We assessed sex differences in the sweat gland response to changes in exercise intensity with respect to subjects' physical training status. In total, 37 subjects participated (10 trained and 10 untrained females, and 8 trained and 9 untrained males). Each subject cycled continuously at 35, 50 and 65% of their maximal O 2 uptake (V O 2 max ) for 60 min at an ambient temperature of 30• C and a relative humidity of 45%. The mean local sweating rate (SR) on the forehead, chest, back, forearm and thigh was significantly greater in the trained subjects than in the untrained subjects of both sexes. The degree of the increase in SR with physical training was greater in males than in females at higher levels of exercise intensity. This increase in SR depended primarily on an increase in the sweat output per gland (SGO) in both sexes. However, control of the SR increase with increasing exercise intensity was altered by training in females, i.e. the increase in SR from exercise at 50 to 65%V O 2 max depended only on an increase in SGO in trained females and males and untrained males, but it depended on increases in activated sweat glands and the SGO in untrained females. It was concluded that training improved the sweating response, and a sex difference was observed in the degree of improvement in the sweating response due to physical training. This sex difference became more pronounced with increasing exercise intensity. A sex difference was observed in the control of sweating rate to an increase in exercise intensity, i.e. the maximal activated sweat gland responses of untrained females required a higher body temperature or work intensity than the other groups.

PurposeThe present study examined sex differences in the sweat gland response to acetylcholine (ACh) in physically trained and untrained male and female subjects.MethodsSweating responses were induced on the forearm and thigh in resting subjects by ACh iontophoresis using a 10% solution at 2 mA for 5 min at 26°C and 50% relative humidity.ResultsThe ACh-induced sweating rate (SR) on the forearm and thigh was greater in physically trained male (P < 0.001 for the forearm and thigh, respectively) and female (P = 0.08 for the forearm, P < 0.001 for the thigh) subjects than in untrained subjects of both sexes. The SR was also significantly greater in physically trained males compared to females at both sites (P < 0.001) and in untrained males compared to females on the thigh (P < 0.02) only, although the degree of difference was greater in trained subjects than in untrained subjects. These sex differences can be attributed to the difference in sweat output per gland rather than the number of activated sweat glands.ConclusionWe conclude that physical training enhances the ACh-induced SR in both sexes but that the degree of enhancement is greater in male than in female subjects. The effects of physical training and sex on the SR may be due to changes in peripheral sensitivity to ACh and/or sweat gland size.

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The purposes of this study were (1) to evaluate changes in blood flow in the brachial artery and basilic vein of the upper arm with a rise in internal temperature during passive heating; and (2) to investigate the contributions of blood velocity and anteroposterior vessel diameter to these blood flow changes. Ten subjects rested in the supine position between a pair of tube-lined sheets. Thermoneutral water was circulated through the tubes to keep a mean skin temperature (Tsk) of 34-35 degrees C, and then hot water was circulated to maintain Tsk of 37-38 degrees C. The blood velocity and diameter in the brachial artery and basilic vein were continuously monitored by Doppler ultrasound technique and used to calculate blood flow. Blood flow in the brachial artery and basilic vein increased linearly as the oral temperature (T(or)) rose by < or =0.6 degrees C. The magnitude of the change in blood flow did not differ significantly between the two vessels. In addition, plots of DeltaT(or) versus blood flow yielded slopes that did not differ significantly between the brachial artery and the basilic vein. As T (or) increased, blood velocity, but not diameter, also increased. In conclusion, blood flow in the brachial artery and the basilic vein increased linearly as the internal temperature variable T (or) increased < or =0.6 degrees C. In both vessels, the passive heating-induced increases in blood flow resulted primarily from a change in blood velocity, rather than from a change in diameter.

