Adaptations and mechanisms of human heat acclimation: Applications for competitive athletes and sports.

Exercise heat acclimation induces physiological adaptations that improve thermoregulation, attenuate physiological strain, reduce the risk of serious heat illness, and improve aerobic performance in warm-hot environments and potentially in temperate environments. The adaptations include improved sweating, improved skin blood flow, lowered body temperatures, reduced cardiovascular strain, improved fluid balance, altered metabolism, and enhanced cellular protection. The magnitudes of adaptations are determined by the intensity, duration, frequency, and number of heat exposures, as well as the environmental conditions (i.e., dry or humid heat). Evidence is emerging that controlled hyperthermia regimens where a target core temperature is maintained, enable more rapid and complete adaptations relative to the traditional constant work rate exercise heat acclimation regimens. Furthermore, inducing heat acclimation outdoors in a natural field setting may provide more specific adaptations based on direct exposure to the exact environmental and exercise conditions to be encountered during competition. This review initially examines the physiological adaptations associated with heat acclimation induction regimens, and subsequently emphasizes their application to competitive athletes and sports.

Consensus recommendations on training and competing in the heat.

Exercising in the heat induces thermoregulatory and other physiological strain that can lead to impairments in endurance exercise capacity. The purpose of this consensus statement is to provide up-to-date recommendations to optimize performance during sporting activities undertaken in hot ambient conditions. The most important intervention one can adopt to reduce physiological strain and optimize performance is to heat acclimatize. Heat acclimatization should comprise repeated exercise-heat exposures over 1-2 weeks. In addition, athletes should initiate competition and training in a euhydrated state and minimize dehydration during exercise. Following the development of commercial cooling systems (e.g., cooling vest), athletes can implement cooling strategies to facilitate heat loss or increase heat storage capacity before training or competing in the heat. Moreover, event organizers should plan for large shaded areas, along with cooling and rehydration facilities, and schedule events in accordance with minimizing the health risks of athletes, especially in mass participation events and during the first hot days of the year. Following the recent examples of the 2008 Olympics and the 2014 FIFA World Cup, sport governing bodies should consider allowing additional (or longer) recovery periods between and during events for hydration and body cooling opportunities when competitions are held in the heat.

Consensus recommendations on training and competing in the heat.

Exercising in the heat induces thermoregulatory and other physiological strain that can lead to impairments in endurance exercise capacity. The purpose of this consensus statement is to provide up-to-date recommendations to optimise performance during sporting activities undertaken in hot ambient conditions. The most important intervention one can adopt to reduce physiological strain and optimise performance is to heat acclimatise. Heat acclimatisation should comprise repeated exercise-heat exposures over 1-2 weeks. In addition, athletes should initiate competition and training in a euhydrated state and minimise dehydration during exercise. Following the development of commercial cooling systems (eg, cooling-vest), athletes can implement cooling strategies to facilitate heat loss or increase heat storage capacity before training or competing in the heat. Moreover, event organisers should plan for large shaded areas, along with cooling and rehydration facilities, and schedule events in accordance with minimising the health risks of athletes, especially in mass participation events and during the first hot days of the year. Following the recent examples of the 2008 Olympics and the 2014 FIFA World Cup, sport governing bodies should consider allowing additional (or longer) recovery periods between and during events, for hydration and body cooling opportunities, when competitions are held in the heat.

Expanded prediction equations of human sweat loss and water needs.

