Training in a Hot Environment Fails to Elicit Changes in the Blood Oxidative Stress Response.

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.

Blood oxidative stress and post-exercise recovery are unaffected byhypobaric and hypoxic environments.

Hypobaria and hypoxia exert independent effects on oxidative stress during exercise, while combined effectson the post-exercise recovery period remain unclear.Accordingly, this study examined the recovery period during lab-simulated hypoxic and hypobaric conditions following exercise-induced oxidative stress. Participants (n=13) performed 60-minutes of cycling (70% watts max) in a normobaric normoxic environment followed by a four-hour recovery under three conditions; 1000m normobaric normoxia (NN, 675mmHg), 4400m normobaric hypoxia (NH, 675mmHg), or 4400m hypobaric hypoxia (HH, 440mmHg). Blood samples collected at Pre, Post, 2-Hours (2-HR), and 4-Hours (4-HR) post-exercise were analyzed fora potential increase in biochemical modifications of proteins(protein carbonyls, PC; 3-nitrotyrosines, 3NT) lipids (lipid hydroperoxides, LOOH; 8-isoprostanes, 8-ISO), and antioxidant capacity (FRAP, TEAC). Gene transcripts (EPAS, HMOX1, SOD2, NFE2L2) were quantified by qRT-PCR from muscle biopsies taken Pre and Post exercise. Hypoxia and hypobaria had no effect throughout recovery. Post-exercise TEAC (p=0.041), FRAP (p=0.013), and 8-ISO (p=0.044) increased, while PC (p=0.002) and 3-NT (p=0.032) were decreased. LOOH was lower in Post (p=0.018) NH trial samples. Exercise-dependent increases occurred in NFE2L2 (p=0.003), HMXO1 (p<0.001), SOD2 (p=0.046), and EPAS (p=0.038). Exercise recovery under conditions of NH and HH did not impact blood oxidative stress or redox-sensitive gene transcripts.

Thermoregulation During Extended Exercise in the Heat: Comparisons of Fluid Volume and Temperature.

OBJECTIVE: This study aimed to determine the physiological and thermoregulatory responses of individuals exercising in the heat (US military red flag conditions, wet-bulb globe temperature 31.5-32.2ºC) while consuming varied volumes of ambient temperature water and ice slurry. METHODS: Participants (N = 12) walked on a treadmill for 3 hours at approximately 40% peak aerobic capacity in a hot environment while consuming ambient temperature (35.5°C) water (W), ice slurry (0°C, two-thirds shaved ice and one-third water) at a ratio of 2 g·kg(-1) body mass every 10 minutes (FS), and reduced volume ice slurry as described at a rate of 1 g·kg(-1) body mass every 10 minutes (HS). Trials were completed at least 14 days apart, in a randomized, repeated measures design. RESULTS: Percent body weight loss was higher during the HS trial (1.8 ± 0.01%) compared with FS (0.5 ± 0.01%; P < .001) and W (0.6 ± 0.01%; P < .001). Mean rectal temperature at 3 hours was lower during FS (37.8 ± 0.7°C) compared with HS (38.1 ± 0.8°C) and W (38.2 ± 0.8°C) (P = .04 vs HS, and P = .005 vs W, main effect for trial). No differences were found in rectal temperature between HS and W. Heart rate was lower at the end of the third hour during FS (141 ± 10 beats/min) compared with HS (157 ± 19 beats/min) and W (154 ± 18 beats/min) (P = .001 and P = .007, respectively, time × trial interaction). There were no differences in heart rate between HS and W. CONCLUSIONS: The temperature of consumed fluids may be as important as the volume for the management of thermoregulation and other physiological responses for extended work in hot environments.

Graded hypoxia and blood oxidative stress during exercise recovery.

