may contribute to skeletal muscle fatigue. Therefore, we examined whether raised extracellular K⁺ concentration ([K⁺]o) (4 to 11 mM) interacts with lowered glycogen to reduce force production. Isometric contractions were evoked in isolated mouse soleus muscles (37°C) using direct supramaximal field stimulation. (1) Glycogen declined markedly in non‐fatigued muscle with >2 h exposure in glucose‐free physiological saline compared with control solutions (11 mM glucose), i.e. to <45% control. (2) Severe glycogen depletion was associated with increased 5′‐AMP‐activated protein kinase activity, indicative of metabolic stress. (3) The decline of peak tetanic force at 11 mM [K⁺]o was exacerbated from 67% initial at normal glycogen to 22% initial at lowered glycogen. This was due to a higher percentage of inexcitable fibres (71% vs. 43%), yet without greater sarcolemmal depolarisation or smaller amplitude action potentials. (4) Returning glucose while at 11 mM [K⁺]o increased both glycogen and force. (5) Exposure to 4 mM [K⁺]o glucose‐free solutions (15 min) did not increase fatiguability during repeated tetani; however, after recovery there was a greater force decline at 11 mM [K⁺]o at lower than normal glycogen. (6) An important exponential relationship was established between relative peak tetanic force at 11 mM [K⁺]o and muscle glycogen content. These findings provide direct evidence of a synergistic interaction between raised [K⁺]o and lowered muscle glycogen as the latter shifts the peak tetanic force–resting EM relationship towards more negative resting EM due to lowered sarcolemmal excitability, which hence may contribute to muscle fatigue. image
Key points
Diminished muscle glycogen levels and raised extracellular potassium concentrations ([K⁺]o) occur simultaneously during intense exercise and together may contribute to muscle fatigue.
Prolonged exposure of isolated non‐fatigued soleus muscles of mice to glucose‐free physiological saline solutions markedly lowered muscle glycogen levels, as does fatigue then recovery in glucose‐free solutions. For both approaches, the subsequent decline of maximal force at 11 mM [K⁺]o, which mimics interstitial [K⁺] levels during intense exercise, was exacerbated at lowered compared with normal glycogen. This was mainly due to many more muscle fibres becoming inexcitable.
We established an important relationship that provides evidence of a synergistic interaction between raised [K⁺]o and lowered glycogen content to reduce force production.
This paper indicates that partially lowered muscle glycogen (and/or metabolic stress) together with elevated interstitial [K⁺] interactively lowers muscle force, and hence may diminish performance especially during repeated high‐intensity exercise.
... A tired athlete may have less energy to exert themselves during practice or a game. Exercise-induced fatigue, which is attributable to many factors, including the accumulation of reactive oxygen species, inflammation, and muscle glycogen depletion, affects athletic performance [1][2][3][4]. However, fatigue and the mechanism leading to the perception of fatigue are not fully elucidated. ...
... The advancement of sport and exercise nutrition (SEN) as a recognised sub-discipline of sport and exercise science (SES) began in the late 1960s, following the pioneering work of Scandinavian scientists who investigated the role of muscle glycogen and carbohydrate availability on exercise capacity and performance (1)(2)(3)(4). More than 50 years on, the application of sports nutrition research is now recognised as paramount to the wellbeing and performance of athletes (5). ...
Evidence-based practice is a systematic approach to decision-making developed in the 1990s to help healthcare professionals identify and use the best available evidence to guide clinical practice and patient outcomes amid a plethora of information in often challenging, time-constrained circumstances. Today’s sports nutrition practitioners face similar challenges, as they must assess and judge the quality of evidence and its appropriateness to their athlete, in the often chaotic, time-pressed environment of professional sport. To this end, we present an adapted version of the evidence-based framework to support practitioners in navigating their way through the deluge of available information and guide their recommendations to athletes whilst also reflecting on their practice experience and skills as evidence-based practitioners, thus, helping to bridge the gap between science and practice in sport and exercise nutrition.
... It is well established that muscle glycogen availability is highly related to performance and fatigue in prolonged submaximal exercise (18,21). It is proposed to consume 1-4 gr.kgBM -1 of carbohydrates (CHO) 1-4 h before an endurance event, in order to provide high CHO availability and maximize endurance performance (5). ...
The aim of this study was to investigate the metabolic responses of the timing of preexercise carbohydrate feeding. Nine moderately trained runners, 7 men, and 2 women, performed an incremental test to exhaustion followed by three 6 min running trials at 75% VO2max on the treadmill. The submaximal runs were performed after ingestion a placebo solution (PLA) one hour before or CHO solution 1gr.kgBM-1 one (CHO60) or two hours (CHO120) before the trial. All trials were performed at least 2 days apart in a double-blind cross-over design following an overnight fast. The results showed no significant differences in physiological parameters (VO2, RER, HR) and CHO metabolism between the three conditions. Blood glucose concentration immediately before the 6-min trials was higher after CHO60 (1.22±0.23 gr.L-1) compared to CHO120 (0.93±0.10 gr.L-1) conditions (p=0.007, η2= 0.567). These findings suggest that preexercise timing of CHO ingestion results in significantly different blood glucose concentrations prior to submaximal running, with no further metabolic and physiological alterations.
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... Since patterns of glycogen utilization and glycogen contents at task failure do not seem to be different between athletes and nonathletes, the present findings can likely be applied to athletes. 42,43,49 The potential for an acute loss of body mass may be greatest in athletes known to possess extraordinarily high resting muscle glycogen levels compared with untrained individuals (~800 vs. ~400 mmol·kg −1 DW). 43 A reduction in muscle glycogen content from 800 mmol·kg −1 DW to 400 mmol·kg −1 DW could theoretically induce a weight loss of up to 2.5 kg in a 75 kg athlete, which should be expected to improve performance in weight-bearing sports provided that glycogen availability is not critically low. ...
Performance in short-duration sports is highly dependent on muscle glycogen, but the total degradation is only moderate and considering the water-binding property of glycogen, unnecessary storing of glycogen may cause an unfavorable increase in body mass. To investigate this, we determined the effect of manipulating dietary carbohydrates (CHO) on muscle glycogen content, body mass and short-term exercise performance. In a cross-over design twenty-two men completed two maximal cycle tests of either 1-min (n = 10) or 15-min (n = 12) duration with different pre-exercise muscle glycogen levels. Glycogen manipulation was initiated three days prior to the tests by exercise-induced glycogen-depletion followed by ingestion of a moderate (M-CHO) or high (H-CHO) CHO-diet. Subjects were weighed before each test, and muscle glycogen content was determined in biopsies from m. vastus lateralis before and after each test. Pre-exercise muscle glycogen content was lower following M-CHO than H-CHO (367 mmol · kg-1 DW vs. 525 mmol · kg-1 DW, P < 0.00001), accompanied by a 0.7 kg lower body mass (P < 0.00001). No differences were observed in performance between diets in neither the 1-min (P = 0.33) nor the 15-min (P = 0.99) test. In conclusion, pre-exercise muscle glycogen content and body mass was lower after ingesting moderate compared with high amounts of CHO, while short-term exercise performance was unaffected. This demonstrates that adjusting pre-exercise glycogen levels to the requirements of competition may provide an attractive weight management strategy in weight-bearing sports, particularly in athletes with high resting glycogen levels.
... Carbohydrate consumption during prolonged aerobic exercise is a common nutritional recommendation for maintaining blood glucose concentrations and sparing muscle or liver glycogen, which may delay fatigue and improve physical performance [1][2][3]. The use of carbohydrate as an energy substrate to support physical performance may be optimized when a ketone monoester (KE) supplement is consumed in combination with carbohydrate before and during exercise [4,5]. ...
Background:
Increasing β-hydroxybutyrate (βHB) availability through ketone monoester plus carbohydrate supplementation is suggested to enhance physical performance by sparing glucose use during exercise. However, no studies have examined the effect of ketone supplementation on glucose kinetics during exercise.
Objective:
This exploratory study primarily aimed to determine the effect of ketone monoester plus carbohydrate (KE + CHO) supplementation on glucose oxidation and physical performance and during steady-state exercise compared with carbohydrate (CHO).
