Post-exercise thermal homeostasis as a function of changes in pre-exercise core temperature

We have previously reported that, following continuous exercise, a prolonged elevated plateau of esophageal temperature (T _es) was directly related to the T _es at the time of cutaneous vasodilation (Th_dil) during exercise. In order to investigate the hypothesis that the factors which result in an increase of the post-exercise Thdil and define the post-exercise T _es elevation are related to pre-exercise T _es, nine healthy, young [24.0 (1.9) years], non-training males rested at 29°C, 50% humidity for > 1 h (control). They then completed three successive cycles of 15 min treadmill running at 70% maximal oxygen consumption ( ) followed by 30 min rest. Esophageal, rectal (T _re) and skin (T _sk) temperatures and forearm cutaneous blood flow were recorded at 5-s intervals throughout. Laser-Doppler flowmetry of forearm skin blood flow was used to identify the Thdil during exercise. Pre-exercise T _es was 36.74 (0.25)°C and post-exercise Tes fell to stable and significant (P < 0.05) elevations above pre-exercise values at 37.22(0.27)°C, 37.37(0.27)°C and 37.48(0.26)°C following each successive work bout respectively. Correspondingly, Th_dil during each work bout rose in proportion to, and was not different than, the post-exercise T _es in the following recovery [37.20(0.23)°C, 37.41(0.24)°C and 37.58(0.24)°C]. Although the increases were less with each successive exercise bout, the differences between each exercise bout, in terms of post-exercise Tes and Th_dil values, were significant (P < 0.05). These results reinforce our previous observations of elevations in Th_dil and post-exercise Tes after a single exercise bout and lead to the tentative conclusions that (1) pre-exercise Test has a direct influence on Thdil and post-exercise Test and (2) the exercise-induced increase of Th_dil persists into recovery, influencing post-exercise thermal recovery.     

The effect of ambient temperature and exercise intensity on post-exercise thermal homeostasis

We have previously demonstrated a prolonged (65?min or longer) elevated plateau of esophageal temperature (T _es ) (0.5–0.6°C above pre-exercise values) in humans following heavy dynamic exercise (70% maximal oxygen consumption, V˙O_2max) at a thermoneutral temperature (T _a) of 29°C. The elevated T _es value was equal to the threshold T _es at which active skin vasodilation was initiated during exercise (Th_dil). A subsequent observation, i.e., that successive exercise/recovery cycles (performed at progressively increasing pre-exercise T _es levels) produced parallel increases of Th_dil and the post-exercise T _es, further supports a physiological relationship between these two variables. However, since all of these tests have been conducted at the same T _a (29°C) and exercise intensity (70% V˙O_2max) it is possible that the relationship is limited to a narrow range of T _a/exercise intensity conditions. Therefore, five male subjects completed 18?min of treadmill exercise followed by 20?min of recovery in the following T _a/exercise intensity conditions: (1) cool with light exercise, T _a?=?20°C, 45% V˙O_2max (CL); (2) temperature with heavy exercise, T _a?=?24°C, 75% O_{2 max} (TH); (3) warm with heavy exercise, T _a?=?29°C, 75% V˙O_2max (WH); and (4) hot with light exercise, T _a?=?40°C, 45% V˙O_2max (HL). An abrupt decrease in the forearm-to-finger temperature gradient (T _fa??T _fi) was used to identify the Th_dil during exercise. Mean pre-exercise T _es values were 36.80, 36.60, 36.72, and 37.20°C for CL, TH, WH, and HL conditions respectively. T _es increased during exercise, and end post-exercise fell to stable values of 37.13, 37.19, 37.29, and 37.55°C for CL, TH, WH, and HL trials respectively. Each plateau value was significantly higher than pre-exercise values (P?dil values (i.e., 37.20, 37.23, 37.37, and 37.48°C for CL, TH, WH, and HL) were comparable to the post-exercise T _es values for each condition. The relationship between Th_dil and post-exercise T _es remained intact in all T _a/exercise intensity conditions, providing further evidence that the relationship between these two variables is physiological and not coincidental.     

