Heat strain evaluation of chemical protective garments.

BACKGROUND: The purpose of this study was to compare thermoregulatory and subjective responses of 12 test subjects (10 male, 2 female) wearing 5 different Joint Service Lightweight Integrated Suit Technology (JSLIST) prototype and 3 different currently fielded control chemical/ biological (CB) protective overgarments. METHODS: The overgarments were compared while subjects attempted to complete 100 min of moderate exercise (400 W) in an environmental chamber (35 degrees C/50% rh). Rectal temperature (Tre), skin temperature, heart rate, sweating rate, and test time, as well as subjective symptoms of heat illness were measured. Data were analyzed for times earlier than 100 min because subjects were not usually able to complete the 100-min trials. RESULTS: At 50 min, of the 3 controls, the Army/Air Force Battledress Overgarment (BDO) imposed significantly greater heat strain (indicated by Tre 37.90 degrees C) than the Marine Saratoga (SAR) (Tre 37.68 degrees C) and Navy Chemical Protective Overgarment (CPO) (Tre 37.69 degrees C). The JSLIST prototype garments imposed heat strain (50 min Tre 37.73-37.86 degrees C) as well as subjective perception of heat strain, that ranged between the warmest and coolest controls. CONCLUSIONS: In the environmental and exercise test conditions of this study, we did not find the five JSLIST overgarments to be consistently different from one another. Subjects in the control garments were and felt generally warmer (BDO) or cooler (SAR, CPO) than in the JSLIST prototype garments.

Physiologic tolerance to uncompensable heat: intermittent exercise, field vs laboratory.

PURPOSE: This study determined whether exercise (30 min)-rest (10 min) cycles alter physiologic tolerance to uncompensable heat stress (UCHS) when outdoors in the desert. In addition, the relationship between core temperature and exhaustion from heat strain previously established in laboratory studies was compared with field studies. METHODS: Twelve men completed four trials: moderate intensity continuous exercise (MC), moderate intensity exercise with intermittent rest (MI), hard intensity continuous exercise (HC), and hard intensity exercise with intermittent rest (HI). UCHS was achieved by wearing protective clothing and exercising (estimated at 420 W or 610 W) outdoors in desert heat. RESULTS: Heat Stress Index values were 200%, 181%, 417%, and 283% for MC, MI, HC, and HI, respectively. Exhaustion from heat strain occurred in 36 of 48 trials. Core temperatures at exhaustion averaged 38.6 +/- 0.5 degrees, 38.9 +/- 0.6 degrees, 38.9 +/- 0.7 degrees, and 39.0 +/- 0.7 degrees C for MC, MI, HC, and HI, respectively. Core temperature at exhaustion was not altered (P > 0.05) by exercise intensity or exercise-rest cycles and 50% of subjects incurred exhaustion at core temperature of 39.4 degrees C. These field data were compared with laboratory and field data collected over the past 35 years. Aggregate data for 747 laboratory and 131 field trials indicated that 50% of subjects incurred exhaustion at core temperatures of 38.6 degrees and 39.5 degrees C, respectively. When heat intolerant subjects (exhaustion < 38.3 degrees C core temperature) were removed from the analysis, subjects from laboratory studies (who underwent short-term acclimation) still demonstrated less (0.8 degrees C) physiological tolerance than those from field studies (who underwent long-term acclimatization). CONCLUSION: Exercise-rest cycles did not alter physiologic tolerance to UCHS. In addition, subjects from field studies demonstrate greater physiologic tolerance than subjects from laboratory studies.

Heat strain imposed by toxic agent protective systems.

