Finger vasodilation correlates better with tympanic than esophageal temperature

The relationship of finger blood flow (FBF) measured by venous occlusion plethysmography to tympanic temperature (Tty) was compared with that of FBF to esophageal temperature (Tes) during exercise at 50% VO2max for 40 min at an ambient temperature of 25 degrees C. The relationship of FBF to Tes showed an inflexion as Tes increased during exercise. The slope of the regression line showing the relationship between FBF and Tes was initially moderate, and then suddenly became steeper at the inflexion point. The relationship of FBF to Tty, however, was linear, without an inflexion. The results suggest that finger vasodilation during moderate exercise correlates better with tympanic than esophageal temperature.     

Effects of facial fanning on local exercise performance and thermoregulatory responses during hyperthermia

To investigate the effects of hyperthermia and facial fanning during hyperthermia on hand-grip exercise performance and thermoregulatory response, we studied eight male subjects, aged 20-53 years. Subjects exercised at 20% of maximal hand-grip strength in the sitting position under three conditions: normothermia (NT), hyperthermia without fanning (HT-nf) or with fanning at 5.5 m X sec-1 wind speed (HT-f). Hyperthermia (0.5 degrees C higher oesophageal temperature than in NT) was induced by leg immersion in water at 42 degrees C. Mean exercise performance was markedly reduced from 716 contractions (NT) to 310 (HT-nf) by hyperthermia (P less than 0.01) and significantly (P less than 0.05) improved to 431 (HT-f) by facial fanning. Hyperthermic exercise was accompanied by significant increases in forearm blood flow (71%) and the local sweat rate on the thigh (136%) at the end of exercise compared with that in NT. Heart rate (HR) and rating of perceived exertion (RPE) increased during exercise and were higher in HT-nf than in NT at any given time of exercise. Oesophageal, tympanic (Tty) and mean skin temperatures were also significantly higher in HT-nf than in NT. Facial fanning caused a marked decrease in forehead skin temperature (1.5-2.0 degrees C) and a slight decrease in Tty, HR and PRE compared with that in HT-nf at any given time of exercise. These results suggested that hyperthermia increased thermoregulatory demands and reduced exercise performance. Facial fanning caused decreases in face skin and brain temperatures, and improved performance.     

Precedence of head homoeothermia over trunk homoeothermia in dehydrated men

Three male humans were subjected repeatedly to 20 min exercise on a bicycle ergometer: twice when hydrated normally and twice when dehydrated. Tympanic (Tty) and oesophageal (Tes) temperatures were recorded and sweat rates on forehead and back were measured. Dehydration did not change the forehead sweat rate, but on the back it reduced significantly, resulting in an increase of Tes. However, Tty was decreased by dehydration. 20 min after the end of exercise subjects were allowed to drink water in order to trigger the potohidrotic response. A potohidrotic response was noted on the back of dehydrated subjects only. It is concluded that dehydration results in active inhibition of sweating on the body but not on the forehead, where evaporation is needed for selective cooling of the brain.     

Effect of saline infusion during exercise on thermal and circulatory regulations

To quantify the effect of an acute increase in plasma volume (PV) on forearm blood flow (FBF), heart rate (HR), and esophageal temperature (Tes) during exercise, we studied six male volunteers who exercised on a cycle ergometer at 60% of maximal aerobic power for 50 min in a warm [(W), 30 degrees C, less than 30% relative humidity (rh)] or cool environment [(C), 22 degrees C, less than 30% rh] with isotonic saline infusion [Inf(+)] or without infusion [Inf(-)]. The infusion was performed at a constant rate of 0.29 ml.kg body wt-1.min-1 for 20-50 min of exercise to mimic fluid intake during exercise. PV decreased by approximately 5 ml/kg body wt within the first 10 min of exercise in all protocols. Therefore, PV in Inf(-) was maintained at the same reduced level by 50 min of exercise in both ambient temperatures, whereas PV in Inf(+) increased toward the preexercise level and recovered approximately 4.5 ml/kg body wt by 50 min in both temperatures. The restoration of PV during exercise suppressed the HR increase by 6 beats/min at 50 min of exercise in W; however, infusion had no effect on HR in C. In W, FBF in Inf(+) continued to increase linearly as Tes rose to 38.1 degrees C by the end of exercise, whereas FBF in Inf(-) plateaued when Tes reached approximately 37.7 degrees C. The infusion in C had only a minor effect on FBF.(ABSTRACT TRUNCATED AT 250 WORDS)     

No evidence for brain stem cooling during face fanning in humans.