Short-term exercise training does not improve whole-body heat loss when rate of metabolic heat production is considered

We evaluated the effects of an 8-week exercise training program in previously sedentary individuals on whole-body heat balance during exercise at a constant rate of metabolic heat production. Prior to and after 8 weeks of training, ten participants performed 60-min of cycling exercise at a constant rate of heat production (~450 W) followed by 60-min of recovery, at 30°C and 15% relative humidity. Rate of total heat loss was measured directly by whole-body calorimetry, while rate of metabolic heat production was measured simultaneously by indirect calorimetry. Esophageal (T _es), skin blood flow (SkBF) and local sweat rate (LSR) were also measured continuously. The 8-week exercise training program elicited a 10% increase in maximal aerobic capacity (P < 0.001). Furthermore, exercise training reduced (P ≤ 0.05) baseline (37.10 ± 0.28 vs. 36.95 ± 0.24°C) and end-exercise (37.85 ± 0.30 vs. 37.55 ± 0.20°C) values for T _es as well as onset thresholds for LSR (37.23 ± 0.26 vs. 36.96 ± 0.22°C, P < 0.001) and SkBF (37.16 ± 0.38 vs. 36.83 ± 0.26°C, P < 0.001). However, these improvements in thermoregulatory function did not translate into a greater rate of total heat loss between the pre- and post-training exercise trials (P = 0.762). Furthermore, there were no differences in SkBF (P = 0.546) and LSR (P = 0.475) from pre- to post-training. Although physical training resulted in significant improvements of cardiorespiratory and thermoregulatory functions, these adaptations did not improve whole-body and local heat loss responses during exercise performed at a given rate of metabolic heat production.     

A comparison of human thermoregulatory response following dynamic exercise and warm-water immersion

We tested the hypothesis that the prolonged elevated plateau of esophageal temperature (T _es) following moderate exercise is a function of some exercise-related factors and not the increase in heat content andT _es during exercise, by comparing the response to increaseT _es during exercise (endogenous heating) and warm-water immersion (exogenous heating). Nine healthy, young [24.0 (1.9) years] subjects performed two separate experiments: (1) 15 min of treadmill exercise at 70% and 15 min rest in a climatic chamber at 29°C, followed by 15 min of immersion in a 42°C water bath and a further 60 min of recovery in the climatic chamber [exercise-water (EW)]; and (2) 15 min of immersion in a 42°C water bath followed by 60 min of recovery in the climatic chamber [water-only (WO)]. Esophageal (T _es) and skin (T _sk) temperatures were recorded at 5-s intervals throughout. TheT _ea at which the forearm to finger temperature gradient (T _fa-T _fi) abruptly decreases was used to identify the threshold for forearm cutaneous vessel dilation (Th_dil) during exercise. Pre-exerciseT _es values were 36.64°C and 36.74°C for EW and WO respectively. The EW post-exerciseT _ea value fell to a stable level of 37.12°C and this value differed by 0.48°C (P < 0.05) from baseline, but was similar to Th_dil (37.09°C). Despite a 1.2°C increase inT _es during the subsequent warm-water immersion,T _es returned to the post-exercise value (37.11°C). The WO post-immersionT _es fell to a stable plateau of 36.9°C, which was not statistically different from the pre-immersion T_es. The data for both warm-water treatments support the hypothesis that increases inT _es and heat content alone are not the primary mechanisms for the post-exercise elevation inT _es and Th_dil. These data also support our previous observation that the exercise-induced elevation in Th_dil persists into recovery.     