This study evaluated physiological heat strain from two developmental toxic agent protective systems compared with the standard Toxicological Agent Protective (TAP) suit during exercise-heat stress. Eight subjects (six men, two women) completed three experimental trials, at 38 degrees C, 30% rh, wearing: 1) Self Contained Toxic Environment Protective Outfit (STEPO) with rebreather (STEPO-R); 2) STEPO with tether (STEPO-T) or 3) the standard TAP. The STEPO systems provided effective body cooling of: STEPO-R, 200 +/- 36 W; and STEPO-T, 186 +/- 59 W. TAP had no cooling. All experimental trials used treadmill walking at 0.89 m x s(-1), 0% grade at exercise/rest cycles of 20/10 min for 240 min. Metabolic rates for the treatments were: STEPO-R, 298 +/- 26 W; STEPO-T, 299 +/- 34 W; and TAP, 222 +/- 40 W. Rate of heat storage was less (p < 0.05) in STEPO-R (37 +/- 8 W x m(-2)) and STEPO-T (38 +/- 12 W x m(-2)) than in TAP (77 +/- 15 W x m(-2)). Sweating rate was less (p < 0.05) in STEPO-T (10.0 +/- 4.8 g x min(-1)) than in TAP (23.8 x 11.4 g x min(-1)). There was no difference between STEPO-R (12.3 +/- 5.6 g min(-1)) and the other two uniform systems. Subjects did not complete targeted exposure times of 240 min. Exposure time was longer (p < 0.05) in STEPO-R (83 +/- 22 min) and STEPO-T (106 +/- 39 min) than in TAP (46 +/- 10 min). Predicted time to 39.0 degrees C was less (p < 0.05) in TAP (69 +/- 20 min) than in either STEPO-R (226 +/- 124 min) or STEPO-T (244 +/- 170 min). The results of this study show that cooling in STEPO significantly reduced heat storage relative to TAP. The new generation toxic cleanup uniform systems effectively reduced heat stress and increased work capabilities compared with the standard TAP suit.

Thermoregulation during cold exposure after several days of exhaustive exercise.

This study examined the hypothesis that several days of exhaustive exercise would impair thermoregulatory effector responses to cold exposure, leading to an accentuated core temperature reduction compared with exposure of the same individual to cold in a rested condition. Thirteen men (10 experimental and 3 control) performed a cold-wet walk (CW) for up to 6 h (6 rest-work cycles, each 1 h in duration) in 5 degrees C air on three occasions. One cycle of CW consisted of 10 min of standing in the rain (5.4 cm/h) followed by 45 min of walking (1.34 m/s, 5.4 m/s wind). Clothing was water saturated at the start of each walking period (0.75 clo vs. 1.1 clo when dry). The initial CW trial (day 0) was performed (afternoon) with subjects rested before initiation of exercise-cold exposure. During the next 7 days, exhaustive exercise (aerobic, anaerobic, resistive) was performed for 4 h each morning. Two subsequent CW trials were performed on the afternoon of days 3 and 7, approximately 2.5 h after cessation of fatiguing exercise. For controls, no exhaustive exercise was performed on any day. Thermoregulatory responses and body temperature during CW were not different on days 0, 3, and 7 in the controls. In the experimental group, mean skin temperature was higher (P < 0.05) during CW on days 3 and 7 than on day 0. Rectal temperature was lower (P < 0.05) and the change in rectal temperature was greater (P < 0.05) during the 6th h of CW on day 3. Metabolic heat production during CW was similar among trials. Warmer skin temperatures during CW after days 3 and 7 indicate that vasoconstrictor responses to cold, but not shivering responses, are impaired after multiple days of severe physical exertion. These findings suggest that susceptibility to hypothermia is increased by exertional fatigue.

Cross validation of USARIEM heat strain prediction models. U.S. ARMY Research Institute of Environmental Medicine.

HYPOTHESIS: This study was a cross validation of three heat strain prediction models developed at the U.S. Army Research Institute of Environmental Medicine: the ARIEM, HSDA, and ARIEM-EXP models ability to predict core temperature. METHODS: Seven heat-acclimated subjects completed twelve experimental tests, six in each of two hot climates, at three exercise intensities and two uniform configurations in each climate. RESULTS: Experimental results showed physiological responses as expected with heat strain increasing with work load and level of protective clothing, but with similar heat strain between the two environments matched for wet bulb, globe index. Neither the ARIEM or HSDA model closely predicted core temperatures over the course of the experiment, due mostly to an abrupt initial rise in core temperature in both models. A proportionality constant in the ARIEM-EXP buffered some of this abrupt rise. CONCLUSIONS: Comparisons of the core temperature and tolerance times data with the three models led to the conclusions that for healthy males: 1) the ARIEM and HSDA models provide conservative safety limits as a result of predicting rapid initial increases in core temperature; 2) the ARIEM-EXP most closely represents core temperature responses; 3) the ARIEM-EXP requires modifications with an alternate proportionality coefficient to increase accuracy for low metabolic cost exercise; 4) all of the models require additional input from existing research on tolerance to heat strain to better predict tolerance times; and 5) additional models should be examined to investigate the transient state of the body as it is affected by environment, clothing and exercise.

Exertional fatigue, sleep loss, and negative energy balance increase susceptibility to hypothermia.