Methods:
Using a randomized, crossover design (ClinicalTrials.gov, NCT04737694), twelve men consumed KE+CHO (573 mg KE/kg body mass, 110 g glucose) or CHO (110 g glucose) before and during 90 minutes of steady-state treadmill exercise (54±3% V̇O2peak) wearing a weighted vest (30% body mass; 25±3 kg). Glucose oxidation and turnover were determined using indirect calorimetry and stable isotopes. Participants performed an unweighted time to exhaustion (TTE; 85% V̇O2peak) after steady-state exercise, and a weighted (25±3 kg) 6.4 km time trial (TT) the next day after consuming a bolus of KE+CHO or CHO. Data were analyzed by paired t-tests and mixed model ANOVA.
Results:
βHB concentrations were higher (P<0.05) after exercise [2.1 mM(95% CI: 1.6, .6)] and the TT [2.6 mM(2.1, 3.1)] in KE+CHO compared with CHO. TTE was lower [-104 s(-201,-8)] and TT performance was slower [141 s(19,262)] in KE+CHO than CHO (P<0.05). Exogenous [-0.01 g/min (-0.07, 0.04)] and plasma [-0.02 g/min(-0.08,0.04)] glucose oxidation and metabolic clearance rate (MCR [0.38 mg·kg-1·min-1(-0.79,1.54)]) were not different, and glucose rate of appearance [-0.51 mg·kg-1·min-1(-0.97,-0.04)] and disappearance [-0.50 mg·kg-1·min-1(-0.96,-0.04)] were lower (P<0.05) in KE+CHO compared with CHO during steady-state exercise.
Conclusion:
Rates of exogenous and plasma glucose oxidation and MCR were not different between treatments during steady-state exercise in the current study suggesting blood glucose utilization is similar between KE+CHO and CHO. KE+CHO supplementation also results in lower physical performance compared with CHO.
... From 1896 to 2008, athletes competing in the Olympics demonstrated trends for increased carbohydrate intake in 1976 and a predominant shift toward high-carbohydrate low-fat (HCLF) diets in the 1996 Olympic games (1)(2)(3). This shift in athlete food preference toward carbohydrates was cited to be driven by (i) increased user consciousness of healthy food choice to optimized performance (1,4,5); (ii) the importance of muscle glycogen as the preferable metabolic fuel during exercise of either high intensity or long duration low intensity (6)(7)(8)(9)(10)(11)(12) following the emergence of muscle biopsy techniques in 1960s (13); (iii) anaplerotic theory in which depleted muscle glycogen attenuates mitochondrial oxaloacetate concentrations and thus reduced mitochondrial capacity to oxidize fatty acids (14); (iv) multiple studies illustrating carbohydrate ingestion delayed or reversed fatigue by maintaining blood glucose homeostasis (15)(16)(17); (v) "cross-over effect" (18)(19)(20) in which exercise of increasing intensity becomes increasingly dependent on carbohydrate oxidation since fat oxidation effectively ceases at any exercise intensity ≥ 85% VO 2max (18)(19)(20)(21)(22); (vi) clinical trials of high-fat diets resulting in impaired performance in both recreational (23) and elite athletes (i.e., Olympic class) (24)(25)(26). ...
High carbohydrate, low fat (HCLF) diets have been the predominant nutrition strategy for athletic performance, but recent evidence following multi-week habituation has challenged the superiority of HCLF over low carbohydrate, high fat (LCHF) diets, along with growing interest in the potential health and disease implications of dietary choice. Highly trained competitive middle-aged athletes underwent two 31-day isocaloric diets (HCLF or LCHF) in a randomized, counterbalanced, and crossover design while controlling calories and training load. Performance, body composition, substrate oxidation, cardiometabolic, and 31-day minute-by-minute glucose (CGM) biomarkers were assessed. We demonstrated: (i) equivalent high-intensity performance (@∼85%VO2max), fasting insulin, hsCRP, and HbA1c without significant body composition changes across groups; (ii) record high peak fat oxidation rates (LCHF:1.58 ± 0.33g/min @ 86.40 ± 6.24%VO2max; 30% subjects > 1.85 g/min); (iii) higher total, LDL, and HDL cholesterol on LCHF; (iv) reduced glucose mean/median and variability on LCHF. We also found that the 31-day mean glucose on HCLF predicted 31-day glucose reductions on LCHF, and the 31-day glucose reduction on LCHF predicted LCHF peak fat oxidation rates. Interestingly, 30% of athletes had 31-day mean, median and fasting glucose > 100 mg/dL on HCLF (range: 111.68-115.19 mg/dL; consistent with pre-diabetes), also had the largest glycemic and fat oxidation response to carbohydrate restriction. These results: (i) challenge whether higher carbohydrate intake is superior for athletic performance, even during shorter-duration, higher-intensity exercise; (ii) demonstrate that lower carbohydrate intake may be a therapeutic strategy to independently improve glycemic control, particularly in those at risk for diabetes; (iii) demonstrate a unique relationship between continuous glycemic parameters and systemic metabolism.
... However, ATP turnover in muscle fibers is tightly regulated and subject to multiple homeostatic mechanisms, such that reductions in ATP content during acute fatigue can be small or modest [84,85]. Glycogen provides an important energy source for ATP production in myofibers, and depletion of glycogen content can also be used as an experimental indicator of muscle fatigue, particularly in the context of sustained exercise [86,87]. Significant reductions in glycogen content in hindlimb muscles (soleus, plantaris, and vastus lateralis muscles) and diaphragm have been reported immediately following treadmill running [88]. ...
Muscle fatigue is the diminution of force required for a particular action over time. Fatigue may be particularly pronounced in aging muscles, including those used for swallowing actions. Because risk for swallowing impairment (dysphagia) increases with aging, the contribution of muscle fatigue to age-related dysphagia is an emerging area of interest. The use of animal models, such as mice and rats (murine models) allows experimental paradigms for studying the relationship between muscle fatigue and swallowing function with a high degree of biological precision that is not possible in human studies. The goal of this article is to review basic experimental approaches to the study of murine tongue muscle fatigue related to dysphagia. Traditionally, murine muscle fatigue has been studied in limb muscles through direct muscle stimulation and behavioral exercise paradigms. As such, physiological and bioenergetic markers of muscle fatigue that have been validated in limb muscles may be applicable in studies of cranial muscle fatigue with appropriate modifications to account for differences in muscle architecture, innervation ratio, and skeletal support. Murine exercise paradigms may be used to elicit acute fatigue in tongue muscles, thereby enabling study of putative muscular adaptations. Using these approaches, hypotheses can be developed and tested in mice and rats to allow for future focused studies in human subjects geared toward developing and optimizing treatments for age-related dysphagia.
... [2][3][4][5] Particularly relevant with respect to muscle performance is the observation that glycogen availability is critical for delaying fatigue during exercise in humans at exercise intensities corresponding to 60%-80% of maximal oxygen uptake (V_O 2 max). 6,7 Glycogen availability is also important for muscle performance during repeated contractions in isolated rodent muscle preparations under defined conditions. 8,9 During prolonged submaximal exercise in humans, glycogen is degraded and can reach very low levels or even depletion. ...
Initially it was believed that phosphorylase was responsible for both glycogen breakdown and synthesis in the living cell. The discovery of glycogen synthase and McArdle's disease (lack of phosphorylase activity), together with the high Pi/glucose 1-P ratio in skeletal muscle, demonstrated that glycogen synthesis could not be attributed to reversal of the phosphorylase reaction. Rather, glycogen synthesis was attributable solely to the activity of glycogen synthase, subsequent to the transport of glucose into the cell. However, the well-established observation that phosphorylase was inactivated (i.e., dephosphorylated) during the initial recovery period after prior exercise, when the rate of glycogen accumulation is highest and independent of insulin, suggested that phosphorylase could play an active role in glycogen accumulation. But the quantitative contribution of phosphorylase inactivation was not established until recently, when studying isolated murine muscle preparations during recovery from repeated contractions at temperatures ranging from 25-35°C. Thus, in both slow-twitch, oxidative and fast-twitch, glycolytic muscles, inactivation of phosphorylase accounted for 45–75% of glycogen accumulation during the initial hours of recovery following repeated contractions. Such data indicate that phosphorylase inactivation may be the most important mechanism for glycogen accumulation under defined conditions. These results support the initial belief that phosphorylase plays a quantitative role in glycogen formation in the living cell. However, the mechanism is not via activation of phosphorylase, but rather via inactivation of the enzyme.