Intense exercise increases the post-exercise threshold for sweating

We demonstrated previously that esophageal temperature (T _es) remains elevated by ≈0.5°C for at least 65?min after intense exercise. Following exercise, average skin temperature (T _avg) and skin blood flow returned rapidly to pre-exercise values even though T _es remained elevated, indicating that the T _es threshold for vasodilation is elevated during this period. The present study evaluates the hypothesis that the threshold for sweating is also increased following intense exercise. Four males and three females were immersed in water (water temperature, T _w?=?42°C) until onset of sweating (Immersion 1), followed by recovery in air (air temperature, T _a?=?24°C). At a T _a of 24°C, 15?min of cycle ergometry (70% VO_2max) (Exercise) was then followed by 30?min of recovery. Subjects were then immersed again (T _w?=?42°C) until onset of sweating (Immersion 2). Baseline T _es and T _skavg were 37.0 (0.1)°C and 32.3 (0.3)°C, respectively. Because the T _skavg at the onset of sweating was different during Exercise [30.9 (0.3)°C] than during Immersion 1 and Immersion 2 [36.8 (0.2)°C and 36.4 (0.2)°C, respectively] a corrected core temperature, T _es (calculated), was calculated at a single designated skin temperature, T _{sk(designated)}, as follows: T _{es(calculated)}?=?T _es?+?[β/(1?β)][T _skavg?T _{sk(designated)}]. The T _{sk(designated)} was set at 36.5°C (mean of Immersion 1 and Immersion 2 conditions) and β represents the fractional contribution of T _skavg to the sweating response (β for sweating?=?0.1). While T _{es(calculated)} at the onset of sweating was significantly lower during exercise [36.7 (0.2)°C] than during Immersion 1 [37.1 (0.1)°C], the threshold of sweating during Immersion 2 [37.3 (0.1)°C] was greater than during both Exercise and Immersion 1 (P?相似文献   

Evidence of a greater onset threshold for sweating in females following intense exercise

We evaluated the hypothesis that females would show a greater postexercise hypotension and concurrently a greater increase in the onset threshold for sweating. Fourteen subjects (7 males and 7 females) of similar age, body composition, and fitness status participated in the study. Esophageal temperature was monitored as an index of core temperature while sweat rate was measured by using a ventilated capsule placed on the upper back. Subjects cycled at either 60% (moderate) or 80% (intense) of peak oxygen consumption followed by 20-min recovery. Subjects then donned a liquid-conditioned suit used to regulate mean skin temperature. The skin was then heated (∼4.3°C·h⁻¹) until sweating occurred. Esophageal temperatures were similar to baseline before the start of whole body warming for all conditions. The postexercise threshold values for sweating following moderate and intense exercise were an esophageal temperature increase of 0.10 ± 0.02 and 0.22 ± 0.04°C, respectively for males, and 0.15 ± 0.03 and 0.34 ± 0.01°C, respectively for females. All were elevated above baseline resting (P < 0.05) and a significant sex-related difference was observed for sweating threshold values following intense exercise (P < 0.05). This was paralleled by a greater decrease in mean arterial pressure in females at the end of the 20-min recovery (P < 0.05). In conclusion, females demonstrate a greater postexercise onset threshold for sweating, which is paralleled by a greater postexercise hypotensive response following intense exercise.     

Safe cooling limits from exercise-induced hyperthermia

We evaluated the cooling rate of hyperthermic subjects, as measured by three estimates of deep core temperatures (esophageal, rectal and aural canal temperatures), during immersion in a range of water temperatures. The objective of the study was to compare the three indices of core temperature and define safe cooling limits when using rectal temperature to avoid the development of hypothermia. On 4 separate days, seven subjects (four males, three females) exercised for 45.4±4.1 min at 65% at an ambient temperature of 39°C, RH: 36.5%, until rectal temperature (T _re) increased to 40.0°C (39.5°C for two subjects). Following exercise, the subjects were immersed in a circulated water bath controlled at 2, 8, 14 and 20°C until T _re returned to 37.5°C. When T _re reached normothermia during the cooling period (37.5±0.05°C), both esophageal (T _es) (35.6±1.3°C) and aural canal (T _ac) (35.9±0.9°C) temperatures were approaching or reaching hypothermia, particularly during immersion in 2°C water (T _es=34.5±1.2°C). On the basis of the heat loss data, the heat gained during the exercise was fully eliminated after 5.4±1.5, 7.9±2.9, 10.4±3.8 and 13.1±2.8 min of immersion in 2, 8, 14 and 20°C water, respectively, with the coldest water showing a significantly faster cooling rate. During the immersion in 2°C water, a decrease of only 1.5°C in T _re resulted in the elimination of 100% of the heat gained during exercise without causing hypothermia. This study would therefore support cooling the core temperature of hyperthermic subjects to a rectal temperature between 37.8°C (during immersion in water >10°C) and 38.6°C (during immersion in water <10°C) to eliminate the heat gained during exercise without causing hypothermia.     

