Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Heat Illness: 2024 Update.

The Wilderness Medical Society (WMS) convened an expert panel in 2011 to develop a set of evidence-based guidelines for the recognition, prevention, and treatment of heat illness. The current panel retained 5 original members and welcomed 2 new members, all of whom collaborated remotely to provide an updated review of the classifications, pathophysiology, evidence-based guidelines for planning and preventive measures, and recommendations for field- and hospital-based therapeutic management of heat illness. These recommendations are graded based on the quality of supporting evidence and the balance between the benefits and risks or burdens for each modality. This is an updated version of the WMS clinical practice guidelines for the prevention and treatment of heat illness published in Wilderness & Environmental Medicine. 2019;30(4):S33-S46.

Twenty-Four Percent of Wildland Firefighters Reach Critical Levels of Serum Creatine Kinase During 80-Hour Critical Training.

INTRODUCTION: Wildland firefighters (WLFFs) must undergo a 2-wk critical training (CT) period prior to deployment to the field. This stress may result in clinical risks, including severe muscle damage and rhabdomyolysis. We aimed to document the effects of WLFFs' CT on physiologic markers of muscle damage and soreness. METHODS: Two interagency hotshot crews (n=25) were followed during spring 2022 for 80 h of training. Activity counts as well as records of upper-body (US) and lower-body (LS) muscle soreness were collected daily. Body weight (BW) and skinfold measurements were recorded on Day 1 (D1) and D11 to estimate body fat (BF) and lean body weight (LBW). Blood was collected on D1 and D11 to measure muscle and liver damage markers. RESULTS: Critical training resulted in significant elevations in creatine kinase (CK) (216.9±57.4 U/L vs 5166.4±1927.8 U/L, P=0.017) and lactate dehydrogenase (LDH) (175.5±4.0 IU/L vs 340.0±42.6 IU/L, P=0.001) despite no significant changes in BW, BF, LBW, cortisol, or testosterone. Main effects of time were seen in US and LS, peaking on D11 (US: 5.2±0.4 cm, P<0.001; LS: 5.5±0.4 cm, P<0.001). Those who spent the most minutes with activity counts of >1500 counts/min showed the greatest increase in CK and LDH. CONCLUSIONS: These data suggest that WLFFs undergo significant physiologic stressors, resulting in muscle soreness and damage during CT, with 6 of the 25 subjects reaching critical levels of serum CK. It appears that much of the muscle damage and soreness occurred because of unaccustomed WLFF job-specific tasks.

Wildland Firefighter Critical Training Elicits Positive Adaptations to Markers of Cardiovascular and Metabolic Health.

INTRODUCTION: The purpose of this study was to identify physiologic changes in body composition and resting metabolic markers of health across 2 wk of critical training (CT) in wildland firefighters (WLFFs). METHODS: Twenty-two male and 3 female participants were recruited from 2 hotshot crews across the western United States prior to the 2022 fire season and monitored over their 80-h CT. Body weight (BW) and skinfolds were recorded before and after CT to estimate body fat (BF) and lean body weight (LBW). Blood was analyzed for changes in hematocrit, hemoglobin, plasma volume, and resting values of a lipid and metabolic panel. RESULTS: The high physical demands of CT resulted in improvements in total cholesterol (-19.3 mg/dL, P<0.001), triglycerides (-34.4 mg/dL, P<0.001), low-density lipoprotein cholesterol (-18.1 mg/dL, P<0.001), very-low-density lipoprotein cholesterol (-5.2 mg/dL, P<0.001), high-density lipoprotein cholesterol (+4.0 mg/dL, P=0.002), non-high-density lipoprotein cholesterol (-19.3 mg/dL, P<0.001), and fasting glucose (-4.3 mg/dL, P=0.008) from before CT to after CT. Significant decreases in hemoglobin and hematocrit were also seen (P<0.001) with corresponding increases in estimated plasma volume (+6.1%, P<0.001). These alterations were seen despite maintenance of BW, LBW, and BF. Lower pretraining BF was associated with a greater magnitude of improvements in fasting glucose and cholesterol markers. CONCLUSIONS: The observed improvements in baseline metabolic and cardiovascular markers along with plasma volume expansion suggest a positive response to the physical stress of WLFF CT. It appears that higher preseason fitness was associated with greater adaptations to the CT stressor.

Cardiovascular and Blood Oxidative Stress Responses to Exercise and Acute Woodsmoke Exposure in Recreationally Active Individuals.