... I n response to scientific evidence highlighting nutrition's integral role in supporting athletic performance and overall health, collegiate athletic programs are increasingly adding nutrition services to their athletic medicine and sports performance departments. [1][2][3] From more simplistic early 20th-century evidence demonstrating that dietary carbohydrate and fat influence exercise performance, 4 dietary proteins affect skeletal muscle adaptation, 5 and carbohydrate manipulation enhances exercise capacity 6 to new, 21st-century scientific perspectives indicating greater metabolic and nutritional complexities for athlete readiness, sport performance, recovery, and health, 2,7 sports nutrition research 8 continues to identify an increasing need for highly skilled sports nutrition professionals and the provision of sports nutrition services. Accordingly, this professional expertise should be supplied by registered dietitian nutritionists (RDNs) using oncampus student health services, off-campus providers, or, preferably, position(s) within athletic departments. ...
Collegiate athletic programs are increasingly adding nutrition services to interdisciplinary sports medicine and sports performance departments in response to scientific evidence highlighting nutrition's integral role in supporting athletic performance and overall health. Registered Dietitian Nutritionists (RDNs) specializing in sports dietetics (ie, sports RDNs) and credentialed Board-certified Specialists in Sports Dietetics (CSSDs) are the preferred nutrition service providers for these programs. Their extensive training and proficiency in medical nutrition therapy, education and behavioral counseling, food-service management, exercise physiology, physical performance, and administration, as defined by the ''Standards of Practice and ''Standards of Professional Performance'' for Registered Dietitian Nutritionists in Sports Nutrition and Human Performance,'' make these practitioners uniquely qualified to deliver the breadth of care required in the collegiate setting. Therefore, this document, guided by a multidisciplinary panel, introduces four sports nutrition models through which any collegiate athletic program can deliver sports RDN-directed nutrition services. In each model, the most effective staffing and scope of service are indicated and reviewed. In addition, recommended organizational structures for sports RDN are provided that best support the delivery of the model's nutrition services in a variety of collegiate athletic programs and organizational settings. Lastly, future research initiatives and nutrition interventions to help improve the standard of care through these sport nutrition models are explored.
... It is plausible that substrate utilisation (respiratory quotient) is different between genotypes. Greater reliance on carbohydrate as a fuel source is closely linked to exercise time to exhaustion during an endurance-based test (Bagby et al., 1978;Hermansen et al., 1967); therefore, we postulate that if the respiratory quotient was indeed affected by loss of Trem2, this would have manifested in time to exhaustion. Future experiments would benefit from indirect calorimetry to determine maximal oxygen consumption and respiratory exchange ratios (e.g. ...
Triggering receptor expressed on myeloid cells 2 (Trem2) is highly expressed on myeloid cells and is involved in cellular lipid homeostasis and inflammatory processes. Trem2 deletion in mice (Trem2−/−) evokes adipose tissue dysfunction, but its role in worsening obesity‐induced metabolic dysfunction has not been resolved. Here we aimed to determine the causal role of Trem2 in regulating glucose homeostasis and insulin sensitivity in mice. Nine‐week‐old male and female littermate wild‐type (WT) and Trem2−/− mice were fed a low‐ or high‐fat diet for 18 weeks and phenotyped for metabolic function. Diet‐induced weight gain was similar between genotypes, irrespective of sex. Consistent with previous reports, we find that loss of Trem2 causes massive adipocyte hypertrophy and an attenuation in the lipid‐associated macrophage transcriptional response to obesity. In contrast to published data, we find that loss of Trem2 does not worsen metabolic function in obese mice. No differences in intraperitoneal glucose tolerance (ipGTT), oral GTT or mixed meal substrate control, including postprandial glucose, non‐esterified fatty acids, insulin or triglycerides, were found between WT and Trem2−/− animals. Similarly, no phenotypic differences existed when animals were challenged with stressors on metabolic demand (i.e. acute exercise or environmental temperature modulation). Collectively, we report a disassociation between adipose tissue remodelling caused by loss of Trem2 and whole‐body metabolic homeostasis in obese mice. The complementary nature of experiments conducted gives credence to the conclusion that loss of Trem2 is unlikely to worsen glucose homeostasis in mice. image
... Additionally, depletion in phosphocreatine (Hultman et al., 1991), glycogen (Hermansen et al., 1967) and oxygen uptake (Matsuura et al., 2011) could equally contribute to peripheral fatigue by reducing ATP availability which is a key factor of muscular contraction. However, the definition of fatigue itself and its categorisation into peripheral and central components seems to be restrictive (Enoka & Duchateau, 2016;St Clair Gibson et al., 2018). ...
This PhD investigated the importance of sleep in the recovery processes of rugby union players. Study 1 found students and student-athletes presented low sleep quality assessed with the Pittsburgh Sleep Quality (65% ≤5 indicating poor sleep quality). Moreover, student-athletes presented a higher intra-individual variability (small to moderate). In study 2, different age groups of rugby union players presented low total sleep time (≤7 hours) and efficiency (≤85%). However, only small differences in sleep schedule were observed between age groups. Study 2 investigated the validity of self-reported sleep parameters and found a large mean bias (87 min) when compared with actigraphy for sleep duration. Additionally, unclear relationships with subjective sleep quality were found. Study 3 investigated the validity, reliability and sensitivity of a standardised run (i.e. Running Load Index). The results demonstrated a large relationship with leg stiffness (r=0.62) and with a coefficient of variation of 11.5%. Moreover, a large increase in Running Load Index was found after a week of training highlighting its sensitivity. Study 4 highlighted a later fall asleep and wake up time, shorter total sleep time and lower subjective sleep quality post-match. Moreover, collisions, travel time and kick-off time explained most of the changes in sleep compared with match load. Despite, a decrease in perceived wellness (small to very large) and neuromuscular function (small) were observed, sleep had marginal effect on their respective changes. The effect of acute sleep extension on recovery was investigated in Study 5. The results suggested that such as strategy has beneficial effects on cognitive function (i.e. Stroop task). Altogether the results from this PhD suggest that acute changes in sleep post-match affect mainly perceptual and cognitive measures rather than neuromuscular function. Nevertheless, more work is necessary to consider the effect of chronic lack of sleep on post-match recovery.
... During exercise, glycogen is utilized and can be depleted to very low levels often reaching one-fifth to one-sixth of the pre-exercise level . This is observed in humans, who are unable to withstand exercise at or above moderate intensity for a prolonged time when the stores are depleted to very low levels (<150 mmol kg À1 dw) compared to pre-exercise levels of 500-900 mmol kg À1 dw (Bergström et al. 1967;Hermansen et al. 1967) even with carbohydrate supplementation during the exercise (Coyle et al. 1986;Rauch et al. 1995). Therefore, the understanding of factors affecting the graded utilization of glycogen during exercise is key to avoid unforeseen glycogen-dependent muscle fatigue. ...
