Role of changes in insulin and glucagon in glucose homeostasis in exercise.

This experiment was performed to determine if plasma glucose homeostasis is maintained in normal human volunteers during light exercise (40% maximal oxygen consumption [VO2 max]) when changes in insulin and glucagon are prevented. Hormonal control was achieved by the infusion of somatostatin, insulin, and glucagon. Glucose kinetics and oxidation rates were determined with stable isotopic tracers of glucose, and by indirect calorimetry. Two different rates of replacement of insulin and glucagon were used; in one group, insulin was clamped at 19.8 +/- 2.6 microU/ml (high-insulin group), and in the other group insulin was clamped at 9.2 +/- 1.3 microU/ml (low-insulin group). Glucagon was maintained at 261 +/- 16.2 and 124 +/- 6.4 pg/ml, respectively, in the high-insulin and low-insulin groups. Without hormonal control, plasma glucose homeostasis was maintained during exercise because the increase in glucose uptake was balanced by a corresponding increase in glucose production. When changes in insulin and glucagon were prevented, plasma glucose concentration fell, particularly in the high-insulin group. Glucose uptake increased to a greater extent than when hormones were not controlled, and glucose production did not increase sufficiently to compensate. The increase in glucose uptake in the hormonal control groups was associated with an increased rate of glucose oxidation. When euglycemia was maintained by glucose infusion in the hormonal control subjects, the modest increase in glucose production that otherwise occurred was prevented. It is concluded that during light exercise there must be a reduction in insulin concentration and/or an increase in glucagon concentration if plasma glucose homeostasis is to be maintained. If such changes do not occur, hypoglycemia, and hence exhaustion, may occur.

Moderate-intensity aerobic training improves glucose tolerance in aging independent of abdominal adiposity.

OBJECTIVE: To test the hypothesis that training-related improvements in glucose and insulin responses to an oral glucose tolerance test (OGTT) are independent of changes in abdominal adiposity. DESIGN: Adiposity and responses to an OGTT were measured before and after a 4-month randomized, controlled aerobic training program. SETTING: An academic medical institution. PARTICIPANTS: Sixteen healthy older (73+/-1 year) men and women. INTERVENTION: Both the training (T) (n=9) and control (C) (n=7) groups exercised 4 times a week for 60-minute sessions. T exercised on mini-trampolines at 55 to 65% of HRmax (determined from a graded treadmill test) for 1 month and then at 75% for 3 months; C engaged in supervised stretching and yoga. MEASUREMENTS: At baseline and follow-up, we estimated abdominal fat (from computed tomography and anthropometry), plasma glucose, and serum insulin responses to the OGTT and fasting concentrations of free fatty acids (FFA). RESULTS: Aerobic training resulted in a 16% increase in VO2 peak and a 24% decrease in FFA in the T group (P < .05), but training had no effect on abdominal fat. In the T group, the glucose response curve shifted to the left, and the incremental area under the glucose curve decreased by 25% (P < .05). This improvement in glucose response occurred, however, only in those with impaired glucose tolerance at baseline and without any observed change in insulin response. No change in any variables occurred in the C group. CONCLUSIONS: Our data suggest that moderate-intensity aerobic training has a favorable effect on glucose tolerance in older people, independent of changes in abdominal adiposity.

Forearm skin and muscle vasoconstriction during lower body negative pressure.

In view of conflicting reports of skeletal muscle and skin blood flow participation in baroreceptor-mediated reflexes, we studied the effects of graded lower body negative pressure (LBNP) on cutaneous and muscular components of forearm blood flow (FBF) in seven male subjects at 28 degrees C. FBF was measured by venous occlusion plethysmography and cutaneous flow by laser-Doppler velocimetry, the difference being the muscular flow. Mean FBF decreased by 39 and 56% from control at LBNP of 20 and 50 Torr, respectively. Skin flow decreased linearly with graded LBNP contributing 32% of the decrease of total blood flow at 20 Torr and then 50% of total decrease of blood flow at 50 Torr. Conversely, the decrease in muscle flow represented 68% of the total decrease at LBNP of 20 Torr and then 50% of the total decrease at LBNP of 50 Torr. We concluded that both skin and muscle circulations participate in sustained peripheral vasoconstriction during LBNP, with muscle flow achieving near maximum vasoconstriction by 20 Torr and skin showing a graded vasoconstriction to decreases in LBNP.