The cutaneous vasodilation and sweating responses of prepubertal children to heat stress were examined. Seven prepubertal boys (9-11 years old) and 9 young men (20-24 years old) were seated wearing only swimming trunks while the air temperature (T(a)) was linearly increased from 28 degrees C to 40 degrees C over 50 min and then maintained at 40 degrees C for an additional 10 min. Skin temperature, cutaneous vascular conductance (CVC), and local sweating rate (m(sw)) were measured at multiple sites on the body. The boys had a significantly greater mean surface area-to-mass ratio compared with the young men. The rectal temperature did not change in either group with increasing T(a), although it was significantly higher in the boys. During the first half of the exposure period, when T(a) was less than the mean skin temperature (T(sk)), the boys had significantly higher CVC on the chest and significantly lower m(sw) on the chest and thigh as compared with the young men. During the latter half of the exposure, when heat stress was increased as T(a) exceeded mean T(sk), the boys had significantly higher mean T(sk), greater CVC on the chest and finger, greater rate of increase in the CVC on the forehead and finger, lower m(sw) on the chest and thigh, greater increase in heart rate, and higher thermal sensation. The mean body temperature at the onset of sweating was significantly greater in the boys than in the men. These results suggest that, compared with young men, prepubertal boys manifest greater physiological and perceptual strain under heat stress induced by T(a) exceeding mean T(sk), which is most probably attributable to a combination of lower evaporative heat loss, as evidenced by lower m(sw), and greater heat gain owing to a larger surface area-to-mass ratio. The maturation-related differences in heat loss responses vary according to body site.

Edited by: Philip Atherton New Findings r What is the central question of this study?Non-thermal factors (e.g. muscle metaboreflex) contribute to the sweating response during exercise. Although it is well recognized that the sweating responses caused by core temperature elevation in prepubertal children and the elderly are attenuated compared with young adults, it is unknown whether non-thermal sweating is also attenuated in these populations. r What is the main finding and its importance?The non-thermal sweating response during isometric hand-grip exercise and isolated muscle metaboreflex were attenuated in prepubertal children compared with young adults in a non-uniform manner over the body, but only during the muscle metaboreflex in the elderly. This may explain the maturation-and ageing-related decline of sweating during exercise.The purpose of the present study was to investigate sweating responses to isometric hand-grip (IH) exercise and muscle metaboreflex in prepubertal children and the elderly. In hot conditions (ambient temperature, 35°C; relative humidity, 45%), 13 healthy young adults, 10 prepubertal children and 10 elderly subjects (aged 20.4 ± 1.2, 11.4 ± 0.5 and 63.5 ± 3.1 years, respectively) repeated a three hand-grip exercise protocol that consisted of 1 min IH exercise at 15, 30 or 45% of maximal voluntary contraction (MVC) followed by 2 min postexercise forearm occlusion. Local sweat rates (SRs) on the forehead, chest, forearm, thigh and palm were continuously measured (ventilated capsule method). The forehead SR in prepubertal children during IH exercise at 45% MVC was significantly lower than that of young adults (0.26 ± 0.22 and 0.08 ± 0.15 mg cm −2 min −1 for young adults and children, respectively; P < 0.05) but not of the elderly at any exercise intensities. The SR on the chest (0.22 ± 0.22 and −0.01 ± 0.05 mg cm −2 min −1 for young adults and children, respectively), forearm (0.14 ± 0.12 and 0.03 ± 0.04 mg cm −2 min −1 ) and thigh (0.13 ± 0.10 and 0.02 ± 0.03 mg cm −2 min −1 ) during postexercise occlusion at 45% MVC was significantly lower in children than in young adults (P < 0.05). Elderly subjects showed a significantly lower SR on the forearm (0.04 ± 0.04 and 0.01 ± 0.02 mg cm 215 Non-thermal sweating in prepubertal children and the elderly (P < 0.05). These results suggest that sweating responses to IH exercise and muscle metaboreflex were underdeveloped in prepubertal children and that ageing attenuates the response to the muscle metaboreflex in a way that is not consistent across the body.

