Influence of exercise training with thigh compression on heat-loss responses.

We investigated the effect of thigh compression, which accelerates activation of central command and muscle metabo- and mechanoreceptors, on the adaptation of sweating and cutaneous vascular responses during exercise heat acclimation. Nine non-heat-acclimated male subjects were acclimated to heat (32 °C and 50% RH) while cycling [50% of maximum oxygen uptake ( V ˙ O 2 m a x )] 60 min/day for 7 days (control group). The experimental group (n = 9) conducted the same training while the proximal thighs were compressed by a cuff at 60 mmHg. V ˙ O 2 m a x , acetylcholine-induced forearm sweating rate (iontophoresis), and mean sweating and cutaneous vascular responses on the forehead, chest, and forearm (SRmean and CVCmean ) during passive heating were evaluated before and after training. Training significantly increased V ˙ O 2 m a x while did not affect acetylcholine-induced sweating rates in either group. Training significantly decreased Tb thresholds for SRmean and CVCmean during passive heating without the alternations of sensitivities in both groups. Although SRmean during passive heating at a given ΔTb was not improved in either group, CVCmean was significantly (P < 0.05) attenuated after exercise training only in experimental group. Our results indicate that thigh cuff compression during exercise heat acclimation does not influence adaptation of the sweating response but attenuate cutaneous vasodilation.

Changes in eccrine sweating on the glabrous skin of the palm and finger during isometric exercise.

AIM: The goals of this study were to investigate changes in the sweating and cutaneous vascular responses on the palm and the volar aspect of the index finger during sustained static exercise of increasing intensity and to determine whether the former can be attributed to altered sweat gland activity. METHODS: Five male and five female subjects performed maximal voluntary handgrip contractions (MVC: right hand) for 60 s at 20, 35 and 50% MVC (ambient temperature 25 °C, relative humidity 50%). RESULTS: The sweat rate and the number of activated sweat glands on the non-exercised hand showed intensity-dependent increases (P < 0.05). At 35 and 50% MVC, finger sweat secretion was significantly higher than on the palm, which was primarily associated with the number of activated sweat glands (P < 0.05). In addition, there was a marked simultaneous decrease in the cutaneous vascular conductance for the finger at 35 and 50% MVC (P < 0.05), but not for the palm. CONCLUSION: Our results suggest that a difference exists between intensity-dependent increases of sudomotor responses within more than one glabrous skin site. Specifically, markedly greater sweating occurs on the volar finger than on the palmar surface during sustained static exercise. These differences in sweat rate mainly resulted from changes in the number of activated sweat glands. In addition, intra-segment variations in cutaneous blood flow on the glabrous hand are shown.

Autonomic heart rate regulation during mild dynamic exercise in humans: insights from respiratory sinus arrhythmia.

To better understand the neural mechanism of heart rate (HR) regulation during dynamic exercise, the responses of HR and the magnitude of respiratory R-R interval variation were examined during exercise and recovery at mild intensities in humans. Eight subjects performed 3-min constant load cycle exercises in a semi-supine position at work rates of 25, 50, and 100 W. The respiratory interval was fixed at 4 s. Peak-to-valley variation in R-R interval caused by respiration was measured breath-by-breath and standardized for tidal volume (DeltaRRst, a noninvasive index of the degree of parasympathetic cardiac control). At all work rates the HR increased significantly from 2.5 s after the beginning of exercise (p <0.05) and decreased temporarily and slightly at around 15 s, and the DeltaRRst varied almost inversely. The HR and the DeltaRRst until 12.5 s after the beginning of exercise changed independently of work rate (ANOVA, p=0.27 and p=0.08). The HR-DeltaRRst relationship at the initial phase of exercise (for 12.5 s) was almost the same at all work rates. These results suggest that the initial HR response to exercise is strongly parasympathetically regulated independently of work rate. The HR recovered slower than the DeltaRRst at 50 and 100 W. On the HR-DeltaRRst relationship, the HR during recovery was significantly higher than during exercise at 1/3, 1/2, and 2/3 levels of pre-exercise DeltaRRst at 50 and 100 W and at the 1/3 level at 25 W (p < 0.05). At 25 W, the difference in HR at the 1/3 level was 5.5 beats.min(-1), and the HR increase to exercise was 21.2 beats.min(-1). We suggest that a HR regulatory system responds slower than a cardiac parasympathetic system to exercise, a cardiac sympathetic system, is activated even during mild exercise in humans.