The purpose of this study was to determine how chronic exertional fatigue and sleep deprivation coupled with negative energy balance affect thermoregulation during cold exposure. Eight men wearing only shorts and socks sat quietly during 4-h cold air exposure (10 degreesC) immediately after (<2 h, A) they completed 61 days of strenuous military training (energy expenditure approximately 4,150 kcal/day, energy intake approximately 3,300 kcal/day, sleep approximately 4 h/day) and again after short (48 h, SR) and long (109 days, LR) recovery. Body weight decreased 7.4 kg from before training to A, then increased 6.4 kg by SR, with an additional 6.4 kg increase by LR. Body fat averaged 12% during A and SR and increased to 21% during LR. Rectal temperature (Tre) was lower before and during cold air exposure for A than for SR and LR. Tre declined during cold exposure in A and SR but not LR. Mean weighted skin temperature (Tsk) during cold exposure was higher in A and SR than in LR. Metabolic rate increased during all cold exposures, but it was lower during A and LR than SR. The mean body temperature (0.67 Tre + 0.33 Tsk) threshold for increasing metabolism was lower during A than SR and LR. Thus chronic exertional fatigue and sleep loss, combined with underfeeding, reduced tissue insulation and blunted metabolic heat production, which compromised maintenance of body temperature. A short period of rest, sleep, and refeeding restored the thermogenic response to cold, but thermal balance in the cold remained compromised until after several weeks of recovery when tissue insulation had been restored.

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.

Role of thermal factors on aerobic capacity improvements with endurance training.

This investigation studied the importance of the rise in body temperature during exercise for aerobic capacity adaptations produced by endurance training. The approach used was to compare training effects produced by subjects exercising in hot (35 degrees C) water vs. cold (20 degrees C) water. Hot water was used to potentiate, and cold water to blunt, the rise in body temperature during exercise. Eighteen young men trained by cycle-ergometer exercise at 60% of maximal oxygen uptake (VO2max) while immersed to the neck in either hot (HWT, n = 9) or cold (CWT, n = 9) water for 60 min, 5 days/wk, for 8 wk. Before and after training, VO2max, erythrocyte volume, plasma volume, and vastus lateralis citrate synthase activity were measured. Training increased (P < 0.01) VO2max by 13%, with no difference between HWT and CWT in the magnitude of the effect. Erythrocyte volume increased 4% (P < 0.01) with training, with no difference between HWT and CWT in the magnitude of the effect. Plasma volume remained unchanged by training in both the HWT and CWT groups. Last, vastus lateralis citrate synthase activity increased by 38% with training, but there was no difference between HWT and CWT in the training effect. Thus, exercise-induced body temperature elevations are not an important stimulus for the aerobic adaptations to moderate-intensity endurance training.

Heat exchange after cholinolytic and oxime therapy in protective clothing.

The effect of the currently fielded therapeutic antidotal (DRUG) combination (a cholinolytic, 2 mg of atropine sulfate, and an oxime, 600 mg of pralidoxime chloride) in combination with chemical protective Mission Oriented Protective Posture clothing (MOPP IV) was studied. Eight healthy male subjects participated in intermittent light physical activity (1.4-2.1 kcal/minute) in two distinct environments: 35 degrees C, 60% rh (95 degrees F, HOT) and 13 degrees C, 44% rh (55 degrees F, COOL). Subjects were exposed once to HOT wearing MOPP (CON) and once wearing MOPP after DRUG. Similarly, each subject was exposed to COOL wearing MOPP and MOPP after DRUG. Rectal temperature (Tre) and mean weighted skin temperature (Tsk) were not different between DRUG and CON during COOL. Exposure time during COOL was 350 minutes. Tre averaged .5 degrees C higher in DRUG than CON in HOT. The rate of core temperature increase was 2 times faster in DRUG than CON in HOT. Tsk was 1.0 degrees C higher in DRUG experiments in HOT. Whole-body sweating rate was 40% lower (p less than .05) in DRUG than CON experiments in HOT. Heart rate was 27 beats/minute higher by 30 minutes post-injection in DRUG at 35 degrees C. Exposure time was 213 +/- 30 minutes in CON and 190 +/- 38 minutes in DRUG at 35 degrees C. These data indicate the currently fielded therapeutic antidotal drug combination increases thermal strain in subjects exposed to a hot environment when wearing protective clothing. The results are applicable to subjects performing light, intermittent work. At higher work intensities, these findings of increased thermal strain would be exacerbated.

Evaluation of three commercial microclimate cooling systems.

