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.

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.

Forearm vascular responses to baroreceptor unloading at the onset of dynamic exercise.

To determine the extent to which reflexes accompanying muscular exercise (associated with central command) interact with cardiopulmonary (CP) baroreceptor-mediated reflexes controlling forearm vascular resistance (FVR), we examined the forearm vasoconstrictor response at the onset of dynamic exercise, with and without CP baroreflex unloading, in 10 physically active men. CP baroreceptors were unloaded by application of lower body negative pressure (LBNP) at rest and during five 4-min bouts of supine exercise at 25 and 32 degrees C. Exercise intensities were 10 (essentially no load) and 100 W, and LBNP was applied at -10, -20, -30, and -40 mmHg during rest and at -20 and -40 mmHg during exercise. Resting FVR was 33.0 +/- 3.2 and 14.0 +/- 2.7 resistance units, and cardiac stroke volume (SV) was 117 +/- 7 and 126 +/- 9 ml/beat at 25 and 32 degrees C, respectively. We found a linear relationship between the increase in FVR and decrease in SV during LBNP; the slope of the relationship was significantly lower at 32 degrees C (FVR = 51.7-0.29SV) than at 25 degrees C (FVR = 123-0.79SV). At the onset of 100-W exercise without LBNP, FVR increased significantly to 50.2 +/- 9.0 and 21.2 +/- 3.2 units at 25 and 32 degrees C, respectively, whereas SV was unchanged. Application of -40-mmHg LBNP reduced SV significantly to 68 +/- 5 and 71 +/- 6 ml/beat and increased FVR significantly to 89.0 +/- 11.3 and 36.3 +/- 7.6 units at 25 and 32 degrees C, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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.

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.

Plasma volume expansion in humans after a single intense exercise protocol.

We used intense intermittent exercise to produce a 10% expansion of plasma volume (PV) within 24 h and tested the hypothesis that PV expansion is associated with an increase in plasma albumin content. The protocol consisted of eight 4-min bouts of exercise at 85% maximal O2 uptake with 5-min recovery periods between bouts. PV, plasma concentrations of albumin and total protein (TP), and plasma osmolality were measured before and during exercise and at 1, 2, and 24 h of recovery from exercise. During exercise, PV decreased by 15%, while plasma TP and albumin content remained at control levels. At 1 h of recovery, plasma albumin content was elevated by 0.17 +/- 0.04 g/kg body wt, accounting for the entire increase in plasma TP content. PV returned to control level at 1 h of recovery without fluid intake by the subjects, despite a 820 +/- 120-g reduction in body weight. At 2 h of recovery, plasma TP content remained significantly elevated, and plasma TP and albumin concentration were significantly elevated. At 24 h of recovery, PV was expanded by 4.5 +/- 0.7 ml/kg body wt (10 +/- 1%), estimated from hematocrit and hemoglobin changes, and by 3.8 +/- 1.3 ml/kg body wt (8 +/- 3%), measured by Evans blue dye dilution. Plasma albumin content was increased by 0.19 +/- 0.05 g/kg body wt at 24 h of recovery. If 1 g of albumin holds 18 ml of water, this increase in plasma albumin content can account for a 3.4-ml/kg body wt expansion of the PV. No significant changes in plasma osmolality occurred during recovery, but total plasma osmotic content increased in proportion to PV.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Cardiovascular and renal function during exercise-induced blood volume expansion in men.

To test the hypothesis that reduced baroreflex sensitivity is a direct result of exercise, we measured forearm vascular conductance (FVC) responses to graded lower body negative pressure (LBNP) 2, 20, and 44 h after intense exercise. Eight 4-min bouts of exercise at 85% of maximum oxygen uptake produced 3.5 +/- 0.7 and 3.9 +/- 1.0% blood volume (BV) expansions at 20 and 44 h of recovery, respectively. BV was unchanged from control values 2 h after exercise. The reduction in FVC was significantly less than control values during 30 and 40 mmHg of LBNP at 2 and 20 h of recovery, respectively, whereas heart rate and cardiac stroke volume responses were unchanged. Thus, a reduced FVC response to LBNP preceded BV expansion, demonstrating that exercise itself can elicit an attenuation of baroreflex function. To test the hypothesis that volume sensitivity of renal function is attenuated by intense exercise, we measured cardiovascular variables, plasma hormone concentrations, and renal output. At 20 h of recovery, resting mean arterial blood pressure and cardiac output were increased by 6 +/- 1 mmHg and 0.6 +/- 0.2 l/min, respectively, but resting plasma aldosterone and overnight Na+ excretion rate were unchanged. At 44 h of recovery, plasma aldosterone was decreased by 26 +/- 9% and overnight Na+ excretion rate was increased by 51 +/- 26%. Thus, appropriate endocrine and renal responses to increased BV were delayed until 44 h of recovery. Our findings suggest that a postexercise attenuation of baroreflex function participates in the induction of BV expansion by intense exercise.