The purpose of the present study was to test our hypothesis that unloading the carotid baroreceptors alters the threshold and gain of the muscle metaboreflex in humans. Ten healthy subjects performed a static handgrip exercise at 50% of maximum voluntary contraction. Contraction was sustained for 15, 30, 45, and 60 s and was followed by 3 min of forearm circulatory arrest, during which forearm muscular pH is known to decrease linearly with increasing contraction time. The carotid baroreceptors were unloaded by applying 0.1-Hz sinusoidal neck pressure (oscillating from +15 to +50 mmHg) during ischemia. We estimated the threshold and gain of the muscle metaboreflex by analyzing the relationship between the cardiovascular responses during ischemia and the amount of work done during the exercise. In the condition with unloading of the carotid baroreceptors, the muscle metaboreflex thresholds for mean arterial blood pressure (MAP) and total vascular resistance (TVR) corresponded to significantly lower work levels than the control condition (threshold for MAP: 795 ± 102 vs. 662 ± 208 mmHg and threshold for TVR: 818 ± 213 vs. 572 ± 292 kg·s, < 0.05), but the gains did not differ between the two conditions (gain for MAP: 4.9 ± 1.7 vs. 4.4 ± 1.6 mmHg·kg·s·100 and gain for TVR: 1.3 ± 0.8 vs. 1.3 ± 0.7 mmHg·l·min·kg·s·100). We conclude that the carotid baroreflex modifies the muscle metaboreflex threshold in humans. Our results suggest the carotid baroreflex brakes the muscle metaboreflex, thereby inhibiting muscle metaboreflex-mediated pressor and vasoconstriction responses. We found that unloading the carotid baroreceptors shifts the pressor threshold of the muscle metaboreflex toward lower metabolic stimulation levels in humans. This finding indicates that, in the normal loading state, the carotid baroreflex inhibits the muscle metaboreflex pressor response by shifting the reflex threshold to higher metabolic stimulation levels.

Reducing blood flow to working muscles during dynamic exercise causes metabolites to accumulate within the active muscles and evokes systemic pressor responses. Whether a similar cardiovascular response is elicited with normal blood flow to exercising muscles during dynamic exercise remains unknown, however. To address that issue, we tested whether cardiovascular responses are affected by increases in blood flow to active muscles. Thirteen healthy subjects performed dynamic plantarflexion exercise for 12 min at 20%, 40%, and 60% of peak workload (EX20, EX40, and EX60) with their lower thigh enclosed in a negative pressure box. Under control conditions, the box pressure was the same as the ambient air pressure. Under negative pressure conditions, beginning 3 min after the start of the exercise, the box pressure was decreased by 20, 45, and then 70 mmHg in stepwise fashion with 3-min step durations. During EX20, the negative pressure had no effect on blood flow or the cardiovascular responses measured. However, application of negative pressure increased blood flow to the exercising leg during EX40 and EX60. This increase in blood flow had no significant effect on systemic cardiovascular responses during EX40, but it markedly attenuated the pressor responses otherwise seen during EX60. These results demonstrate that during mild exercise, normal blood flow to exercising muscle is not a factor eliciting cardiovascular responses, whereas it elicits an important pressor effect during moderate exercise. This suggests blood flow to exercising muscle is a major determinant of cardiovascular responses during dynamic exercise at higher than moderate intensity. integrated circulatory regulation; neural cardiovascular regulation; muscle metaboreflex DURING DYNAMIC EXERCISE, INCREASED skeletal muscle blood flow is essential to ensure an appropriate supply of O 2 to the active muscles and to remove the metabolic byproducts and generated heat. This exercise-induced skeletal muscle hyperemia is thought to be initially elicited by local mechanical and metabolic factors and to be modulated by neural cardiovascular regulatory mechanisms (8,41). Neural mechanisms also act to increase cardiac output (CO) and to redistribute blood flow from inactive regions to support the increase in skeletal muscle flow. This neural cardiovascular regulation is thought to be mediated by central command (41), as well as by feedback transmitted via afferent nerves (group III and IV fibers), innervating the working skeletal muscles, which are sensitive to mechanical (the so-called muscle mechanoreflex) and metabolic changes (the so-called muscle metaboreflex) (26,33,34,37,42), and are modulated via the arterial and cardiopulmonary baroreflexes (23,41,42).Reducing the blood flow to working muscles during dynamic exercise causes accumulation of metabolites within the active muscles and evokes muscle metaboreflex-mediated increases in sympathetic nerve activity, heart rate (HR), and systemic blood pressure (1,5,12,19,29,30,35,42). In addition, the reduced b...