Disturbance of thermal homeostasis during post-exercise hyperthermia

The response of core temperature to exercise was investigated during recovery in order to avoid the antagonistic competition between exercise and thermal reflexes for the same effector systems which control skin blood flow. Five healthy, non-training males [mean (SD) age, 23.8 (2.04) years] were habituated to 29° C at relative 50% humidity for more than 2 h and then exercised by treadmill running at about 75% maximum oxygen uptake for 18 min. They then remained at 29° C for up to 65 min of recovery. Oesophageal (T _es), rectal (T _re) and skin temperatures (T _sk) were recorded at 5-s intervals throughout. The abrupt fall of temperature gradient from the forearm to finger was used to identify the T _es for skin vessel dilatation (T _dil) during exercise. Mean (SE) Ts rose from a resting value of 36.67 (0.15)° C to 38.22 (0.24)° C, mean T _re rose from 37.09 (0.25)° C to 38.23 (0.15)° C, and T _dil occurred at 37.39 (0.32)° C. Within 10 min of recovery mean T _es fell to 37.31 (0.24)° C, where it remained a significant 0.64° C above its pre-exercise (PrEx) level (P0.018) but insignificantly different from T _dil for the remaining 55 min of recovery. Meanwhile, T _re fell gradually throughout recovery to 37.64 (0.18)° C. The T _sk at all non-acral sites except the thigh had recovered to PrEx levels by 20–30 min post-exercise (PoEx). The rapid PoEx fall of T _es to the level of T _dil and the subsequent plateau above PrEx values suggests that heat dissipation during recovery was primarily passive once T _es had fallen to T _dil, even though T _es and T _re were significantly elevated. The relationship of these results to the set-point and load error concepts of thermal control is discussed.These data have been presented at the Canadian Physiological Society Winter meeting, January 1993, but have not been previously published     

Rectal and esophageal temperatures during upper- and lower-body exercise

This study investigated the question: is core temperature measurement influenced by whether exercise involves predominantly upper- or lower-body musculature? Healthy men were allocated to three groups: treadmill ergometry (T) n=4, cycle ergometry (C) n=6 and arm crank ergometry (AC) n=5. Subjects underwent an incremental exercise test to exhaustion on an exercise-specific ergometer to determine maximum/peak oxygen consumption (V˙O_2max). One week later subjects exercised for 36?min on the same ergometer at approximately 65% V˙O_2max while temperatures at the rectum (T _re) and esophagus (T _es) were simultaneously measured. The V˙O_2max (l?·?min^?1) for groups T [4.76 (0.50)] and C [4.35 (0.30)] was significantly higher than that for the AC group [2.61 (0.24)]. At rest, T _re was significantly higher than T _es in all groups (P<0.05). At the end of submaximal exercise in the C group, T _re [38.32 (0.11)°C] was significantly higher than T _es [38.02 (0.12)°C, P<0.05]. No significant differences between T _re and T _es at the end of exercise were noted for AC and T groups. The temperature difference (T _diff) between T _re and T _es was dissimilar at rest in the three groups; however, by the end of exercise T _diff was approximately 0.2°C for each of the groups, suggesting that at the end of steady-state exercise T _re can validly be used to estimate core temperature.     

Post-exercise cold water immersion: effect on core temperature and melatonin responses

To study the effect of post-exercise cold water immersion (CWI) on core temperature and melatonin responses, 10 male cyclists completed two evening (~1800 hours) cycling trials followed by a 15-min CWI (14 °C) or warm water immersion (WWI; 34 °C), and were then monitored for 90 min post-immersion. The exercise trial involved 15 min at 75 % peak power, followed by a 15 min time trial. Core (rectal) temperature was not different between the two conditions pre-exercise (~37.4 °C), post-exercise (~39 °C) or immediately post-immersion (~37.7 °C), but was significantly (p < 0.05) below pre-exercise levels at 60 and 90 min post-immersion in both conditions. Core temperature was significantly lower after CWI than WWI at 30 min (36.84 ± 0.24 vs. 37.42 ± 0.40 °C, p < 0.05) and 90 min (36.64 ± 0.24 vs. 36.95 ± 0.43 °C, p < 0.05) post-immersion. Salivary melatonin levels significantly increased (p < 0.05) from post-exercise (~5 pM) to 90 min post-immersion (~8.3 pM), but were not different between conditions. At 30 and 90 min post-immersion heart rate was significantly lower (~5–10 bpm, p < 0.01) after CWI than WWI. These results show that undertaking either CWI or WWI post-exercise in the evening lowers core temperature below baseline for at least 90 min; however, the magnitude of decrease is significantly greater following CWI. The usual evening increase in melatonin is unaffected by exercise or post-exercise water immersion undertaken between ~1800 and ~2000 hours.     