Enhancement of parasympathetic cardiac activity during activation of muscle metaboreflex in humans.

We measured the changes in heart rate (HR) variability estimated from the standard deviation of the R-R intervals to evaluate cardiac parasympathetic tone noninvasively before and during activation of muscle metaboreflex induced by postexercise muscle ischemia. Eight healthy male subjects performed sustained handgrip at 50% maximal voluntary contraction followed by forearm occlusion. Mean arterial pressure, cardiac stroke volume, and ratio of cardiac preejection period to left ventricular ejection time (PEP/LVET) were also measured. During the 2-min occlusion after 60 s of handgrip with voluntary respiration, HR variability and mean arterial pressure were significantly increased from baseline (54.4 +/- 6.1 to 80.1 +/- 12.8 ms and 81 +/- 1 to 99 +/- 3 mmHg, respectively) and PEP/LVET was decreased from resting level of 0.404 +/- 0.022 to 0.363 +/- 0.036. During occlusion and recovery, HR did not change from baseline level in any experiment. There was no influence of occlusion itself or of cessation of exercise per se on any parameters. Although overall enhanced HR variability was seen, probably due to lower breathing frequency and larger tidal volume, similar results were also obtained from an experiment with controlled respiration, showing that the increase in HR variability was not due to the changes in tidal volume or breathing frequency during occlusion. In conclusion, the HR variability is increased during activation of the muscle metaboreflex induced by postexercise muscle ischemia in humans. This finding shows that the parasympathetic cardiac tone is enhanced during activation of the muscle metaboreflex in humans and balances enhanced cardiac sympathetic activity to result in an unchanged HR.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Effect of hypovolemia on forearm vascular resistance control during exercise in the heat.

To determine the influence of hypovolemia on the control of forearm vascular resistance (FVR) during dynamic exercise, we studied five physically active men during 60 min of supine cycle ergometer exercise bouts at 35 degrees C in control (normovolemic) and hypovolemic conditions. Hypovolemia was achieved by 3 days of diuretic administration and resulted in an average decrease in plasma volume of 15.9%. Relative to normovolemia, hypovolemia caused an attenuation of the progressive rise in forearm blood flow (P less than 0.05) and an increase in heart rate (P less than 0.05) during exercise. Because mean arterial blood pressure during hypovolemic exercise was well maintained, the attenuation of forearm blood flow was due entirely to a relative increase in FVR. At the onset of dynamic exercise, FVR was increased significantly in control and hypovolemic conditions by 13.2 and 27.1 units, respectively. The increase in FVR was significantly different between control and hypovolemic conditions as well. We attributed the increased vasoconstrictor bias during hypovolemia to cardiopulmonary baroreceptor unloading and/or an increased sensitivity to cardiopulmonary baroreceptor unloading. We concluded that reduced blood flow to the periphery during exercise in the hypovolemic condition was caused entirely by an increase in vascular resistance, thereby preserving arterial blood pressure and adequate perfusion to the organs requiring increased flow.

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.

Comparison of the forearm and calf blood flow response to thermal stress during dynamic exercise.