INTRODUCTION: Those who work and recreate outdoors experience woodsmoke exposure during fire season. Exercise during woodsmoke exposure harms the cardiovascular system, but the acute physiologic and biochemical responses are understudied. The purpose of this pilot laboratory-based study was to examine the effect of exercise during woodsmoke exposure on acute indicators of cardiovascular function, including heart rate variability (HRV), pulse wave velocity (PWV), blood pressure (BP), augmentation index (AIx), and blood oxidative stress. METHODS: Ten participants performed 2 moderate-intensity exercise (70% V˙O2 max) trials (clean air 0 µg·m-3, woodsmoke 250 µg·m-3) in a crossover design. HRV, PWV, BP, AIx, and blood oxidative stress were measured before, after, and 90 min after exercise for each trial. Blood oxidative stress was quantified through lipid damage (LOOH, 8-ISO), protein damage (3-NT, PC), and antioxidant capacity (TEAC). RESULTS: A 45-min woodsmoke exposure combined with moderate-intensity exercise did not result in a statistically significant difference in HRV, PWV, BP, AIx, or oxidative stress (P>0.05). CONCLUSIONS: Despite the known deleterious effects of smoke inhalation, moderate-intensity aerobic exercise while exposed to woodsmoke particulate matter (250 µg·m-3) did not result in a statistically significant difference in HRV, PWV, or blood oxidative stress in this methodologic context. Although findings do not negate the negative impact of woodsmoke inhalation, additional research approaches are needed to better understand the acute effects of smoke exposure on the cardiovascular system.

Short term heat acclimation reduces heat stress, but is not augmented by dehydration.

Heat acclimation lowers physiological strain when exercising in the heat, and may be enhanced by promoting dehydration during acclimation. The purpose was to compare fluid intake during heat acclimation by promoting dehydration (DEH=0.5 mL kg-1 15 min-1, ~2.4% dehydration per acclimation session) compared to euhydration (EUH=2.0 mL kg-1 15 min-1, ~1.4% dehydration per acclimation session) following four heat acclimation bouts on thermal strain, and exercise performance. Thirteen males completed 90 min heat stress tests (HST) at 50% VO2max (40 °C, 30%RH) before and after three 90 min heat acclimation trials, involving consecutive bouts with 4-fold less fluid (DEH) or EUH. DEH and EUH trials were separated by 48 h and assigned in a random crossover design separated by a 5 week washout. Wildland firefighter (WLFF) Nomex: shirt, pants, and a cotton T-shirt baselayer were worn. Peak core temperature (Tc) from the HST significantly decreased following both DEH (39.5 ±â€¯0.1-39.0 ±â€¯0.1 °C: P < 0.001) and EUH acclimation (39.5 ±â€¯0.1-38.9 ±â€¯0.1 °C: P < 0.001). HR, RPE, physiological strain index (PSI), and total work (J) completed in a graded exercise test to exhaustion were improved (P < 0.001) in effect for acclimation, but not different when comparing DEH or EUH fluid delivery. SBF was unchanged (P = 0.313). Sweat rate increased greater following DEH (1.52 ±â€¯0.06-1.89 ±â€¯0.09 L h-1) compared to EUH acclimation (1.57 ±â€¯0.06-1.79 ±â€¯0.08 L h-1: P = 0.015). Resting plasma volume increased in effect for acclimation (P = 0.002). Aldosterone decreased in effect for acclimation (P < 0.001) at rest and following exercise, and total protein was unaffected (P = 0.83). In conclusion, short-term heat acclimation (~360 min) attenuates heat stress, and improves exercise capacity in the heat, and was not impaired nor improved by promoting DEH during acclimation.

Comparison of Sports Drink Versus Oral Rehydration Solution During Exercise in the Heat.

INTRODUCTION: This study compared 2 commercially available beverages, an oral rehydration solution (ORS; 60.9 mM Na+; 3.4% carbohydrate) and a sports drink (SDS; 18.4 mM Na+; 5.9% carbohydrate), on hydration and metabolism during submaximal exercise in the heat. METHODS: Ten male subjects completed two 90-min exercise trials (39ºC, 30%) of walking at 50% VO2max followed by a 30-min rest period in the heat while wearing wildland firefighter personal protective clothing. After 45 min of exercise, fluid delivery by either ORS or SDS replaced 150% of sweat loss. Subjects continued the exercise for 45 additional minutes followed by a 30-min rest period. Blood samples were collected pre-exercise (0 min), post-exercise (90 min), and post-trial (120 min) to measure plasma volume (%) and blood glucose (mg·dL-1). Expired gases were collected twice for 3 min for substrate oxidation. RESULTS: The sweat rate and percent dehydration did not differ between the groups (P=0.86 and P=0.79, respectively). Changes in plasma volume did not differ (P=0.55). Hemoglobin levels significantly increased in both groups post-trial (P=0.009). Blood glucose was significantly greater post-trial in SDS versus ORS (116±19 vs 103±13 mg·dL-1, respectively; P=0.01). Fat oxidation was lower post-exercise in SDS vs ORS (0.38±0.1 vs 0.47±0.2 g·min-1, respectively; P=0.049). CONCLUSIONS: These data indicate no difference in fluid retention between ORS or SDS when supplemented during exercise in the heat. This implies that fluid volume, and not drink contents, may be more important when ingested during exercise in a hot environment.