The Institute of Medicine expressed a need for improved sweating rate (msw) prediction models that calculate hourly and daily water needs based on metabolic rate, clothing, and environment. More than 25 years ago, the original Shapiro prediction equation (OSE) was formulated as msw (g.m(-2).h(-1))=27.9.Ereq.(Emax)(-0.455), where Ereq is required evaporative heat loss and Emax is maximum evaporative power of the environment; OSE was developed for a limited set of environments, exposures times, and clothing systems. Recent evidence shows that OSE often overpredicts fluid needs. Our study developed a corrected OSE and a new msw prediction equation by using independent data sets from a wide range of environmental conditions, metabolic rates (rest to 500 observations) by using a variety of metabolic rates over a range of environmental conditions (ambient temperature, 15-46 degrees C; water vapor pressure, 0.27-4.45 kPa; wind speed, 0.4-2.5 m/s), clothing, and equipment combinations and durations (2-8 h). Data are expressed as grams per square meter per hour and were analyzed using fuzzy piecewise regression. OSE overpredicted sweating rates (P<0.003) compared with observed msw. Both the correction equation (OSEC), msw=147.exp (0.0012.OSE), and a new piecewise (PW) equation, msw=147+1.527.Ereq-0.87.Emax were derived, compared with OSE, and then cross-validated against independent data (21 males and 9 females; >200 observations). OSEC and PW were more accurate predictors of sweating rate (58 and 65% more accurate, P<0.01) and produced minimal error (standard error estimate<100 g.m(-2).h(-1)) for conditions both within and outside the original OSE domain of validity. The new equations provide for more accurate sweat predictions over a broader range of conditions with applications to public health, military, occupational, and sports medicine settings.

Exercise associated hyponatraemia: quantitative analysis to understand the aetiology.

BACKGROUND: The development of symptomatic hyponatraemia consequent on participation in marathon and ultraendurance races has led to questions about its aetiology and prevention. OBJECTIVES: To evaluate: (a) the assertion that sweat sodium losses cannot contribute to the development of hyponatraemia during endurance exercise; (b) the adequacy of fluid replacement recommendations issued by the International Marathon Medical Directors Association (IMMDA) for races of 42 km or longer; (c) the effectiveness of commercial sports drinks, compared with water, for attenuating plasma sodium reductions. METHODS: A mathematical model was used to predict the effects of different drinking behaviours on hydration status and plasma sodium concentration when body mass, body composition, running speed, weather conditions, and sweat sodium concentration were systematically varied. RESULTS: Fluid intake at rates that exceed sweating rate is predicted to be the primary cause of hyponatraemia. However, the model predicts that runners secreting relatively salty sweat can finish ultraendurance exercise both dehydrated and hyponatraemic. Electrolyte-containing beverages are predicted to delay the development of hyponatraemia. The predictions suggest that the IMMDA fluid intake recommendations adequately sustain hydration over the 42 km distance if qualifiers-for example, running pace, body size-are followed. CONCLUSIONS: Actions to prevent hyponatraemia should focus on minimising overdrinking relative to sweating rate and attenuating salt depletion in those who excrete salty sweat. This simulation demonstrates the complexity of defining fluid and electrolyte consumption rates during athletic competition.

Fluid and electrolyte supplementation for exercise heat stress.

During exercise in the heat, sweat output often exceeds water intake, resulting in a body water deficit (hypohydration) and electrolyte losses. Because daily water losses can be substantial, persons need to emphasize drinking during exercise as well as at meals. For persons consuming a normal diet, electrolyte supplementation is not warranted except perhaps during the first few days of heat exposure. Aerobic exercise is likely to be adversely affected by heat stress and hypohydration; the warmer the climate the greater the potential for performance decrements. Hypohydration increases heat storage and reduces a person's ability to tolerate heat strain. The increased heat storage is mediated by a lower sweating rate (evaporative heat loss) and reduced skin blood flow (dry heat loss) for a given core temperature. Heat-acclimated persons need to pay particular attention to fluid replacement because heat acclimation increases sweat losses, and hypohydration negates the thermoregulatory advantages conferred by acclimation. It has been suggested that hyperhydration (increased total body water) may reduce physiologic strain during exercise heat stress, but data supporting that notion are not robust. Research is recommended for 3 populations with fluid and electrolyte balance problems: older adults, cystic fibrosis patients, and persons with spinal cord injuries.

Effects of pyridostigmine bromide on human thermoregulation during cold water immersion.