Altitude exposure and exercise elicit oxidative stress in blood; however, exercise recovery at 5000 m attenuates oxidative stress. The purpose was to determine the altitude threshold at which blood oxidative stress is blunted during exercise recovery. Twelve males 18-28 years performed four-cycle ergometry bouts (60 min, 70% VO2max, at 975 m). In a randomised counterbalanced crossover design, participants recovered 6 h at 0, 1667, 3333 and 5000 m in a normobaric hypoxia chamber (recovery altitudes were simulated by using a computerised system in an environmental chamber by lowering the partial pressure of oxygen to match that of the respective altitude). Oxygen saturation was monitored throughout exercise recovery. Blood samples obtained pre-, post-, 1 h post- and 5 h post-exercise were assayed for ferric-reducing antioxidant plasma, Trolox equivalent antioxidant capacity, uric acid, lipid hydroperoxides and protein carbonyls. Muscle biopsies obtained pre and 6 h were analysed by real-time polymerase chain reaction to quantify expression of hemeoxgenase 1, superoxide dismutase 2 and nuclear factor (euthyroid-derived 2)-like factor. Pulse oximetry data were similar during exercise, but decreased for the three highest recovery elevations (0 m = 0%, 1667 m = -3%; 3333 m = -7%; 5000 m = -17%). A time-dependent oxidative stress occurred following exercise for all variables, but the two highest recovery altitudes partially attenuated the lipid hydroperoxide response (0 m = +135%, 1667 m = +251%, 3333 m = +99%; 5000 m = +108%). Data may indicate an altitude threshold between 1667 and 3333 m, above which the oxidative stress response is blunted during exercise recovery.

The Effect of Environmental Temperature on Glucose and Insulin After an Oral Glucose Tolerance Test in Healthy Young Men.

OBJECTIVE: The purpose of this study was to compare glucose and insulin responses during an oral glucose tolerance test (OGTT) in cold (C), neutral (N), and hot (H) environments. METHODS: Eleven males completed three 4-hour climate-controlled OGTT trials (C, 7.2°C; N, 22°C; and H, 43°C). Participants remained semireclined for 60 minutes before ingesting a 1.8 g/kg glucose beverage. Skin and rectal core temperatures were continuously monitored. Blood was collected just before glucose ingestion (time 0) and at 15, 30, 60, 90, 120, and 180 minutes, and analyzed for serum glucose, insulin, hematocrit, and hemoglobin. Expired gases were collected upon entering the chamber (-60 minutes), before glucose ingestion (0 minutes), and at 60, 120, and 180 minutes to determine V(O2) and respiratory exchange ratio. RESULTS: Rectal core temperature was greater in the H condition compared with both C and N (P < .001). Rectal core temperature was not different between C and N, whereas skin temperature was different across all trials (H greater than N greater than C). The V(O2) was greater in C than in both H and N during all time points. Carbohydrate oxidation was greater in C compared with H and N (P < 0.001). Glucose was higher during H compared with C and N (P ≤ 0.002). Glucose was elevated in C compared with N. Insulin was higher in H compared with C (P = 0.009). Area under the curve for serum glucose was greater in H compared with C and N (P ≤ 0.001); however, there was no significant difference in area under the curve for insulin. CONCLUSIONS: These data indicate that after an OGTT, glucose and insulin are elevated in a hot environment.

Postexercise Glycogen Recovery and Exercise Performance is Not Significantly Different Between Fast Food and Sport Supplements.

A variety of dietary choices are marketed to enhance glycogen recovery after physical activity. Past research informs recommendations regarding the timing, dose, and nutrient compositions to facilitate glycogen recovery. This study examined the effects of isoenergetic sport supplements (SS) vs. fast food (FF) on glycogen recovery and exercise performance. Eleven males completed two experimental trials in a randomized, counterbalanced order. Each trial included a 90-min glycogen depletion ride followed by a 4-hr recovery period. Absolute amounts of macronutrients (1.54 ± 0.27 g·kg-1 carbohydrate, 0.24 ± 0.04 g·kg fat-1, and 0.18 ±0.03g·kg protein-1) as either SS or FF were provided at 0 and 2 hr. Muscle biopsies were collected from the vastus lateralis at 0 and 4 hr post exercise. Blood samples were analyzed at 0, 30, 60, 120, 150, 180, and 240 min post exercise for insulin and glucose, with blood lipids analyzed at 0 and 240 min. A 20k time-trial (TT) was completed following the final muscle biopsy. There were no differences in the blood glucose and insulin responses. Similarly, rates of glycogen recovery were not different across the diets (6.9 ± 1.7 and 7.9 ± 2.4 mmol·kg wet weight- 1·hr-1 for SS and FF, respectively). There was also no difference across the diets for TT performance (34.1 ± 1.8 and 34.3 ± 1.7 min for SS and FF, respectively. These data indicate that short-term food options to initiate glycogen resynthesis can include dietary options not typically marketed as sports nutrition products such as fast food menu items.