Sweating responses to a sustained static exercise is dependent on thermal load in humans.

The purpose of this project was to test the hypothesis that internal temperature modulates the sweating response to sustained handgrip exercise. Ten healthy male subjects immersed their legs in 43 degrees C water for 30-40 min at an ambient temperatures of 30 degrees C and a relative humidity of 50%. Sweating responses to 50% maximal voluntary contraction isometric handgrip exercise (IH) were measured following the onset of sweating (i.e. following slight increases in internal temperature), and after more pronounced increases in internal temperature. Oesophageal temperature (Tes) was significantly lower during the first bout of exercise (37.54 +/- 0.07 degrees C) relative to the second bout (37.84 +/- 0.12 degrees C; P < 0.05). However, the increase in mean sweating rate (SR) from both the chest and forearm (non-glabrous skin) was significantly greater during the first IH bout relative to the second bout (P < 0.05). Increases in mean arterial blood pressure and palm SR (glabrous skin) did not differ significantly between exercise bouts, while heart rate and rating of perceived effort were significantly greater during the second bout of IH. As Tes and mean skin temperature did not change during either bout of exercise, the changes in SR from non-glabrous skin between the bouts of IH were likely because of non-thermal factors. These data suggest that sweating responses from non-glabrous skin during IH vary depending on the magnitude of thermal input as indicated by differing internal temperatures between bouts of IH. Moreover, these data suggest that the contribution of non-thermal factors in governing sweating from non-glabrous skin may be greatest when internal temperature is moderate (37.54 degrees C), but has less of an effect after greater elevations in internal temperature (i.e. 37.84 degrees C).

Sweating response in physically trained men to sustained handgrip exercise in mildly hyperthermic conditions.

To investigate the effects of physical training on heat loss response to sustained handgrip exercise (non-thermal factors), we compared the sweating response during isometric handgrip exercise to mild hyperthermia in physically trained and untrained subjects. Seven trained and untrained male subjects (maximal oxygen uptake 62.7 +/- 2.4 and 42.7 +/- 1.6 mL kg-1 min-1, respectively, P < 0.05) performed isometric handgrip exercises at 20, 35 and 50% maximal voluntary contraction (MVC) for 60 s. The study was conducted in a climatic chamber with a regulated ambient temperature of 35 degrees C and relative humidity of 50% to induce sweating response at rest by rising skin temperature without a marked change in internal temperature. Sublingual and mean skin temperatures (thermal factors) in both trained and untrained groups were essentially constant throughout all exercise intensities. Changes in heart rate, mean arterial blood pressure, and rating of perceived exertion with increased exercise intensity were similar in both groups. Sweating rate (SR) on the limbs (mean value of forearm and thigh) was significantly greater in the trained group than in the untrained group at 50% MVC (P < 0.05). In addition, the slopes of the relationship between increased SR and exercise intensity (% MVC) on the trunk (chest) and limbs were significantly greater in the trained group than in the untrained group (P < 0.05). Our results suggest that the sweating response caused by non-thermal factors against a background of changing thermal factors was enhanced by physical training. It is also thought that the enhanced sweating response may be especially evident on the limbs than on the trunk, such as improvement of sweating response associated with thermal factors.

Effects of rhythmic muscle compression on arterial blood pressure at rest and during dynamic exercise in humans.