Muscle glycogen is an important fuel source for contracting skeletal muscle, and it is well documented that exercise performance is impaired when the muscle’s stores of glycogen are exhausted. The role of carbohydrate (CHO) availability on exercise performance has been known for more than a century, while the specific role of muscle glycogen for muscle function has been known for half a century. Nonetheless, the precise cellular and molecular mechanisms by which glycogen availability regulates cell function and contractile-induced fatigue are unresolved. Alterations of pre-exercise muscle glycogen reserves by dietary and exercise manipulations or modifying the degree of dependency on endogenous glycogen during exercise have collectively established a close relationship between muscle glycogen and the resistance to fatigue. It is also apparent that glycogen availability regulates rates of muscle glycogenolysis and resynthesis, muscle glucose uptake, key steps in excitation-contraction coupling, and exercise-induced cell signaling regulating training adaptation. The present review provides both a historical and contemporary overview of the effects of exercise on muscle glycogen metabolism, addressing factors affecting glycogen use during exercise as well as the evolving concepts of how glycogen and glycolysis are integrated with cell function, skeletal muscle fatigue, and training adaptation.KeywordsGlycogenolysis, glycogen particleDietExerciseE-C coupling, fatigue, performance
... of carbohydrate, or glycogen. The amount of muscle Likewise, more women aged 51 and over who were hig h glycogens directly affects endurance capabilities, or the time sugars consumers met two-thirds of the RDA for folacin, an athlete may effectively perform during an event (Ahlborg et vitam in B6, vitamin C and vitamin A than did low sugar s al., 1967;Bergstron et al., 1967;Hermansen et al., 1967). consu mers their age. ...
... The importance of muscle glycogen availability during prolonged exercise has received much attention over the last 50 years (13-15) and a strong association has been reported between muscle glycogen depletion, impaired muscle performance, and fatigue (16)(17)(18)(19)(20)(21). In contrast, little attention has been paid to the contribution of liver glycogen during exercise. ...
Muscle glycogen depletion has been proposed as one of the main causes of fatigue during exercise. However, few studies have addressed the contribution of liver glycogen to exercise performance. Using a low-intensity running protocol, here we analyzed exercise capacity in mice overexpressing protein targeting to glycogen (PTG) specifically in the liver (PTGOE mice), which show a high concentration of glycogen in this organ. PTGOE mice showed improved exercise capacity, as determined by the distance covered and time ran in an extenuating endurance exercise compared to control mice. Moreover, fasting decreased exercise capacity in control mice but not in PTGOE mice. After exercise, liver glycogen stores were totally depleted in control mice, but PTGOE mice maintained significant glycogen levels even in fasting conditions. Additionally, PTGOE mice displayed an increased hepatic energy state after exercise compared to control mice. Exercise caused a reduction in blood glucose concentration in control mice that was less pronounced in PTGOE mice. No changes were found in the levels of blood lactate, plasma free fatty acids, or ß-hydroxybutyrate. Plasma glucagon was elevated after exercise in control mice, but not in PTGOE mice. Exercise-induced changes in skeletal muscle were similar in both genotypes. These results identify hepatic glycogen as a key regulator of endurance capacity in mice, an effect that may be exerted through the maintenance of blood glucose levels.
... Indeed, the development of methods to measure its presence and location within the muscle cell provided the first major advances in the science and practice of sports nutrition [14]. The first measurements of muscle glycogen were made possible by the introduction of the percutaneous biopsy technique to sports science in the late 1960s [15][16][17]. Subsequent modification of the technique included the addition of suction to increase the size of the sample collected [18] and movement of the location of the muscle site by 2 cm for subsequent biopsies to avoid the artefact of damage from the first [19]. This protocol is still used today, and is considered the "gold standard" for assessment of muscle glycogen stores, while acknowledging the invasiveness of the procedure and its downstream limitations on the subjects and environments in which it might be safely and logistically performed. ...
Researchers and practitioners in sports nutrition would greatly benefit from a rapid, portable, and non-invasive technique to measure muscle glycogen, both in the laboratory and field. This explains the interest in MuscleSound®, the first commercial system to use high-frequency ultrasound technology and image analysis from patented cloud-based software to estimate muscle glycogen content from the echogenicity of the ultrasound image. This technique is based largely on muscle water content, which is presumed to act as a proxy for glycogen. Despite the promise of early validation studies, newer studies from independent groups reported discrepant results, with MuscleSound® scores failing to correlate with the glycogen content of biopsy-derived mixed muscle samples or to show the expected changes in muscle glycogen associated with various diet and exercise strategies. The explanation of issues related to the site of assessment do not account for these discrepancies, and there are substantial problems with the premise that the ratio of glycogen to water in the muscle is constant. Although further studies investigating this technique are warranted, current evidence that MuscleSound® technology can provide valid and actionable information around muscle glycogen stores is at best equivocal.
... The reliance on this substrate over fats increases exponentially with exercise intensity, measured by analysis of respiratory quotient [15]. The reintroduction of the needle muscle biopsy technique in the late 1960s [12,30,31] provided direct measurements of intramuscular substrate utilisation. Subsequent non-invasive methods such as magnetic resonance spectroscopy [32] and contemporary isotope methodologies [29] also advance our understanding of muscle metabolism. ...
The human body requires energy to function. Adenosine triphosphate (ATP) is the cellular currency for energy-requiring processes including mechanical work (i.e., exercise). ATP used by the cells is ultimately derived from the catabolism of energy substrate molecules—carbohydrates, fat, and protein. In prolonged moderate to high-intensity exercise, there is a delicate interplay between carbohydrate and fat metabolism, and this bioenergetic process is tightly regulated by numerous physiological, nutritional, and environmental factors such as exercise intensity and du- ration, body mass and feeding state. Carbohydrate metabolism is of critical importance during prolonged endurance-type exercise, reflecting the physiological need to regulate glucose homeostasis, assuring optimal glycogen storage, proper muscle fuelling, and delaying the onset of fatigue. Fat metabolism represents a sustainable source of energy to meet energy demands and preserve the ‘limited’ carbohydrate stores. Coordinated neural, hormonal and circulatory events occur during prolonged endurance-type exercise, facilitating the delivery of fatty acids from adipose tissue to the working muscle for oxidation. However, with increasing exercise intensity, fat oxidation declines and is unable to supply ATP at the rate of the exercise demand. Protein is considered a subsidiary source of energy supporting carbohydrates and fat metabolism, contributing to approximately 10% of total ATP turnover during prolonged endurance-type exercise. In this review we present an overview of substrate metabolism during prolonged endurance-type exercise and the regulatory mechanisms involved in ATP turnover to meet the energetic demands of exercise.
... Since early studies by Christensen and Hansen [1] demonstrated new insights into the role of fat and carbohydrate metabolism during exercise, a strong relationship between muscle glycogen and performance during prolonged exercise has been well established [2][3][4][5][6][7]. In contrast, the effect of glycogen content on high-intensity (defined here as ≥ 100% VO 2max ) exercise performance is more ambiguous. ...
Muscle glycogen is the main substrate during high-intensity exercise and large reductions can occur after relatively short durations. Moreover, muscle glycogen is stored heterogeneously and similarly displays a heterogeneous and fiber-type specific depletion pattern with utilization in both fast- and slow-twitch fibers during high-intensity exercise, with a higher degradation rate in the former. Thus, depletion of individual fast- and slow-twitch fibers has been demonstrated despite muscle glycogen at the whole-muscle level only being moderately lowered. In addition, muscle glycogen is stored in specific subcellular compartments, which have been demonstrated to be important for muscle function and should be considered as well as global muscle glycogen availability. In the present review, we discuss the importance of glycogen metabolism for single and intermittent bouts of high-intensity exercise and outline possible underlying mechanisms for a relationship between muscle glycogen and fatigue during these types of exercise. Traditionally this relationship has been attributed to a decreased ATP resynthesis rate due to inadequate substrate availability at the whole-muscle level, but emerging evidence points to a direct coupling between muscle glycogen and steps in the excitation–contraction coupling including altered muscle excitability and calcium kinetics.
... PA has been the cure for a healthy life and longevity since ~450 BC [216]. In the 1960s, with the technological advancements, the first scientific papers began publishing and provided mechanistic insight into how acute or chronic exercise could make a remarkable and paradigm shift in human physiology [217][218][219]. Although the existing literature attributes the health benefits of PA to reduced adiposity, increased cardiorespiratory fitness, reduced levels of circulating lipids, and the maintenance of muscle mass [220], the exact molecular mechanisms by which PA promotes human health is not fully elucidated. ...