Work patterns dictate energy demands and thermal strain during wildland firefighting.

OBJECTIVE: The purpose of this investigation was to characterize the effects of self-selected work activity on energy expenditure, water turnover, and thermal strain during wildland fire suppression. A secondary aim was to contrast current data with data collected 15 years ago using similar methods to determine whether job demands have changed. METHODS: Participants (n=15, 26±3 years, 179±6 cm, 78.3±8.6 kg) were monitored for 3 days for total energy expenditure, water turnover, core and chest skin temperature, physical activity, and heart rate. Participants arrived to the mobile laboratory each morning, submitted a nude weight, ingested a temperature transmitter, provided a urine sample, and were equipped with a physiological and activity monitor. Participants completed live wildland fire suppression during their work shifts. RESULTS: Mean core temperature was 37.6°±0.2°C, mean chest skin temperature was 34.1°±1.0°C, mean heart rate was 112±13 beats/min, and the mean physiological strain index score was 3.3±1.0. Wildland firefighters spent 49±8%, 39±6%, and 12±2% in the sedentary, light, and moderate-vigorous intensity categories, respectively. The mean total energy expenditure was 19.1±3.9 MJ/d, similar to 1997 (17.5±6.9 MJ/d). The mean water turnover in 2012 was 9.5±1.7 L/d, which was higher (P<.05) compared with 1997-98 (7.0±1.7 L/d). CONCLUSIONS: Wildland firefighters do not induce consistently high cardiovascular and thermal strain while completing arduous work in a hot environment despite fairly high chest skin temperatures. The total energy expenditure in the current study suggests job demands are similar to those of 15 years ago, while the increased water turnover may reflect a change in drinking habits.

Effects of commercially available pneumatic compression on muscle glycogen recovery after exercise.

The purpose of this study was to investigate the effects of pneumatic compression pants on postexercise glycogen resynthesis. Active male subjects (n = 10) completed 2 trials consisting of a 90-minute glycogen depleting ride, followed by 4 hours of recovery with either a pneumatic compression device (PCD) or passive recovery (PR) in a random counterbalanced order. A carbohydrate beverage (1.8 g·kg bodyweight) was provided at 0 and 2 hours after exercise. Muscle biopsies (vastus lateralis) were obtained immediately and 4 hours after exercise for glycogen analyses. Blood samples were collected throughout recovery to measure glucose and insulin. Eight fingerstick blood samples for lactate were collected in the last 20 minutes of the exercise period and during the initial portion of the recovery period. Heart rate was monitored throughout the trial. During the PCD trial, subjects recovered using a commercially available recovery device (NormaTec PCD) operational at 0-60 and 120-180 minutes into recovery period. The same PCD was worn during the PR trial but was not turned on to create pulsatile pressures. There was no difference in muscle glycogen resynthesis during the recovery period (6.9 ± 0.8 and 6.9 ± 0.5 mmol·kg wet wt·h for the PR and PCD trials, respectively). Blood glucose, insulin, and lactate concentrations changed with respect to time but were not different between trials (p > 0.05). The use of PCD did not alter the rate of muscle glycogen resynthesis, blood lactate, or blood glucose and insulin concentrations associated with a postexercise oral glucose load.

Seasonal heat acclimatization in wildland firefighters.