Self-paced intermittent-sprint performance and pacing strategies following respective pre-cooling and heating

This study examined the effects of pre-exercise cooling and heating on neuromuscular function, pacing and intermittent-sprint performance in the heat. Ten male, team sport athletes completed three randomized, counterbalanced conditions including a thermo-neutral environment (CONT), whole body submersion in an ice bath (ICE) and passive heating in a hot environment (HEAT) before 50 min of intermittent-sprint exercise (ISE) in the heat (31 + 1°C). Exercise involved repeated 15 m maximal sprints and self-paced exercise of varying intensities. Performance was measured by sprint times and distance covered during self-paced exercise. Maximal isometric contractions were performed to determine the maximal voluntary torque (MVT), activation (VA) and contractile properties. Physiological measures included heart rate (HR), core (T _core) and skin (T _skin) temperatures, capillary blood and perceptual ratings. Mean sprint times were slower during ICE compared to HEAT (P < 0.05). Total distance covered was not different between conditions, but less distance was covered during HEAT in 31–40 min compared to CONT, and 41–50 min compared to ICE (P < 0.05). MVT was reduced post-exercise compared to post-intervention in CONT and HEAT. VA was reduced post-intervention in HEAT compared to CONT and ICE, and post-exercise compared to ICE (P < 0.05). HR, T _core and T _skin during exercise were lower in ICE compared to CONT and HEAT (P < 0.05). Sprint times and distance covered were not affected by ICE and HEAT conditions compared to CONT. However, initial sprint performance was slowed by pre-cooling, with improvements following passive heating possibly due to altered contractile properties. Conversely, pre-cooling improved exercise intensities, whilst HEAT resulted in greater declines in muscle recruitment and ensuing distance covered.     

Expired air temperature during prolonged exercise in cool- and hot-humid environments

The purpose of this investigation was to measure expired air temperature under cool- and hot-humid environmental conditions at rest and during prolonged exercise to: (1) establish if significant increases in body core temperature affected expired air temperature, and (2) to determine if the temperature setting for heating the pneumotachometer in an open-circuit system requires adjustment during prolonged exercise tests to account for changes in expired air temperature. Six male distance runners completed two tests in cool-humid [dry bulb temperature (T _db) 15.5 (SD 1.3)°C, wet bulb temperature (T _wb) 12.1 (SD 1.4)°C] and hot-humid [T _db 31.6 (SD 0.6)°C, T _wb 24.9 (SD 0.6)°C, black globe temperature (T _g) 34.3 (SD 0.3)°C] environments, running at a velocity corresponding to 65% [67.1 (SD 2.82)%] of their maximal oxygen uptake. Rectal temperature and expired air temperatures were compared at rest, and after 30 min and 60 min of exercise for each environment. The main finding of this investigation was a significant (P?相似文献   

Short-term exercise-heat acclimation enhances skin vasodilation but not hyperthermic hyperpnea in humans exercising in a hot environment