This study was designed to examine the hypothesis that a rhythmic mechanical compression of muscles would affect systemic blood pressure regulation at rest and during dynamic exercise in humans. We measured the changes in mean arterial pressure (MAP) occurring (a) at rest with pulsed (350 ms pulses at 50 pulses min(-1)) or static compression (50 and 100 mmHg) of leg muscles with or without upper thigh occlusion, and (b) during 12-min supine bicycle exercise (75 W, 50 r.p.m.) with or without pulsed compression (50, 100, 150 mmHg) of the legs in synchrony with the thigh extensor muscle contraction. At rest with thigh occlusion, MAP increased by 4-8 mmHg during static leg compression, and by 5-9 mmHg during pulsed leg compression. This suggests that at rest pulsed leg compression elicits a reflex pressor response of similar magnitude to that evoked by static compression. During dynamic exercise without leg compression, MAP (having risen initially) gradually declined, but imposition of graded pulsed leg compression prevented this decline, the MAP values being significantly higher than those recorded without pulsed leg compression by 7-10 mmHg. These results suggest that the rhythmic increase in intramuscular pressure that occurs during dynamic exercise evokes a pressor response in humans.

Spontaneous wheel running attenuates cardiovascular responses to stress in rats.

We investigated the effect of chronic, 10-week spontaneous wheel running (SWR) exercise on stress-induced cardiovascular responses in free-moving male rats, using a biotelemetry system. During cage-switch stress or immobilization stress, blood pressure and heart rate were significantly increased in both the SWR (P<0.001 for each stress) and control groups (P<0.001 for each stress). However the blood pressure response was attenuated significantly in the SWR group (P<0.001) during cage-switch stress, and the blood pressure and heart rate responses were attenuated significantly in the SWR group (P<0.0001 and 0.01, respectively) during immobilization stress. The plasma norepinephrine (NE) response induced by immobilization stress tended to be attenuated in the SWR group, but the groups showed no significant differences in the plasma NE and epinephrine (E) responses to both stresses. These results suggest that daily SWR in rats has beneficial effects in suppressing excessive blood pressure and heart rate responses induced by two different types of stress. The mechanisms responsible for the greater resistance to these stresses in the SWR rats should be investigated further.

Effects of exercise intensity on the sweating response to a sustained static exercise.

To investigate how the sweating response to a sustained handgrip exercise depends on changes in the exercise intensity, the sweating response to exercise was measured in eight healthy male subjects. Each subject lay in the supine position in a climatic chamber (35 degrees C and 50% relative humidity) for approximately 60 min. This exposure caused sudomotor activation by increasing skin temperature without a marked change in internal temperature. After this period, each subject performed isometric handgrip exercise [15, 30, 45, and 60% maximal voluntary contraction (MVC)] for 60 s. Although esophageal and mean skin temperatures did not change with a rise in exercise intensity and were similar at all exercise intensities, the sweating rate (SR) on the forearm increased significantly (P < 0.05) from baseline (0.094 +/- 0.021 mg. cm(-2). min(-1) at 30% MVC, 0.102 +/- 0.022 mg. cm(-2). min(-1) at 45% MVC, 0.059 +/- 0.009 mg. cm(-2). min(-1) at 60% MVC) in parallel with exercise intensity above exercise intensity at 30% MVC (0.121 +/- 0.023 mg. cm(-2). min(-1) at 30% MVC, 0.242 +/- 0.051 mg. cm(-2). min(-1) at 45% MVC, 0.290 +/- 0.056 mg. cm(-2). min(-1) at 60% MVC). Above 45% MVC, SR on the palm increased significantly from baseline (P < 0.05). Although SR on the forearm and palm tended to increase with a rise in exercise intensity, there was a difference in the time courses of SR between sites. SR on the palm showed a plateau after abrupt increase, whereas SR on the forearm increased progressively during exercise. These results suggest that the increase in SR with the increase in sustained handgrip exercise intensity is due to nonthermal factors and that the magnitude of these factors during the exercise may be responsible for the magnitude of SR.

Reflex control of the cutaneous circulation during passive body core heating in humans.

