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Lactic acid accumulation during running at submaximal aerobic demands
Abstract
Four running tests were performed by five, normal, male adults on a motor driven treadmill. After determination of the max [latin capital V with dot above]o2 they ran on different days for 30 minutes at 82-89% max[latin capital V with dot above]o2, 40 minutes at 74-79% max[latin capital V with dot above]o2 and 60 minutes at 67-74% max[latin capital V with dot above]o2. Gas exchange determinations and basilic vein lactate measurements were made for selected one-minute intervals over the duration of the runs. Periodic pH determinations, heart rates and rectal temperatures were monitored. In running at 82-89% max[latin capital V with dot above]o2 the venous lactate levels were observed to continuously increase over the duration of the 30 minute performances for all subjects (peak mean 82.5mg%). Running at 74-79% max[latin capital V with dot above]o2 resulted in an elevation. of lactate that generally plateaued around 45mg% by the 20th minute of the 40 minute performances. At 67-74% max[latin capital V with dot above]o2 a small increase in lactate occured (means ranged from 18 to 29mg%) which was sustained over the 60 minute performances. The results indicate that blood LA is elevated over the duration of 30 to 60 minute runs in proportion to the aerobic demands in excess of 65 to 70% of maximum. This suggests that LA is continuously produced in work requiring 65 to 90% max[latin capital V with dot above]o2 even when a reasonably steady state of O2 consumption is attained. (C)1970The American College of Sports Medicine
... Most of the studies that have reported a V O 2 slow component were performed during cycling (12). However, the V O 2 slow component has also been reported during running but only for prolonged tests (20-30 min) (18,25). No data are available on the behavior of the V O 2 slow component during a submaximal running test leading to fatigue. ...
... Whipp (29) suggested that the more rapidly the slow component projects toward V O 2 , the shorter the tolerable duration of the exercise test. In the study by Nagle et al. (18), the subjects did not reach their V O 2 max and were not completely exhausted. In the present study as well, many subjects did not reach their V O 2 max during running but were completely exhausted at the end of the test. ...
... . O 2max . [215][216][217][218][219][220][221][222][223][224] However, some authors have observed a MLSS at 65% of V . O 2max , [225] while others reported intensities equal to or above 85% of V . ...
... . O 2max . [151,155,166,215,228,229] The intention is to establish the highest exercise intensity where [La -] b increases by no more than 1.0 mmol/L between 10 to 30 minutes. [184] McLellan and Jacobs [230] proposed a slightly different algorithm to determine MLSS. ...
... Most of the studies that have reported a V O 2 slow component were performed during cycling (12). However, the V O 2 slow component has also been reported during running but only for prolonged tests (20-30 min) (18,25). No data are available on the behavior of the V O 2 slow component during a submaximal running test leading to fatigue. ...
... Whipp (29) suggested that the more rapidly the slow component projects toward V O 2 , the shorter the tolerable duration of the exercise test. In the study by Nagle et al. (18), the subjects did not reach their V O 2 max and were not completely exhausted. In the present study as well, many subjects did not reach their V O 2 max during running but were completely exhausted at the end of the test. ...
The purpose of this study was to examine the influence of the type of exercise (running vs. cycling) on the O2 uptake V(O2) slow component. Ten triathletes performed exhaustive exercise on a treadmill and on a cycloergometer at a work rate corresponding to 90% of maximal VO2 (90% work rate maximal V(O2)). The duration of the tests before exhaustion was superimposable for both type of exercises (10 min 37 s +/- 4 min 11 s vs. 10 min 54 s +/- 4 min 47 s for running and cycling, respectively). The V(O2) slow component (difference between V(O2) at the last minute and minute 3 of exercise) was significantly lower during running compared with cycling (20.9 +/- 2 vs. 268.8 +/- 24 ml/min). Consequently, there was no relationship between the magnitude of the V(O2) slow component and the time to fatigue. Finally, because blood lactate levels at the end of the tests were similar for both running (7.2 +/- 1.9 mmol/l) and cycling (7.3 +/- 2.4 mmol/l), there was a clear dissociation between blood lactate and the V(O2) slow component during running. These data demonstrate that 1) the V(O2) slow component depends on the type of exercise in a group of triathletes and 2) the time to fatigue is independent of the magnitude of the V(O2) slow component and blood lactate concentration. It is speculated that the difference in muscular contraction regimen between running and cycling could account for the difference in the V(O2) slow component.
... Considering the absence of the V O 2 slow component in running despite continuous blood lactate accumulation, this present study is in accordance with that of Nagle et al. [28] who underlined that during running "lactic acid is produced in work requiring 65 -90 % of V O 2 max even when a reasonably steady state of V O 2 is attained" (duration 30 min at 86.4 ± 2.6 % of V O 2 max). Costill [15] reported that three highly trained distance runners (V O 2 max > 70 ml/kg/min) were able to sustain a V O 2 steady-state at 90 % of V O 2 max for more than 25 minutes (10 km performed on treadmill) with end blood lactate of 5 mM. ...
... Whipp [42] suggested that the more rapidly the slow component projects toward V O 2 max, the shorter the tolerable duration of the exercise test. In Nagle et al.'s study [28], subjects did not reach their V O 2 max and were not completely exhausted. In the present study, both cases existed since during running subjects did not reach their V O 2 max, but were completely exhausted and in cycling, they reached their V O 2 max and were exhausted, too (after the same duration). ...
The purpose of this study was to compare the effect of two different types of cyclic severe exercise (running and cycling) on the VO2 slow component. Moreover we examined the influence of cadence of exercise (freely chosen [FF] vs. low frequency [LF]) on the hypothesis that: 1) a stride frequency lower than optimal and 2) a pedalling frequency lower than FF one could induce a larger and/or lower VO2 slow component. Eight triathletes ran and cycled to exhaustion at a work-rate corresponding to the lactate threshold + 50% of the difference between the work-rate associated with VO2max and the lactate threshold (delta 50) at a freely chosen (FF) and low frequency (LF: - 10 % of FF). The time to exhaustion was not significantly different for both types of exercises and both cadences (13 min 39 s, 15 min 43 s, 13 min 32 s, 15 min 05 s for running at FF and LF and cycling at FF and LF, respectively). The amplitude of the VO2 slow component (i.e. difference between VO2 at the last and the 3rd min of the exercise) was significantly smaller during running compared with cycling, but there was no effect of cadence. Consequently, there was no relationship between the magnitude of the VO2 slow component and the time to fatigue for a severe exercise (r = 0.20, p = 0.27). However, time to fatigue was inversely correlated with the blood lactate concentration for both modes of exercise and both cadences (r = - 0.42, p = 0.01). In summary, these data demonstrate that: 1) in subjects well trained for both cycling and running, the amplitude of the VO2 slow component at fatigue was larger in cycling and that it was not significantly influenced by cadence; 2) the VO2 slow component was not correlated with the time to fatigue. If the nature of the linkage between the VO2 slow component and the fatigue process remains unclear, the type of contraction regimen depending on exercise biomechanic characteristics seems to be determinant in the VO2 slow component phenomenon for a same level of training.
... [213] In most studies, the MLSS is located between 70 and 80% of V . O 2max .215216217218219220221222223224 However, some authors have observed a MLSS at 65% of V . ...
... O 2max . [151,155,166,215,228,229] The intention is to establish the highest exercise intensity where [La – ] b increases by no more than 1.0 mmol/L between 10 to 30 minutes. [184] McLellan and Ja- cobs [230] proposed a slightly different algorithm to determine MLSS. ...
Physiological testing of elite athletes requires the correct identification and assessment of sports-specific underlying factors. It is now recognised that performance in long-distance events is determined by maximal oxygen uptake (V(2 max)), energy cost of exercise and the maximal fractional utilisation of V(2 max) in any realised performance or as a corollary a set percentage of V(2 max) that could be endured as long as possible. This later ability is defined as endurance, and more precisely aerobic endurance, since V(2 max) sets the upper limit of aerobic pathway. It should be distinguished from endurance ability or endurance performance, which are synonymous with performance in long-distance events. The present review examines methods available in the literature to assess aerobic endurance. They are numerous and can be classified into two categories, namely direct and indirect methods. Direct methods bring together all indices that allow either a complete or a partial representation of the power-duration relationship, while indirect methods revolve around the determination of the so-called anaerobic threshold (AT). With regard to direct methods, performance in a series of tests provides a more complete and presumably more valid description of the power-duration relationship than performance in a single test, even if both approaches are well correlated with each other. However, the question remains open to determine which systems model should be employed among the several available in the literature, and how to use them in the prescription of training intensities. As for indirect methods, there is quantitative accumulation of data supporting the utilisation of the AT to assess aerobic endurance and to prescribe training intensities. However, it appears that: there is no unique intensity corresponding to the AT, since criteria available in the literature provide inconsistent results; and the non-invasive determination of the AT using ventilatory and heart rate data instead of blood lactate concentration ([La(-)](b)) is not valid. Added to the fact that the AT may not represent the optimal training intensity for elite athletes, it raises doubt on the usefulness of this theory without questioning, however, the usefulness of the whole [La(-)](b)-power curve to assess aerobic endurance and predict performance in long-distance events.