The purpose of this study was to determine changes in physiological markers of heat acclimatization across a 4-month wildland fire season. Wildland firefighters (WLFF) (n=12) and non-WLFF (n=14) were assessed pre- and post-season for body mass, percent body fat, and peak VO2. Both groups completed a 60-min heat stress trial (walking at 50% of peak VO2) in a climate controlled chamber (43.3 °C, 33% RH) pre and post-fire season (May through September). During the trials, core (Tc) and skin (Tsk) temperatures, heart rate (HR), physiological strain index (PSI), and rating of perceived exertion (RPE) were measured. There were no differences pre or post-season between the WLFF and non-WLFF groups in body mass, percent body fat, or peak V.O2. During the 73 days where the WLFF were involved in direct wildland fire suppression, daily high temperature for the WLFF was higher compared to the non-WLFF, 30.6 ± 5.4 °C and 26.9 ± 6.1 °C, respectively, p<0.05. Tc was lower at post-season compared to pre-season (p<0.05) for the WLFF at 30, 45, and 60 min (pre 30, 45, and 60: 37.9 ± 0.3, 38.3 ± 0.3 and 38.5 ± 0.3 °C, respectively; post 30, 45, and 60: 37.8 ± 0.3, 38.1 ± 0.3 and 38.2 ± 0.4 °C, respectively). For WLFF, PSI was lower (p<0.05) at 15, 30, 45, and 60 min at post-season compared to pre-season (4.2 ± 0.7, 5.6 ± 0.9, 6.5 ± 0.9, and 7.1 ± 1.1 for 15, 30, 45, and 60 min pre-season, respectively; 3.6 ± 0.8, 4.9 ± 1.0, 5.7 ± 1.2, 6.3 ± 1.3 for 15, 30, 45, and 60 min post-season, respectively). For WLFF, RPE was lower during the post-season trial at 30, 45, and 60 min (pre 30, 45, and 60: 11.7 ± 1.4, 12.3 ± 1.2, and 13.5 ± 1.4, respectively; post 30, 45, and 60: 10.7 ± 1.2, 11.3 ± 1.3, and 11.9 ± 1.5, respectively), p<0.05. There were no differences between pre and post-season for the non-WLFF for Tc and PSI, but RPE was lower at 15 min during the pre-season trial. WLFFs demonstrated significant decreases in Tc, PSI, and RPE during controlled heat stress after the season. Since an age and fitness-matched control group experienced no indication of heat acclimatization, it is suggested that the long-term occupational heat exposure accrued by the WLFFs was adequate to incur heat acclimatization.

Human skeletal muscle mRNAResponse to a single hypoxic exercise bout.

BACKGROUND: The ability to physically perform at high altitude may require unique strategies to acclimatize before exposure. The effect of acute hypoxic exposure on the metabolic response of the skeletal muscle may provide insight into the value of short-term preacclimatization strategies. OBJECTIVE: To determine the human skeletal muscle response to a single acute bout of exercise in a hypoxic environment on metabolic gene expression. METHODS: Eleven recreationally active male participants (24 ± 4 years, 173 ± 20 cm, 82 ± 12 kg, 15.2 ± 7.1% fat, 4.0 ± 0.6 L/min maximal oxygen consumption) completed two 1-hour cycling exercise trials at 60% of peak power followed by 4 hours of recovery in ambient environmental conditions (975 m) and at normobaric hypoxic conditions simulating 3000 m in a randomized counterbalanced order. Muscle biopsies were obtained from the vastus lateralis before exercise and 4 hours after exercise for real-time polymerase chain reaction analysis of select metabolic genes. RESULTS: Gene expression of hypoxia-inducible factor 1 alpha, cytochrome c oxidase subunit 4, peroxisome proliferator-activated receptor gamma coactivator 1 alpha, hexokinase, phosphofructokinase, mitochondrial fission 1, and mitofusin-2 increased with exercise (P < .05) but did not differ with hypoxic exposure (P > .05). Optic atrophy 1 did not increase with exercise or differ between environmental conditions (P > .05). CONCLUSIONS: The improvements in mitochondrial function reported with intermittent hypoxic training may not be explained by a single acute hypoxic exposure, and thus it appears that a longer period of preacclimatization than a single exposure may be required.

A reduced core to skin temperature gradient, not a critical core temperature, affects aerobic capacity in the heat.

