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Fold change from pre-exercise rest in PGC-1α mRNA at 4 h after exercise at the pre-training and post-training time-points. *p < 0.05 from pre-exercise (1.00 fold change). †p < 0.05 from 20 °C. Data are mean ± SE
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IntroductionPGC-1a has been termed the master regulator of mitochondrial biogenesis. The exercise-induced rise in PGC-1a transcription is blunted when acute exercise takes place in the heat. However, it is unknown if this alteration has functional implications after heat acclimation and exercise training.PurposeTo determine the impact of 3 weeks of...
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Abstract
Purpose: Age-related muscle deconditioning is characterized by a loss of muscle mass and functional capacities, involving oxidative stress and chronic inflammation. Carnosol (CA), a natural polyphenol extracted from rosemary has shown antioxidant and anti-inflammatory effects in several type of tissues. The purpose of this study was to de...
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... Nevertheless, a single bout of aerobic cycling exercise (50 % W max ) at 33°C in untrained individuals reduced PGC1-α mRNA expression compared to exercise at 20°C [103]. Additionally, three weeks of exercise (matched at a rating of perceived exertion of 15) in the heat did not increase PGC1-α mRNA expression compared to similar exercise in temperate conditions [104]. Crucially, in these studies, the impact of exercise intensity cannot be overlooked. ...
... Crucially, in these studies, the impact of exercise intensity cannot be overlooked. In the former [104], power output was significantly reduced during exercise in hot conditions. In the case of the latter implementing walking exercise [105], the exercise intensity may have been insufficient to induce increases in PGC-1α or markers of mitochondrial biogenesis [106]. ...
Inducing a heat-acclimated phenotype via repeated heat stress improves exercise capacity and reduces athletes̓ risk of hyperthermia and heat illness. Given the increased number of international sporting events hosted in countries with warmer climates, heat acclimation strategies are increasingly popular among endurance athletes to optimize performance in hot environments. At the tissue level, completing endurance exercise under heat stress may augment endurance training adaptation, including mitochondrial and cardiovascular remodeling due to increased perturbations to cellular homeostasis as a consequence of metabolic and cardiovascular load, and this may improve endurance training adaptation and subsequent performance. This review provides an up-to-date overview of the metabolic impact of heat stress during endurance exercise, including proposed underlying mechanisms of altered substrate utilization. Against this metabolic backdrop, the current literature highlighting the role of heat stress in augmenting training adaptation and subsequent endurance performance will be presented with practical implications and opportunities for future research.
... Participants arrived at the laboratory every weekday (Monday-Friday) for three weeks to complete the exercise training sessions. The training sessions consisted of 60 min of cycle ergometery at an intensity rated at 15 (hard) on the Borg Rating of Perceived Exertion (RPE) scale as previously described (Borg, 1973;McGlynn et al., 2022;Slivka et al., 2021). Participants were instructed to adjust exercise intensity to maintain an RPE of 15 throughout the training period. ...
... All training sessions were conducted in the assigned environmental temperature. The heart rate and core body temperature were continuously monitored during each training session and these data have been previously published (McGlynn et al., 2022;Slivka et al., 2021). ...
Environmental temperature can impact exercise-induced blood oxidative stress; however, the effects of heat acclimation on this response have not been fully elucidated. The purpose of the study was to investigate the effects of hot (33°C) and room temperature (20°C) environments on post-exercise blood oxidative stress responses following 15 temperature acclimation sessions. Untrained participants (n = 38, 26 7 years, VO2peak = 38.0 7.2 years) completed 15 temperature acclimation sessions of a cycling bout at an intensity perceived as “hard” in either a hot (33°C) or room temperature (20°C) environment. Pre and post acclimation exercise tolerance trials were conducted, which involved cycling at 50% Wpeak for one hour. Blood sampling occurred before exercise, immediately after, two hours, and four hours after the exercise tolerance trials. Blood samples were analyzed for oxidative stress markers including lipid hydroperoxides, 8-isoprostanes, protein carbonyls, 3-nitrotyrosine, ferric-reducing ability of plasma, and Trolox-equivalent antioxidant capacity. Exercise-dependent increases were observed in lipid hydroperoxides, Trolox-equivalent antioxidant capacity, and ferric-reducing ability of plasma (p < 0.001). Considering exercise-induced elevations in markers of blood oxidative stress, there were no differences observed between environmental temperatures before or after the acclimation training period.