This study examined the effects of an oral 30-mg dose of pyridostigmine bromide (PYR) on thermoregulatory and physiological responses of men undergoing cold stress. Six men were immersed in cold water (20 degrees C) for up to 180 min on two occasions, once each 2 h after ingestion of PYR and 2 h after ingestion of a placebo. With PRY, erythrocyte cholinesterase inhibition was 33 +/- 12% (SD) 110 min postingestion (10 min preimmersion) and 30 +/- 7% at termination of exposure (mean 117 min). Percent cholinesterase inhibition was significantly related to lean body mass (r = -0.91, P less than 0.01). Abdominal discomfort caused termination in three of six PYR experiments but in none of the control experiments (mean exposure time 142 min). During immersion, metabolic rate, ventilatory volume, and respiratory rate increased significantly (P less than 0.05) over preimmersion levels and metabolic rate increased with duration of immersion (P less than 0.01) in both treatment but did not differ between conditions. PYR had no significant effect on rectal temperature, mean body temperature, thermal sensations, heart rate, plasma cortisol, or change in plasma volume. It was concluded that a 30-mg dose of PYR does not increase an individual's susceptibility to hypothermia during cold water immersion; however, in combination with cold stress, PYR may result in marked abdominal cramping and limit cold tolerance.

Control of thermoregulatory sweating is altered by hydration level and exercise intensity.

The purpose of this study was to examine the thermoregulatory sweating control parameters of threshold temperature and sensitivity to determine whether 1) these variables were altered by hypohydration level and exercise intensity and 2) these alterations, if present, were additive and independent. Nine heat-acclimated men completed a matrix of nine trials: three exercise intensities of 25, 45, and 65% maximal O2 uptake and three hydration levels, i.e., euhydration and hypohydration (Hy) at 3 and 5% of body weight. During each trial, subjects attempted 50 min of treadmill exercise in a warm room (30 degrees C dry bulb, 50% relative humidity) while esophageal temperature and upper arm sweating rate were continuously measured. Hypohydration was achieved by exercise and fluid restriction the day preceding the trials. The following new findings were made: 1) threshold temperature increased in graded manner with hypohydration level (approximately 0.06 degree C/% Hy); 2) sensitivity decreased in a graded manner with hypohydration level (approximately 0.06 units/%Hy); 3) threshold temperature was not altered by exercise intensity; and 4) sensitivity increased from low- to moderate- and high-intensity exercise. We conclude that both hypohydration level and exercise intensity produce independent effects on control of thermoregulatory sweating.

Impact of muscle injury and accompanying inflammatory response on thermoregulation during exercise in the heat.

This study examined whether muscle injury and the accompanying inflammatory responses alter thermoregulation during subsequent exercise-heat stress. Sixteen subjects performed 50 min of treadmill exercise (45-50% maximal O(2) consumption) in a hot room (40 degrees C, 20% relative humidity) before and at select times after eccentric upper body (UBE) and/or eccentric lower body (LBE) exercise. In experiment 1, eight subjects performed treadmill exercise before and 6, 25, and 30 h after UBE and then 6, 25, and 30 h after LBE. In experiment 2, eight subjects performed treadmill exercise before and 2, 7, and 26 h after LBE only. UBE and LBE produced marked soreness and significantly elevated creatine kinase levels (P < 0.05), but only LBE increased (P < 0.05) interleukin-6 levels. In experiment 1, core temperatures before and during exercise-heat stress were similar for control and after UBE, but some evidence for higher core temperatures was found after LBE. In experiment 2, core temperatures during exercise-heat stress were 0.2-0.3 degrees C (P < 0.05) above control values at 2 and 7 h after LBE. The added thermal strain after LBE (P < 0.05) was associated with higher metabolic rate (r = 0.70 and 0.68 at 2 and 6-7 h, respectively) but was not related (P > 0.05) to muscle soreness (r = 0.47 at 6-7 h), plasma interleukin-6 (r = 0.35 at 6-7 h), or peak creatine kinase levels (r = 0.22). Local sweating responses (threshold core temperature and slope) were not altered by UBE or LBE. The results suggest that profuse muscle injury can increase body core temperature during exercise-heat stress and that the added heat storage cannot be attributed solely to increased heat production.