... As such, theV o 2 sc has most commonly been identified during cycle ergometry where the external work rate can be most accurately set and maintained (35,38,42,43,48,115,118,127,131,160,192,303,316,330,476,561,606,609,610,646,686,795). However, this behavior is also evident for running (e.g., 121,125,347,539,707), rowing (377,632), and isometric exercise (e.g., 664,739). ...
... The undissoci-ing graded load protocols or single steps at a conated lactic acid may diffuse across the cell mem-stant load of long duration (≥10 minutes) and near complete recovery between the steps. [26] However, 50% and 90% of V O2. [10, [94][95][96] The accumulation of the duration and size of the intensity increments lactate is only evident after 10 minutes if the running have been found to influence the value of the lactate speed is only slightly greater than at the velocity threshold. [91] associated with maximal lactate steady state (vMLSS). ...
The maximal lactate steady state (MLSS) is defined as the highest blood lactate concentration (MLSSc) and work load (MLSSw) that can be maintained over time without a continual blood lactate accumulation. A close relationship between endurance sport performance and MLSSw has been reported and the average velocity over a marathon is just below MLSSw. This work rate delineates the low-to high-intensity exercises at which carbohydrates contribute more than 50% of the total energy need and at which the fuel mix switches (crosses over) from predominantly fat to predominantly carbohydrate. The rate of metabolic adenosine triphosphate (ATP) turnover increases as a direct function of metabolic power output and the blood lactate at MLSS represents the highest point in the equilibrium between lactate appearance and disappearance both being equal to the lactate turnover. However, MLSSc has been reported to demonstrate a great variability between individuals (from 2–8 mmol/L) in capillary blood and not to be related to MLSSw. The fate of enhanced lactate clearance in trained individuals has been attributed primarily to oxidation in active muscle and gluconeogenesis in liver. The transport of lactate into and out of the cells is facilitated by monocarboxylate transporters (MCTs) which are transmembrane proteins and which are significantly improved by training. Endurance training increases the expression of MCT1 with intervariable effects on MCT4. The relationship between the concentration of the two MCTs and the performance parameters (i.e. the maximal distance run in 20 minutes) in elite athletes has not yet been reported. However, lactate exchange and removal indirectly estimated with velocity constants of the individual blood lactate recovery has been reported to be related to time to exhaustion at maximal oxygen uptake.
... In exercising vertebrates anaerobic fermentation supplements aerobic ATP production, increasing the scope for activity (Bennett, 1978(Bennett, , 1980. Lactate accumulates in the blood primarily under three exercise conditions: (1) early in submaximal exercise during the O2 deficit period (Cerretelli et al. 1979;Gleeson, 1980), (2) during Vo2s S at submaximal work intensities greater than 50% maximal V02 (Nagle et al. 1970;Seeherman, Taylor, Maloiy & Armstrong, 1981) and (3) at work levels exceeding maximal V02 (Margaria et al. 1963;Bennett, 1978). Lactate is probably produced in exercising crustaceans under similar conditions. ...
The fiddler crab, Uca pugilator, used sideways octapedal locomotion during 15 min of treadmill exercise. At each velocity tested (0·06, 0·11 and 0·16 km h−1), oxygen consumption showed only a modest, sluggish elevation; a ‘steady-state’ was never attained. The highest recorded, 0·22 ml O2g−1 h−1, was 4·4 times the resting rate. Net whole body lactate (WBL) was found to increase at a constant rate throughout the exercise period.
During recovery, and WBL removal followed a similar time course and returned to pre-exercise rates in 30–45 min. Although the fate of lactate after exercise is unknown for crustaceans, calculations suggest that not enough oxygen is consumed by the crab during recovery to oxidize lactate completely to CO2 and H2O. A gluconeogenic fate is compatible with the data.
As running velocity was increased, increased only slightly, while the net rate of WBL production showed a substantial elevation. At low velocity aerobic metabolism accounted for 60 % of the ATP produced when aerobic metabolism and anaerobic fermentation are considered. Anaerobic fermentation dominated at medium and high velocity and produced 60 and 70 % of the ATP, respectively.
The minimum cost of transport, the least amount of energy required to transport a given mass a distance, was determined using both aerobic and anaerobic sources. This estimation of locomotion economy for Uca pugilator was within the range predicted for a vertebrate of a similar mass.
... As such, theV o 2 sc has most commonly been identified during cycle ergometry where the external work rate can be most accurately set and maintained (35,38,42,43,48,115,118,127,131,160,192,303,316,330,476,561,606,609,610,646,686,795). However, this behavior is also evident for running (e.g., 121,125,347,539,707), rowing (377,632), and isometric exercise (e.g., 664,739). ...
Muscular exercise requires transitions to and from metabolic rates often exceeding an order of magnitude above resting and places prodigious demands on the oxidative machinery and O2-transport pathway. The science of kinetics seeks to characterize the dynamic profiles of the respiratory, cardiovascular, and muscular systems and their integration to resolve the essential control mechanisms of muscle energetics and oxidative function: a goal not feasible using the steady-state response. Essential features of the O2 uptake (VO2) kinetics response are highly conserved across the animal kingdom. For a given metabolic demand, fast VO2 kinetics mandates a smaller O2 deficit, less substrate-level phosphorylation and high exercise tolerance. By the same token, slow VO2 kinetics incurs a high O2 deficit, presents a greater challenge to homeostasis and presages poor exercise tolerance. Compelling evidence supports that, in healthy individuals walking, running, or cycling upright, VO2 kinetics control resides within the exercising muscle(s) and is therefore not dependent upon, or limited by, upstream O2-transport systems. However, disease, aging, and other imposed constraints may redistribute VO2 kinetics control more proximally within the O2-transport system. Greater understanding of VO2 kinetics control and, in particular, its relation to the plasticity of the O2-transport/utilization system is considered important for improving the human condition, not just in athletic populations, but crucially for patients suffering from pathologically slowed VO2 kinetics as well as the burgeoning elderly population. © 2012 American Physiological Society. Compr Physiol 2:933-996, 2012.
... Although blood sampling during cycle ergometer work is a common laboratory technique, the collection of serial venous blood samples while treadmill running has been reported only briefly earlier (32,33,35), while the precise methodology has never been fully elucidated. Therefore considerable pilot work was employed in order to refine the technique for this specific laboratory application. ...
Thesis (Ph. D. - Animal Physiology)--University of Arizona, 1982. Includes bibliographical references (leaves 74-77). Microfiche. s
... As such, theV o 2 sc has most commonly been identified during cycle ergometry where the external work rate can be most accurately set and maintained (35,38,42,43,48,115,118,127,131,160,192,303,316,330,476,561,606,609,610,646,686,795). However, this behavior is also evident for running (e.g., 121,125,347,539,707), rowing (377,632), and isometric exercise (e.g., 664,739). ...
The objective of the book is to discuss the principal determinants of oxygen uptake dynamics which is essential to developing exercise performance and improving quality of life for patients, especially those with cardio-respiratory diseases. A broad review of the current knowledge about this relatively less studied field is provided by this book. Incidentally, it updates the reader about how a person can use his/her aerobic energy system more effectively in order to fatigue gradually and be able to endure more physical activity. It also discusses the effects of exercise training in speeding up oxygen uptake kinetics, and the effects of ageing and a selection of conditions in slowing oxygen dynamics and declining exercise capacity.
... As such, theV o 2 sc has most commonly been identified during cycle ergometry where the external work rate can be most accurately set and maintained (35,38,42,43,48,115,118,127,131,160,192,303,316,330,476,561,606,609,610,646,686,795). However, this behavior is also evident for running (e.g., 121,125,347,539,707), rowing (377,632), and isometric exercise (e.g., 664,739). ...