The prevalence of obesity continues to rise worldwide despite evidence-based public health recommendations. The promise to adopt a healthy lifestyle is increasingly important for tackling this global epidemic. Calorie restriction or regular exercise or a combination of the two is accepted as an effective strategy in preventing or treating obesity. Furthermore, the benefits conferred by regular exercise to overcome obesity are attributed not only to reduced adiposity or reduced levels of circulating lipids but also to the proteins, peptides, enzymes, and metabolites that are released from contracting skeletal muscle or other organs. The secretion of these molecules called cytokines in response to exercise induces browning of white adipose tissue by increasing the expression of brown adipocyte-specific genes within the white adipose tissue, suggesting that exercise-induced cytokines may play a significant role in preventing obesity. In this review, we present research-based evidence supporting the effects of exercise and various diet interventions on preventing obesity and adipose tissue health. We also discuss the interplay between adipose tissue and the cytokines secreted from skeletal muscle and other organs that are known to affect adipose tissue and metabolism.
The impacts of carbohydrate (CHO) availability on time to task failure (TTF) and physiological responses to exercise at the maximal lactate steady state (MLSS) have not been studied. Ten participants (3 females, 7 males) completed this double blinded, placebo-controlled study that involved a ramp incremental test, MLSS determination, and four TTF trials at MLSS, all performed on a cycle ergometer. Using a combination of nutritional (CHO [7g/kg] and placebo [PLA; 0g/kg] drinks) and exercise interventions (no exercise [REST] and glycogen reducing exercise [EX]), the four conditions were expected to differ in pre-exercise CHO availability (REST CHO > REST PLA > EX CHO > EX PLA ). TTF at MLSS was not improved by CHO loading, as REST CHO (57.1 [16.6] min) and REST PLA (57.1 [15.6] min) were not different (p=1.00); however, TTF was ~50% shorter in EX conditions compared to REST conditions on average (p < 0.05), with EX CHO (39.1 [9.2] min) ~90% longer than EX PLA (20.6 [6.9] min; p < 0.001). There were effects of condition for all perceptual and cardiometabolic variables when compared at isotime (p<0.05) and TF (p<0.05), except for ventilation, perceptual responses, and neuromuscular function measures, which were not different at TF (p>0.05). Blood lactate concentration was stable in all conditions for participants who completed 30 min of exercise. These findings indicate that TTF at MLSS is not enhanced by pre-exercise CHO supplementation, but recent intense exercise decreases TTF at MLSS even with CHO supplementation. Extreme fluctuations in diet and strenuous exercise that reduce CHO availability should be avoided before MLSS determination.
Background
Physique athletes are ranked by a panel of judges against the judging criteria of the corresponding division. To enhance on-stage presentation and performance, competitors in certain categories (i.e. bodybuilding and classic physique) achieve extreme muscle size and definition aided by implementing acute “peaking protocols” in the days before competition. Such practices can involve manipulating nutrition and training variables to increase intramuscular glycogen and water while minimising the thickness of the subcutaneous layer. Carbohydrate manipulation is a prevalent strategy utilised to plausibly induce muscle glycogen supercompensation and subsequently increase muscle size. The relationship between carbohydrate intake and muscle glycogen saturation was first examined in endurance event performance and similar strategies have been adopted by physique athletes despite the distinct physiological dissimilarities and aims between the sports.
Objectives
The aim of this narrative review is to (1) critically examine and appraise the existing scientific literature relating to carbohydrate manipulation practices in physique athletes prior to competition; (2) identify research gaps and provide direction for future studies; and (3) provide broad practical applications based on the findings and physiological reasoning for coaches and competitors.
Findings
The findings of this review indicate that carbohydrate manipulation practices are prevalent amongst physique athletes despite a paucity of experimental evidence demonstrating the efficacy of such strategies on physique performance. Competitors have also been observed to manipulate water and electrolytes in conjunction with carbohydrate predicated on speculative physiological mechanisms which may be detrimental for performance.
Conclusions
Further experimental evidence which closely replicates the nutritional and training practices of physique athletes during peak week is required to make conclusions on the efficacy of carbohydrate manipulation strategies. Quasi-experimental designs may be a feasible alternative to randomised controlled trials to examine such strategies due to the difficulty in recruiting the population of interest. Finally, we recommend that coaches and competitors manipulate as few variables as possible, and experiment with different magnitudes of carbohydrate loads in advance of competition if implementing a peaking strategy.
Background
Exercise mimetics is a proposed class of therapeutics that specifically mimics or enhances the therapeutic effects of exercise. Muscle glycogen and lactate extrusion are critical for physical performance. The mechanism by which glycogen and lactate metabolism are manipulated during exercise remains unclear. This study aimed to assess the effect of miR‐92b on the upregulation of exercise training‐induced physical performance.
Methods
Adeno‐associated virus (AAV)‐mediated skeletal muscle miR‐92b overexpression in C57BLKS/J mice, and global knockout of miR‐92b mice were used to explore the function of miR‐92b in glycogen and lactate metabolism in skeletal muscle. AAV‐mediated UGP2 or MCT4 knockdown in WT or miR‐92 knockout mice was used to confirm whether miR‐92b regulates glycogen and lactate metabolism in skeletal muscle through UGP2 and MCT4. Body weight, muscle weight, grip strength, running time and distance to exhaustion, and muscle histology were assessed. The expression levels of muscle mass‐related and function‐related proteins were analysed by immunoblotting or immunostaining.
Results
Global knockout of miR‐92b resulted in normal body weight and insulin sensitivity, but higher glycogen content before exercise exhaustion (0.8538 ± 0.0417 vs. 1.043 ± 0.040, ** P = 0.0087), lower lactate levels after exercise exhaustion (4.133 ± 0.2589 vs. 3.207 ± 0.2511, * P = 0.0279), and better exercise capacity (running distance to exhaustion, 3616 ± 86.71 vs. 4231 ± 90.29, *** P = 0.0006; running time to exhaustion, 186.8 ± 8.027 vs. 220.8 ± 3.156, ** P = 0.0028), as compared with those observed in the control mice. Mice skeletal muscle overexpressing miR‐92b (both miR‐92b‐3p and miR‐92b‐5p) displayed lower glycogen content before exercise exhaustion (0.6318 ± 0.0231 vs. 0.535 ± 0.0194, ** P = 0.0094), and higher lactate accumulation after exercise exhaustion (4.5 ± 0.2394 vs. 5.467 ± 0.1892, * P = 0.01), and poorer exercise capacity (running distance to exhaustion, 4005 ± 81.65 vs. 3228 ± 149.8, *** P <0.0001; running time to exhaustion, 225.5 ± 7.689 vs. 163 ± 6.476, ** P = 0.001). Mechanistic analysis revealed that miR‐92b‐3p targets UDP‐glucose pyrophosphorylase 2 (UGP2) expression to inhibit glycogen synthesis, while miR‐92b‐5p represses lactate extrusion by directly target monocarboxylate transporter 4 (MCT4). Knockdown of UGP2 and MCT4 reversed the effects observed in the absence of miR‐92b in vivo.
Conclusions
This study revealed regulatory pathways, including miR‐92b‐3p/UGP2/glycogen synthesis and miR‐92b‐5p/MCT4/lactate extrusion, which could be targeted to control exercise capacity.
Endurance athletes have traditionally been advised to consume high carbohydrate intake before, during and after exercise to support high training loads and facilitate recovery. Accumulating evidence suggests periodically training with low carbohydrate availability, termed “train-low”, augments skeletal oxidative adaptations. Comparably, to account for increased carbohydrate utilisation during exercise in hot environmental conditions, nutritional guidelines advocate high carbohydrate intake. Recent evidence suggests heat stress induces oxidative adaptation in skeletal muscle, augmenting mitochondrial adaptation during endurance training. This thesis aimed to assess the efficacy of training with reduced carbohydrate and the impact of elevated ambient temperatures on performance and metabolism. Chapter 4 demonstrated 3 weeks of Sleep Low-Train Low (SL-TL) improves performance when prescribed and completed remotely. Chapter 5 implemented SL-TL in hot and temperate conditions, confirming SL-TL improves performance and substrate metabolism, whilst additional heat stress failed to enhance performance in hot and temperate conditions following the intervention. Chapters 6 and 7 optimised and implemented a novel in vitro skeletal muscle exercise model combining electrical pulse stimulation and heat stress. Metabolomics analysis revealed an ‘exercise-induced metabolic response, with no direct metabolomic impact of heat stress. Chapter 8 characterised the systemic metabolomic response to acute exercise in the heat following SL-TL and heat stress intervention revealing distinct metabolic signatures associated with exercise under heat stress.