The purpose of this study was to determine the impact of the core to skin temperature gradient during incremental running to volitional fatigue across varying environmental conditions. A secondary aim was to determine if a "critical" core temperature would dictate volitional fatigue during running in the heat. 60 participants (n=49 male, n=11 female; 24±5 yrs, 177±11 cm, 75±13 kg) completed the study. Participants were uniformly stratified into a specific exercise temperature group (18 °C, 26 °C, 34 °C, or 42 °C) based on a 3-mile run performance. Participants were equipped with core and chest skin temperature sensors and a heart rate monitor, entered an environmental chamber (18 °C, 26 °C, 34 °C, or 42 °C), and rested in the seated position for 10 min before performing a walk/run to volitional exhaustion. Initial treadmill speed was 3.2 km h(-1) with a 0% grade. Every 3 min, starting with speed, speed and grade increased in an alternating pattern (speed increased by 0.805 km h(-1), grade increased by 0.5%). Time to volitional fatigue was longer for the 18 °C and 26 °C group compared to the 42 °C group, (58.1±9.3 and 62.6±6.5 min vs. 51.3±8.3 min, respectively, p<0.05). At the half-way point and finish, the core to skin gradient for the 18 °C and 26 °C groups was larger compared to 42 °C group (halfway: 2.6±0.7 and 2.0±0.6 vs. 1.3±0.5 for the 18 °C, 26 °C and 42 °C groups, respectively; finish: 3.3±0.7 and 3.5±1.1 vs. 2.1±0.9 for the 26 °C, 34 °C, and 42 °C groups, respectively, p<0.05). Sweat rate was lower in the 18 °C group compared to the 26 °C, 34 °C, and 42 °C groups, 3.6±1.3 vs. 7.2±3.0, 7.1±2.0, and 7.6±1.7 g m(-2) min(-1), respectively, p<0.05. There were no group differences in core temperature and heart rate response during the exercise trials. The current data demonstrate a 13% and 22% longer run time to exhaustion for the 18 °C and 26 °C group, respectively, compared to the 42 °C group despite no differences in beginning and ending core temperatures or baseline 3-mile run time. This capacity difference appears to result from a magnified core to skin gradient via an environmental temperature advantageous to convective heat loss, and in part from an increased sweat rate.

Acute hypoxia and exercise-induced blood oxidative stress.

Hypoxic exercise is characterized by workloads decrements. Because exercise and high altitude independently elicit redox perturbations, the study purpose was to examine hypoxic and normoxic steady-state exercise on blood oxidative stress. Active males (n = 11) completed graded cycle ergometry in normoxic (975 m) and hypoxic (3,000 m) simulated environments before programing subsequent matched intensity or workload steady-state trials. In a randomized counterbalanced crossover design, participants completed three 60-min exercise bouts to investigate the effects of hypoxia and exercise intensity on blood oxidative stress. Exercise conditions were paired as such; 60% normoxic VO(2)peak performed in a normoxic environment (normoxic intensity-normoxic environment, NI-NE), 60% hypoxic VO(2)peak performed in a normoxic environment (HI-NE), and 60% hypoxic VO(2)peak performed in a hypoxic environment (HI-HE). Blood plasma samples drawn pre (Pre), 0 (Post), 2 (2HR) and 4 (4HR) hr post exercise were analyzed for oxidative stress biomarkers including ferric reducing ability of plasma (FRAP), trolox equivalent antioxidant capacity (TEAC), lipid hydroperoxides (LOOH) and protein carbonyls (PCs). Repeated-measures ANOVA were performed, a priori significance of p ≤ .05. Oxygen saturation during the HI-HE trial was lower than NI-NE and HI-NE (p < .05). A Time × Trial interaction was present for LOOH (p = .013). In the HI-HE trial, LOOH were elevated for all time points post while PC (time; p = .001) decreased post exercise. As evidenced by the decrease in absolute workload during hypoxic VO(2)peak and LOOH increased during HI-HE versus normoxic exercise of equal absolute (HI-NE) and relative (NI-NE) intensities. Results suggest acute hypoxia elicits work decrements associated with post exercise oxidative stress.

Exercise-induced oxidative stress and hypoxic exercise recovery.