We tested the hypothesis that short-term exercise-heat acclimation (EHA) attenuates hyperthermia-induced hyperventilation in humans exercising in a hot environment. Twenty-one male subjects were divided into the two groups: control (C, n = 11) and EHA (n = 10). Subjects in C performed exercise-heat tests [cycle exercise for ~75 min at 58% [(V)\dot]_{\textO 2 \textpeak} \dot{V}_{{{\text{O}}_{{ 2 {\text{peak}}}} }} (37°C, 50% relative humidity)] before and after a 6-day interval with no training, while subjects in EHA performed the tests before and after exercise training in a hot environment (37°C). The training entailed four 20-min bouts of exercise at 50% [(V)\dot]_{\textO 2 \textpeak} \dot{V}_{{{\text{O}}_{{ 2 {\text{peak}}}} }} separated by 10 min of rest daily for 6 days. In C, comparison of the variables recorded before and after the no-training period revealed no changes. In EHA, the training increased resting plasma volume, while it reduced esophageal temperature (T _es), heart rate at rest and during exercise, and arterial blood pressure and oxygen uptake ( [(V)\dot]_\textO2 \dot{V}_{{{\text{O}}_{2} }} ) during exercise. The training lowered the T _es threshold for increasing forearm vascular conductance (FVC), while it increased the slope relating FVC to T _es and the peak FVC during exercise. It also lowered minute ventilation ( [(V)\dot]_\textE \dot{V}_{\text{E}} ) during exercise, but this effect disappeared after removing the influence of [(V)\dot]_\textO2 \dot{V}_{{{\text{O}}_{2} }} on [(V)\dot]_\textE \dot{V}_{\text{E}} . The training did not change the slope relating ventilatory variables to T _es. We conclude that short-term EHA lowers ventilation largely by reducing metabolism, but it does not affect the sensitivity of hyperthermia-induced hyperventilation during submaximal, moderate-intensity exercise in humans.     

Impact of a protective vest and spacer garment on exercise-heat strain

Protective vests worn by global security personnel, and weighted vests worn by athletes, may increase physiological strain due to added load, increased clothing insulation and vapor resistance. The impact of protective vest clothing properties on physiological strain, and the potential of a spacer garment to reduce physiological strain, was examined. Eleven men performed 3 trials of intermittent treadmill walking over 4 h in a hot, dry environment (35°C, 30% rh). Volunteers wore the US Army battledress uniform (trial B), B + protective vest (trial P), and B + P + spacer garment (trial S). Biophysical clothing properties were determined and found similar to many law enforcement, industry, and sports ensembles. Physiological measurements included core (T _c), mean skin (T _sk) and chest (T _chest) temperatures, heart rate (HR), and sweating rate (SR). The independent impact of clothing was determined by equating metabolic rate in all trials. In trial P, HR was +7 b/min higher after 1 h of exercise and +19 b/min by the fourth hour compared to B (P < 0.05). T _c (+0.30°C), T _sk (+1.0°C) and Physiological Strain Index were all higher in P than B (P < 0.05). S did not abate these effects except to reduce T _sk (P > S) via a lower T _chest (−0.40°C) (P < 0.05). SR was higher (P < 0.05) in P and S versus B, but the magnitude of differences was small. A protective vest increases physiological strain independent of added load, while a spacer garment does not alter this outcome.     

Skin cooling aids cerebrovascular function more effectively under severe than moderate heat stress

Skin surface cooling has been shown to improve orthostatic tolerance; however, the influence of severe heat stress on cardiovascular and cerebrovascular responses to skin cooling remains unknown. Nine healthy males, resting supine in a water-perfusion suit, were heated to +1.0 and +2.0°C elevation in body core temperature (T _c). Blood flow velocity in the middle cerebral artery (transcranial Doppler ultrasound), mean arterial pressure (MAP; photoplethysmography), stroke volume (SV; Modelflow), total peripheral resistance (TPR; Modelflow), heart rate (HR; ECG) and the partial pressure of end-tidal carbon dioxide (P_ETCO₂) were measured continuously during 1-min baseline and 3-min lower body negative pressure (LBNP, −15 mm Hg) when heated without and again with skin surface cooling. Nine participants tolerated +1°C and six participants reached +2°C. Skin cooling elevated (P = 0.004) MAP ~4% during baseline and LBNP at +1°C T _c. During LBNP, skin cooling increased SV (9%; P = 0.010) and TPR (0.9 mm Hg L⁻¹ min, P = 0.013) and lowered HR (13 b min⁻¹, P = 0.012) at +1°C T _c and +2°C T _c collectively. At +2°C T _c, skin cooling elevated P_ETCO₂ ~4.3 mm Hg (P = 0.011) and therefore reduced cerebral vascular resistance ~0.1 mm Hg cm⁻¹ s at baseline and LBNP (P = 0.012). In conclusion, skin cooling under severe heating and mild orthostatic stress maintained cerebral blood flow more effectively than it did under moderate heating, in conjunction with elevated carbon dioxide pressure, SV and arterial resistance.     