... Based on this study, it may not be appropriate to assume that heat stress and exercise are ineffective at inducing PGC1-⍺ expression post-exercise. Further evidence from Slivka et al. (2021) reported that following a single bout of aerobic cycling exercise at 33ºC, untrained individuals had reduced PGC1-⍺ expression compared to participants who completed the exercise at 20ºC (Slivka et al., 2021). Three weeks of exercise in the heat did not increase PGC1-⍺ expression compared to exercise in temperate conditions. ...
... Based on this study, it may not be appropriate to assume that heat stress and exercise are ineffective at inducing PGC1-⍺ expression post-exercise. Further evidence from Slivka et al. (2021) reported that following a single bout of aerobic cycling exercise at 33ºC, untrained individuals had reduced PGC1-⍺ expression compared to participants who completed the exercise at 20ºC (Slivka et al., 2021). Three weeks of exercise in the heat did not increase PGC1-⍺ expression compared to exercise in temperate conditions. ...
... In vivo, mitochondrial adaptation was greatest in exercise and heat compared to either condition alone in rat muscle (Tamura et al., 2014). Data from human exercise studies remain equivocal and rarely applicable to trained populations and contrary to cell and animal evidence, PGC-1⍺ expression was suppressed following 3-h recovery in the heat (33ºC) in moderately trained individuals (Slivka et al., 2012), impairing improvements in V O2peak following 3 weeks of RPE clamped heat acclimation (Slivka et al., 2021). In contrast, Maunder et al. (2021c) reported increased mitochondrial protein activity (citrate synthase), corresponding to improved performance in temperate conditions when exercise is matched relative to cardiovascular demand during heat acclimation in endurance-trained individuals (Maunder et al., 2021b). ...
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.
... However, best practices to optimize heat acclimation are still unclear. Although previous evidence suggests that exercising while enduring heat stress has a detrimental effect [3,4], the majority show favorable alterations [4][5][6][7][8][9][10][11]. Acute extended exercise in the heat can impede performance by altering the extracellular fluid (reduced plasma volume) and amplifying cardiovascular stress (increased heart rate). ...
... Res. Public Health 2022, 19, 5554 2 of 15 conditions and a steeper rise in core temperature, leading to impaired performance and a sub-optimal training day [3,11,12]. Heat acclimation can directly combat these detrimental physiological alterations [3,[5][6][7][8][9][10][11]. ...
... Public Health 2022, 19, 5554 2 of 15 conditions and a steeper rise in core temperature, leading to impaired performance and a sub-optimal training day [3,11,12]. Heat acclimation can directly combat these detrimental physiological alterations [3,[5][6][7][8][9][10][11]. After acclimation, evidence suggests that an increase in plasma volume [3,5,[7][8][9] allows for an attenuated strain on the cardiovascular system and a reduced submaximal heart rate [3,6,8,11]. ...
Recent aerobic exercise training in the heat has reported blunted aerobic power improvements and reduced mitochondrial-related gene expression in men. It is unclear if this heat-induced blunting of the training response exists in females. The purpose of the present study was to determine the impact of 60 min of cycling in the heat over three weeks on thermoregulation, gene expression, and aerobic capacity in females. Untrained females (n = 22; 24 ± 4yoa) were assigned to three weeks of aerobic training in either 20 °C (n = 12) or 33 °C (n = 10; 40%RH). Maximal aerobic capacity (39.5 ± 6.5 to 41.5 ± 6.2 mL·kg−1·min−1, p = 0.021, ηp2 = 0.240, 95% CI [0.315, 3.388]) and peak aerobic power (191.0 ± 33.0 to 206.7 ± 27.2 W, p < 0.001, ηp2 = 0.531, 95% CI [8.734, 22.383]) increased, while the absolute-intensity trial (50%VO2peak) HR decreased (152 ± 15 to 140 ± 13 b·min−1, p < 0.001, ηp2 = 0.691, 95% CI [15.925, 8.353]), but they were not different between temperatures (p = 0.440, p = 0.955, p = 0.341, respectively). Independent of temperature, Day 22 tolerance trial skin temperatures decreased from Day 1 (p = 0.006, ηp2 = 0.319, 95% CI [1.408, 0.266), but training did not influence core temperature (p = 0.598). Average sweat rates were higher in the 33 °C group vs. the 20 °C group (p = 0.008, ηp2 = 0.303, 95% CI [67.9, 394.9]) but did not change due to training (p = 0.571). Pre-training PGC-1α mRNA increased 4h-post-exercise (5.29 ± 0.70 fold change, p < 0.001), was lower post-training (2.69 ± 0.22 fold change, p = 0.004), and was not different between temperatures (p = 0.455). While training induced some diminished transcriptional stimulus, generally the training temperature had little effect on genes related to mitochondrial biogenesis, mitophagy, and metabolic enzymes. These female participants increased aerobic fitness and maintained an exercise-induced PGC-1α mRNA response in the heat equal to that of room temperature conditions, contrasting with the blunted responses previously observed in men.