Hypohydration and thermoregulation in cold air.

This study examined the effects of hypohydration on thermoregulation during cold exposure. In addition, the independent influences of hypohydration-associated hypertonicity and hypovolemia were investigated. Nine male volunteers were monitored for 30 min at 25 degrees C, then for 120 min at 7 degrees C, under three counterbalanced conditions: euhydration (Eu), hypertonic hypohydration (HH), and isotonic hypohydration (IH). Hypohydration was achieved 12 h before cold exposure by inducing sweating (HH) or by ingestion of furosemide (IH). Body weight decrease (4.1 +/- 0.2%) caused by hypohydration was similar for HH and IH, but differences (P < 0.05) were found between HH and IH in plasma osmolality (292 +/- 1 vs. 284 +/- 1 mosmol/kgH2O) and plasma volume reduction (-8 +/- 2 vs. -18 +/- 3%). Heat debt (349 +/- 14 among) did not differ (P > 0.05) among trials. Mean skin temperature decreased throughout cold exposure during Eu but plateaued after 90 min during HH and IH. Forearm-finger temperature gradient tended (P = 0.06) to be greater during Eu (10.0 +/- 0.7 degrees C) than during HH or IH (8.9 +/- 0.7 degrees C). This suggests weaker vasoconstrictor tone during hypohydration than during Eu. Final mean skin temperature was higher for HH than for Eu or IH (23.5 +/- 0.3, 22.6 +/- 0.4, and 22.9 +/- 0.3 degrees C, respectively), and insulation was lower on HH than on IH (0.13 +/- 0.01 vs. 0.15 +/- 0.01 degree C.W-1.m-2, respectively), but not with Eu (0.14 +/- 0.01 degree C.W-1.m-2). This provides some evidence that hypertonicity impairs the vasoconstrictor response to cold. Although mild hypohydration did not affect body heat balance during 2-h whole body exposure to moderate cold, hypohydration-associated hypertonicity may have subtle effects on vasoconstriction that could become important during a more severe cold exposure.

Cooling different body surfaces during upper and lower body exercise.

The effect of varying the body surface area being cooled by a liquid microclimate system was evaluated during exercise heat-stress conditions. Six male subjects performed a total of six exercise (O2 uptake = 1.2 l/min) tests in a hot environment (ambient temperature = 38 degrees C, relative humidity = 30%) while dressed in clothing having low moisture permeability and high insulation. Each subject completed two upper body exercise (U; arm crank) tests: 1) with only the torso surface (T) cooled; and 2) with the surfaces of both the torso and upper arms (TA) cooled [coolant temperature at the inlet (Ti) was 20 degrees C for all upper body tests]. Each subject also completed four lower body exercise (L; walking) tests: 1) with only the T cooled (Ti = 20 degrees C); 2) with only the T cooled (Ti = 26 degrees C); 3) with torso, upper arm, and thigh surface (TAT) cooled (Ti = 20 degrees C); and 4) with TAT cooled (Ti = 26 degrees C). During U exercise, TA cooling had no effects compared with cooling only T. During L exercise, sweat rates, heart rates, and rectal temperature (Tre) changes were less with TAT cooling compared with cooling only the T. Altering Ti had no effect on Tre changes, but higher heart rates were observed with 26 than with 20 degrees C. These data indicate that cooling arms during upper body exercise provides no thermoregulatory advantage, although cooling the thigh surfaces during lower body exercise does provide an advantage.

Human thermoregulatory responses to cold air are altered by repeated cold water immersion.