Control of sweating during the human menstrual cycle

Summary Thermoregulatory responses were studied in seven women during two separate experimental protocols in the follicular (F, days 4–7) phase and during the luteal (L, days 19–22) phase of the menstrual cycle. Continuous measurements of esophageal temperature (T _es), mean skin temperature ( ), oxygen uptake and forearm sweating ( ) were made during all experiments. Protocol I involved both passive heat exposure (3 h) and cycle exercise at ∼80% peak during which the environmental chamber was controlled atT _a=50.0° C, rh=14% (P _w=1.7 kPa). In protocol II subjects were tested during thirty-five minutes of exercise at ∼85% peak atT _a=35° C and rh=25% (P _w=1.4 kPa). The normal L increase in restingT _es (≈0.3° C) occurred in all seven subjects. was higher during L than F in all experiments conducted at 50° C. During exercise and passive heat exposure, theT _es threshold for sweating was higher in L, with no change in the thermosensitivity (slope) of toT _es between menstrual cycle phases. This rightward or upward shift inT _es threshold for initiation of sweating averaged 0.5° C for all experiments. The data indicate the luteal phase modulation in the control of sweating in healthy women is also apparent during severe exercise and/or heat stress.     

Thermoregulatory responses to ice-slush beverage ingestion and exercise in the heat

We compared the effects of an ice-slush beverage (ISB) and a cool liquid beverage (CLB) on cycling performance, changes in rectal temperature (T _re) and stress responses in hot, humid conditions. Ten trained male cyclists/triathletes completed two exercise trials (75 min cycling at ~60% peak power output + 50 min seated recovery + 75% peak power output × 30 min performance trial) on separate occasions in 34°C, 60% relative humidity. During the recovery phase before the performance trial, the athletes consumed either the ISB (mean ± SD −0.8 ± 0.1°C) or the CLB (18.4 ± 0.5°C). Performance time was not significantly different after consuming the ISB compared with the CLB (29.42 ± 2.07 min for ISB vs. 29.98 ± 3.07 min for CLB, P = 0.263). T _re (37.0 ± 0.3°C for ISB vs. 37.4 ± 0.2°C for CLB, P = 0.001) and physiological strain index (0.2 ± 0.6 for ISB vs. 1.1 ± 0.9 for CLB, P = 0.009) were lower at the end of recovery and before the performance trial after ingestion of the ISB compared with the CLB. Mean thermal sensation was lower (P < 0.001) during recovery with the ISB compared with the CLB. Changes in plasma volume and the concentrations of blood variables (i.e., glucose, lactate, electrolytes, cortisol and catecholamines) were similar between the two trials. In conclusion, ingestion of ISB did not significantly alter exercise performance even though it significantly reduced pre-exercise T _re compared with CLB. Irrespective of exercise performance outcomes, ingestion of ISB during recovery from exercise in hot humid environments is a practical and effective method for cooling athletes following exercise in hot environments.     

Shivering endurance and fatigue during cold water immersion in humans

An important component of survival time during cold exposure is shivering endurance. Nine male and three female healthy and fit subjects [mean (SD) age 24.8 (6.3) years, body mass 71.7 (13.2) kg, height 1.75 (0.10) m, body fat 22.7 (7.4)%] were immersed to the upper chest level in cold water for periods ranging from 105 to 388 min on two occasions to test a prediction of shivering endurance. The water was cooled from 20 to 8°C during the first 15 min of immersion and subsequently rewarmed (<20°C) to elicit a near constant submaximal shivering response. The data were divided according to moderate (M) and high (H) levels of shivering intensity. Respective mean total immersion times were 250 (75) and 199 (80) min (P=0.086) at different average shivering intensities of 61 (10) and 69 (8)% relative to maximal shivering (P<0.001). Blood plasma glucose concentration increased during the immersion [from 3.44 (0.54) pre- to 3.94 (0.60) mmol·l^–1 post-immersion (P=0.037)] and levels were higher during M (P=0.012). When compared to a model prediction of shivering endurance, shivering activity continued well beyond the predicted endurance times in 18 out of the 24 trials. The average rates of oxygen consumption over the entire immersion period were lower (P=0.002) during M [0.93 (0.20) l·min^–1] compared to H [1.05 (0.21) l·min^–1), and while these rates did not change during the last 90 min of immersion, there was an increase in fat oxidation. There were no trial differences in the average esophageal (T _es) and mean skin temperatures during the entire immersion period (36.0 and 18.0°C, respectively), yet T _es decreased (P=0.003) approximately 0.4°C during the last 90 min of immersion. When the shivering intensity was normalized to account for this decrease, a significant downward trend of approximately 17%·h^–1 in the normalized shivering intensity was found after the predicted end of shivering endurance. These results suggest that shivering drive, and not shivering intensity per se, decreased during the latter stages of the immersion. Underlying mechanisms such as fatigue and habituation for this diminishing cold sensitivity are discussed. Electronic Publication     