The impact of body core heating on the interaction between the cutaneous and central circulation during blood pressure challenges was examined in eight adults. Subjects were exposed to -10 to -90 mmHg lower body negative pressure (LBNP) in thermoneutral conditions and -10 to -60 mmHg LBNP during heat stress. We measured forearm vascular conductance (FVC; ml. min(-1). 100 ml(-1). mmHg(-1)) by plethysmography; cutaneous vascular conductance (CVC) by laser-Doppler techniques; and central venous pressure, arterial blood pressure, and cardiac output by impedance cardiography. Heat stress increased FVC from 5.7 +/- 0.9 to 18.8 +/- 1.3 conductance units (CU) and CVC from 0.21 +/- 0.07 to 1.02 +/- 0.20 CU. The FVC-CVP relationship was linear over the entire range of LBNP and was shifted upward during heat stress with a slope increase from 0. 46 +/- 0.10 to 1.57 +/- 0.3 CU/mmHg CVP (P < 0.05). Resting CVP was lower during heat stress (6.3 +/- 0.6 vs. 7.7 +/- 0.6 mmHg; P < 0. 05) but fell to similar levels during LBNP as in normothermic conditions. Data analysis indicates an increased capacity, but not sensitivity, of peripheral baroreflex responses during heat stress. Laser-Doppler techniques detected thermoregulatory responses in the skin, but no significant change in CVC occurred during mild-to-moderate LBNP. Interestingly, very high levels of LBNP produced cutaneous vasodilation in some subjects.

Involvement of central beta-adrenoceptors in the tachycardia induced by water immersion stress in rats.

The purpose of the present study was to investigate whether central beta-adrenoceptors are involved in stress-induced cardiovascular responses in rats. Using a biotelemetry system, blood pressure and heart rate were measured at rest and during stress induced by immersion in 1 cm-deep water. Intracerebroventricular (i.c.v.) injections of a nonselective beta-adrenoceptor antagonist, DL-propranolol (5 or 50 microg), significantly and dose dependently attenuated the tachycardia induced by water immersion stress (drug-induced reduction of tachycardia at 5 min after the start of stress: 61.4 +/- 13.2% for 5 microg, 72.5 +/- 8.2% for 50 microg). The same doses of DL-propranolol had no effect on the resting heart rate. Injection (i.c.v.) of a lower dose (5 microg) of D-propranolol--which has a lower potency as a beta-adrenoceptor antagonist than DL-propranolol, but a similar local anesthetic, membrane-stabilizing activity--did not attenuate the stress-induced tachycardia, although a higher dose (50 microg) did. Intravenous administration of DL-propranolol (5 or 50 microg) significantly attenuated the stress-induced tachycardia (drug-induced reduction of tachycardia at 5 min after the start of stress: 20.0 +/- 7.5% for 5 microg, 42.4 +/- 3.4% for 50 microg). However, the attenuation was much smaller than in the i.c.v. DL-propranolol-injected group. The i.c.v. injection of the 50 microg dose of DL-propranolol significantly augmented both the resting blood pressure and the pressor response to water immersion stress, whereas the lower dose (5 microg) had no effect. The i.c.v. injection of 50 microg D-propranolol also augmented, although not significantly, the resting blood pressure and the pressor response to stress. These results suggest that central beta-adrenoceptors are involved in the tachycardia induced by water immersion stress in rats.

Human cardiovascular and humoral responses to moderate muscle activation during dynamic exercise.

We examined the hypothesis that activation of the muscle metaboreflex during dynamic exercise would augment influences tending to cause a rise in arginine vasopressin, plasma renin activity, and catecholamines during dynamic exercise in humans. Ten healthy adults performed 30 min of supine cycle ergometer exercise at approximately 50% of peak oxygen consumption with or without moderate muscle metaboreflex activation by application of 35 mmHg lower body positive pressure (LBPP). Application of LBPP during the first 15 or last 15 min of exercise increased mean arterial blood pressure, plasma lactate concentration, and minute ventilation, indicating an activation of the muscle metaboreflex. These changes were rapidly reversed when LBPP was removed. During exercise at this intensity, LBPP augmented the release of arginine vasopressin and catecholamines but not of plasma renin activity. These results suggest that, although in humans hormonal responses are induced by moderate activation of the muscle metaboreflex during dynamic exercise, the thresholds for these responses may not be uniform among the various glands and hormones.