... Mitochondria are highly concentrated in skeletal muscle and can undergo damage when the ATP demand is elevated (e.g., a stressor like exercise and/or temperature) via increased production of ROS. Gene expression data has suggested that exercise, when paired with cold and hot ambient temperatures, may have different transcriptional influences [10][11][12][13][14][15][16][17]. More specifically, the pairing of exercise and cold ambient temperature may act in a mitochondrial-enhancing manner through the upregulation of the gene PGC1α and its mitochondrial biogenesis-related downstream targets [10,11,15,16]. ...
... More specifically, the pairing of exercise and cold ambient temperature may act in a mitochondrial-enhancing manner through the upregulation of the gene PGC1α and its mitochondrial biogenesis-related downstream targets [10,11,15,16]. Whereas exercise in hot ambient conditions may blunt these same mitochondrial-related benefits [10][11][12]17]. However, the exact mechanisms for these altered gene expression results are unclear. ...
... Under the American College of Sports Medicine stratification, all participants were considered "low risk" for cardiovascular disease-related events. Samples and descriptive data used in this study are a sub-set obtained from a larger project focused on exercise and temperature acclimation over a longer training period [16,17]. Two participants were removed from analysis due to extreme variation in reference genes and thus the inability to meet the assumption of reference gene stability. ...
A reduced mitochondrial DNA (mtDNA) copy number, the ratio of mitochondrial DNA to genomic DNA (mtDNA:gDNA), has been linked with dysfunctional mitochondria. Exercise can acutely induce mtDNA damage manifested as a reduced copy number. However, the influence of a paired (exercise and temperature) intervention on regional mtDNA (MINor Arc and MAJor Arc) are unknown. Thus, the purpose of this study was to determine the acute effects of exercise in cold (7 °C), room temperature (20 °C), and hot (33 °C) ambient temperatures, on regional mitochondrial copy number (MINcn and MAJcn). Thirty-four participants (24.4 ± 5.1 yrs, 87.1 ± 22.1 kg, 22.3 ± 8.5 %BF, and 3.20 ± 0.59 L·min−1 VO2peak) cycled for 1 h (261.1 ± 22.1 W) in either 7 °C, 20 °C, or 33 °C ambient conditions. Muscle biopsy samples were collected from the vastus lateralis to determine mtDNA regional copy numbers via RT-qPCR. mtDNA is sensitive to the stressors of exercise post-exercise (MIN fold change, −1.50 ± 0.11; MAJ fold change, −1.70 ± 0.12) and 4-h post-exercise (MIN fold change, −0.82 ± 0.13; MAJ fold change, −1.54 ± 0.11). The MAJ Arc seems to be more sensitive to heat, showing a temperature-trend (p = 0.056) for a reduced regional copy number ratio after exercise in the heat (fold change −2.81 ± 0.11; p = 0.019). These results expand upon our current knowledge of the influence of temperature and exercise on the acute remodeling of regional mtDNA.
Heat adaptation (HA) is a popular strategy to combat the negative effects of thermal stress. The HA literature has expanded since a 2016 meta-analysis, and we provide an updated meta-analysis, incorporating 39 additional studies and advanced analysis.
Following Pubmed searches, full-text original articles using human participants were reviewed using the four-stage PRISMA process. Data were extracted by at least two of the authors. Hedges’ g effect sizes, 95% confidence intervals, and prediction intervals were calculated. Correlations were run where appropriate.
One hundred and thirty-five total articles (96 previous, 39 new) were reviewed. Medium-term (8–14 days), active, constant work HA regimens remain the most common despite a recent focus on isothermal, passive, and short-term (≤ 7 days) alternatives. HA still improves subsequent exercise performance and capacity in the heat (g = 0.7), reduces resting core temperature (g = − 0.6) and heart rate (g = − 0.5), and increases sweat rate (g = 0.4) but the effect sizes are lower than previously reported. HA has a moderate or larger effect (g > 0.5) on lowering sweat onset temperature, mean heart rate, sweat sodium and chloride concentrations, resting thermal sensation, and thirst sensation, and increasing resting plasma volume. There is considerable heterogeneity within the data for most variables.
HA regimens can reduce physiological and perceptual strain and improve subsequent exercise performance and capacity in the heat. Longer regimens may be more effect than shorter ones, but the data are lacking. Passive HA is a practical, effective alternative to active HA.