This paper offers a brief synopsis of the five preceding papers which constitute the proceedings of the symposium "Mechanistic basis of the slow component of VO2 kinetics during heavy exercise." The key features have been taken from each paper and a coherent position regarding the site and potential underlying mechanisms for the "excess" VO2 is presented. The hypothesis is developed that some aspect of fiber type recruitment patterns might be responsible for this phenomenon. Elucidation of the precise determinants of VO2 during heavy exercise is fundamental to our understanding of muscle energetics. Furthermore, certain patient populations, whose exercise tolerance is limited by impaired cardiovascular and/or respiratory capacity, may benefit from interventions designed to constrain the magnitude of the VO2 slow component.
... As such, theV o 2 sc has most commonly been identified during cycle ergometry where the external work rate can be most accurately set and maintained (35,38,42,43,48,115,118,127,131,160,192,303,316,330,476,561,606,609,610,646,686,795). However, this behavior is also evident for running (e.g., 121,125,347,539,707), rowing (377,632), and isometric exercise (e.g., 664,739). ...
Technical limitations have precluded measurement of the V(O(2)) profile within contracting muscle (mV(O(2))) and hence it is not known to what extent V(O(2)) dynamics measured across limbs in humans or muscles in the dog are influenced by transit delays between the muscle microvasculature and venous effluent. Measurements of capillary red blood cell flux and microvascular P(O(2)) (P(O(2)m)) were combined to resolve the time course of mV(O(2)) across the rest-stimulation transient (1 Hz, twitch contractions). mV(O(2)) began to rise at the onset of contractions in a close to monoexponential fashion (time constant, J = 23.2 +/- 1.0 sec) and reached it's steady-state value at 4.5-fold above baseline. Using computer simulation in healthy and disease conditions (diabetes and chronic heart failure), our findings suggest that: (1) mV(O(2)) increases essentially immediately (< 2 sec) following exercise onset; (2) within healthy muscle the J blood flow (thus O(2) delivery, J Q(O(2)m)) is faster than JmV(O(2)) such that oxygen delivery is not limiting, and 3) a faster P(O(2)m) fall to a P(O(2)m) value below steady-state values within muscle from diseased animals is consistent with a relatively sluggish Q(O(2)m) response compared to that of mV(O(2)).
... [26] However, 50% and 90% of ˙ VO2. [10,[94][95][96] The accumulation of the duration and size of the intensity increments lactate is only evident after 10 minutes if the running have been found to influence the value of the lactate speed is only slightly greater than at the velocity threshold. [91] associated with maximal lactate steady state (vMLSS). ...
The maximal lactate steady state (MLSS) is defined as the highest blood lactate concentration (MLSSc) and work load (MLSSw) that can be maintained over time without a continual blood lactate accumulation. A close relationship between endurance sport performance and MLSSw has been reported and the average velocity over a marathon is just below MLSSw. This work rate delineates the low- to high-intensity exercises at which carbohydrates contribute more than 50% of the total energy need and at which the fuel mix switches (crosses over) from predominantly fat to predominantly carbohydrate. The rate of metabolic adenosine triphosphate (ATP) turnover increases as a direct function of metabolic power output and the blood lactate at MLSS represents the highest point in the equilibrium between lactate appearance and disappearance both being equal to the lactate turnover. However, MLSSc has been reported to demonstrate a great variability between individuals (from 2-8 mmol/L) in capillary blood and not to be related to MLSSw. The fate of enhanced lactate clearance in trained individuals has been attributed primarily to oxidation in active muscle and gluconeogenesis in liver. The transport of lactate into and out of the cells is facilitated by monocarboxylate transporters (MCTs) which are transmembrane proteins and which are significantly improved by training. Endurance training increases the expression of MCT1 with intervariable effects on MCT4. The relationship between the concentration of the two MCTs and the performance parameters (i.e. the maximal distance run in 20 minutes) in elite athletes has not yet been reported. However, lactate exchange and removal indirectly estimated with velocity constants of the individual blood lactate recovery has been reported to be related to time to exhaustion at maximal oxygen uptake.
... As such, theV o 2 sc has most commonly been identified during cycle ergometry where the external work rate can be most accurately set and maintained (35,38,42,43,48,115,118,127,131,160,192,303,316,330,476,561,606,609,610,646,686,795). However, this behavior is also evident for running (e.g., 121,125,347,539,707), rowing (377,632), and isometric exercise (e.g., 664,739). ...
The purpose of this paper is to provide an introduction to the study of oxygen uptake (VO(2)) dynamics or kinetics. Following the onset of exercise, both muscle and pulmonary VO(2) rise in a near-exponential fashion towards the anticipated "steady-state" VO(2) demand. However, it can take 2-4 min, or even longer at higher work rates, before this steady state is attained. Slow VO(2) kinetics increase the so-called O(2) deficit and obligate a greater contribution from anaerobic mechanisms of ATP production (involving the breakdown of muscle high energy phosphates and lactate production from glycogen) to meet the ATP requirement of the exercise task. A primary goal in this area of research is therefore to elucidate the physiological mechanisms which control and/or limit the rate at which muscle VO(2) increases following the onset of exercise. At higher intensities of exercise, a continued increase in both muscle and pulmonary VO(2) is observed with time despite the external work rate remaining constant. This continued rise in VO(2), beyond the anticipated steady-state requirement for the work rate, has been termed the VO(2) "slow component," and establishing the mechanistic basis for this phenomenon is another important goal of research in this field. This paper provides an overview of some of the factors which might contribute to both the fundamental and slow phases of the VO(2) kinetics and, in so doing, provides general background material for the more specific papers that follow.
Cette thèse avait pour ambition de contribuer à la compréhension des effets des variables de contrôle sur la performance, que sont le temps, la vitesse, la perception de l'effort (article 1), la distance (article 2) ainsi que V̇O2 et la fréquence cardiaque (article 3). Nous avons pu réaliser ce travail en utilisant les nouvelles possibilités qu'offrent les nouvelles technologies affranchissant le physiologiste du tapis roulant tout en disposant de la possibilité de contrôler par Bluetooth® toutes les variables physiologiques. Nous avons mis en évidence que : 1) les athlètes étaient capables d'adapter et de reproduire des réponses physiologiques non seulement en intensité mais en durée (article 1), 2) lorsque la variable de contrôle est la distance avec une mise en situation de compétition, la contribution de l'énergie à V̇O2max était relativement identique en proportion de l'énergie aérobie et ce, du 100 au 10,000m (article 2). Il y aurait donc un continuum énergétique allant du sprint au 10 kilomètres qui pourrait être une information intégrée dans l'organisme de façon centrale (demi-fond et fond) ou métabolique (sprint), 3) Enfin, nous avons montré que même dans un effort assez long (12 minutes) et maximal, le coureur tirait bénéfice d'une aide de contrôle « physiologique » par la fréquence cardiaque ou V̇O2 pour parvenir à sa meilleure performance. En conclusion, ce travail de thèse propose une méthodologie dans laquelle le coureur devient autonome dans le choix de sa stratégie de vitesse en s'affranchissant des calculs de vitesse cible à partir des seuils physiologiques, V̇O2max et autres facteurs physiologiques rendus limitants en cela.
There appear to be no differences in the aerobic demands of running at submaximal speeds between males and females who are of relatively equal ability and fitness. That the effects of fractional utilization during submaximal running may produce measurable differences in V(O2 submax) at given speeds of running is not clear and should be investigated using trained males and females of both equal and widely different V(O2max) values. It appears that the comparison of regression curves relating running speed and V(O2) for different speed ranges is clearly a hazardous practice. This is true whether subjects are of the same or opposite sex. The data presented in Figure 2 indicate that the use of speeds below 200 m/min produces a particularly flat regression curve and calculation of the energy demands of running at higher speeds based on data collected at very slow speeds would greatly underestimate the energy requirements of the faster running. A quadratic regression equation should be used when sufficient data are available. The following regression equations best fit the present data: Y = 14.77 + 0.059x + 0.000279x2, where y = V(O2) (ml/kg.min) and x = speed (m/min), and y = 83.74 + 2.798x + 0.014288x2, where y = speed (m/min) and x = V(O2) (ml/kg.min). The differences in male and female running performances at middle and long distance races are mainly attributable to differences in V(O2max). This being the case, and in the absence of other yet-to-be-detected sex differences that might be important particularly in marathon running, females of the caliber presently competing in middle distance races should be capable of marathon times in the range of 2 hours 20 minutes to 2 hours 30 minutes.