Three commercially available microclimate cooling systems were evaluated for their ability to reduce heat stress in men exercising in a hot environment while wearing high insulative, low permeability clothing. Five male volunteers performed three 180-min experiments (three repeats of 10 min rest, 50 min walking at 440 watts) in an environment of 38 degrees C dry bulb (Tdb), 12 degrees C dew point (Tdp). The cooling systems were: 1) ILC Dover Model 19 Coolvest (ILC), mean inlet temperature 5.0 degrees C; 2) LSSI Coolhead (LSSI), mean inlet temperature 14.5 degrees C; and 3) Thermacor Cooling Vest (THERM), mean inlet temperature 28.3 degrees C. Endurance time (ET), heart rate (HR), rectal temperature (Tre), mean skin temperature (Tsk), sweating rate (SR), rated perceived exertion (RPE), and thermal sensation (TS) were measured. A computer model prediction of ET with no cooling was 101 min. ET was greater (p less than 0.01) with ILC (178 min) than THERM (131 min) which was greater (p less than 0.01) than LSSI (83 min). The subjects self terminated on all LSSI tests because of headaches. Statistical analyses were performed on data collected at 60 min to have values on all subjects. There were no differences in HR, Tre, SR, or TS values among the cooling vests. The subjects' Tsk was lower (p less than 0.05) for the LSSI than THERM; and RPE values were higher (p less than 0.05) for LSSI than the other two vests. These data suggest an improved physiological response to exercise heat stress with all three commercial systems with the greatest benefit in performance time provided by the ILC cooling system.

Thermoregulatory responses of middle-aged and young men during dry-heat acclimation.

Thermoregulatory responses during heat acclimation were compared between nine young (mean age 21.2 yr) and nine middle-aged men (mean age 46.4 yr) who were matched (P greater than 0.05) for body weight, surface area, surface area-to-weight ratio, percent body fat, and maximal aerobic power. After evaluation in a comfortable environment (22 degrees C, 50% relative humidity), the men were heat acclimated by treadmill walking (1.56 m/s, 5% grade) for two 50-min exercise bouts separated by 10 min of rest for 10 consecutive days in a hot dry (49 degrees C ambient temperature, 20% relative humidity) environment. During the first day of heat exposure performance time was 27 min longer (P less than 0.05) for the middle-aged men, whereas final rectal and skin temperatures and heart rate were lower, and final total body sweat loss was higher (P less than 0.05) compared with the young men. These thermoregulatory advantages for the middle-aged men persisted for the first few days of exercise-heat acclimation (P less than 0.05). After acclimation no thermoregulatory or performance time differences were observed between groups (P greater than 0.05). Sweating sensitivity, esophageal temperature at sweating onset, and the sweating onset time did not differ (P greater than 0.05) between groups either pre- or postacclimatization. Plasma osmolality and sodium concentration were slightly lower for the young men both pre- and postacclimatization; however, both groups had a similar percent change in plasma volume from rest to exercise during these tests.(ABSTRACT TRUNCATED AT 250 WORDS)

Human thermoregulation after atropine and/or pralidoxime administration.

The effects of intramuscular saline (control), atropine (2 mg), and/or pralidoxime (600 mg) on heat exchange was evaluated in four healthy males during seated, cycle exercise (55% Vo2 peak) in a temperate environment (Ta = 30.3 degrees C, Pw = 1.0 kPa). Esophageal (Tes), rectal (Tre), and mean skin temperatures (Tsk), and chest and forearm sweating (ms) were continuously measured. Skin blood flow (FBF) from the forearm was measured twice each minute by venous occlusion plethysmography. Whole body sweating was calculated from weight changes. The expected result of atropine injection, decreased eccrine sweating (-60%, p less than 0.05) and elevated esophageal (+0.4 degree C, p less than 0.05) and skin temperatures (+2.1 degrees C, p less than 0.05) was observed relative to control. Heart rate (+28 b X min-1) and FBF (+9 ml X 100 ml-1 X min-1) were higher after atropine. Pralidoxime, in general, did not affect the core and skin temperature responses to the exercise differently from control; however, a slightly elevated FBF (+3 ml X 100 cc-1 X min-1, 33%) compensated for the reduction in whole body sweating (-45%, p less than 0.05] that we observed. The combination of the drugs resulted in significantly higher esophageal (0.4 degree C) and skin (0.9 degree C) temperatures than atropine alone, as has been previously shown. The thermoregulatory disadvantage of inhibited sweating by atropine was partially compensated for by enhanced skin blood flow in this environment where Ta less than Tsk. Pralidoxime was shown to decrease whole body sweating, by a mechanism as yet unexplained.