Nocturnal hormonal responses to resistance exercise

The effects of resistance exercise on the nocturnal responses of cortisol (CO), testosterone (TEST), human growth hormone (hGH), and thyroid hormones (T₃, T₄) were examined in eight trained weight lifters. Each subject completed two trials using a counterbalanced design: a control, no exercise trial (CON) and a heavy resistance exercise session of three sets of six exercises to exhaustion (RE). The exercise session took place between 1900 and 2000 hours. Blood was sampled prior to and at 20-min intervals after RE. For both trials blood was sampled at hourly intervals from 2100 hours until 0700 hours. The hGH and CO concentrations were increased up to 40-min post-exercise (P < 0.05), but returned to resting levels 1 h post-exercise. Nocturnal hGH concentration was not affected by RE (P > 0.26) and peaked at 0200 hours and declined until 0700 hours. Similarly, the CO responses were similar between the trails (P > 0.14). This CO concentrations declined from 2200 hours until 0100 hours, then increased steadily until 0700 hours. The TEST concentrations during both trials rose steadily from 2200 hours until 0700 hours; however, the rise in TEST from 0500–0700 hours during RE was greater than during the CON trails (P = 0.059). The T₃ concentrations were unchanged by exercise and were similar at all times between trails. The T₄ concentrations were elevated for 20 min after RE; however nocturnal T₄ concentrations were lower after RE than during CON. These results would suggest that bGH and CO may have limited nocturnal reactivity to resistance exercise. However, the nocturnal alterations of TEST and T4 after resistance exercise, although small, may have implications for muscle anabolism.     

Effects of human menstrual cycle on thermoregulatory vasodilation during exercise

Summary To investigate the effects of the menstrual cycle and of exercise intensity on the relationship between finger blood flow (FBF) and esophageal temperature (T_es), we studied four women, aged 20–32 years. Subjects exercised at 40% and 70% in the semi-supine posture at an ambient temperature of 20 C. Resting T_es was higher during the luteal phase than the follicular phase (P<0.01). There were no significant differences between the two phases in FBF, oxygen consumption, carbon dioxide production, heart rate or minute ventilation at rest and during exercise, respectively. Each regression line of the FBF-T_es relationship consists of two distinct segments of FBF change to T_es (slope 1 and 2). FBF increased at a threshold T_es for vasodilation ([T_{es 0}]) and the rate of FBF rise became greater at another T_es above this threshold ([T_{es 0}']). For both levels of exercise, [T_{es 0}] and [T_{es 0}'] were shifted upward during the luteal phase, but the slopes of the FBF-T_es relationship were almost the same in the two phases of the menstrual cycle. Increasing exercise intensity induced a significant decrease in slope 1 of the FBF-T_es relationship during the follicular (P<0.01) and the luteal phases (P<0.02), respectively. These results show that the set-point temperature may be shifted towards a higher level during the luteal phase of the menstrual cycle during exercise and that, as in males, the thermoregulatory vasodilator response is attenuated by increasing exercise-induced vasoconstrictor tone in proportion to exercise intensity during both phases of the menstrual cycle when heat storage is insufficient in women.Supported in part by Grant-in-Aid for Scientific Research from the Ministry of Education, Science and Culture of Japan (grant no. 57770137)