To examine the hypothesis that the skin blood flow response to body heating is not uniform over the entire body surface, we compared forearm (FBF) and calf (CBF) blood flow responses to an increase in core temperature (esophageal temperature, Tes) during dynamic exercise. We studied 13 physically active men during semi-recumbent one leg exercise and/or intermittent supine cycle exercise at 35 degrees C. During 30 min of one leg exercise, Tes, FBF, and CBF in the nonactive leg increased from 36.94 +/- 0.09 degrees C, 5.7 +/- 1.2, and 5.6 +/- 0.6 ml.(min.100 ml)-1 at rest to 37.97 +/- 0.10 degrees C, 27.0 +/- 2.4, and 11.1 +/- 0.8 ml.(min.100 ml)-1, respectively. The increase in blood flow per unit increase in Tes was much less in the calf than in the forearm. The ratio of the peak to resting blood flow averaged 6.5 in the forearm and 2.5 in the calf. During 60 min of intermittent supine two leg exercise, Tes, FBF, and CBF increased from 36.96 +/- 0.06 degrees C, 7.9 +/- 1.5, and 5.6 +/- 0.7 ml.(min.100 ml)-1 at rest to 37.91 +/- 0.07 degrees C, 23.6 +/- 3.0, and 11.4 +/- 1.9 ml.(min.100 ml)-1, respectively. Skin blood flow (SkBF) in the forearm and calf was estimated by using a simple cylindrical model, assuming skin thickness and resting muscle blood flow to be 0.2 cm and 2 ml.(min.100 ml)-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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.

Cardiopulmonary baroreflex control of forearm vascular resistance after acute blood volume expansion.

We report the stimulus-response characteristics of cardiopulmonary (CP) baroreflex control of forearm vascular resistance (FVR) in young adult male volunteers before and after: 1) blood volume expansion (8 ml/kg infusion of 5% human serum albumin solution, n = 5) and 2) a redistribution of blood volume toward the heart (6 degrees head-down tilt (HDT), n = 6). We assessed the relationship between reflex stimulus (i.e., changes in central venous pressure (CVP] and response (i.e., FVR) during unloading of CP mechanoreceptors with lower body negative pressure (0 to -20 mm Hg). Changes in CVP were estimated from changes in venous pressure of a large peripheral vein of the dependent arm with the subject in the right lateral decubitus position. In all conditions, reflex forearm vasoconstriction occurred in response to a reduction in estimated CVP. The absolute change in FVR per unit of CVP was reduced from -4.24 +/- 1.68 to -2.15 +/- 1.16 units/mm Hg (p less than 0.05) following blood volume expansion but was similar before (-3.34 +/- 0.89 units/mm Hg) and during 6 degrees HDT (-3.30 +/- 0.92 units/mm Hg). The reduced sensitivity of the CP baroreflex following volume expansion was manifested primarily as a smaller FVR response to LBNP (p less than 0.05). Blood volume expansion and 6 degrees HDT increased resting estimated CVP by 1.5 and 0.9 mm Hg, respectively (p less than 0.05) and resting levels of FVR decreased slightly.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of dynamic exercise on cardiovascular regulation during lower body negative pressure.

The purpose of this study was to compare the cardiovascular control mechanisms that defend arterial blood pressure against blood pooling between rest and moderate dynamic exercise. We studied ten physically active men during rest and five 12-min graded supine cycle ergometer exercise bouts with and without application of LBNP in 25 degrees C and 35 degrees C. Exercise intensities were 10, 50, and 100 watts (W), each for 4 min, and LBNP was applied at 0 (control), -20, -40, and -60 mm Hg in 25 degrees C and -40 mm Hg in 35 degrees C. At rest, cardiac stroke volume (SV) decreased from 120 +/- 5 ml during control to 94 +/- 6, 67 +/- 5 and 49 +/- 3 ml during -20, -40, and -60 mm Hg LBNP, respectively, and to 55 +/- 3 ml during -40 mm Hg at 35 degrees C. Exercise elevated SV toward the control level during LBNP due to muscle pumping action. Heart rate (HR) did not increase significantly during application of LBNP until SV decreased by 20-25 ml during LBNP, both during rest and exercise. The magnitude of HR increase per decrease in SV, once an increase in HR occurred, was similar between rest and exercise, regardless of exercise intensity. The change in total peripheral resistance (TPR) with respect to SV was linear, confirming that peripheral vascular adjustments were proportional to changes in the heart's preload. The slopes of the TPR-SV relation were similar during rest and exercise, although shifted to the left with increasing exercise intensity.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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.