Near-infrared monitoring of tissue oxygenation during application of lower body pressure at rest and during dynamical exercise in humans.

During the application of a wide range of graded lower body pressures (LBP) (-50 to 50 mmHg), we examined how (1) the tissue oxygenation in the lower and upper parts of the body changes at rest, and (2) how tissue oxygenation changes in the lower extremities during dynamical leg exercise. We used near-infrared spectroscopy (NIRS) to measure the changes induced by LBP in total Hb content and Hb oxygenation in seven subjects. At rest, total Hb increased and Hb oxygenation decreased in the thigh muscles during -25 and -50 mmHg LBP, while both decreased during +25 and +50 mmHg LBP. However, in the forearm muscles during graded LBP, the pattern of change in total Hb was the reverse of that in the thigh. Measurements from the forehead showed changes only during +50 mmHg LBP. These results demonstrated that the pattern of change in total Hb and Hb oxygenation differed between upper and lower parts with graded LBP at rest. During dynamical leg exercise, total Hb and Hb oxygenation in the thigh muscles decreased during stepwise increases in LBP above -25 mmHg, Hb oxygenation decreasing markedly during +50 mmHg LBP. These results suggest that during dynamical exercise (i) LBP at +25 mmHg or more causes a graded decline in blood volume and/or flow in the thigh muscles, and (ii) especially at +50 mmHg LBP, the O2 content may decrease markedly in active muscles. Our results suggest that NIRS can be used to monitor in a non-invasive and continuous fashion the changes in oxygenation occurring in human skeletal muscles and head during the graded changes in blood flow and/or volume caused by changes in external pressure and secondary reflexes both at rest and during dynamical exercise.

Mechanism for the posture-specific plasma volume increase after a single intense exercise protocol.

To test the hypothesis that exercise-induced hypervolemia is a posture-dependent process, we measured plasma volume, plasma albumin content, and renal function in seven healthy subjects for 22 h after single upright (Up) or supine (Sup) intense (85% peak oxygen consumption rate) exercise. This posture was maintained for 5 h after exercise. Plasma volume decreased during exercise but returned to control levels by 5 h of recovery in both postures. By 22 h of recovery, plasma volume increased 2.4 +/- 0.8 ml/kg in Up but decreased 2.1 +/- 0.8 ml/kg in Sup. The plasma volume expansion in Up was accompanied by an increase in plasma albumin content (0.11 +/- 0.04 g/kg; P < 0.05). Plasma albumin content was unchanged in Sup. Urine volume and sodium clearance were lower in Up than Sup (P < 0.05) by 5 h of recovery. These data suggest that increased plasma albumin content contributes to the acute phase of exercise-induced hypervolemia. More importantly, the mechanism by which exercise influences the distribution of albumin between extra- and intravascular stores after exercise is altered by posture and is unknown. We speculate that factors associated with postural changes (e.g., central venous pressure) modify the increase in plasma albumin content and the plasma volume expansion after exercise.

Modulation of the thermoregulatory sweating response to mild hyperthermia during activation of the muscle metaboreflex in humans.

1. To investigate the effect of the muscle metaboreflex on the thermoregulatory sweating response in humans, eight healthy male subjects performed sustained isometric handgrip exercise in an environmental chamber (35 C and 50 % relative humidity) at 30 or 45 % maximal voluntary contraction (MVC), at the end of which the blood circulation to the forearm was occluded for 120 s. The environmental conditions were such as to produce sweating by increase in skin temperature without a marked change in oesophageal temperature. 2. During circulatory occlusion after handgrip exercise at 30 % MVC for 120 s or at 45 % MVC for 60 s, the sweating rate (SR) on the chest and forearm (hairy regions), and the mean arterial blood pressure were significantly above baseline values (P < 0.05). There were no changes from baseline values in the oesophageal temperature, mean skin temperature, or SR on the palm (hairless regions). 3. During the occlusion after handgrip exercise at 30 % MVC for 60 s and during the occlusion alone, none of the measured parameters differed from baseline values. 4. It is concluded that, under mildly hyperthermic conditions, the thermoregulatory sweating response on the hairy regions is modulated by afferent signals from muscle metaboreceptors.