The interpeak latencies (IPLs) of the acoustically evoked brain stem potentials depend on brain stem temperature. This was used to see whether face fanning during hyperthermia lowers brain stem temperature. In 15 subjects, three thermally stable conditions were maintained by a water bath. In each condition the IPLs were determined in 10 separate trials. In condition A esophageal temperature (Tes) was 36.9 +/- 0.3 degrees C and increased to 38.6 +/- 0.2 degrees C in condition B. In conditions A and B the head was enclosed in a ventilated hood (air temperature 38 degrees C, relative humidity 100%) to suppress any direct heat loss from the head. From conditions A to B the IPL at peaks I-V decreased by 0.146 ms/degrees C change in Tes, reflecting a change in brain stem temperature. In condition C the hood was removed and the face was fanned by a cold air-stream (8-15 degrees C, 4-10 m/s) to maximize direct heat loss from the head. Skin temperature at the sweating forehead decreased from 38 to 23 degrees C, whereas Tes in condition C was maintained at the same level as in condition B (38.5 +/- 0.2 degrees C). The IPL at peaks I-V showed no difference between conditions B and C. It is concluded that face fanning in hyperthermic subjects does not dissociate brain stem temperature from Tes.     

Effect of exercise hemoconcentration and hyperosmolality on exercise responses

We investigated the effects of a decrease in plasma volume (PV) and an increase in plasma osmolality during exercise on circulatory and thermoregulatory responses. Six subjects cycled at approximately 65% of their maximum O2 uptake in a warm environment (30 degrees C, 40% relative humidity). After 30 min of control (C) exercise (no infusion), PV decreased 13.0%, or 419 +/- 106 (SD) ml, heart rate (HR) increased to 167 +/- 3 beats/min, and esophageal temperature (Tes) rose to 38.19 +/- 0.09 degrees C (SE). During infusion studies (INF), infusates were started after 10 min of exercise. The infusates contained 5% albumin suspended in 0.45, 0.9, or 3.0% saline. The volume of each infusate was adjusted so that during the last 10 min of exercise PV was maintained at the preexercise level and osmolality was allowed to differ. HR was significantly lower (10-16 beats/min) during INF than during C. Tes was reduced significantly during INF, with trends for increased skin blood flow and decreased sweating rates. No significant differences in HR, Tes, or sweating rate occurred between the three infusion conditions. We conclude that the decrease in PV, which normally accompanies moderate cycle exercise, compromises circulatory and thermal regulations. Increases in osmolality appear to have small if any effects during such short-term exercise.     

Rectal and rectal vs. esophageal temperatures in paraplegic men during prolonged exercise