Role of cardiopulmonary baroreflexes during dynamic exercise.

To examine the role of cardiopulmonary (CP) mechanoreceptors in the regulation of arterial blood pressure during dynamic exercise in humans, we measured mean arterial pressure (MAP), cardiac output (Q), and forearm blood flow (FBF) during mild cycle ergometer exercise (77 W) in 14 volunteers in the supine position with and without lower-body negative pressure (LBNP). During exercise, MAP averaged 103 +/- 2 mmHg and was not altered by LBNP (-10, -20, or -40 mmHg). Steady-state Q during exercise was reduced from 10.2 +/- 0.5 to 9.2 +/- 0.5 l/min (P less than 0.05) by application of -10 mmHg LBNP, whereas heart rate (97 +/- 3 beats/min) was unchanged. MAP was maintained during -10 mmHg LBNP by an increase in total systemic vascular resistance (TSVR) from 10.3 +/- 0.5 to 11.4 +/- 0.6 U and forearm vascular resistance (FVR) from 17.5 +/- 1.9 to 23.3 +/- 2.6 U. The absence of a reflex tachycardia or reduction in arterial pulse pressure during -10 mmHg LBNP supports the hypothesis that the increase in TSVR and FVR results primarily from the unloading of CP mechanoreceptors. Because CP mechanoreceptor unloading during exercise stimulates reflex circulatory adjustments that act to defend the elevated MAP, we conclude that the elevation in MAP during exercise is regulated and not merely the consequence of differential changes in Q and TSVR. In addition, a major portion of the reduction in FBF in our experimental conditions occurs in the cutaneous circulation. As such, these data support the hypothesis that CP baroreflex control of cutaneous vasomotor tone is preserved during mild dynamic exercise.

Involvement of sodium retention hormones during rehydration in humans.

We investigated the relation between involuntary dehydration and the mechanisms affecting Na+ retention in the body, focusing on the renin-angiotensin-aldosterone system. Six adult males were dehydrated to 2.3% of their body weight by an exercise-heat regimen, followed by rehydration (180 min) with tap water (H2O-R) or 0.45% NaCl solution (Na-R). We measured plasma renin activity (PRA) and aldosterone levels (PA) before dehydration (control), after dehydration, and at 60, 120, and 180 min of rehydration. During the 3-h rehydration period, subjects, restored 51% of the water lost during H2O-R and 71% during Na-R (P less than 0.05). Plasma volume was reduced by an average of 4.5% after dehydration. After 180 min of rehydration, plasma volume restoration during Na-R was to 174% of that lost, and during H2O-R it was to 78% of that lost. We found significant correlations between the change in plasma volume and PRA (r = -0.70, P less than 0.001) and between PRA and PA (r = 0.71, P less than 0.001). In both recovery conditions, PRA increased significantly after dehydration (P less than 0.05) and decreased almost to the control level by 180 min of rehydration, at which time the plasma volume deficit was restored. The change in PA paralleled that in PRA. The rate of sodium excretion was correlated with PA levels in both groups (r = -0.58, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Shift in body fluid compartments after dehydration in humans.