In brief: Physiologic testing represents one of the “high tech” parts of many contemporary sports programs. Some think it gives a big advantage to the Eastern Bloc countries; others think it is nothing more than fluff. Physiologic testing provides some good ways for coaches to identify talent or measure progress. It also helps them to view athletes in a unique way and provides a context for understanding recent scientific findings so that those might be used to enhance the athletes' performance.
Being a competitive distance runner is, in part, attributable to a high VO2max. However running economy (RE) is a more robust indicator of distance running performance among endurance athletes of similar VO2max levels. The purpose of this study was to examine the influence of unshod (barefoot) vs. shod (wearing shoes) running on RE (expressed as mL * kg-1 * min-1) during three 5-minute submaximal running trials representing 65, 75, and 85% of VO2max. Other physiologic and perceptual variables such as respiratory exchange ratio (RER), lactate, heart rate (HR), and ratings of perceived exertion (RPE) were also chosen as dependent variables. We measured VO2max in fourteen recreationally active, trained distance female runners (age = 27.6 ± 1.6 yrs; height = 163.3 ± 1.7 cm; weight = 57.8 ± 1.9 kg) who were completely inexperienced with unshod running. Following initial testing, each subject was randomized to either unshod or shod for days 2 and 3. We analyzed the data with a 2-way (condition by intensity) repeated measures ANOVA. Submaximal oxygen consumption was significantly reduced at 85% of VO2max (P = 0.018), indicating an improvement in RE, but not during the 65% or 75% trials (P > 0.05, both). No other dependent measure was different between unshod and shod conditions. Our results indicate that the immediate improvement to RE while barefoot occurs at a relatively high fraction of maximal oxygen consumption. For the recreational or competitive distance runner, training or competing while barefoot may be a useful strategy to improve endurance performance.
For exercise modalities such as cycling which recruit a substantial muscle mass, muscle oxygen uptake (V̇O2) is the primary determinant of pulmonary V̇O2. Indeed, the kinetic complexities of pulmonary V̇O2 associated with exercise onset and the non-steady states of heavy (>lactate threshold) and severe [>asymptote of power-time relationship for high intensity exercise (Ẇ)] exercise reproduce with close temporal and quantitative fidelity those occurring across the exercising muscles. For moderate (<lactate threshold) exercise and also rapidly incremental work tests, pulmonary (and muscle) V̇O2 increases as a linear function of work rate (≈9 to 11 ml O2/W/min) in accordance with theoretical determinations of muscle efficiency (≈30%). In contrast, for constant load exercise performed in the heavy and severe domains, a slow component of the V̇O2 response is manifest and pulmonary and muscle V̇O2 increase as a function of time as well as work rate beyond the initial transient associated with exercise onset.
In these instances, muscle efficiency is reduced as the V̇O2 cost per unit of work becomes elevated, and in the severe domain, this V̇O2 slow component drives V̇O2 to its maximum and fatigue ensues rapidly. At pulmonary maximum oxygen uptake (V̇O2max) during cycling, the maximal cardiac output places a low limiting ceiling on peak muscle blood flow, O2 delivery and thus muscle V̇O2. However, when the exercise is designed to recruit a smaller muscle mass (e.g. leg extensors, 2 to 3kg), mass-specific muscle blood flow and V̇O2 at maximal exercise are 2 to 3 times higher than during conventional cycling. Consequently, for any exercise which recruits more than ≈5 to 6kg of muscle at pulmonary V̇O2max there exists a mitochondrial or V̇O2 reserve capacity within the exercising muscles which cannot be accessed due to oxygen delivery limitations. The implications of these latter findings relate to the design of exercise tests. Specifically, if the purpose of exercise testing is to evaluate the oxidative capacity of a small muscle mass (<5 to 6kg), the testing procedure should be designed to restrict the exercise to those muscles so that a central (cardiac output, muscle O2 delivery) limitation is not invoked. It must be appreciated that exercise which recruits a greater muscle mass will not stress the maximum mass-specific muscle blood flow and V̇O2 but rather the integration of central (cardiorespiratory) and peripheral (muscle O2 diffusing capacity) limitations.
Purpose.
The aim of this review is to make a critical analysis of the operational concepts associated with aerobic endurance, presented as direct and indirect methods.
Current knowledge and key points.
Aerobic endurance is the capacity to maintain a high fraction of the maximal oxygen uptake (VO2max) during a long period of time. In so far as it is a determinant of the performance in long-distance events, and is independant of VO2max, aerobic endurance has to be assessed with specific tools.
Future prospects and projects.
The operational concepts associated with aerobic endurance are numerous, but most of them provide a partial description of the phenomenon. Direct methods allow one to observe the reduction of the fraction of utilisation of VO2max with time, but the equations proposed in the literature don't give individual values. Indirect methods allow this possibility, but their accuracy is not sufficient to optimise the choice of training intensities.
In 1967, Margaria and coworkers presented results showing that blood lactate levels never increased during submaximal constant load exercises when the V02 steady state was reached (Saiki et al. 1967). The aim of the present study was to verify whether blood lactate steady state (LA = O) occurred at exercise intensity close to maximal aerobic power as found by Margaria et al (1963) with only two subjects. Ten physically active but untrained subjects randomly performed three 30-min constant load treadmill exercises at running speeds corresponding to 90% VO2max, or 0.5 km·h−1 below or above that intensity. Blood samples (ear lobe) were taken every 5 min (exercise was stopped) during, the 30-min exercises. Individual time course of blood lactate levels between the first 10 or 15 minutes and the following minutes showed 3 patterns of blood lactate level changes: LA = O, or decreased (LA < O) and increased (LA > O) blood lactate levels. Four subjects exhibited LA < 0 at 10. 9 ± 1.6 km·h−1 or 90.1 ± 4.9% VO2max (table I and fig 1). LA = 0 was found in 9 subjects at 11.8 ± 1.4 km·h−1 or 90.3 ± 4.6% VO2max (table 1 and fig 1). LA > 0 (> 0.5 mmol·L−1) was found in 8 subjects at 12.7 ± 1.3 km·h−1 92.2 ± 3.9% de V02 max (table 1 and fig 1). With our experimental conditions, we showed that LA = 0 (fig 2) was found in untrained subjects at an exercise intensity higher than usually shown in the literature (60–80% VO2max; Oyono-Enguelle et al, 1990; Billat et al, 1994) but not as high as Margaria found some thirty years ago (90–100% VO2max; Saiki et al. 1967).
Elevated oxygen uptake (V˙O2) during moderate-intensity running following a bout of interval running training has been studied previously. To further investigate this phenomenon, the V˙O2 response to high-intensity exercise was examined following a bout of interval running. Well-trained endurance runners were split into an experimental group [maximum oxygen uptake, V˙O2max
4.73 (0.39) l · min−1] and a reliability group [V˙O2max
4.77 (0.26) l · min−1]. The experimental group completed a training session (4 × 800 m at 1 km · h−1 below speed at V˙O2max
, with 3 min rest between each 800-m interval). Five minutes prior to, and 1 h following the training session, subjects completed 6 min 30 s of constant speed, high-intensity running designed to elicit 40% Δ (where Δ is the difference between V˙O2 at ventilatory threshold and V˙O2max
; tests 1 and 2, respectively). The slow component of V˙O2 kinetics was quantified as the difference between the V˙O2 at 6 min and the V˙O2 at 3 min of exercise, i.e. ΔV˙O2(63). The ΔV˙O2(63) was the same in two identical conditions in the reliability group [mean (SD): 0.30 (0.10) l · min−1 vs 0.32 (0.13) l · min−1]. In the experimental group, the magnitude of the slow component of V˙O2 kinetics was increased in test 2 compared with test 1 by 24.9% [0.27 (0.14) l · min−1 vs 0.34 (0.08) l · min−1, P < 0.05]. The increase in ΔV˙O2(63) in the experimental group was observed in the absence of any significant change in body mass, core temperature or blood lactate concentration, either at the start or end of tests 1 or 2. It is concluded that similar mechanisms may be responsible for the slow component of V˙O2 kinetics and for the fatigue following the training session. It has been suggested previously that this mechanism may be linked primarily to changes within the active limb, with the recruitment of alternative and/or additional less efficient fibres.