Metabolic Demand of Hiking in Wildland Firefighting.

INTRODUCTION: The objective of this study was to document characteristics of hiking during wildland firefighter (WLFF) training and wildfire suppression. For the first time, the overall physical demands during wildland firefighting were evaluated in the field using global positioning systems coupled with wireless physiological monitoring and load carriage prediction models. METHODS: Male (n=116) and female (n=15) interagency hotshot crew and type II WLFFs on wildfires volunteered for this direct observation study. Participants' heart rate, internal temperature, speed, and elevation gain were monitored throughout training and during wildfire suppression. The Pandolf and Santee equations were used to predict metabolic rate to estimate oxygen consumption of uphill and downhill hiking. RESULTS: Equipment weight varied by crew type (type II: 24±9 kg and interagency hotshot crew: 28±6 kg; P<0.05). Grade of terrain was steepest during training hikes, and ingress hikes were statistically different from egress and training hikes (ingress: 4±9%, shift: 4±9%, egress: 1±8%, training hikes: 10±9%; P<0.01). Estimated oxygen consumption was highest during ingress hikes and was significantly different from all other hike types on fire assignments (ingress: 22±12, shift: 19±12, egress: 19±12 mL·kg-1·min-1; P=0.01). Oxygen consumption was higher during training hikes (34±14 mL·kg-1·min-1) than during job-related hikes (P<0.01). CONCLUSIONS: The greatest metabolic demand during wildfire assignments occurred during ingress hikes. On average, this was close to the estimated metabolic demand of the job qualification arduous pack test. However, greater metabolic demand occurred for periods during both shift (on the job) and training hikes. These data quantify the demands associated with actual wildland performance of WLFFs and can help define future work capacity testing and training procedures.

Lung function measures following simulated wildland firefighter exposures.

Across the world, biomass smoke is a major source of air pollution and is linked with a variety of adverse health effects. This is particularly true in the western U.S. where wood smoke from wildland forest fires are a significant source of PM2.5. Wildland firefighters are impacted as they experience elevated PM2.5 concentrations over extended periods of time, often occurring during physical exertion. Various epidemiological studies have investigated wood smoke impacts on human health, including occupational field exposures experienced by wildland firefighters. As there are numerous challenges in carrying out these field studies, having the ability to research the potential health impacts to this occupational cohort in a controlled setting would provide important information that could be translated to the field setting. To this end, we have carried out a simulated wildland firefighter exposure study in a wood smoke inhalation facility. Utilizing a randomized crossover trial design, we exposed 10 participants once to clean filtered-air, 250 µg/m3, and 500 µg/m3 wood stove-generated wood smoke PM2.5. Participants exercised on a treadmill at an absolute intensity designed to simulate wildland firefighting for 1.5 hr. In addition to measured PM2.5 smoke concentrations, mean levels of CO2, CO, and % relative humidity were continuously monitored and recorded and were representative of occupational "real-world" exposures. Pulmonary function was measured at three time points: before, immediately after, and 1-hr post-exposure. Although there were some reductions in FVC, FEV1, and FVC:FEV1 measures, results of the spirometry testing did not show significant changes in lung function. The development of this wood smoke inhalational facility provides a platform to further address unique research questions related to wood smoke exposures and associated adverse health effects.

Impact of extreme exercise at high altitude on oxidative stress in humans.

Exercise and oxidative stress research continues to grow as a physiological subdiscipline. The influence of high altitude on exercise and oxidative stress is among the recent topics of intense study in this area. Early findings indicate that exercise at high altitude has an independent influence on free radical generation and the resultant oxidative stress. This review provides a detailed summary of oxidative stress biochemistry as gleaned mainly from studies of humans exercising at high altitude. Understanding of the human response to exercise at altitude is largely derived from field-based research at altitudes above 3000 m in addition to laboratory studies which employ normobaric hypoxia. The implications of oxidative stress incurred during high altitude exercise appear to be a transient increase in oxidative damage followed by redox-sensitive adaptations in multiple tissues. These outcomes are consistent for lowland natives, high altitude acclimated sojourners and highland natives, although the latter group exhibits a more robust adaptive response. To date there is no evidence that altitude-induced oxidative stress is deleterious to normal training or recovery scenarios. Limited evidence suggests that deleterious outcomes related to oxidative stress are limited to instances where individuals are exposed to extreme elevations for extended durations. However, confirmation of this tentative conclusion requires further investigation. More applicably, altitude-induced hypoxia may have an independent influence on redox-sensitive adaptive responses to exercise and exercise recovery. If correct, these findings may hold important implications for athletes, mountaineers, and soldiers working at high altitude. These points are raised within the confines of published research on the topic of oxidative stress during exercise at altitude.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.