This study investigated the rectal (Tre), esophageal (Tes), and skin (Tsk) temperature changes in a group of trained traumatic paraplegic men pushing their own wheelchairs on a motor-driven treadmill for a prolonged period in a neutral environment. There were two experiments. The first experiment (Tre and Tsk) involved a homogeneous group (T10-T12/L3) of highly trained paraplegic men [maximum O2 uptake (VO2max) 47.5 +/- 1.8 ml.kg-1.min-1] exercising for 80 min at 60-65% VO2max.Tre and Tsk (head, arm, thigh, and calf) and heart rate (HR) were recorded throughout. O2 uptake (VO2), minute ventilation (VE), CO2 production (VCO2), and heart rate (HR) were recorded at four intervals. During experiment 1 significant changes in HR and insignificant changes in VCO2, VE, and VO2 occurred throughout prolonged exercise. Tre increased significantly from 37.1 +/- 0.1 degrees C (rest) to 37.8 +/- 0.1 degrees C after 80 min of exercise. There were only significant changes in arm Tsk. Experiment 2 involved a nonhomogeneous group (T5-T10/T11) of active paraplegics (VO2max 39.9 +/- 4.3 ml.kg-1.min-1) exercising at 60-65% VO2max for up to 45 min on the treadmill while Tre and Tes were simultaneously recorded. Tes rose significantly faster than Tre during exercise (dT/dt 20 min: Tes 0.050 +/- 0.003 degrees C/min and Tre 0.019 +/- 0.005 degrees C/min), and Tes declined significantly faster than Tre at the end of exercise. Tes was significantly higher than Tre at the end of exercise. Our results suggest that during wheelchair propulsion by paraplegics, Tes may be a better estimate of core temperature than Tre.     

Effect of positive-pressure breathing on cardiovascular and thermoregulatory responses to exercise

Five healthy male volunteers performed 20 min of both seated and supine cycle-ergometer exercise (intensity, 50% maximal O2 uptake) in a warm environment (Tdb = 30 degrees C, relative humidity = 40-50%) with and without breathing 10 cmH2O of continuous positive airway pressure (CPAP). The final esophageal temperature (Tes) at the end of 20 min of seated exercise was significantly higher during CPAP (mean difference = 0.18 +/- 0.04 degree C, P less than 0.05) compared with control breathing (C). The Tes threshold for forearm vasodilation was significantly higher (P less than 0.05) during seated CPAP exercise than C (C = 37.16 +/- 0.13 degrees C, CPAP = 37.38 + 0.12 degree C). The highest forearm blood flow (FBF) at the end of exercise was significantly lower (P less than 0.05) during seated exercise with CPAP (mean +/- SE % difference from C = -30.8 +/- 5.8%). During supine exercise, there were no significant differences in the Tes threshold, highest FBF, or final Tes with CPAP compared with C. The added strain on the cardiovascular system produced by CPAP during seated exercise in the heat interacts with body thermoregulation as evidenced by elevated vasodilation thresholds, reduced peak FBF, and slightly higher final esophageal temperatures.     

Influence of menstrual cycle on thermoregulatory, metabolic, and heart rate responses to exercise at night

Ten women [mean maximal O2 uptake (VO2max), 2.81 l X min-1] exercised for 15 min on a cycle ergometer in the middle of the luteal phase (L) and in the early follicular phase (F) of the menstrual cycle at the same constant work rates (mean 122 W) and an ambient temperature of 18 degrees C. Serum progesterone averaged 44.7 nmol X l-1 in L and 0.7 nmol X l-1 in F. After a 4-h resting period, exercise was performed between 3 and 4 A.M., when the L-F core temperature difference is maximal. Preexercise esophageal (Tes), tympanic (Tty), and rectal (Tre) temperatures averaged 0.6 degrees C higher in L. During exercise Tes, Tty, and Tre averaged 0.5 degrees C higher. The thresholds for chest sweating and cutaneous vasodilation (heat clearance technique) at the thumb and forearm were elevated in L by an average of 0.47 degrees C, related to mean body temperature (Tb(es) = 0.87Tes + 0.13Tskin), Tes, Tty, or Tre. The above-threshold chest sweat rate and cutaneous heat clearances were also increased in L. The mean exercise heart rate was 170.0 beats X min-1 in L and 163.8 beats X min-1 in F. The mean exercise VO2 in L (2.21 l X min-1) was 5.2% higher than in F (2.10 l X min-1), the metabolic rate was increased in L by 5.6%, but the net efficiency was 5.3% lower. No significant L-F differences in the respiratory exchange ratio and postexercise plasma lactate were demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)     

Postexercise hypotension causes a prolonged perturbation in esophageal and active muscle temperature recovery