The effects of repeated cold water immersion on thermoregulatory responses to cold air were studied in seven males. A cold air stress test (CAST) was performed before and after completion of an acclimation program consisting of daily 90-min cold (18 degrees C) water immersion, repeated 5 times/wk for 5 consecutive wk. The CAST consisted of resting 30 min in a comfortable [24 degrees C, 30% relative humidity (rh)] environment followed by 90 min in cold (5 degrees C, 30% rh) air. Pre- and postacclimation, metabolism (M) increased (P less than 0.01) by 85% during the first 10 min of CAST and thereafter rose slowly. After acclimation, M was lower (P less than 0.02) at 10 min of CAST compared with before, but by 30 min M was the same. Therefore, shivering onset may have been delayed following acclimation. After acclimation, rectal temperature (Tre) was lower (P less than 0.01) before and during CAST, and the drop in Tre during CAST was greater (P less than 0.01) than before. Mean weighted skin temperature (Tsk) was lower (P less than 0.01) following acclimation than before, and acclimation resulted in a larger (P less than 0.02) Tre-to-Tsk gradient. Plasma norepinephrine increased during both CAST (P less than 0.002), but the increase was larger (P less than 0.004) following acclimation. These findings suggest that repeated cold water immersion stimulates development of true cold acclimation in humans as opposed to habituation. The cold acclimation produced appears to be of the insulative type.

Effects of body mass and morphology on thermal responses in water.

Ten male volunteers were divided into two groups based on body morphology and mass. The large-body mass (LM) group (n = 5) was 16.3 kg heavier and 0.22 cm2 X kg-1 X 10(-2) smaller in surface area-to-mass ratio (AD X wt-1) (P less than 0.05) than the small-body mass (SM) group (n = 5). Both groups were similar in total body fat and skinfold thicknesses (P greater than 0.05). All individuals were immersed for 1 h in stirred water at 26 degrees C during both rest and one intensity of exercise (metabolic rate approximately 550 W). During resting exposures metabolic rate (M) and rectal temperature (Tre) were not different (P greater than 0.05) between the LM and SM groups at min 60. Esophageal temperature (Tes) was higher (P less than 0.05) for the SM group at min 60, although the change in Tes during the 60 min between groups was similar (LM, -0.4 degrees C; SM, -0.2 degrees C). Tissue insulation (I) was lower (P less than 0.05) for SM (0.061 degrees C X m-2 X W-1) compared with the LM group (0.098 degrees C X m-2 X W-1). During exercise M, Tre, Tes, and I were not different (P greater than 0.05) between groups at min 60. These data illustrate that a greater body mass between individuals increases the overall tissue insulation during rest, most likely as a result of a greater volume of muscle tissue to provide insulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of skeletal muscle glycogen on passive rewarming after hypothermia.

To examine the influence of muscle glycogen on the thermal responses to passive rewarming subsequent to mild hypothermia, eight subjects completed two cold-water immersions (18 degrees C), followed by 75 min of passive rewarming (24 degrees C air, resting in blanket). The experiments followed several days of different exercise-diet regimens eliciting either low (LMG; 141.0 +/- 10.5 mmol.kg.dry wt-1) or normal (NMG; 526.2 +/- 44.2 mmol.kg.dry wt-1) prewarming muscle glycogen levels. Cold-water immersion was performed for 180 min or to a rectal temperature (Tre) of 35.5 degrees C. In four subjects (group A, body fat = 20 +/- 1%), postimmersion Tre was similar to preimmersion Tre for both trials (36.73 +/- 0.18 vs. 37.26 +/- 0.18 degrees C, respectively). Passive rewarming in group A resulted in an increase in Tre of only 0.13 +/- 0.08 degrees C. Conversely, initial rewarming Tre for the other four subjects (group B, body fat = 12 +/- 1%) averaged 35.50 +/- 0.05 degrees C for both trials. Rewarming increased Tre similarly in group B during both LMG (0.76 +/- 0.25 degrees C) and NMG (0.89 +/- 0.13 degrees C). Afterdrop responses, evident only in those individuals whose body core cooled during immersion (group B), were not different between LMG and NMG. These data support the contention that Tre responses during passive rewarming are related to body insulation. Furthermore these results indicate that low muscle glycogen levels do not impair rewarming time nor alter after-drop responses during passive rewarming after mild-to-moderate hypothermia.