Hypoxia due to altitude diminishes performance and alters exercise oxidative stress responses. While oxidative stress and exercise are well studied, the independent impact of hypoxia on exercise recovery remains unknown. Accordingly, we investigated hypoxic recovery effects on post-exercise oxidative stress. Physically active males (n = 12) performed normoxic cycle ergometer exercise consisting of ten high:low intensity intervals, 20 min at moderate intensity, and 6 h recovery at 975 m (normoxic) or simulated 5,000 m (hypoxic chamber) in a randomized counter-balanced cross-over design. Oxygen saturation was monitored via finger pulse oximetry. Blood plasma obtained pre- (Pre), post- (Post), 2 h post- (2Hr), 4 h post- (4Hr), and 6 h (6Hr) post-exercise was assayed for Ferric Reducing Ability of Plasma (FRAP), Trolox Equivalent Antioxidant Capacity (TEAC), Lipid Hydroperoxides (LOOH), and Protein Carbonyls (PC). Biopsies from the vastus lateralis obtained Pre and 6Hr were analyzed by real-time PCR quantify expression of Heme oxygenase 1 (HMOX1), Superoxide Dismutase 2 (SOD2), and Nuclear factor (euthyroid-derived2)-like factor (NFE2L2). PCs were not altered between trials, but a time effect (13 % Post-2Hr increase, p = 0.044) indicated exercise-induced blood oxidative stress. Plasma LOOH revealed only a time effect (p = 0.041), including a 120 % Post-4Hr increase. TEAC values were elevated in normoxic recovery versus hypoxic recovery. FRAP values were higher 6Hr (p = 0.045) in normoxic versus hypoxic recovery. Exercise elevated gene expression of NFE2L2 (20 % increase, p = 0.001) and SOD2 (42 % increase, p = 0.003), but hypoxic recovery abolished this response. Data indicate that recovery in a hypoxic environment, independent of exercise, may alter exercise adaptations to oxidative stress and metabolism.

Accelerometry and salivary cortisol response during Air Force Special Tactics Officer selection.

BACKGROUND: Special Tactics Officer (STO) selection is conducted to select officers to enter the combat controller training pipeline. The aims were to determine physical activity patterns, estimate energy expenditure, and identify whether return and/or unsuccessful candidates demonstrated differences in cortisol responses compared to non-selected and/or first-time attendees. METHODS: Participants completed the STO selection, consisting of 5 days of physical and mental challenges. Participants were equipped with ActiCals®, and saliva samples were collected throughout the STO selection. RESULTS: Average activity counts were 684 ± 200 counts∙min-1, with no group differences. Estimated energy expenditure was 4,105 ± 451 kcal∙day-1. Cortisol was elevated following extended physical training but returned to baseline during rest. Return candidates had significantly lower cortisol responses compared to first-timers, 0.43 ± 0.06 µg∙dl-1 versus 0.76 ± 0.18 µg∙dl-1, respectively, p < 0.05. CONCLUSIONS: An individual's salivary cortisol response to the stresses incurred during the STO selection has the potential to be incorporated into the entire picture of a candidate's performance and ability to handle stress.

Skeletal muscle metabolic gene response to carbohydrate feeding during exercise in the heat.

BACKGROUND: Heat stress down-regulates mitochondrial function, while carbohydrate supplementation attenuates the exercise induced stimulation of mitochondrial biogenesis in humans. The effects of exogenous carbohydrate during exercise in the heat on metabolic mRNA have not been investigated in humans. The purpose of this study was to determine the impact of exercise with and without carbohydrate supplementation on skeletal muscle metabolic response in the heat. METHODS: Eight recreationally active males (4.05 ± 0.2 L.min-1) completed 2 trials which included 1 hr of cycling at 70% workload max and 3 hr recovery in a hot environment. Both trials were conducted in a climate controlled environmental chamber (38°C and 40% RH). The trials differed by the consumption of either a 6% carbohydrate (CHO) containing beverage (8 ml.kg-1.hr-1) or placebo (P) during exercise in random order. Muscle biopsies were obtained from the vastus lateralis before exercise, immediately post-exercise and at the end of the 3 hr recovery period. Muscle was analyzed for muscle glycogen and mRNA related to metabolic and mitochondrial development (MFN2, PGC-1α, GLUT4, UCP3). Expired gases were measured to determine whole body substrate use during exercise. RESULTS: Carbohydrate oxidation and muscle glycogen utilization did not differ between trials, whereas fat oxidation was elevated during exercise in P. Exercise caused an increase in PGC-1α, and GLUT4 (P < 0.05) independent of exogenous carbohydrate provision. Carbohydrate consumption attenuated the mRNA response in UCP3 (P < 0.05). CONCLUSIONS: This study indicates that the provision of exogenous carbohydrate attenuates the stimulation of mRNA expression of UCP3 following exercise in the heat.