El Umbral Anaerobio (UAn) viene siendo un tema de permanente actualidad desde que Wasserman y McIlroy acuñaron el término en 1964, debido a su indudable importancia en el ámbito de las ciencias de la educación física y el deporte y de la medicina clínica, y a la controversia existente en relación con el concepto, la terminología utilizada y los métodos empleados para su determinación. Partiendo de la hipótesis de que la mayoría de definiciones dadas hasta ahora del UAn son operacionales y no conceptuales, y de que los diferentes umbrales propuestos no son sino diferentes efectos producidos por una misma causa, hemos planteado el presente trabajo con los principales objetivos de: 1) separar y diferenciar en el tiempo a través de un trabajo incremental (ergoforesis) la mayor parte de los umbrales lácticos, ventilatorios y cardiovasculares propuestos en la literatura científica; 2) intentar determinar su origen común; 3) ajustar la terminología; y 4) comprobar el grado de relación existente entre los umbrales y la percepción del esfuerzo realizado. Los resultados de nuestro trabajo han mostrado que: 1) los diferentes UAn no tienen ninguna relación causa efecto entre ellos y que, por tanto, son diferentes manifestaciones procedentes de un origen común; 2) el origen de dichas manifestaciones reside en el aumento de la tasa glucolítica; 3) el término umbral anaerobio probablemente no refleja lo acontecido durante un ejercicio incremental; y 4) no existe una buena relación entre los umbrales ventilatorios 1 y 2 y la sensación percibida del esfuerzo realizado.
De acuerdo con la literatura científica, la frecuencia del acortamiento de los isquiotibiales, está relacionado con factores genéticos, hábitos diarios y actividades deportivas. Sin embargo, con las numerosas metodologías de tratamiento propuestas en la literatura se hace difícil establecer cuál de ellas resulta ser la más efectiva. En este trabajo se llevó a cabo meta-análisis sobre la eficacia de los tratamientos para la ganancia de flexibilidad en los músculos isquiotibiales. La búsqueda de la literatura permitió identificar 41 estudios, 39 publicados y 2 no publicados, entre 1930 y 2007, que cumplieron con los criterios de inclusión, totalizando 85 comparaciones entre grupo tratado y control. El índice del tamaño del efecto utilizado fue la diferencia de medias estandarizada. Los tratamientos obtuvieron una efectividad estadísticamente significativa (d+ = 1,054). El estiramiento muscular, más la combinación de estiramiento más calentamiento resultaron ser los tratamientos más efectivos. La relación entre el tamaño del efecto con las demás variables de tratamiento, de sujeto, metodolíogicas y extrínsecas, también fueron examinadas. El sesgo de publicación no fue una amenaza contra la validez de los resultados. Los tratamientos son más eficaces cuando: son empleados en sujetos del género femenino; cuanto más jóvenes sean los sujetos; y cuando se utiliza un número mayor de semanas de tratamiento. SUMMARY According to the scientific literature, the frequency of the shortened hamstring, is related to genetic factors, daily habits and sports activities. In spite of the found treatment methodologies diversity is difficult to establish which of them is more effective. In this paper we carried out a meta-analysis about the efficacy of the treatment for the increase the flexibility in the hamstring muscle. The searched of the literature enabled us identify 41 studies, 39 published and 2 no published, between 1930 and 2007, that fulfilled our the selection criteria, giving a total 85 comparisons between a treated an a control group. The effect size index was the standardized mean difference in the posttest. The treatments obtained a statistically significant effectiveness (d+ = 1,054). The stretching and stretching plus warming -up resulted to be the treatment more effective. The relationship of others treatment, subjects, methodological and extrinsic variables with the effect size were also examined. The publication bias was not a threat against the validity of the results. The treatments are more efficient when: they are applied in subjects of the feminine gender; the more young be the subjects and when a greater number of weeks of treatment are utilized
Five male subjects performed three successive incremental work tests on an electronically braked cycle ergometer. The first and second tests were separated by thirty minutes of rest, the second and third by three minutes of maximum work. During the third test, venous blood lactate concentrations were still decreasing at work rates where they were increasing during the first two tests. The work rate at which rapid increases in lactate concentrations occurred during the final test coincided with the work rate where rapid increases occurred in the two initial tests. It was concluded that this point represented a threshold where a balance existed between removal and release of lactate from and into the plasma compartment, and did not coincide with the anaerobic threshold. It is postulated that steady state work at levels above this threshold would result in a continuous increase in venous lactate concentration.
Seven untrained male subjects were studied for the effects of mild warm-up on oxygen uptake and lactic acid production. Each subject completed two standardized workloads on a bicycle ergometer requiring 75% of their physical work capacity. Protocols of the two tests consisted of either no warm-up or a 4-min warm-up preceding a 5-min exercise at approximately 80% of their maximal oxygen uptake.
The contrasting protocols did not reveal any significant differences between heart rate, lactic acid, and oxygen uptake. The dominant influence on the metabolic processes was the absolute workload of the tasks and not the presence or absence of preliminary related activity. It was concluded that an untrained individual lacks the cardiovascular and cellular adaptations necessary to demonstrate metabolic benefits from warm-up.
To determine whether the activity of playing squash is sufficiently intense to promote and/or maintain cardiovascular fitness, the heart rate response of ten male subjects (aged 20 to 53 years), was monitored continuously via radio telemetry for a 45-minute playing session. The mean heart rate for the total time of play was determined and intensity was calculated using the Karvonen method of potential heart rate. Maximum heart rate was determined with a continuous, graded bicycle ergometer test. Prior to and 5 minutes after squash play, fingertip blood samples were obtained for lactate analysis. The mean heart rate intensity of squash play was 77.2 ± 6.1 %. Intensities as high as 96% were recorded for 5-minute periods during the playing session. The average game heart rate was attained by the 10th minute of play. Thereafter, a heart rate fluctuation of only six beats was observed for the remaining 35 minutes. Postexercise lactate concentrations ranged from 11 to 57 mg% with a mean of 24.5 ± 13.8 mg%. The ball was in play 58% of the time with an average of 10.9 hits per minute. It was concluded that playing squash is an activity that results in heart rate responses of sufficient intensity to elicit aerobic training effects and does not produce high lactic acid concentrations.