In summary, this thesis provides data supporting the application of the SL-TL strategy during endurance training to augment adaptation. Data also highlights the impact of exercise, environmental temperature and substrate availability on skeletal muscle metabolism and the systemic metabolome. Together, these data provide practical support for the efficacy of the SL-TL strategy to improve performance and adaptation whilst casting doubt on the utility of this approach in hot environments in endurance-trained athletes.
Physical inactivity is a scourge to human health, promoting metabolic disease and muscle wasting. Interestingly, multiple ecological niches have relaxed investment into physical activity, providing an evolutionary perspective into the effect of adaptive physical inactivity on tissue homeostasis. One such example, the Mexican cavefish Astyanax mexicanus, has lost moderate-to-vigorous activity following cave colonization, reaching basal swim speeds ~3.7-fold slower than their river-dwelling counterpart. This change in behavior is accompanied by a marked shift in body composition, decreasing total muscle mass and increasing fat mass. This shift persisted at the single muscle fiber level via increased lipid and sugar accumulation at the expense of myofibrillar volume. Transcriptomic analysis of laboratory-reared and wild-caught cavefish indicated that this shift is driven by increased expression of pparγ —the master regulator of adipogenesis—with a simultaneous decrease in fast myosin heavy chain expression. Ex vivo and in vivo analysis confirmed that these investment strategies come with a functional trade-off, decreasing cavefish muscle fiber shortening velocity, time to maximal force, and ultimately maximal swimming speed. Despite this, cavefish displayed a striking degree of muscular endurance, reaching maximal swim speeds ~3.5-fold faster than their basal swim speeds. Multi-omic analysis suggested metabolic reprogramming, specifically phosphorylation of Pgm1-Threonine 19, as a key component enhancing cavefish glycogen metabolism and sustained muscle contraction. Collectively, we reveal broad skeletal muscle changes following cave colonization, displaying an adaptive skeletal muscle phenotype reminiscent to mammalian disuse and high-fat models while simultaneously maintaining a unique capacity for sustained muscle contraction via enhanced glycogen metabolism.
In diesem Kapitel werden zunächst 3 häufig diskutierte Trainingswirkungsmodelle gefolgt von trainingsinduzierten Anpassungen aerob bedeutsamer Strukturen und Funktionen des menschlichen Organismus beschrieben. Anhand von Simulationsberechnungen wird aufgezeigt, wie sich Änderungen der maximalen Sauerstoffaufnahme bei Konstanz der maximalen Laktatbildungsrate auf das Laktatverhalten im Blut auswirken. Gleiche Berechnungen werden für die Variation der maximalen Laktatbildungsrate bei Konstanz der maximalen Sauerstoffaufnahme vorgenommen. Es wird dargelegt, wie üblicherweise anhand von Ankerpunkten auf der Laktatleistungskurve Trainingsbereichskategorien zugeordnet werden, auf deren Basis konkrete Trainingspläne erstellt werden. Anschließend wird aufgezeigt, welche Probleme bei dem üblichen Vorgehen auftreten können. Mit der Darstellung des Einsatzes von Laktatmessungen in der kardialen Rehabilitation und bei Beta-Blocker-Medikation sowie beim Krafttraining schließt das Kapitel.
David G. Allen looks at new research from the Nielsen lab.
We here discuss metabolic causes of skeletal muscle fatigue with focus on peripheral fatigue, that is, negative transient effects on muscle contractility manifested as decreased force production, reduced shortening speed and/or slowed relaxation. We specifically address the following fatigue-related metabolic changes: (1) [ATP] normally remains almost constant but might decrease to critically low levels in severe fatigue where the accompanying transient increase in [ADP] would reduce shortening speed and hence power output. (2) The increase in inorganic phosphate ions (Pi) during intense exercise has a central role in fatigue by reducing the myofibrillar force generating capacity and Ca2+ sensitivity and by attenuating sarcoplasmic reticulum (SR) Ca2+ release. (3) Acidosis occurs during intense exercise and may depress myofibrillar contractile function; its importance is currently debated. (4) Increases in reactive oxygen/nitrogen species during intense exercise can induce long-lasting protein modifications that delay the recovery after exercise. (5) The depletion of intramyofibrillar glycogen during prolonged exercise is well correlated with decreased force due to impaired SR Ca2+ release. Thus, several metabolic alterations contribute to skeletal muscle fatigue, and the relative importance of these depends on factors such as the type of exercise, muscle fibre composition and the training status of the exercising individual.
The source of energy utilized during physical activity has been of intense scientific interest for at least two centuries. This chapter briefly describes how (and why) each of the three major macronutrients—i.e., protein, carbohydrate, and fat—has alternately had their moments in the sun. Specifically, although until the 1860s protein was considered to be the only fuel used during exercise, first carbohydrate, then fat, and then again carbohydrate held sway from the 1860s until World War II, from World War II until the late 1960s, and from the late 1960s to ca. 1990, respectively. It is now widely recognized, however, that contracting muscle relies upon a mixture of carbohydrate, fat, and even a small amount of protein to provide its energy needs, with the relative importance of each varying with the exercise intensity and duration, the characteristics (e.g., nutritional state, physical fitness) of the individual, etc. Thus, although substrate metabolism during exercise is now understood in greater detail than ever before, the overall picture has come full circle to that described by Zuntz at the start of the twentieth century.
Sickle cell disease (SCD) is a group of hemoglobin disorders sharing a nucleotide mutation in the β-globin gene, such as homozygous sickle cell anaemia (SS) and sickle cell-hemoglobin C disease (SC), with various clinical severities. SCD patients are characterized by a limited exercise capacity caused by cardio-
vascular abnormalities but skeletal muscle implication remains unclear. Recently, few studies characterized skeletal muscle in SS patients and showed an amyotrophy, a profound microvasculature remodeling and a decreased maximal strength however an exercise-induced skeletal muscle dysfunction are yet to described in SCD patients. It was also hypothesized that oxidative stress may be increased and participate in the skeletal muscle abnormalities observed in SCD patients. Chronic aerobic exercise is known to increase the antioxidant capacity in the skeletal muscle, but the effects of this type exercise have not been described in the skeletal muscle of SCD patients. Hence, the aim of this thesis work is 1) to characterize skeletal muscle function
during exercise in S/S et S/C patients and 2) to study the effects of chronic exercise on pro/antioxidant balance in the skeletal muscle of transgenic sickle cell mice. In a first study it was shown that S/S and S/C patients exhibit a profound skeletal muscle dysfunction characterized by an increased fatigability of the quadriceps. Also, the skeletal muscle dysfunction seems to be explained by intramuscular alterations specific to sickle cell disease rather than the clinical severity. In a second study, Townes sickle cell mice performed 8 weeks of moderate aerobic exercise and we observed an altered response of pro/antioxidant balance in the skeletal muscle of S/S mice. To conclude, the results of this work strengthen the idea that skeletal muscle is key
therapeutic target in the exercise rehabilitation of sickle cell disease patients.
Individuals may opt to follow a plant-based diet for a variety of reasons, such as religious practices, health benefits or concerns for animal or environmental welfare. Such diets offer a broad spectrum of health benefits including aiding in the prevention and management of chronic diseases. In addition to health benefits, a plant-based diet may provide performance-enhancing effects for various types of exercise due to high carbohydrate levels and the high concentration of antioxidants and phytochemicals found in a plant-based diet. However, some plant-based foods also contain anti-nutrional factors, such as phytate and tannins, which decrease the bioavailability of key nutrients, such as iron, zinc, and protein. Thus, plant-based diets must be carefully planned to ensure adequate intake and absorption of energy and all essential nutrients. The current narrative review summarizes the current state of the research concerning the implications of a plant-based diet for health and exercise performance. It also outlines strategies to enhance the bioavailability of nutrients, sources of hard-to-get nutrients, and sport supplements that could interest plant-based athletes.