Skin temperature and heart rate can be used to estimate physiological strain during exercise in the heat in a cohort of fit and unfit males.

OBJECTIVE: To evaluate the previously developed physiological strain index (PSI) model using heart rate and skin temperature to provide further insight into the detection and estimation of thermal and physiological heat strain indices. A secondary aim was to characterize individuals who excel in their performance in the heat. METHODS: 56 male participants completed 2 walking trials (3.5 miles per hour, 5% grade) in controlled environments of 43.3 °C and 15.5 °C (40% humidity). Core and skin temperature, along with heart rate and PSI, were continually monitored during exercise. Participants completed a physical fitness test. RESULTS: The logistic regression model exhibited 4 false positives and 1 false negative at the 40% decision boundary. The "Not at Risk" group (N = 33) had higher body weight (84 ± 13 vs. 77 ± 10 kg, respectively) compared to the "At Risk" (N = 23) group, p < 0.05. The "Not at Risk" group had a faster 3-mile run time compared to the "At Risk" group (21:53 ± 3:13 vs. 25:16 ± 2:37, respectively), p < 0.05. During the Heat Trial, the "At Risk" group had a higher rating of perceived exertion at 60 and 90 minutes compared to the "Not at Risk" group (13.5 ± 2.8 vs. 11.5 ± 1.8 and 14.8 ± 3.2 vs. 12.2 ± 2.0 for "At Risk" vs. "Not at Risk" at 60 and 90 minutes, respectively), p < 0.05. CONCLUSIONS: The previously developed model relating heart rate and skin temperature to PSI is highly accurate at assessing heat risk status. Participants classified as "At Risk" had lower physical performance scores and different body weights compared to the "Not at Risk" group and perceived themselves as working harder during exercise in the heat.

Environmental temperature and exercise-induced blood oxidative stress.

Previous research findings indicate that environmental temperature can influence exercise-induced oxidative-stress responses, although the response to variable temperatures is unknown. The purpose of this study was to investigate the effect of warm, cold, and "neutral," or room, environmental temperatures on the blood oxidative stress associated with exercise and recovery. Participants (N = 12, age 27 ± 5 yr, VO2max = 56.7 ± 5.8 ml · kg-1 · min-1, maximal cycle power output = 300 ± 39 W) completed 3 exercise sessions consisting of a 1-hr ride at 60% Wmax, at 40% relative humidity in warm (33 °C), cold (7 °C), and room-temperature environments (20 °C) in a randomized crossover fashion. Rectal core temperature was monitored continually as participants remained in the respective trial temperature throughout a 3-hr recovery. Blood was collected preexercise and immediately, 1 hr, and 3 hr postexercise and analyzed for oxidative-stress markers including ferric-reducing ability of plasma (FRAP), Trolox-equivalent antioxidant capacity (TEAC), lipid hydroperoxides, and protein carbonyls. Core temperature was significantly elevated by all exercise trials, but recovery core temperatures reflected the given environment. FRAP (p < .001), TEAC (p < .001), and lipid hydroperoxides (p < .001) were elevated after warm exercise while protein carbonyls were not altered (p > .05). These findings indicate that moderate-intensity exercise and associated recovery in a warm environment elicits a blood oxidative-stress response not observed at comparable exercise performed at lower temperatures.

Effects of post-exercise recovery in a cold environment on muscle glycogen, PGC-1α, and downstream transcription factors.