The tolerable work duration (t) for high-intensity cycling is well described as a hyperbolic function of power (W): W = (W'.t-1) + Wa, where Wa is the upper limit for sustainable power (lying between maximum W and the threshold for sustained blood [lactate] increase, theta lac), and W' is a constant which defines the amount of work which can be performed greater than Wa. As training increases the tolerable duration of high-intensity cycling, we explored whether this reflected an alteration of Wa, W' or both. Before and after a 7-week regimen of intense interval cycle-training by healthy males, we estimated ( ) theta lac and determined maximum O2 uptake (mu VO2); Wa; W'; and the temporal profiles of pulmonary gas exchange, blood gas, acid-base and metabolic response to constant-load cycling at and above Wa. Although training increased theta lac (24%), mu VO2 (15%) and Wa (15%), W' was unaffected. For exercise at Wa, a steady state was attained for VO2, [lactate] and pH both pre- and post-training, despite blood [norepinephrine] and [epinephrine] ([NE], [E]) and rectal temperature continuing to rise. For exercise greater than Wa, there was a progressive increase in VO2 (resulting in mu VO2 at fatigue), [lactate], [NE], [E] and rectal temperature, and a progressive decrease for pH. We conclude that the increased endurance capacity for high-intensity exercise following training reflects an increased W asymptote of the W-t relationship with no effect on its curvature; consequently, there is no appreciable change in the amount of work which can be performed above Wa.(ABSTRACT TRUNCATED AT 250 WORDS)
Exercise performed above the lactate threshold (OLa) produces a slowly-developing phase of oxygen uptake (VO2) kinetics which elevates VO2 above that predicted from the sub-OLa VO2-work rate relationship. This phenomenon has only been demonstrated, to date, in subjects who were relatively homogeneous with respect to fitness. This investigation therefore examined whether this behaviour occurred at a given absolute VO2 or whether it was a characteristic of supra-OLa exercise in a group of subjects with over a threefold range of OLa (990-3000 ml O2.min-1) and peak VO2 (1600-5260 ml O2.min-1). Twelve healthy subjects performed: 1) exhausting incremental cycle ergometer exercise for estimation of OLa (OLa) and peak VO2, and 11) a series of constant-load tests above and below OLa for determination of the VO2 profile and efficiency of work. During all tests expired ventilation, VO2 and carbon dioxide production were monitored breath-by-breath. The efficiency of work determined during incremental exercise (28.1 +/- 0.7%, means +/- SE, n = 12) did not differ from that determined during sub-OLa constant-load exercise (27.4 +/- 0.5%, p greater than 0.05). For constant-load exercise, VO2 rose above that predicted, from the sub-OLa VO2-work rate relationship, for all supra-OLa work rates. This was evident above 990 ml O2.min-1 in the least fit subject but only above 3000 ml O2.min-1 in the fittest subject. As a consequence the efficiency of work was reduced from 27.4 +/- 0.5% for sub-OLa exercise to 22.6 +/- 0.4% (p less than 0.05) at the lowest supra-OLa work rate (i.e. OLa + 20 W, on average).(ABSTRACT TRUNCATED AT 250 WORDS)
The oxygen uptake kinetics during constant-load exercise when sitting on a bicycle ergometer were determined in 7 untrained subjects by measuring breath-by-breath\(\dot V_{{\text{O}}_{\text{2}} } \) during continuous exercise to volitional exhaustion (mean endurance time=1160±172 s) at a pedal frequency of 70 revolutions · min−1. The power output, averaging 189,5 W, was set at 82.5% of that eliciting the individual\(\dot V_{{\text{O}}_{{\text{2}} {\text{max}}} } \) during a 5 min incremental exercise test. Throughout the exercise period, the\(\dot V_{{\text{O}}_{\text{2}} } \) kinetics could be appropriately described by a two-component exponential equation of the form:$$\dot V_{{\text{O}}_{\text{2}} } (t) = Y_a [1 - \exp ( - k_a t)] + Y_b [1 - \exp ( - k_b t)]$$ where\(\dot V_{{\text{O}}_{\text{2}} } \) is net oxygen consumption andt the time from work onset.\(\dot V_{{\text{O}}_{\text{2}} } \) measured at the end of exercise was close to\(\dot V_{{\text{O}}_{{\text{2}} {\text{max}}} } \) (98%\(\dot V_{{\text{O}}_{{\text{2}} {\text{max}}} } \)) and the mean values ofY
a
,k
a
,Y
b
andk
b
amounted to 1195 ml O2 · min−1, 0.034s−1, 1562 ml O2 · min−1, and 0.005 s−1 respectively. The initial rate of increase in\(\dot V_{{\text{O}}_{\text{2}} } \) predicted from the above equation is slower than that calculated, for the same work intensity, on the basis of the data obtained by Morton (1985) in trained subjects. For t>480 s, however, the two models yield substantially equal results.
To compare the results obtained by incremental or constant work load exercises in the evaluation of endurance conditioning, a 20-week training programme was performed by 9 healthy human subjects on the bicycle ergometer for 1 h a day, 4 days a week, at 70-80% VO2max. Before and at the end of the training programme, (1) the blood lactate response to a progressive incremental exercise (18 W increments every 2nd min until exhaustion) was used to determine the aerobic and anaerobic thresholds (AeT and AnT respectively). On a different day, (2) blood lactate concentrations were measured during two sessions of constant work load exercises of 20 min duration corresponding to the relative intensities of AeT (1st session) and AnT (2nd session) levels obtained before training. A muscle biopsy was obtained from vastus lateralis at the end of these sessions to determine muscle lactate. AeT and AnT, when expressed as % VO2max, increased with training by 17% (p less than 0.01) and 9% (p less than 0.05) respectively. Constant workload exercise performed at AeT intensity was linked before training (60% VO2max) to a blood lactate steady state (4.8 +/- 1.4 mmol.l-1) whereas, after training, AeT intensity (73% VO2max) led to a blood lactate accumulation of up to 6.6 +/- 1.7 mmol.l-1 without significant modification of muscle lactate (7.6 +/- 3.1 and 8.2 +/- 2.8 mmol.kg-1 wet weight respectively). It is concluded that increase in AeT with training may reflect transient changes linked to lower early blood lactate accumulation during incremental exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
This study investigated the relationship of individual anaerobic thresholds to oxygen debt. Anaerobic threshold speed (VTAM) was determined for 21 male university students using a continuous ramp treadmill protocol. The onset of anaerobiosis was determined by visual inspection of excess CO2 elimination. The following week, all subjects ran at the treadmill speed 3.3 m.sec-1 for 10 minutes (this speed split the group into two halves). Recovery oxygen consumption was monitored after this run. Application of double exponential equations by computer and subsequent integration was used to calculate total, alactic, and lactic oxygen debts. Subjects who ran above their VTAM (group L-VTAM) had significantly (p less than .05) higher total, lactic and alactic debts compared to subjects who ran below their VTAM (group H-VTAM). The total debt demonstrated a significant (p less than .05) negative correlation (r = .77) to VTAM in group L-VTAM. This appears to be due to increasing lactic debt, that was also significantly (p less than .05) negatively correlated (r = -.73) to VTAM. Group H-VTAM did not exhibit this characteristic. This study demonstrates that VTAM, as determined by excess CO2 elimination, is a critical factor in determining oxygen debt and therefore, work above this point (which results in the onset of metabolic acidosis) may limit the optimal running speed for a given distance.
Blood lactate concentration (LA) was measured in 4 female and 3 male well-trained subjects before and during 30 min of continuous treadmill running at 4 different speeds, demanding about 30, 60, 70 and 80% of the individuals' maximal oxygen uptake (Vo2 max). The same subjects also performed in another series of experiments where maximal intermittent exercise preceded 30 min of running at the same 4 speeds, or resting in a chair. During continuous running, starting from resting conditions, the blood LA increased only slightly up to a critical Ievel (i.e. 60—80%) of Vo2-max. From then on, a pronounced lactate production may occur. During the maximal intermittent exercise, blood LA increased to 130—220 mg/100 ml. In the recovery period, i.e. continuous running at the same 4 speeds, or resting in a chair, blood LA decreased towards resting values. The lactate removal rate was calculated from the rectilinear part of the curves describing the changes in LA with time, and expressed as mg/100 ml X min. The lactate removal rate was higher during exercise than during rest, and increased with increasing work load up to the same critical level (i.e. 60—80% of Vo2 max), beyond which a reduction was observed. The highest removal rate was 8 mg lactate/100 ml x min at 63% of Vo2 max (average values). These results indicate that human skeletal muscle possesses a pronounced capacity to oxidize lactate. Therefore, a production of lactate is possible even with no increase in the blood LA. These results also indicate that the skeletal muscle, rather than the liver, may be regarded as the main site for lactate removal during exercise.
The purpose of this study was to determine if pace changes similar to those experienced in competition could affect the relative contribution of aerobic and anaerobic processes to overall energy utilization during running. In particular, does a fast start in the mile race increase the energy supplied aerobically during the first three-quarters of a mile such that the lactate formation is reduced prior to the usual rapid last quarter? Eight subjects (middle and long distance runners) ran three-quarters of a mile on a treadmill according to a fast-medium-very slow (F-M-S) and a slow-medium-slow pace. The two paces were performed in a random order and the total running times were equal. No significant differences were found between the two paces for oxygen uptake during the runs, for the 15-min recovery oxygen and for the post-exercise peak lactate values. Although several world class milers have employed a fast-medium-slow-fast pace, the present data concerning the relative contribution of different energy sources do not explain why this might be the best pacing technique.
During this study the relationships between venous lactate concentration and accociated changes in respiratory gas exchange were investigated. Five men performed two successive incremental exercise tests to exhaustion on an electronically braked cycle ergometer. These tests were separated by a 5 min rest period. During the initial test venous lactate concentrations showed a characteristic curvilinear increase and the anaerobic threshold (AT1) was determined conventionally. During the second test lactate concentrations were still decreasing at higher work rates than the AT1, and a second anaerobic threshold (AT2) was determined as the point where lactate concentrations again increased. The departure from linearity of the ventilatory response to both exercise tests occurred at a similar work rate, irrespective of whether venous lactate concentrations were increasing or decreasing. Carbon dioxide production was similar during the two exercise tests. The anaerobic thresholds as determined by respiratory gas analysis (ATR) were therefore similar for both tests. Results of this study indicate that changing venous lactate concentrations were not responsible for the ventilatory drive which occurred at the ATR. The venous lactate response to work at a constant rate determined within the range AT1-AT2 was also investigated. It was concluded that the lactate response to constant work rate will vary predictably at work rates falling within the AT1 to AT2 range. At AT1 no increase in venous lactate concentrations occurred, while at AT2 these increased progressively, and the test was terminated at varying times (12-15 min) due to subject exhaustion. At work rates determined from the ATR venous lactate concentrations varied according to the placement of the ATR within the AT1 AT2 range.