Since ancient times, the health benefits of regular physical activity/exercise have been recognised and the classic studies of Morris and Paffenbarger provided the epidemiological evidence in support of such an association. Cardiorespiratory fitness, often measured by maximal oxygen uptake, and habitual physical activity levels are inversely related to mortality. Thus, studies exploring the biological bases of the health benefits of exercise have largely focused on the cardiovascular system and skeletal muscle (mass and metabolism), although there is increasing evidence that multiple tissues and organ systems are influenced by regular exercise. Communication between contracting skeletal muscle and multiple organs has been implicated in exercise benefits, as indeed has other inter-organ "cross-talk". The application of molecular biology techniques and 'omics' approaches to questions in exercise biology has opened new lines of investigation to better understand the beneficial effects of exercise and, in so doing, inform the optimisation of exercise regimens and the identification of novel therapeutic strategies to enhance health and well-being.
El objetivo general de la investigación fue determinar la influencia que tiene la maduración biológica en el rendimiento anaeróbico de luchadores adolescentes en formación. Se trata de un diseño no experimental, de campo, de nivel correlacional–causal, prospectivo y transversal. Se seleccionaron un total de 29 luchadores cuyas características físicas fueron (media±DS), edad: 14,99±1,83años, masa corporal: 54,68±16,80kg, estatura: 161,06±12,78cm, adiposidad: 12,09±4,11%, IMC: 20,58±3,79kg/m2, experiencia deportiva: 3,66±2,27años, pertenecientes al estado Barinas. La maduración se estimó mediante los criterios de Tanner. El rendimiento anaeróbico se evaluó con la prueba de Wingate de miembros inferiores y superiores. Los resultados indicaron correlaciones significativas moderadas y altas entre: los estados de madurez con la Pmáx y Pprom absoluta y relativa de miembros inferiores y superiores (p<0.05). La fatigabilidad (%IF) de miembros inferiores no mostró relación alguna con los estados de madurez, ni con las categorías de maduración púber y pospúber. Sin embargo, el %IF de miembros superiores develó una correlación moderada con los estados de madurez y la categoría pospúber (p<0.01). Se encontró una correlación alta entre la categoría de madurez púber con la Pmáx y Pprom absoluta y relativa de miembros inferiores (p<0.01) y relación moderada entre la categoría pospúber con solo la Pmáx(abs.) (p<0.01). La Pmáx(abs.) y Pprom(rel.) de miembros superiores presentó una relación moderada con la clasificación púber (p<0.05) y la pospúber tuvo una correlación alta con la Pmáx(abs.), Pprom(abs.) y Pprom(rel.) (p<0.01). En conclusión, la maduración biológica se ve influenciada en el rendimiento anaeróbico de luchadores adolescentes en formación.
Descriptores: luchadores, maduración biológica, rendimiento anaeróbico.
A rise in body core temperature and loss of body water via sweating are natural consequences of prolonged exercise in the heat. This review provides a comprehensive and integrative overview of how the human body responds to exercise under heat stress and the countermeasures that can be adopted to enhance aerobic performance under such environmental conditions. The fundamental concepts and physiological processes associated with thermoregulation and fluid balance are initially described, followed by a summary of methods to determine thermal strain and hydration status. An outline is provided on how exercise-heat stress disrupts these homeostatic processes, leading to hyperthermia, hypohydration, sodium disturbances and in some cases exertional heat illness. The impact of heat stress on human performance is also examined, including the underlying physiological mechanisms that mediate the impairment of exercise performance. Similarly, the influence of hydration status on performance in the heat and how systemic and peripheral hemodynamic adjustments contribute to fatigue development is elucidated. This review also discusses strategies to mitigate the effects of hyperthermia and hypohydration on exercise performance in the heat, by examining the benefits of heat acclimation, cooling strategies and hyperhydration. Finally, contemporary controversies are summarized and future research directions provided.
Although the majority of patients with acute or chronic pulmonary disease and respiratory failure do not have respiratory muscle disease or dysfunction at the outset of their clinical condition, most if not all do not have a normal respiratory musculature at the time of respiratory failure, especially those who have had a chronic course. Indeed, a large number of alterations in the muscle structure and metabolism occur as a result of a chronic load. Most of these changes are compensatory, but some may be maladaptive and deleterious to function. In addition, the compensatory mechanisms can be limited, and it is now believed that respiratory failure is at least in part exaggerated, or initiated, by the failure of the respiratory musculature. Therefore, the failure of these muscles can lead to hypoventilation, apnea, poor gas exchange, and clinically serious cardiovascular consequences.
Although research efforts have increased in the past several years, there is still a great deal to learn about the function of the respiratory musculature under stress. Some of the notable questions are: 1) What is the relation between inspiratory muscles (for example, the diaphragm and the intercostals) and the muscles of the airways during loaded breathing and in the presence of respiratory failure? 2) How does the differential respiratory output to the various motor neuron pools change and evolve during the chronic loaded breathing? 3) What kind of compensatory mechanisms (for example, humoral, biochemical, neural, or mechanical) can the respiratory muscles use to preserve function? 4) What is the relation between the nutritional status of the individual and its effect on the function of these muscles? and 5) What effect(s) do the changes associated with chronic pulmonary disease (for example, hypoxia, hypercapnea) have on respiratory muscle metabolism and function? This is an exciting area of research that has enormous potential for clinical applicability, and we believe that we are just at the very beginning.
Zusammenfassung
1.
Es wird keine Veränderung in der Stickstoff-, Kreatinin- und Kreatinausscheidung beobachtet, wenn man von Ruhe - zu intensiven Arbeitsbedingungen übergeht, und zwar auch dann nicht, wenn infolge von Fasten und vorhergegangener Arbeit die Kohlehydratreserven im Organismus auf ganz niedrige Werte gesunken sind, so daß auch die Arbeitsfähigkeit der Versuchspersonen bedeutend herabgesetzt ist.
2.
Daraus wird gefolgert, daß die im Organismus enthaltenen stickstoffhaltigen Substanzen höchstwahrscheinlichweder direkt von den tätigen Muskeln,noch durch die dazwischenliegende Bildung von Kohlehydraten zu energetischen Zwecken verwendet werden können.
3.
In einem Versuch ist während des Bergabsteigens bei niedrigem Calorienverbrauch eine Zunahme der Wasser- und Stickstoffausscheidung durch die Nieren, im Gegensatz zu den während des Ganges auf ebenem Terrain und während des Hinaufsteigens gemachten Beobachtungen bei bedeutend höheren energetischen Umsatz beobachtet worden. Diese Erscheinung wird auf Kreislaufveränderungen im Nierengebiet während des Herabsteigens zurückgeführt.
4.
Obwohl kein direktes Verhältniszwischen der Stickstoff- und der Kreatininausscheidung besteht, so besteht trotzdem ein deutlicher Zusammenhang dieser zwei Funktionen, im Gegensatz zu den gegenwärtigen Theorien über die verschiedene Bedeutung und über die funktionelle Unabhängigkeit des Kreatininstoffwechseis (endogener Stickstoffwechsel) gegenüber dem Gesamtstickstoffwechsel (exogener Stickstoffwechsel).
5.
Bei der unter aeroben Bedingungen geleisteten Arbeit ist die Ausscheidung von Säureradikalen von der Arbeitsintensität ganz unabhängig, was den Beweis liefert, daß es während einer unter solchen Bedingungen geleisteten Arbeit nicht zu einer Anhäufung von sauren Substanzen im Blut oder in den Geweben kommt.