Effects of atropine on thermoregulatory responses to exercise in different environments.

The thermoregulatory effects of atropine (2 mg im) were examined in six heat-acclimated subjects during exercise in three environments, which provided different evaporative capacities, but similar heat stress as indicated by the wet bulb, globe temperature index (WBGT). Subjects walked in environments of Ta = 42.3 degrees C, Tdp = 14.6 degrees C, WBGT = 29.1 degrees C (HD); Ta = 33.9 degrees C, Tdp = 23.5 degrees C, WBGT = 28.9 degrees C (WM); Ta = 30.4 degrees C, Tdp = 23.8 degrees C, WBGT = 27.4 degrees C, (WW) after atropine and saline injections. In comparison to saline, atropine elevated rectal temperature (Tre) (p less than 0.05) in HD. Additionally, atropine elevated (p less than 0.01) mean skin temperature (Tsk), and heart rate (HR) in all three environments relative to saline. Whole body sweating rate (msw) was 45% lower (p less than 0.01) in each environment after atropine relative to saline. Exercise time was reduced from saline values (p less than 0.05) by 26.5 min in the HD after atropine. Within the atropine treatments, Tre was higher (p less than 0.05) in HD (0.6 degrees C) than WW, and HR was higher (p less than 0.05) in HD (23 b X min-1) and WM (14 b X min-1) than WW. Tsk was higher (p less than 0.01) in WM than WW (1.2 degrees C) and in HD than WM (1.5 degrees C). Exercise time was 26.5 min longer (p less than 0.05) in WW than HD in the atropine experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Influence of heat stress and acclimation on maximal aerobic power.

Thirteen male volunteers performed cycle ergometer maximal oxygen uptake (VO2max tests) in moderate (21 degrees C, 30% rh) and hot (49 degrees C, 20% rh) environments, before and after a 9-day heat acclimation program. This program resulted in significantly decreased (P less than 0.01) final heart rate (24 bt X min-1) and rectal temperature (0.4 degrees C) from the first to last day of acclimation. The VO2max was lower (P less than 0.01) in the hot environment relative to the moderate environment both before (8%) and after (7%) acclimation with no significant difference (P greater than 0.05) shown for maximal power output (PO max, watts) between environments either before or after acclimation. The VO2max was higher (P less than 0.01) by 4% after acclimation in both environments. Also, PO max was higher (P less than 0.05) after acclimation in both the moderate (4%) and hot (2%) environments. The reduction in VO2max in the hot compared to moderate environment was not related to the difference in core temperature at VO2max between moderate and hot trials, nor was it strongly related with aerobic fitness level. These findings indicate that heat stress, per se, reduced the VO2max. Further, the reduction in VO2max due to heat was not affect be state of heat acclimation, the degree of elevation in core temperature, or level of aerobic fitness.

Effects of heat acclimation on atropine-impaired thermoregulation.

The effects of saline or atropine injection (2 mg, im) on eccrine sweating and performance time in seven healthy male subjects were evaluated during treadmill walking (1.34 m X s-1) in a hot-dry environment (Ta = 49 degrees C, Tdp = 20.5 degrees C) before and after heat acclimation (HA). Mean skin temperature (Tsk), rectal temperature (Tre), and heart rate (HR) were continuously measured. Sweat loss from the skin (Msw) was calculated by changes in body weight. HA resulted in decreased (p less than 0.05) Tre (0.4 degrees C) and HR (17 b X min-1), and increased (p less than 0.05) Msw (16 g X m-2 X h-1) during the saline experiments. Pre-acclimation, Msw was reduced (p less than 0.01) 65% (151 g X m-2 X h-1) with atropine, which resulted in higher (p less than 0.01) Tre (0.4 degrees C) and Tsk (2.8 degrees C). HR was increased 48% (53 b X min-1) by atropine pre-acclimation (p less than 0.01). Post-acclimation, atropine reduced (p less than 0.01) Msw 33% (100 g X m-2 X h-1) and increased (p less than 0.01) HR 63% (62 b X min-1) compared to saline exposures. The change in Tre X min-1 (delta Tre/delta t) was lower (p less than 0.05) in atropine-injected subjects following heat acclimation, and their worktime was improved by an average of 23.5 min (p = 0.08). These data demonstrate that heat acclimation improves the endurance time of atropine-treated subjects in a hot-dry environment. This improvement was, in part, due to the potentiation of sweat gland activity enabling greater evaporative cooling for the same dose of atropine.