Physiological tolerance to uncompensable heat stress: effects of exercise intensity, protective clothing, and climate.

This study determined the influence of exercise intensity, protective clothing level, and climate on physiological tolerance to uncompensable heat stress. It also compared the relationship between core temperature and the incidence of exhaustion from heat strain for persons wearing protective clothing to previously published data of unclothed persons during uncompensable heat stress. Seven heat-acclimated men attempted 180-min treadmill walks at metabolic rates of approximately 425 and 600 W while wearing full (clo = 1.5) or partial (clo = 1.3) protective clothing in both a desert (43 degrees C dry bulb, 20% relative humidity, wind 2.2 m/s) and tropical (35 degrees C dry bulb, 50% relative humidity, wind 2.2 m/s) climate. During these trials, the evaporative cooling required to maintain thermal balance exceeded the maximal evaporative capacity of the environment and core temperature continued to rise until exhaustion from heat strain occurred. Our findings concerning exhaustion from heat strain are 1) full encapsulation in protective clothing reduces physiological tolerance as core temperature at exhaustion was lower (P < 0.05) in fully than in partially clothed persons, 2) partial encapsulation results in physiological tolerance similar to that reported for unclothed persons, 3) raising metabolic rate from 400 to 600 W does not alter physiological tolerance when subjects are fully clothed, and 4) physiological tolerance is similar when subjects are wearing protective clothing in desert and tropical climates having the same wet bulb globe thermometer. These findings can improve occupational safety guidelines for human heat exposure, as they provide further evidence that the incidence of exhaustion from heat strain can be predicted from core temperature.

Thermoregulatory responses to cold water at different times of day.

This study examined how time of day affects thermoregulation during cold-water immersion (CWI). It was hypothesized that the shivering and vasoconstrictor responses to CWI would differ at 0700 vs. 1500 because of lower initial core temperatures (T(core)) at 0700. Nine men were immersed (20 degrees C, 2 h) at 0700 and 1500 on 2 days. No differences (P > 0.05) between times were observed for metabolic heat production (M, 150 W. m(-2)), heat flow (250 W. m(-2)), mean skin temperature (T(sk), 21 degrees C), and the mean body temperature-change in M (DeltaM) relationship. Rectal temperature (T(re)) was higher (P < 0.05) before (Delta = 0.4 degrees C) and throughout CWI during 1500. The change in T(re) was greater (P < 0. 05) at 1500 (-1.4 degrees C) vs. 0700 (-1.2 degrees C), likely because of the higher T(re)-T(sk) gradient (0.3 degrees C) at 1500. These data indicate that shivering and vasoconstriction are not affected by time of day. These observations raise the possibility that CWI may increase the risk of hypothermia in the early morning because of a lower initial T(core).

Thermoregulation during cold exposure: effects of prior exercise.

This study examined whether acute exercise would impair the body's capability to maintain thermal balance during a subsequent cold exposure. Ten men rested for 2 h during a standardized cold-air test (4.6 degrees C) after two treatments: 1) 60 min of cycle exercise (Ex) at 55% peak O(2) uptake and 2) passive heating (Heat). Ex was performed during a 35 degrees C water immersion (WI), and Heat was conducted during a 38.2 degrees C WI. The duration of Heat was individually adjusted (mean = 53 min) so that rectal temperature was similar at the end of WI in both Ex (38.2 degrees C) and Heat (38.1 degrees C). During the cold-air test after Ex, relative to Heat 1) rectal temperature was lower (P < 0.05) from minutes 40-120, 2) mean weighted heat flow was higher (P < 0.05), 3) insulation was lower (P < 0.05), and 4) metabolic heat production was not different. These results suggest that prior physical exercise may predispose a person to greater heat loss and to experience a larger decline in core temperature when subsequently exposed to cold air. The combination of exercise intensity and duration studied in these experiments did not fatigue the shivering response to cold exposure.