The concentration of triglycerides, cholesterol and phospholipids in plasma and in ultracentrifugally separated plasma lipoproteins was studied in normal persons during participation in 1962 and 1963 in a yearly skiracing. The skiing time was around 8–9 hours. In the group studied in 1962 as well as in the 1963 group there was a significant fall in the concentration of triglycerides and phospholipids in plasma. When the 1962 group was studied during ordinary activities with identical caloric intake and at identical times as during the skiing no significant changes were found in the plasma lipids. The most pronounced decreases of the plasma lipids was in the triglyceride fraction and this decrease was directly and highly significantly correlated to the fasting triglyceride concentration. About three quarters of the decrease in triglyceride concentration was due to a decrease in the amount of triglycerides in the very low density lipoproteins. The triglyceride concentration in the low and the high density lipoprotein classes also decreased. The decrease of triglycerides was directly correlated to the fasting level in each lipoprotein class. No significant changes were observed in the cholesterol content of any of the lipoproteins. The phospholipid concentration, however, decreased in all three lipoprotein classes. The most pronounced decrease of phospholipids was found in the high density lipoproteins. Mechanism(s) for these changes in the concentration of the plasma lipids and lipoproteins during prolonged, heavy exercise were discussed.
Using a single injection of indocyanine green dye, estimated hepatic plasma and blood flow were determined in six normal young males during the 30th to 60th min of exercise requiring 10–12 kcal/min (2.04– 2.49 liters O2 per min). Subjects were fasted 15–18 hours. During hepatic flow measurements four determinations of splanchnic A-V differences of triglyceride (TG), free fatty acid (FFA), phospholipid (PL), ketone bodies, and glucose were made from radial arterial and hepatic venous sampling sites. Splanchnic A-V concentration differences for TG and PL varied randomly with time from positive to negative values indicating no net production whereas FFA was uniformly taken up by splanchnic organs at an average rate of 64 μm/min. Average splanchnic ketone body production was 20 mg/min and glucose production averaged 295 mg/min. Complete oxidation by skeletal muscle of lipid substrate released by splanchnic organs could account for less than 5% of total caloric expenditure; glucose production accounted for an average of 10.4%. One to two determinations of splanchnic A-V lactate, CO2, and O2 concentrations in four men indicated continued uptake of lactate (average 50 mg/min) during exercise with RQ values approaching zero.
lipid metabolism; exercise, hepatic blood flow, and metabolism; energy metabolism
Submitted on January 15, 1965
A method has been devised for determination of the glycogen content of human skeletal muscle, obtained with a needle biopsy technique.
The method involves homogenization of the muscle specimens. The protein is precipitated with trichloroacetic acid. After precipitation of the glycogen with alcohol from the supernatant, it is hydrolyzed with sulphuric acid, and then determined as glucose with the orthotoluidine method.
In 96 per cent of healthy subjects, the glycogen content of the quadriceps femoris muscle ranges from 0.95 to 2.0 g/100 g wet muscle (mean 1.39 g). The standard error of the method is 0.05 g/100 g, representing 3.5 per cent of the mean value. The glycogen content of the deltoid muscle (mean 0.98 g/100 g wet muscle) is significantly lower than that of the quadriceps femoris.
A study was also made of the diurnal fluctuations in the muscle glycogen, both under normal conditions and during brief fasting. These fluctuations are found to be small and not uniform.
The type of work was ski running at a constant speed on a 750 m circular track set up on level ground. Four well trained male subjects performed this work to the point of exhaustion. During 150–160 min three of the subjects were able to run at a work intensity which corresponded to an oxygen intake of 3.6‐4.1 l/min. (The oxygen intake for the fourth subject was 3.4‐3.9 l/min during 120 min.) The total energy expenditure during this time was 2,000–3,000 Cal; the pulmonary ventilation rose to a mean of 90 l/min and the heart rate was 160–190 beats/min. By determination of the respiratory metabolism the quantity of oxidized carbohydrates was calculated.
The RQ values remained during the whole run at a practically constant level. One subject, who had reduced his glycogen depot by 445 g, continued to get 55 % of his calorie need from carbohydrates, although hypoglycemic symptoms were present.
The blood lactic acid concentrations at the end of these long periods of work were slightly increased (20 mg %).
IN the clinical field it is of importance to have a rapid and exact method for glucose determinations. In order to avoid the non-specific reduction methods, a coupling reaction was worked out utilizing the conjugation of aldoses and ketoses with meta-aminophenol in acetic acid. After some preliminary experiments1, a routine method was described2. The method has been used for some time in this laboratory and has proved satisfactory; but, because of the necessarily long boiling time of 30 min., and the fact that the whole range of urine sugar concentration cannot be read without dilution of the urine, it was considered an advantage to have a reagent giving a more rapid reaction and a wider range. Many aromatic amines have been tested; of these, one of the most suitable was ortho-toluidine, for which the optimal boiling time is 8 min. (Fig. 1). It gives a blue-green colour with maximum absorption at 6250 A. and is fairly specific for aldosugars (Fig. 2). Blood treated with glucose oxidase gave readings corresponding to 0-4 mgm. glucose per 100 ml. blood. With this reagent glucose quantities of 10-400 µgm. can be read directly in a Beckman B photometer.
Oxygen uptake, heart rate, pulmonary ventilation, and blood lactic acid were studied in five subjects performing maximal work on a bicycle ergometer. After a 10-min warming up period work loads were varied so that exhaustion terminated exercise after about 2—8 min. Peak oxygen uptake and heart rate were practically identical (sd 3.1% and 3 beats/minute, respectively) in the experiments. The heavier the work was and the shorter the work time the higher became the pulmonary ventilation. There was a more rapid increase in the functions studied when the heaviest work loads were performed. It is concluded that aerobic capacity can be measured in a work test of from a few up to about 8 min duration, severity of work determining the actual work time necessary. Duration of work in studies of circulation and respiration during submaximal work should exceed 5 min.
Submitted on June 23, 1961
Four subjects worked on a treadmill or a bicycle ergometer for 180 min at oxygen uptakes of 75% of the individual's max Vo2; after 90 min rest, the exercise was resumed and a maximal work load was tried. Repeated circulatory studies were made. The body weight decreased 3.1 kg (3.2–5.2%), but the reduction in blood volume was less than 5%. During submaximal exercise the major change in the hemodynamic response was a decrease in stroke volume (from 126 to 107 ml). Oxygen uptake and cardiac output increased slightly. There was a decrease of about 10% in systolic, diastolic, and mean arterial blood pressure during the 180 min of exercise. When the work was performed in a supine position there was the same reduction in the stroke volume as in the sitting work position. At the maximal work oxygen uptake, cardiac output, heart rate, and blood pressure attained almost normal values but there was a marked decrease in both work time and blood lactates.
dehydration; blood volume; arterial blood pressure; circulatory reaction
Submitted on January 31, 1964
Ten subjects performed standard exercise tests at two submaximal loads and one maximal load before and 90 min after dehydration caused predominantly by 1) a thermal, 2) a metabolic, and 3) a combined thermal and metabolic heat load applied for 2.5@#X2013;4 hr. Each subject interrupted dehydration so that almost the same decrease in body weight was attained in the three situations (1.7@#X2013;4.6 kg). Oxygen uptake, heart rate, and concentration of blood lactate were measured during the exercise. At the submaximal loads there was no change in oxygen uptake after dehydration but the heart rates were significantly higher (mean difference 13 beats/min) and blood lactates were lower (from 0.5 after (1) to 1.6 (2) mmoles/liter). At the maximal load there were no significant changes in oxygen uptake and heart rate but work times decreased markedly (6@#X2013;4 min) as did blood lactates (14.0@#X2013;10.4 mmoles/liter) especially after exercise dehydration.
physical work capacity
Submitted on January 20, 1964
Source et nature du potential directement utilisé dans le travail musculaire, d'après les échanges respirations, chez l'homme en état d'abstinence
- Chaveau A.
The arterial plasma‐free fatty acid concentration during and after exercise and its regualtion
- Carlsson L. A.
Über die Bedeutung der verschiedene Nährstoff als Energiequelle der Muskelkraft
- Zuntz N.
Arbeitsfähigkeit und Ernährung
- Christensen E. H.
Über die Wirkung von Nystatin auf Bäckerhefe
- Scholz R.