We examined the effect of two levels of exercise-induced hypotension on esophageal (Tes) and active and nonactive muscle temperatures during and following exercise. Seven males performed an incremental isotonic test on a Kin-Com isokinetic apparatus to determine their peak oxygen consumption during bilateral knee extensions (VO2sp). This was followed on separate days by 15-min of isolated bilateral knee extensions at moderate (60% VO2sp) (MEI) and high (80% VO2sp) (HEI) exercise intensities, followed by 90 min of recovery. Muscle temperature was measured with an intramuscular probe inserted in the left vastus medialis (Tvm) and triceps brachii (Ttb) muscles under ultrasound guidance. The deepest sensor (tip) was located approximately 10 mm from the femur and deep femoral artery and from the superior ulnar collateral artery and humerus for the Tvm and Ttb, respectively. Additional sensors were located 15 and 30 mm from the tip with an additional sensor located at 45 mm for the Tvm measurements only. Following exercise, mean arterial pressure (MAP) remained significantly below preexercise rest for the initial 60 min of recovery after MEI and for the duration of the postexercise recovery period after HEI (P< or =0.05). After HEI, significantly greater elevations from preexercise rest were recorded for Tes and all muscle temperatures paralleled a greater decrease in MAP compared with MEI (P< or =0.05). By the end of 90-min postexercise recovery, MAP, Tes, and all muscle temperatures remained significantly greater after HEI than MEI. Furthermore, a significantly shallower muscle temperature profile across Tvm, relative to preexercise rest, was observed at the end of exercise for both HEI and MEI (P< or=0.05), and for 30 min of recovery for MEI and throughout 90 min of recovery for HEI. No significant differences in muscle temperature profile were observed for Ttb. Thus we conclude that the increase in the postexercise hypotensive response, induced by exercise of increasing intensity, was paralleled by an increase in the magnitude and recovery time of the postexercise esophageal and active muscle temperatures.     

Influence of beta-adrenergic blockade on the control of sweating in humans

To evaluate the role of beta-adrenergic receptors in the control of human sweating, we studied six subjects during 40 min of cycle-ergometer exercise (60% maximal O2 consumption) at 22 degrees C 2 h after oral administration of placebo or nonselective beta-blockade (BB, 80 mg propranolol). Internal temperature (esophageal temperature, Tes), mean skin temperature (Tsk), local chest temperature (Tch), and local chest sweat rate (msw) were continuously recorded. The control of sweating was best described by the slope of the linear relationship between msw and Tes and the threshold Tes for the onset of sweating. The slope of the msw-Tes relationship decreased 27% (P less than 0.01), from 1.80 to 1.30 mg X cm-2 X min-1 X degree C-1 during BB. The Tes threshold for sweating (36.8 degrees C) was not altered as the result of BB. These data suggest that BB modified the control of sweating via some peripheral interaction. Since Tsk was significantly (P less than 0.05) reduced during BB exercise, from a control value of 32.8 to 32.2 degrees C, we evaluated the influence of the reduction in local skin temperature (Tsk) in the altered control of sweating. Reductions in Tch accounted for only 45% of the decrease in the slope of the msw-Tes relationship during BB. Since evaporative heat loss requirement during exercise with BB, as estimated from the energy balance equation, was also reduced 18%, compared with control exercise, we concluded that during BB the reduction in sweating at any Tes is the consequence of both a decrease in local Tsk and a direct effect on sweat gland.     

Nonthermoregulatory control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in women.