To investigate the influence of [Na+] in sweat on the distribution of body water during dehydration, we studied 10 volunteer subjects who exercised (40% of maximal aerobic power) in the heat [36 degrees C, less than 30% relative humidity (rh)] for 90-110 min to produce a dehydration of 2.3% body wt (delta TW). After dehydration, the subjects rested for 1 h in a thermoneutral environment (28 degrees C, less than 30% rh), after which time the changes in the body fluid compartments were assessed. We measured plasma volume, plasma osmolality, and [Na+], [K+], and [Cl-] in plasma, together with sweat and urine volumes and their ionic concentrations before and after dehydration. The change in the extracellular fluid space (delta ECF) was estimated from chloride distribution and the change in the intracellular fluid space (delta ICF) was calculated by subtracting delta ECF from delta TW. The decrease in the ICF space was correlated with the increase in plasma osmolality (r = -0.74, P less than 0.02). The increase in plasma osmolality was a function of the loss of free water (delta FW), estimated from the equation delta FW = delta TW - (loss of osmotically active substance in sweat and urine)/(control plasma osmolality) (r = -0.79, P less than 0.01). Free water loss, which is analogous to "free water clearance" in renal function, showed a strongly inverse correlation with [Na+] in sweat (r = -0.97, P less than 0.001). Fluid movement out of the ICF space attenuated the decrease in the ECF space.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of osmolality and plasma volume during rehydration in humans.

To determine how the sodium content of ingested fluids affects drinking and the restoration of the body fluid compartments after dehydration, we studied six subjects during 4 h of recovery from 90-110 min of a heat [36 degrees C, less than 30% relative humidity (rh)] and exercise (40% maximal aerobic power) exposure, which caused body weight to decrease by 2.3%. During the 1st h, subjects rested seated without any fluids in a thermoneutral environment (28 degrees C, less than 30% rh) to allow the body fluid compartments to stabilize. Over the next 3 h, subjects rehydrated ad libitum using tap water and capsules containing either placebo (H2O-R) or 0.45 g NaCl (Na-R) per 100 ml water. During the 3-h rehydration period, subjects restored 68% of the lost water during H2O-R, whereas they restored 82% during Na-R (P less than 0.05). Urine volume was greater in H2O-R than in Na-R; thus only 51% of the lost water was retained during H2O-R, whereas 71% was retained during Na-R (P less than 0.05). Plasma osmolality was elevated throughout the rehydration period in Na-R, whereas it returned to the control level by 30 min in H2O-R (P less than 0.05). Changes in free water clearance followed changes in plasma osmolality. The restoration of plasma volume during Na-R was 174% of that lost. During H2O-R it was 78%, which seemed to be sufficient to diminish volume-dependent dipsogenic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Venous and arterial reflex responses to positive-pressure breathing and lower body negative pressure.

We examined the relative importance of arteriolar and venous reflex responses during reductions in cardiac output provoked by conditions that increase [positive end-expiratory pressure (PEEP)] or decrease [lower body negative pressure (LBNP)] peripheral venous filling. Five healthy subjects were exposed to PEEP (10, 15, 20, and 25 cmH2O) and LBNP (-10, -15, -20, and -25 mmHg) to induce progressive but comparable reductions in right atrial transmural pressure (control to minimum): from 5.9 +/- 0.4 to 1.8 +/- 0.7 and from 6.5 +/- 0.6 to 2.0 +/- 0.2 mmHg with PEEP and LBNP, respectively. Cardiac output (impedance cardiography) fell less during PEEP than during LBNP (from 3.64 +/- 0.21 to 2.81 +/- 0.21 and from 3.39 +/- 0.21 to 2.14 +/- 0.24 l.min-1.m-2 with PEEP and LBNP, respectively), and mean arterial pressure increased. We observed sustained increases in forearm vascular resistance (i.e., forearm blood flow by venous occlusion plethysmography) and systemic vascular resistance that were greater during LBNP: from 19.7 +/- 2.91 to 27.97 +/- 5.46 and from 20.56 +/- 2.48 to 50.25 +/- 5.86 mmHg.ml-1.100 ml tissue-1.min (P < 0.05) during PEEP and LBNP, respectively. Venomotor responses (venous pressure in the hemodynamically isolated limb) were always transient, significant only with the greatest reduction in right atrial transmural pressure, and were similar for LBNP and PEEP. Thus arteriolar rather than venous responses are predominant in blood volume mobilization from skin and muscle, and venoconstriction is not intensified with venous engorgement during PEEP.

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)

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.

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

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

Measurement of plasma volume in rats with use of fluorescent-labeled albumin molecules.