This study investigated the effect of exercise duration on the response dynamics of oxygen consumptionVO2, carbon dioxide outputVCO2, ventilation VE), and cardiac frequency (f
c) following stepped changes in exercise intensity, by manipulating the duration of the pretransition exercise period. A group of 11 healthy men performed a stepped exercise intensity cycling protocol on three separate occasions, each consisting of a stepped increase from 55% to 65% peak oxygen consumptionVO2,peak of 6-min duration, followed by a stepped decrease to 55%VO2,peak of 10-min duration. This stepped protocol was preceded by either 5, 15, or 60 min of cycling at 55%VO2,peak. The response times for each variable were calculated at 10% increments between the prestep baselines and poststep plateaux. Following the stepped increase, the response times forVO2 at the 50%, 60%, 70%, 80%, and 90% relative increments were significantly reduced in the 60-min condition compared to the 15-min condition (P< 0.05); however, the response times forVCO2 andf
c were not significantly altered across the three conditions. No significant differences were found in the response times forVO2,VCO2 andf
c, across the three conditions following the stepped decrease in exercise intensity. It was concluded that the faster response time of aerobic metabolism to a stepped increase in exercise intensity was mediated by increases in active muscle temperature, leading to improved oxygen utilisation.
The aim of the present study was to estimate the importance of lactate steady state velocity (WCL) of the running velocity at maximal oxygen uptake (Va max) and its time to exhaustion (Tlim), in the performance of a half marathon stated by the velocity over 21.1 km sustained by the runners during 1 h 12 min +/- 2 min 27 s. The population consisting of ten sub-elite male long distance runners (32 +/- 4 years old) was homogeneous with regard to their velocities on 21 km (V21 = 17.5 +/- 0.88 km.h-1, coefficient of variation, CV = 5%) and their aerobic maximal speed (Va max) (21.6 +/- 1.2 km.h-1, CV 6%). The fractional utilization of VO2max on 21 km was calculated from their own running economy (oxygen consumed per kilo of body mass and kilometer run (194 +/- 74 ml.kg-1.km-1). V21 represented 83 +/- 5% VO2max (VO2max = 68.1 +/- 4.1 ml.kg-1.min-1) and 81 +/- 3.3% Va max. The velocity corresponding to lactate steady state and called "lactate steady state velocity" (WCL) was measured according to a protocol proposed by CHASSAIN (1986). The subjects ran twenty minutes at a constant velocity representing 70-75% and 85-90% VO2max. Lactatemia was measured at the fifth (Lact 5) and the twentieth minute (Lact 20). Lactate slope was measured for two running velocities in order to determine the velocity (WCL) corresponding to lactate steady state, i.e. the lactate slope is equal to zero.(ABSTRACT TRUNCATED AT 250 WORDS)
The aim of this study was to estimate the characteristic exercise intensity (WCL) which produces the maximal steady state of blood lactate concentration (MLSS) from submaximal intensities of 20 min carried out on the same day and separated by 40 min. Ten fit male adults [maximal oxygen uptake (VO2max) 62 (SD 7) ml.min-1.kg-1] exercised for two 30-min periods on a cycle ergometer at 67% (test 1.1) and 82% of VO2max (test 1.2) separated by 40 min. They exercised 4 days later for 30 min at 82% of VO2max without prior exercise (test 2). Blood lactate was collected for determination of lactic acid concentration every 5 min and heart rate and O2 uptake (VO2) were measured every 30 s. There were no significant differences at the 5th, 10th, 15th, 20th, 25th, or 30th min between VO2, lactacidaemia, and heart rate during tests 1.2 and 2. Moreover, we compared the exercise intensities (WCL) which produced the MLSS obtained during tests 1.1 and 1.2 or during tests 1.1 and 2 calculated from differential values of lactic acid blood concentration ([la-]b) between the 30th and the 5th min or between the 20th and the 5th min. There was no significant difference between the different values of WCL [68 (SD 9), 71 (SD 7, 73 (SD 6), 71 (SD 11)% of VO2max] (ANOVA test, P < 0.05). Four subjects ran for 60 min at their WCL determined from periods performed on the same day (test 1.1 and 1.2) and the difference between the [la-]b at 5 min and at 20 min (delta ([la-]b)) was computed.(ABSTRACT TRUNCATED AT 250 WORDS)
Laboratory and field assessments were made on eighteen male distance runners. Performance data were obtained for distances of 3.2, 9.7, 15, 19.3 km (n = 18) and the marathon (n = 13). Muscle fiber composition expressed as percent of slow twitch fibers (%ST), maximal oxygen consumption (VO2max), running economy (VO2 for a treadmill velocity of 268 m/min), and the VO2 and treadmill velocity corresponding to the onset of plasma lactate accumulation (OPLA) were determined for each subject. %ST (R > or equal to .47), VO2max (r > or equal to .83), running economy (r > or equal to .49), VO2 in ml/kg min corresponding to the OPLA (r > or equal to .91) and the treadmill velocity corresponding to OPLA (r > or equal to .91) were significantly (p < .05) related to performance at all distances. Multiple regression analysis showed that the treadmill velocity corresponding to the OPLA was most closely related to performance and the addition of other factors did not significantly raise the multiple R values suggesting that these other variables may interact with the purpose of keeping plasma lactates low during distance races. The slowest and fastest marathoners ran their marathons 7 and 3 m/min faster than their treadmill velocities corresponding to their OPLA which indicates that this relationship is independent of the competitive level of the runner. Runners appear to set a race pace which allows the utilization of the largest possible VO2 which just avoids the exponential rise in plasma lactate.
The purpose of this investigation was to determine the effects of increasing specific (rowing ergometer) and non-specific (cycle ergometer) workloads on parameters relating to the ventilatory threshold (Tvent) and work efficiency. When highly trained male rowers were tested using non-specific workloads, their %VO2 max values at Tvent were close to those characteristic of untrained subjects (74.6 +/- 6.2% VO2 max). However, when we tested the same subjects using specific workloads, we recorded values typical of highly trained athletes (85.0 +/- 4.4% VO2 max). For the non-specific exercise on the cycle ergometer, we recorded work efficiency values close to those of untrained subjects (22.8 +/- 2.1%); however, for the specific exercise on the rowing ergometer, we recorded much lower values (16.4 +/- 3.1%). Because of the results of the non-specific submaximal exercise tests, we suggest caution in the interpretation of physiological variables that may be sensitive to training status. The evaluation of Tvent and work efficiency as supplementary parameters during laboratory studies will enable researchers to ascertain the effectiveness of the training process used, as well as indicating the specificity of the loading apparatus.
The purpose of this study was to measure the running velocity corresponding to the individual maximal lactate steady-state of a group of 12-year old boys and girls on a treadmill. This running velocity (v MLST) was compared with the maximal aerobic running velocity (v a max) at which maximal oxygen uptake (VO2 max) occurs. Thirteen pupils of the same school whose puberal maturation corresponded to the end of stage 2 and the beginning of stage 3 of Tanner: 6 boys (12.2 years old +/- 0.5, 38.4 +/- 2 kg, 150 +/- 4.8 cm: group 1) and 7 girls (12.3 years old +/- 0.5, 37.6 +/- 6 kg, 151.4 +/- 5.6 cm: group 2) carried out two tests at one week interval. The first test was a maximal incremental test for the determination of VO2 max with Douglas's bag method and v a max. The purpose of the second test was the determination of maximal lactate steadystate velocity (v MLST) With two stages of ten minutes at 60 +/- 5% and 74 +/- 4.5% v a max separated by 40 minutes of complete rest (Billat, 1992); VO2max and v a max were significantly different, equal to 49.4 +/- 7 ml.min-1.kg-1, 40.4 +/- 4.7 ml.min-1.kg-1 and 12.6 +/- 0.2 km.h-1, 11.2 +/- 1.2 km.h-1 for group 1 and 2 respectively (P < 0.05). Moreover, maximal lactate steady state velocity (v MLST) was respectively equal to 64.8 +/- 12.5% and 64.6% +/- 12.5% VO2 max respectively, representing 67.8 +/- 6.2% and 68.8% +/- 8.3% v a max and was not significantly different for group 1 and 2. In conclusion, this study shows that maximal lactate steady-state velocity is not significantly different between young boys and girls of 12 years old, when expressed in fraction of VO2 max or v a max. However, VO2 max and v a max were significantly higher in boys: +27.2 and +11.6% higher respectively.