Human thermoregulatory responses during serial cold-water immersions.

This study examined whether serial cold-water immersions over a 10-h period would lead to fatigue of shivering and vasoconstriction. Eight men were immersed (2 h) in 20 degrees C water three times (0700, 1100, and 1500) in 1 day (Repeat). This trial was compared with single immersions (Control) conducted at the same times of day. Before Repeat exposures at 1100 and 1500, rewarming was employed to standardize initial rectal temperature. The following observations were made in the Repeat relative to the Control trial: 1) rectal temperature was lower and heat debt was higher (P < 0.05) at 1100; 2) metabolic heat production was lower (P < 0.05) at 1100 and 1500; 3) subjects perceived the Repeat trial as warmer at 1100. These data suggest that repeated cold exposures may impair the ability to maintain normal body temperature because of a blunting of metabolic heat production, perhaps reflecting a fatigue mechanism. An alternative explanation is that shivering habituation develops rapidly during serially repeated cold exposures.

Skeletal muscle metabolism during exercise is influenced by heat acclimation.

The influence of heat acclimation on skeletal muscle metabolism during submaximal exercise was studied in 13 healthy men. The subjects performed 30 min of cycle exercise (70% of individual maximal O2 uptake) in a cool [21 degrees C, 30% relative humidity (rh)] and a hot (49 degrees C, 20% rh) environment before and again after they were heat acclimated. Aerobic metabolic rate was lower (0.1 l X min-1; P less than 0.01) during exercise in the heat compared with the cool both before and after heat acclimation. Muscle and plasma lactate accumulation with exercise was greater (P less than 0.01) in the hot relative to the cool environment both before and after acclimation. Acclimation lowered (P less than 0.01) aerobic metabolic rate as well as muscle and plasma lactate accumulation in both environments. The amount of muscle glycogen utilized during exercise in the hot environment did not differ from that in the cool either before or after acclimation. These findings indicate that accumulation of muscle lactate is increased and aerobic metabolic rate is decreased during exercise in the heat before and after heat acclimation; increased muscle glycogen utilization does not account for the increased muscle lactate accumulation during exercise under extreme heat stress; and heat acclimation lowers the aerobic metabolic rate and muscle and blood lactate accumulation during exercise in a cool as well as a hot environment.

Comparison of thermal responses between rest and leg exercise in water.

This study examined both the thermal and metabolic responses of individuals in cool (30 degrees C, n = 9) and cold (18 degrees C, n = 7; 20 degrees C, n = 2) water. Male volunteers were immersed up to the neck for 1 h during both seated rest (R) and leg exercise (LE). In 30 degrees C water, metabolic rate (M) remained unchanged over time during both R (115 W, 60 min) and LE (528 W, 60 min). Mean skin temperature (Tsk) declined (P less than 0.05) over 1 h during R, while Tsk was unchanged during LE. Rectal (Tre) and esophageal (Tes) temperatures decreased (P less than 0.05) during R (delta Tre, -0.5 degrees C; delta Tes, -0.3 degrees C) and increased (P less than 0.05) during LE (delta Tre, 0.4 degrees C; Tsk, 0.4 degrees C). M, Tsk, Tre, and Tes were higher (P less than 0.05) during LE compared with R. In cool water, all regional heat flows (leg, chest, and arm) were generally greater (P less than 0.05) during LE than R. In cold water, M increased (P less than 0.05) over 1 h during R but remained unchanged during LE. Tre decreased (P less than 0.05) during R (delta Tre, -0.8 degrees C) but was unchanged during LE. Tes declined (P less than 0.05) during R (delta Tes, -0.4 degrees C) but increased (P less than 0.05) during LE (delta Tes, 0.2 degrees C). M, Tre, and Tes were higher (P less than 0.05), whereas Tsk was not different during LE compared with R at 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)