The purpose of the study was to examine the effect of 1) active (loadless pedaling), 2) passive (assisted pedaling), and 3) inactive (motionless) recovery modes on mean arterial pressure (MAP), cutaneous vascular conductance (CVC), and sweat rate during recovery after 15 min of dynamic exercise in women. It was hypothesized that an active recovery mode would be most effective in attenuating the fall in MAP, CVC, and sweating during exercise recovery. Ten female subjects performed 15 min of cycle ergometer exercise at 70% of their predetermined peak oxygen consumption followed by 20 min of 1) active, 2) passive, or 3) inactive recovery. Mean skin temperature (Tsk), esophageal temperature (Tes), skin blood flow, sweating, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance (TPR), and MAP were recorded at baseline, end exercise, and 2, 5, 8, 12, 15, and 20 min postexercise. Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler blood flow to MAP. In the active recovery mode, CVC, sweat rate, MAP, CO, and SV remained elevated over inactive values (P < 0.05). The passive mode was equally as effective as the active mode in maintaining MAP. Sweat rate was different among all modes after 12 min of recovery (P < 0.05). TPR during active recovery remained significantly lower than during recovery in the inactive mode (P < 0.05). No differences in either Tes or Tsk were observed among conditions. The results indicate that CVC can be modulated by central command and possibly cardiopulmonary baroreceptors in women. However, differences in sweat rate may be influenced by factors such as central command, mechanoreceptor stimulation, or cardiopulmonary baroreceptors.     

Effect of physical training on basal metabolism. (1). Aging and long-term exercise loaded at a moderate intensity in rats

Effect of training on basal metabolism in rats by means of long-term exercise loaded at a moderate intensity were studied. The Wistar-strain male rats were carefully bred at the room temperature of 23.0 +/- 1 degree C and humidity of 60%. The first physical training was carried out by motor driven treadmill for 8 weeks at a speed of 25 m/min for less than 15 min once daily and 6 times in a week after 4 weeks of birth. Continuously, the second training was carried out for 15 months at the same load of one time per week. Running ability and the recovery of glycogen in exhausted skeletal muscles on period of the first training, loaded from 4 weeks to 12 weeks after birth. There was no change on the basal metabolism between the trained and sedentary control rats. In general, the basal metabolism significantly fell by aging, for instance, 24 months rat's basal metabolism was 63% of 3-4 months rat's. The second training repressed a decline of running ability and rose the recovery of muscle glycogen in rats, though training could not be stopped lowering of basal metabolism in aged rats.     

A second postcooling afterdrop: more evidence for a convective mechanism.

An attempt was made to demonstrate the importance of increased perfusion of cold tissue in core temperature afterdrop. Five male subjects were cooled twice in water (8 degrees C) for 53-80 min. They were then rewarmed by one of two methods (shivering thermogenesis or treadmill exercise) for another 40-65 min, after which they entered a warm bath (40 degrees C). Esophageal temperature (Tes) as well as thigh and calf muscle temperatures at three depths (1.5, 3.0, and 4.5 cm) were measured. Cold water immersion was terminated at Tes varying between 33.0 and 34.5 degrees C. For each subject this temperature was similar in both trials. The initial core temperature afterdrop was 58% greater during exercise (mean +/- SE, 0.65 +/- 0.10 degrees C) than shivering (0.41 +/- 0.06 degrees C) (P < 0.005). Within the first 5 min after subjects entered the warm bath the initial rate of rewarming (previously established during shivering or exercise, approximately 0.07 degrees C/min) decreased. The attenuation was 0.088 +/- 0.03 degrees C/min (P < 0.025) after shivering and 0.062 +/- 0.022 degrees C/min (P < 0.025) after exercise. In 4 of 10 trials (2 after shivering and 2 after exercise) a second afterdrop occurred during this period. We suggest that increased perfusion of cold tissue is one probable mechanism responsible for attenuation or reversal of the initial rewarming rate. These results have important implications for treatment of hypothermia victims, even when treatment commences long after removal from cold water.     

Influence of body temperature on the development of fatigue during prolonged exercise in the heat.