Muscular exercise requires transitions to and from metabolic rates often exceeding an order of magnitude above resting and places prodigious demands on the oxidative machinery and O 2-transport pathway. The science of kinetics seeks to characterize the dynamic profiles of the respiratory, cardiovascular, and muscular systems and their integration to resolve the essential control mechanisms of muscle energetics and oxidative function: a goal not feasible using the steady-state response. Essential features of the O 2 uptake (˙ V O 2) kinetics response are highly conserved across the animal kingdom. For a given metabolic demand, fast ˙ V O 2 kinetics mandates a smaller O 2 deficit, less substrate-level phosphorylation and high exercise tolerance. By the same token, slow ˙ V O 2 kinetics incurs a high O 2 deficit, presents a greater challenge to homeostasis and presages poor exercise tolerance. Compelling evidence supports that, in healthy individuals walking, running, or cycling upright, ˙ V O 2 kinetics control resides within the exercising muscle(s) and is therefore not dependent upon, or limited by, upstream O 2-transport systems. However, disease, aging, and other imposed constraints may redistribute ˙ V O 2 kinetics control more prox-imally within the O 2-transport system. Greater understanding of ˙ V O 2 kinetics control and, in particular, its relation to the plasticity of the O 2-transport/utilization system is considered important for improving the human condition, not just in athletic populations, but crucially for patients suffering from pathologically slowed ˙ V O 2 kinetics as well as the burgeoning elderly population. C 2012 American Physiological Society. Compr Physiol 2:933-996, 2012.
Time over a distance, i.e. speed, is the reference for performance for all events whose rules are based on locomotion in different mechanical constraints. A certain power output has to be maintained during a distance or over time. The energy requirements and metabolic support for optimal performance are functions of the length of the race and the intensity at which it is completed. However, despite the complexity of the regulation of lactate metabolism, blood lactate measurements can be used by coaches for prediction of exercise performance.
The anaerobic threshold, commonly defined as the exercise intensity, speed or fraction of maximal oxygen uptake (V̇O2max) at a fixed blood lactate level or at a maximal lactate steady-state (MLSS), has been accepted as a measure of the endurance. The blood lactate threshold, expressed as a fraction of the velocity associated with V̇O2max, depends on the relationship between velocity and oxygen uptake (V̇O2). The measurement of the post-competition blood lactate in short events (lasting 1 to 2 minutes) has been found to be related to the performance in events (400 to 800m in running). Blood lactate levels can be used to assist with determining training exercise intensity. However, to interpret the training effect on the blood lactate profile, the athlete’s nutritional state and exercise protocol have also to be controlled. Moreover, improvement of fractional utilisation of V̇O2max at the MLSS has to be considered among all discriminating factors of the performance, such as the velocity associated with V̇O2max.
The purpose of the present study was to measure the time-course and degree of cardiovascular and respiratory 'drift' during constant submaximal exercise in the horse. One Thoroughbred and four Morgan mares were instrumented for simultaneous measurement of respiratory and blood gases which also enabled cardiac output (Q) to be calculated. Data were collected at rest, and at 10, 20 and 30 mins during a constant workload which elicited an initial exercising heart rate (HR) of 150 beats/min, and an approximate 15-fold increase in oxygen consumption (VO2). Significant cardiac and respiratory drift during exercise were observed over time so that ventilation increased from 750 +/- 58 to 910 +/- 49 litres/min (21 per cent increase) from the 10 to 30 min time-point (P < 0.05) and HR went from 154 +/- 4 to 173 +/- 9 beats/min (mean +/- se) over the same time period (P < 0.05). Q also rose from 142 +/- 5 to 177 +/- 17 litres/min (P < 0.05) during the same interval while stroke volume (SV) was maintained. Rectal temperature (TR) and mixed venous lactate (LA) also showed significant increases during exercise while PaO2 and PaCO2 remained constant. The results indicate a significant degree of cardiac and respiratory drift in the horse in response to strenuous submaximal exercise. At the constant exercise work rate chosen, a levelling off, or plateauing of the selected parameters of interest was not observed. Therefore if a true exercising 'steady-state' was achieved, it must have occurred very early in the exercise bout.
For exercise modalities such as cycling which recruit a substantial muscle mass, muscle oxygen uptake (VO2) is the primary determinant of pulmonary VO2. Indeed, the kinetic complexities of pulmonary VO2 associated with exercise onset and the non-steady state of heavy (> lactate threshold) and severe [> asymptote of power-time relationship for high intensity exercise (W)] exercise reproduce with close temporal and quantitative fidelity those occurring across the exercising muscles. For moderate (< lactate threshold) exercise and also rapidly incremental work tests, pulmonary (and muscle) VO2 increases as a linear function of work rate (approximately equal to 9 to 11 ml O2/W/min) in accordance with theoretical determinations of muscle efficiency (approximately equal to 30%). In contrast, for constant load exercise performed in the heavy and severe domains, a slow component of the VO2 response is manifest and pulmonary and muscle VO2 increase as a function of time as well as work rate beyond the initial transient associated with exercise onset. In these instances, muscle efficiency is reduced as the VO2 cost per unit of work becomes elevated, and in the severe domain, this VO2 slow component drives VO2 to its maximum and fatigue ensues rapidly. At pulmonary maximum oxygen uptake (VO2max) during cycling, the maximal cardiac output places a low limiting ceiling on peak muscle blood flow, O2 delivery and thus muscle VO2. However, when the exercise is designed to recruit a smaller muscle mass (e.g. leg extensors, 2 to 3kg), mass-specific muscle blood flow and VO2 at maximal exercise are 2 to 3 times higher than during conventional cycling. consequently, for any exercise which recruits more than approximately equal to 5 to 6kg of muscle at pulmonary VO2max, there exists a mitochondrial or VO2 reserve capacity within the exercising muscles which cannot be accessed due to oxygen delivery limitations. The implications of these latter findings relate to the design of exercise tests. Specifically, if the purpose of exercise testing is to evaluate the oxidative capacity of a small muscle mass (< 5 to 6kg), the testing procedure should be designed to restrict the exercise to those muscles so that a central (cardiac output, muscle O2 delivery) limitation is not invoked. It must be appreciated that exercise which recruits a greater muscle mass will not stress the maximum mass-specific muscle blood flow and VO2 but rather the integration of central (cardiorespiratory) and peripheral (muscle O2 diffusing capacity) limitations.
To examine the effects of 6 weeks of exercise training above or below the lactate threshold (LT) on the slow component (SC) of pulmonary oxygen consumption (.VO(2)).
Randomized controlled trial.
University human performance laboratory.
Apparently healthy, untrained men (n = 18).
Subjects were randomized to one of three groups: high-intensity exercise training (HI) [above the LT], moderate-intensity exercise training (MOD) [below the LT], or no exercise training (CON). Exercise groups performed cycle ergometry 4 d/wk for 6 weeks. Total work throughout training was constant between groups.
Maximal cycle ergometry was performed at baseline and after training to assess power output at the LT (WLT), .VO(2) at the LT (.VO(2)LT), and peak .VO(2) (.VO(2)PK). High-intensity, constant-load cycling was performed at baseline and weeks 1, 2, 4, and 6 to assess SC adaptations. WLT, .VO(2)LT, and .VO(2)PK increased after 6 weeks in both exercise groups compared to the CON group (p < 0.05), although there were no differences between the training groups. SC of .VO(2) decreased 44% in the HI group following 1 week of exercise training vs MOD (20%, p < 0.05) and CON (12%, p < 0.01) groups. The SC attenuation was more prominent at all time points in the HI group compared to the MOD group. Total SC attenuation over the 6-week training period did not differ between the HI (71%) and MOD (57%) groups.
Training at HI or MOD produced similar improvements in the LT, .VO(2), and power output at peak exertion when total work output was held constant. Attenuation of the SC with training above and below the LT were similar, although above-LT training promoted faster SC adaptations.
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