We describe a method for measuring plasma volume (PV) in small animals that allows small sample sizes but does not require the use of radioisotopes and thus is a convenient approach for making repeated measurements. Texas Red covalently bound to albumin (TR-A) was used in a typical indicator-dilution technique to measure PV. The relative fluorescent intensity of TR-A is linear to its concentration (up to 0.15 mg/ml) at an excitation lambda of 590 nm and an emission lambda of 610 nm. Catheters were inserted through the right jugular vein of anesthetized rats and threaded into the vena cava. A 0.5-ml control blood sample was taken, a measured quantity of TR-A was injected, and the catheter was flushed with saline. A 0.5-ml postinjection sample was taken 5 min after TR-A injection. PV was calculated by comparing the difference between the relative fluorescent intensity of control and postinjection plasma samples to a standard. The PV of 22 rats [362 +/- 14 (SE) g] was 14.1 +/- 0.4 ml (39.6 +/- 0.9 ml/kg body wt) measured by the TR-A method and 12.8 +/- 0.4 ml (35.9 +/- 1.0 ml/kg body wt) measured by a standard radioiodinated albumin method. There was a strong correlation between PV measured by both methods in the same rat (r = 0.90, P < 0.01). Infusion experiments indicated that the TR-A method can detect acute changes in PV, and repeated measurements of PV made on a chronically instrumented rat demonstrated that the method can reliably measure PV on consecutive days.

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.

Diminished baroreflex control of forearm vascular resistance in physically fit humans.

The stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR) were studied in five unfit [UF, maximal O2 consumption (VO2 max) = 38.5 ml X min-1 X kg-1] and six fit (F, VO2 max = 57.0 ml X min-1 X kg-1) subjects. We assessed the relationship between reflex stimulus, i.e., changes in central venous pressure (CVP) and response, i.e., FVR, during selective unloading of the cardiopulmonary mechanoreceptors with lower body negative pressure (0 to -20 mmHg). The linear relationship between FVR and CVP, the gain of this baroreflex, was significantly diminished in the F subjects, -2.42 +/- 0.57 U/mmHg, compared with the UF, -5.15 +/- 0.58 U/mmHg. Both groups, F and UF, had similar resting values for CVP and FVR; thus the diminished gain in F subjects was not simply an artifact resulting from a shift of the set point along the baroreflex stimulus-response curve. We also found a linear relationship between baroreflex gain and total blood volume (r = 0.59, P less than 0.05). We conclude that the gain of this vascular reflex is attenuated in trained individuals and is related to cardiovascular adaptations, such as an increased blood volume, associated with exercise training.

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

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

Albumin synthesis after intense intermittent exercise in human subjects.

We measured hepatic albumin synthesis in five volunteers (4 men and 1 woman) at 3 and 6 h after recovery from intense exercise. A primed-constant infusion of a stable isotopic tracer of phenylalanine was used to determine hepatic fractional synthetic rate (FSR) and absolute synthetic rate (ASR) of albumin from the enrichment of phenylalanine in albumin. The infusion of the stable isotope tracer began 2 h after upright exercise or upright rest. Albumin FSR and ASR were 6.39 +/- 0.48%/day and 120 +/- 9 mg.kg body wt-1.day-1, respectively, 3-6 h after recovery from exercise; the FSR and ASR on the time control study day were 5.94 +/- 0.47%/day and 104 +/- 9 mg.kg body wt-1.day-1, respectively. The 6 and 16% increases (P < 0.05) in FSR and ASR after exercise were associated with an elevated plasma albumin content at 5 and 6 h of recovery (P < 0.05), an increased total protein content throughout recovery (P < 0.05), and a negative free water clearance (P < 0.05) at 2, 3, and 6.5 h of recovery compared with baseline values; these variables were unchanged from their baselines on the time control study day. Increased albumin content and reduced free water clearance contribute to a retention of fluid within the circulation after intense exercise. The measured increase in albumin synthesis could not account for the entire increase in albumin content at 6 h of recovery from exercise. However, we estimate that if the increased activity was maintained for the next 18 h, it could account for the expected increase in albumin content at 24 h of recovery.

Effect of saline infusion during exercise on thermal and circulatory regulations.