Aerobic fitness and the hypohydration response to exercise-heat stress.

This study examined the influence that aerobic fitness (VO2 max) had on final heart rate (HR), final rectal temperature (Tre), and total body sweat rate (Msw) when subjects exercised while euhydrated and hypohydrated (-5.0% from baseline body weight). Eight male and six female subjects completed four exercise tests both before and after a 10-d heat acclimation program. The tests were a euhydration and a hypohydration exposure conducted in a comfortable (20 degrees C, 40% rh) and in a hot-dry (49 degrees C, 20% rh) environment. Significant differences were not generally found between the genders for HR, Tre and Msw during the tests. In the comfortable environment, HR, Tre and Msw were not generally significantly correlated (p greater than 0.05) with VO2max. In the hot-dry environment, Tre and VO2max were significantly correlated (r = -0.58) when euhydrated before acclimation. HR was significantly related to VO2max before acclimation when eu- (r = -0.61) and hypohydrated (r = -0.60) as well as after acclimation when eu- (r = -0.57) and hypohydrated (r = -0.67). These data indicate that, when euhydrated in the heat, aerobic fitness provides cardiovascular and thermoregulatory benefits before acclimation, but only cardiovascular benefits after acclimation. However, when hypohydrated in the heat, cardiovascular benefits are present for fit subjects both before and after acclimation, but thermoregulatory benefits are not associated with fitness.

Varied and repeated atropine dosages and exercise-heat stress.

Comparisons of physiological responses to 0, 0.5, 1, and 2 mg atropine (IM) were made in seven males (X +/- SD: age, 24 +/- 3 years; ht, 174 +/- 12 cm; wt, 76 +/- 3 kg) while they exercised (approximately 390 W) in a hot-dry (40 degrees C, 20% rh) environment. Responses to 4 mg, as well as repeatability of responses to 2 mg, were studied in two and six of these subjects, respectively. On 8 test days an intramuscular injection of atropine or saline control was administered 20 min before subjects walked on a treadmill for two 50-min bouts. Heart rate (HR) during exercise did not change in the control trial but by min 50 increased during all atropine trials (P less than 0.01). Rectal temperature (Tre) increased (P less than 0.01) in all trials by min 50 and continued increasing (P less than 0.01) in the 2-mg trial during the second exercise bout. For the two subjects tested with all dosages (0.5 - 4 mg atropine), the change in HR and Tre between the atropine and control trials at 50 min of exercise was regressed against the various atropine dosages. The relationship (r = 0.92) for HR was curvilinear while the relationship (r = 0.99) for Tre was linear. Mean weighted skin temperature (Tsk) was relatively constant during exercise and was warmer (P less than 0.05) with increasing atropine dosage. In a repeat 2 mg trial, HR was 6 bt . min-1 lower (P less than 0.05) on the second exposure but Tre was the same (P greater than 0.05) on both days. For subjects walking in the heat, three new observations were: 1) 0.5 mg of atropine resulted in increased HR and Tsk compared to control values; 2) HR was elevated but the magnitude of change decreased with increasing dosage, while the elevation in Tre was consistent with increasing dosage; and 3) rectal temperatures (in trials with and without atropine) were unaffected by previous days of atropine administration.

Fructose and glucose ingestion and muscle glycogen use during submaximal exercise.

Substrate utilization after fructose, glucose, or water ingestion was examined in four male and four female subjects during three treadmill runs at approximately 75% of maximal O2 uptake. Each test was preceded by three days of a carbohydrate-rich diet. The runs were 30 min long and were spaced at least 1 wk apart. Exercise began 45 min after ingestion of 300 ml of randomly assigned 75 g fructose (F), 75 g glucose (G), or control (C). Muscle glycogen depletion determined by pre- and postexercise biopsies (gastrocnemius muscle) was significantly (P less than 0.05) less during the F trial than during C or G. Venous blood samples revealed a significant increase in serum glucose (P less than 0.05) and insulin (P less than 0.01) within 45 min after the G drink, followed by a decrease (P less than 0.05) in serum glucose during the first 15 min of exercise, changes not observed in the C or F trials. Respiratory exchange ratio was higher (P less than 0.05) during the G than C or F trials for the first 5 min of exercise and lower (P less than 0.05) during the C trial compared with G or F for the last 15 min of exercise. These data suggest that fructose ingested before 30 min of submaximal exercise maintains stable blood glucose and insulin concentrations, which may lead to the observed sparing of muscle glycogen.