Effects of posture on cardiovascular responses to lower body positive pressure at rest and during dynamic exercise.

We tested the hypothesis that cardiovascular responses to lower body positive pressure (LBPP) would be dependent on the posture of the subject and also on the background condition (rest or exercise). We measured heart rate (HR), mean arterial blood pressure (MAP), and cardiac stroke volume in eight subjects at rest and during cycle ergometer exercise (76 +/- 3 W) with and without LBPP (25, 50, and 75 mmHg) in the supine and upright positions. At rest, the increase in MAP was proportional to the increase in LBPP and was greater in the supine (6 +/- 2, 15 +/- 3, and 26 +/- 3 mmHg) than in the upright (2 +/- 3, 9 +/- 3, and 17 +/- 3 mmHg) position. During dynamic exercise, the increases in MAP evoked by 25, 50, and 75 mmHg LBPP were greater in the supine (13 +/- 2, 28 +/- 3, and 40 +/- 3 mmHg) than in the upright (7 +/- 3, 12 +/- 3, and 25 +/- 3 mmHg) position. We conclude that the systemic pressure response to LBPP is clearly dependent on the body position, with the larger pressure responses being associated with the supine position both at rest and during dynamic leg exercise.

Cardiovascular and humoral responses to sustained muscle metaboreflex activation in humans.

The cardiovascular and humoral responses to sustained muscle metaboreflex activation were examined in eight male volunteers while they performed two 24-min exercise protocols. Each of these consisted of six 1-min bouts of isometric handgrip exercise (the left and right hands being used alternately) at 50% of maximal voluntary contraction; after each bout, there was either 3-min postexercise occlusion (occlusion protocol) or 3-min rest (control protocol). In the occlusion protocol, mean arterial blood pressure was approximately 25 mmHg higher than during the control protocol, indicating that the muscle metaboreflex was activated during occlusion. During the control protocol, plasma renin activity, plasma vasopressin, and adrenocorticotropic hormone values were not significantly different from the values at rest. During the occlusion protocol, however, plasma renin activity, plasma vasopressin, and adrenocorticotropic hormone were all significantly increased at 25 min. These data demonstrate that, in humans, the sustained activation of the muscle metaboreflex causes the secretion of several hormones originating from different regions.

The influence of exercise intensity on sweating efficiency of the whole body in a mild thermal condition.

To investigate whether the exercise intensity affects sweating efficiency (eta sw) during exercise under mild environmental conditions, six healthy males, aged 22 +/- 2 years, performed three bicycle ergometer exercises at varying intensities (73W: Ex-1, 103W: Ex-2 and 133W: Ex-3) for 40 min under the conditions of 25 degrees C room temperature, 50% relative humidity and 0.3-0.4 m s-1 wind velocity. Heart rate, oxygen consumption, rectal temperature (Tre), mean skin temperature (Tsk; 4 skin sites) and total sweat rate were determined intermittently throughout the experiments. Moreover, heat loss by evaporation (E), radiation (R), convection (C) and eta sw were calculated using the heat balance equations. The findings concerning thermoregulatory parameters under the three experimental conditions were summarized as follows: (1) the higher the exercise intensity, the larger the values of Tre and Tsk at the end of exercise and E, R and C during exercise (2) the mean values +/- SE of eta sw were 55.4 +/- 5.1, 63.2 +/- 5.2 and 58.5 +/- 1.9% for Ex-1, Ex-2 and Ex-3, respectively. The results suggest that exercise intensity would have no effect on eta sw in this mild thermal environment.

Differences in regional sweating responses during exercise between athletes trained on land and in water.