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

Effects of varied air velocity on sweating and evaporative rates during exercise.

This study was designed to determine the extent to which changes in the evaporative power of the environment (Emax) affect sweating and evaporative rates. Six male subjects undertook four 60-min bouts of cycle ergometer exercise at 56% maximal O2 uptake (VO2max).Emax was varied by differences in ambient temperature and airflow; two exercise bouts took place at 24 degrees C and two at 35 degrees C, with air velocity at < 0.2 and 3.0 m/s in both. Total sweat production was estimated from body weight loss, whereas whole body evaporative rate was measured continuously from a Potter beam balance. Body core temperature was measured continuously from a thermocouple in the esophagus (T(es)), with mean skin temperature (Tsk) computed each minute from thermocouples at eight sites. Total body sweat loss was significantly greater (P < 0.05) in the 0.2- than in the 3.0-m/s condition at both 24 and 35 degrees C. Tsk was higher (P < 0.05) in the still-air conditions at both temperatures, but final T(es) was significantly higher (P < 0.05) in still air only in the 35 degrees C environment. Thus the reduced Emax in still air caused a greater heat storage, thereby stimulating a greater total sweat loss. However, in part because of reduced skin wettedness, the slope of the sweat rate-to-T(es) relation at 35 degrees C in the 3.0-m/s condition was 118% that at 0.2 m/s (P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Interaction of local and reflex thermal effects in control of forearm blood flow.

We measured forearm blood flow (ABF) bilaterally on six subjects during 15-min periods of leg exercise and the first 10 min of recovery. One forearm (control) was kept at about 33 degrees C skin temperature in all experiments. In experiments at ambient temperature (Ta) of 15 degrees C, the other arm (experimental) was kept at about 26, 33, and 40 degrees C, respectively, during three successive cycles of exercise and recovery. ABF in the 26 degrees C forearm was linearly related to and averaged 42% of control. The relation of ABF in the 40 degrees C forearm to control ABF showed a bend at control ABF of 4-5 ml X 100 ml-1 X min-1. Below the bend, experimental ABF average 213% of control. Above the bend, experimental ABF averaged 5.09 ml X 100 ml-1 X min-1 above control. In four subjects, after heating the experimental forearm to 40 degrees C, we measured ABF for 25-30 min at rest in Ta of both 15 and 25 degrees C. At 25 degrees C Ta, ABF in the heated forearms rose gradually, but control ABF showed little change. At 15 degrees C Ta, the effect on ABF of local heating to 40 degrees C was much reduced, apparently due to reflex vasoconstrictor signals.

Effect of beta-adrenergic blockade on thermoregulation during exercise.

To resolve conflicting reports concerning the effects of beta-blockade (BB) on thermoregulatory reflexes during exercise, we studied six fit men during 40 min of cycle ergometer exercise at 60% maximum O2 consumption at ambient temperatures of 22 and 32 degrees C. Two hours before exercise, each subject ingested a capsule containing either 80 mg of propranolol or placebo in single-blind fashion. Heart rate at 40 min of exercise was reduced (P less than 0.01) from 125 to 103 beats min at 22 degrees C and 137 to 104 beats min at 32 degrees C, demonstrating effective BB. After 40 min of exercise, esophageal temperature (Tes) was elevated with BB (P less than 0.05) from 37.66 +/- 0.04 to 38.14 +/- 0.03 and 38.13 +/- 0.04 to 38.41 +/- 0.04 degrees C at 22 and 32 degrees C, respectively. The elevated Tes resulted from a reduced core-to-skin heat flux at both temperatures, indicated by a reduction in the slope of the forearm blood flow (FBF)-Tes relationship, and a decrease in maximal FBF. Systolic blood pressure was decreased 20 mmHg with BB (P less than 0.01), whereas diastolic blood pressure was unchanged, reducing arterial pulse pressure (PP). Because PP was decreased and cardiac filling pressure was presumably not reduced (since cardiac stroke volume was elevated), we suggest that at least a part of the relative increase in peripheral vasomotor tone during BB was the consequence of reduced sinoaortic baroreceptor stimulation.