We investigated whether fatigue during prolonged exercise in uncompensable hot environments occurred at the same critical level of hyperthermia when the initial value and the rate of increase in body temperature are altered. To examine the effect of initial body temperature [esophageal temperature (Tes) = 35.9 +/- 0.2, 37.4 +/- 0. 1, or 38.2 +/- 0.1 (SE) degrees C induced by 30 min of water immersion], seven cyclists (maximal O2 uptake = 5.1 +/- 0.1 l/min) performed three randomly assigned bouts of cycle ergometer exercise (60% maximal O2 uptake) in the heat (40 degrees C) until volitional exhaustion. To determine the influence of rate of heat storage (0.10 vs. 0.05 degrees C/min induced by a water-perfused jacket), four cyclists performed two additional exercise bouts, starting with Tes of 37.0 degrees C. Despite different initial temperatures, all subjects fatigued at an identical level of hyperthermia (Tes = 40. 1-40.2 degrees C, muscle temperature = 40.7-40.9 degrees C, skin temperature = 37.0-37.2 degrees C) and cardiovascular strain (heart rate = 196-198 beats/min, cardiac output = 19.9-20.8 l/min). Time to exhaustion was inversely related to the initial body temperature: 63 +/- 3, 46 +/- 3, and 28 +/- 2 min with initial Tes of approximately 36, 37, and 38 degrees C, respectively (all P < 0.05). Similarly, with different rates of heat storage, all subjects reached exhaustion at similar Tes and muscle temperature (40.1-40.3 and 40. 7-40.9 degrees C, respectively), but with significantly different skin temperature (38.4 +/- 0.4 vs. 35.6 +/- 0.2 degrees C during high vs. low rate of heat storage, respectively, P < 0.05). Time to exhaustion was significantly shorter at the high than at the lower rate of heat storage (31 +/- 4 vs. 56 +/- 11 min, respectively, P < 0.05). Increases in heart rate and reductions in stroke volume paralleled the rise in core temperature (36-40 degrees C), with skin blood flow plateauing at Tes of approximately 38 degrees C. These results demonstrate that high internal body temperature per se causes fatigue in trained subjects during prolonged exercise in uncompensable hot environments. Furthermore, time to exhaustion in hot environments is inversely related to the initial temperature and directly related to the rate of heat storage.     

Tympanic temperatures during hemiface cooling

In adult men the left half of the head was covered with thick heat insulation, and the right hemiface was cooled by spraying a mist of water, and vigorous fanning. The subjects were immersed up to the waist in warm water (42 degrees) to achieve hyperthermia. In control sessions the subjects were rendered slightly hypothermic by preliminary exposure to cold. Under the hypothermic condition during right skin cooling, the right Tty remained low as compared with oesophageal temperature, while the left Tty was raised. Under the hyperthermic condition right hemiface cooling maintained not only the right Tty lower than oesophageal but also, to a lesser extent the left Tty, while the skin on the left side was close to core temperature. This latter result cannot be explained by conductive cooling from the skin to the tympanic membrane and implies a vascular cooling of the left Tty originating from the other side of the head. It is concluded that selective cooling of the brain takes place during hyperthermia. The main mechanism is forced vascular convection, but conductive cooling also occurs.     

Exercise thermoregulation after prolonged wakefulness

The effect of 33 h of wakefulness on the control of forearm cutaneous blood flow and forearm sweating during exercise was studied in three men and three women. Subjects exercised for 30 min at 60% peak O2 consumption while seated behind a cycle ergometer (Ta = 35 degrees C, Pw = 1.0 kPa). We measured esophageal temperature (Tes), mean skin temperature, and arm sweating continuously and forearm blood flow (FBF) as an index of skin blood flow, twice each minute by venous occlusion plethysmography. During steady-state exercise, Tes was unchanged by sleep loss. The sensitivity of FBF to Tes was depressed an average of 30% (P less than 0.05) after 33 h of wakefulness with a slight decrease (-0.15 degrees C, P less than 0.05) in the core temperature threshold for vasodilatory onset. Sleep loss did not alter the Tes at which the onset of sweating occurred; however, sensitivity of arm sweating to Tes tended to be lower but was not significant. Arm skin temperature was not different between control and sleep loss experiments. Reflex cutaneous vasodilation during exercise appeared to be reduced by both central and local factors after 33 h of wakefulness.     