We investigated whether there are any differences in regional sweating responses during exercise between athletes trained on land and in water. We measured the local sweating rates on the left forearm (mswf) and the left scapula (msws), body temperatures (mean skin temperature, and rectal temperature Tre) in eight athletes trained on land (five soccer players, one distance runner and two baseball players, L group) and seven athletes trained in water (seven swimmers, W group) during cycle ergometer exercise at 50% maximal oxygen uptake for 40 min. The heart rate and oxygen uptake in the two groups during exercise showed nearly the same pattern of change. The Tre at the end of the exercise were 38.13 (SEM 0.19) degrees C in the L group and 38.26 (SEM 0.34) degrees C in the W group. Although the mswf in the two groups were similar, msws were significantly higher in L than in W at 30, 35 and 40 min of exercise. The msws at any given mean body temperature tended to be greater in L than in W. These results showed that a difference in regional sweating rate during exercise between the athletes trained on land and in water was present on the scapula.

Baroreceptor modulation of cutaneous vasodilator and sudomotor responses to thermal stress in humans.

1. The influence of baroreceptor unloading on cutaneous vasodilatation was investigated in ten human subjects during dynamic supine cycle ergometer exercise at 28 degrees C. Increases in forearm skin blood flow (venous occlusion plethysmography) and arterial blood pressure (non-invasive) were measured and used to calculate forearm vascular conductance while local chest sweating rate was measured by dew-point hygrometry. Subjects performed two similar exercise protocols with and without baroreceptor unloading induced by application of -40 mmHg lower body negative pressure (LBNP). The LBNP condition was reversed (i.e. either removed or applied) after 15 min while exercise continued for an additional 20 min. 2. During exercise without LBNP, the body core temperature threshold for vasodilatation (measured as oesophageal temperature, Tc) averaged 37.06 +/- 0.12 degrees C (+/- S.E.M.) and increased to 37.30 +/- 0.09 degrees C (P < 0.05) during exercise with LBNP. The rate of rise of forearm vascular conductance (FVC) per unit increase in Tc (an expression of thermal sensitivity) and peak FVC at 15 min was significantly attenuated during baroreceptor unloading. These effects were rapidly reversed when LBNP was turned off. 3. Baroreceptor unloading during the first 15 min of exercise attenuated the local chest sweating rate, which was also reversed when LBNP was removed. 4. The time course and quickness in which baroreceptor unloading modulated thermoregulatory control of skin blood flow and local chest sweat rate suggests that the interaction between these two homeostatic mechanisms is primarily neurally mediated. The ability of baroreceptor activity to modulate both control of skin blood flow and sweating suggests a common site of interaction, more proximal than the effector organs, and involving the active vasodilator system.

The sweating responses of athletes trained on land and in water.

In order to examine whether different sweating responses of athletes trained on land and in water may be ascribed to changes in the central sudomotor mechanisms and/or those of the peripheral mechanisms of sweat glands, we measured the local sweating rate at the left forearm (mswf) and the left scapula (msws), the frequence of sweat expulsion (Fsw) and body temperatures (mean skin temperature and rectal temperature: Tre) in six runners and five soccer players (R group) and six swimmers (S group) during progressive thermal stress at rest (2 degrees C increase in ambient temperature every 15 min from 35 to 45 degrees C RH = 30-40%). Tre and heart rate at the end of experiment did not differ significantly between the groups (37.31 +/- 0.04 degrees C, 74.5 +/- 7.9 beats.min-1 in the S group and 37.27 +/- 0.07 degrees C, 71.1 +/- 9.0 beats.min-1 in the R group, respectively). The msws and mswf at any given mean body temperature (Tb) were greater in the S group than in the R group. Although the regression line showing the relationship between Fsw and Tb in the S group was shifted to the left of that in the R group, there was no significant difference in the slope of the lines. The msws-Fsw or mswf-Fsw regression line was not different between the two groups. These results indicate that the higher sweating rate in the S group may be ascribed to a difference in the centrally derived sudomotor neural activity, but not to that in the peripheral mechanisms of sweat gland activity.