PURPOSE: The purpose of this investigation was to determine the impact of post-exercise environmental cold exposure on muscle glycogen, PGC-1α, and downstream transcription factors. METHODS: Eight males cycled for 1h and recovered in either 7 °C (cold) or 20 °C (room temp) environment for 4h. Muscle biopsies were obtained pre, post, and 4h post exercise for the analysis of muscle glycogen and mRNA. During recovery participants consumed 1.8 g kg⁻¹ of body weight of an oral dextrose solution immediately following the post biopsy and 2h into recovery. Blood samples were obtained post exercise and at 30, 60, 120, 150, 180, and 240 min post exercise for the analysis of serum glucose and insulin AUC. RESULTS: Oxygen uptake was lower during room temp than during cold recovery (0.40 ± 0.05 L x min⁻¹ vs. 0.80 ± 0.12 L x min⁻¹; p<0.01). There was no effect of temperature on muscle glycogen recovery or glucose AUC. However, insulin AUC was greater during the room temp trial compared to the cold trial (5139 ± 1412 vs. 4318 ± 1272, respectively; p=0.025). PGC-1α gene expression was higher (p=0.029), but ERRα and NRF2 were lower (p=0.019 and p=0.046, respectively) after recovery in the cold. There were no differences in NRF1 (p=.173) or TFAM (p=0.694). CONCLUSIONS: This investigation shows no effect of a cold recovery environment on glycogen re-synthesis but does demonstrate reduced ERRα and NRF2 mRNA despite elevations in PGC-1α mRNA when recovery post-exercise takes place in a cold environment.

Blood oxidative-stress markers during a high-altitude trek.

UNLABELLED: Oxidative stress occurs as a result of altitude-induced hypobaric hypoxia and physical exercise. The effect of exercise on oxidative stress under hypobaric hypoxia is not well understood. PURPOSE: To determine the effect of high-altitude exercise on blood oxidative stress. Nine male participants completed a 2-d trek up and down Mt Rainer, in North America, at a peak altitude of 4,393 m. Day 1 consisted of steady-pace climbing for 6.25 hr to a final elevation of 3,000 m. The 4,393-m summit was reached on Day 2 in approximately 5 hr. Climb-rest intervals varied but were consistent between participants, with approximately 14 hr of total time including rest periods. Blood samples were assayed for biomarkers of oxidative stress and antioxidant potential at the following time points: Pre (before the trek), 3Kup (at ascent to 3,000 m), 3Kdown (at 3,000 m on the descent), and Post (posttrek at base elevation). Blood serum variables included ferric-reducing antioxidant potential (FRAP), Trolox equivalent antioxidant capacity (TEAC), protein carbonyls (PC), and lipid hydroperoxides. Serum FRAP was elevated at 3Kup and 3Kdown compared with Pre and Post values (p = .004, 8% and 11% increase from Pre). Serum TEAC values were increased at 3Kdown and Post (p = .032, 10% and 18% increase from Pre). Serum PC were elevated at 3Kup and 3Kdown time points (p = .034, 194% and 138% increase from Pre), while lipid hydroperoxides were elevated Post only (p = .004, 257% increase from Pre). CONCLUSIONS: Findings indicate that high-altitude trekking is associated with increased blood oxidative stress.

Water turnover and core temperature on Mount Rainier.

OBJECTIVE: Hydration is an important logistical consideration for persons performing in austere environments because water demands must be balanced with the burden of carrying water. METHODS: Seven novice climbers participated in a study to determine the hydration kinetics and core temperatures associated with a successful summit of Mount Rainier. Ingestible radio-equipped thermometer capsules were swallowed to monitor core temperature, and an oral dose of deuterium (0.12 ± 0.02 g·kg⁻¹ body weight) was administered to determine hydration kinetics. RESULTS: Mean core temperature throughout the 5.5-hour climb to Camp Muir (3000 m) was 37.6 ± 0.3°C. Water turnover was 95.0 ± 17.5 mL·kg⁻¹·24 h⁻¹ over the duration of the 43-hour study. There was a trend for reduced body mass from before (75.9 ± 13.0 kg) to after (74.8 ± 12.5 kg) the climb (P = .06), and urine specific gravity increased from before (1.013 ± 0.002) to after (1.022 ± 0.006) the climb (P = .004). CONCLUSIONS: Hydration demands of climbing Mount Rainier are highly elevated despite modest fluctuations in core temperature. Participants experienced hypohydration but were able to maintain sufficient hydration to successfully summit Mount Rainier and return home safely.