Core threshold temperatures for sweating

To detect shifts in the threshold core temperature (Tc) for sweating caused by particular nonthermal stresses, it is necessary to stabilize or standardize all other environmental and physiological variables which cause such shifts. It is, however, difficult to cause progressive changes in Tc without also causing changes in skin temperature (Tsk). This study compares the technique of body warming by immersion in water at 40 degrees C, and subsequent body cooling in water at 28 degrees C, to determine the core threshold for sweating, with one by which Tc was raised by cycling exercise in air at 20 degrees C, and then lowered by immersion in water at 28 degrees C. The first of these procedures involved considerable shifts in Tsk upon immersion in water at 40 degrees C, and again upon transfer to water at 28 degrees C; the second procedure caused only small changes in Tsk. The onset of sweating at a lower esophageal temperature (Tes) during immersion in water at 40 degrees C (36.9 +/- 0.1 degrees C) than during exercise (37.4 +/- 0.3 degree C) is attributed to the high Tsk since Tes was then unchanged. Likewise, the rapid decline in the sweat rate during immersion at 28 degrees C had the same time course to extinction after the pretreatments. This related more to the Tsk, which was common, than to the levels or rates of change of Tes, which both differed between techniques. Tes fell most rapidly, and thus sweating was extinguished at a lower Tes, following 40 degrees C immersion than following exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Skin blood flow during incremental exercise in a thermoneutral and a hot dry environment

Eight physically fit men performed two incremental bicycle ergometer tests, one in an ambient temperature of 25 degrees C and the other at 40 degrees C. Oesophageal temperature (Tes) increased continuously throughout the tests up to 38.0 and 38.3 degrees C, respectively. In both environments, forearm blood flow (plethysmography) was linearly related to Tes above the Tes threshold for vasodilation, but at the heaviest work loads this relationship was clearly attenuated and therefore indicated skin vasoconstriction, which tended to be more pronounced at 25 degrees C. During recovery at 25 degrees C, in some subjects the forearm blood flow increased above the levels observed at the end of the graded exercise in spite of a decreasing Tes. Skin blood flow, measured by laser Doppler flow meter at the shoulder, was quantitatively different but, on average, seemed to reveal the same response pattern as the forearm blood flow. In spite of the higher level of skin blood flow in the heat, blood lactate accumulation did not differ between the two environments. The present results suggest that there is competition between skin vasoconstriction and vasodilation at heavy work rates, the former having precedence in a thermoneutral environment to increase muscle perfusion. During short-term graded exercise in a hot environment, skin vasoconstriction with other circulatory adjustments seems to be able to maintain adequate muscle perfusion at heavy work levels, but probably not during maximum exercise.     

Core temperature "null zone".

An experimental protocol was designed to investigate whether human core temperature is regulated at a "set point" or whether there is a neutral zone between the core thresholds for shivering thermogenesis and sweating. Nine male subjects exercised on an underwater cycle ergometer at a work rate equivalent to 50% of their maximum work rate. Throughout an initial 2-min rest period, the 20-min exercise protocol, and the 100-min recovery period, subjects remained immersed to the chin in water maintained at 28 degrees C. On completion of the exercise, the rate of forehead sweating (Esw) decayed from a mean peak value of 7.7 +/- 4.2 (SD) to 0.6 +/- 0.3 g.m-2.min-1, which corresponds to the rate of passive transpiration, at core temperatures of 37.42 +/- 0.29 and 37.39 +/- 0.48 degrees C, as measured in the esophagus (Tes) and rectum (Tre), respectively. Oxygen uptake (VO2) decreased rapidly from an exercising level of 2.11 +/- 0.25 to 0.46 +/- 0.09 l/min within 4 min of the recovery period. Thereafter, VO2 remained stable for approximately 20 min, eventually increased with progressive cooling of the core region, and was elevated above the median resting values determined between 15 and 20 min at Tes = 36.84 +/- 0.38 degrees C and Tre = 36.80 +/- 0.39 degrees C. These results indicate that the core temperatures at which sweating ceases and shivering commences are significantly different (P less than 0.001) regardless of whether core temperature is measured within the esophagus or rectum.(ABSTRACT TRUNCATED AT 250 WORDS)