INTRODUCTION

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION REFERENCES

IN HUMANS, THE EVAPORATION of sweat is an important way to lose body heat to control internal temperature during exercise. The thermal factors associated with the sweating response are mainly internal temperature and skin temperature (T_sk), with sweating rate (SR) increasing linearly with a rise in the internal temperature (1, 10, 12, 18, 19, 25). The relationship between SR and internal temperature also shifts to the left with a rise in skin temperature (16). On the other hand, the SR can increase without changes in the internal temperature or skin temperature (13, 14, 28, 29, 34). This response indicates that the change in SR may be due to some mechanisms (nonthermal factors) involving activation of mechanosensitive (8, 14, 28, 29) or metabosensitive (13) receptors in the exercising muscle, central command signals linked with volitional effort (14, 28, 29, 32-34), or emotional or mental stimulation (15, 21, 24). However, the relationship between the sweating response and the magnitude of nonthermal factors is less well understood, although it is well known that body temperature (internal temperature and skin temperature) has a temperature-dependent effect on the sweating response.

Isometric exercise leads to changes in the heart rate (HR), blood pressure, and skin and muscle sympathetic nerve activity (16, 17, 22, 23). The SR also increases during isometric exercise (3, 23). Because brief isometric handgrip exercises do not induce marked increases in the internal temperature or skin temperature in mild hyperthermia (13), any change in SR would likely be due to nonthermal factors. Van Beaumont and Bullard (28) were the first to show that SR could increase without changes in internal temperature and skin temperature and that the increase in SR was dependent on exercise intensity. In their study, however, there were no data on how the SR changed with exercise intensity. Also, Vissing et al. (33) showed that skin sympathetic nerve and electrodermal activity increased with a rise in handgrip exercise intensity in normothermia. Because this study was performed in normothermia, basal sudomotor activity was absent or minimal before the exercise. It has also been reported that the muscle metaboreflex, which is a nonthermal factor, may have different effects on thermoregulatory responses [sweating and skin blood flow (SkBF) responses] between normothermia and hyperthermia or mild hyperthermia in which the sudomotor system is activated (4, 13). Moreover, the effect of muscle metaboreflex on sweating response is different between hairy regions (forearm and chest) and hairless regions (palm) (13). Therefore, it is not known how the sweating response depends on changes in intensity of isometric exercise when the sudomotor system is already activated.

The purpose of this study was to examine how the sweating response to a sustained handgrip exercise depends on changes in the exercise intensity and whether there are any regional differences in sweating responses between hairy and hairless regions. To test this, we measured the sweating responses on the palm and forearm with changes in the intensity of an isometric handgrip exercise in mild hyperthermia, after the sudomotor system had been activated by thermal stimulation (increasing skin temperature) but without marked changes in internal temperature.

	METHODS

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION REFERENCES

Subjects. The experiments were performed on eight healthy male subjects with the following morphometric characteristics: age 23.9 ± 2.5 (SD) yr, height 1.71 ± 0.05 m, and mass 69.0 ± 8.5 kg. Each subject was informed of the purpose of the study and the procedures involved beforehand, and his consent was obtained.

Procedures. The experiments were conducted in an environmental chamber (SR-3000, Nagano Science, Osaka, Japan) maintained at an ambient temperature of 35°C and a humidity of 50% with minimal air movement. We selected these environmental conditions to cause sudomotor activation by increasing skin temperature without a marked change in internal temperature. After entering the chamber, each subject rested in the supine position for ~60 min until his SR reached a steady state. During this time, the instruments for measuring data were attached. After a first 30-min rest, each subject performed two maximal voluntary contractions (MVC) of the right arm using a handgrip dynamometer. We used the higher value to determine the relative workload (%MVC). Subsequently, the subjects rested again for ~30 min, and then baseline data were recorded for 5 min at rest before the isometric handgrip exercise of the right arm. The subject performed 60-s handgrip exercises at 15, 30, 45, and 60% MVC in a random order. In all cases, the subjects used a visual feedback system to maintain the force of the handgrip. Because the movements of respiration influence the skin sympathetic nerve activity (5), we controlled the respiratory frequency at 12 breaths/min during the handgrip exercise. A rest of at least 10 min was allowed between trials. During this rest, the thermoregulatory parameters [SR, SkBF, esophageal temperature (T_es) and skin temperature] return to preexercise levels. Also, the values of T_es and skin temperature before handgrip exercise are similar in all exercise intensities.

Measurements. In all the experiments, the T_es, local skin temperature at eight body sites (chest, forearm, palm, forehead, abdomen, thigh, lower leg, and foot), SR on the forearm and palm, SkBF on the forearm, HR, arterial blood pressure (systolic and diastolic), and rating of perceived effort (RPE) were measured. T_es and local skin temperature were measured with a copper-constantan thermocouple. The tip of the thermocouple was coated with silicone, and it was inserted through the nose to a distance equal to one-quarter of each subject's height. The mean skin temperature () was calculated according to the method of Hardy and DuBois (9). SR at two body sites (left forearm and left palm) was measured continuously by the ventilated capsule method. Dry nitrogen gas was supplied to each capsule (forearm: 7.06 cm², palm: 1.53 cm²) at a rate of 1.5 l/min, and the humidity of the nitrogen gas flowing out of the capsules was measured with a capacitance hygrometer (HMP 133Y, Vaisala, Helsinki, Finland). The time delay of this system for measuring SR was 1 s and was counted for calculating SR. Change in SkBF on the left forearm was estimated continuously by using laser-Doppler velocimetry (ALF21, Advance, Tokyo, Japan). The cutaneous vascular conductance (CVC) was calculated from the ratio of SkBF to mean arterial blood pressure (MAP). The probe for measuring SkBF was placed within 1 cm of the ventilated capsule. The temperatures, SR, and SkBF were recorded every second and stored in a personal computer (PC9801RA, NEC, Tokyo, Japan) with a data logger (HR2300, Yokogawa, Tokyo, Japan).

Statistics. Data were analyzed for a 60-s preexercise period and the final 30 s of each handgrip exercise. The data are given as means ± SE. A one-way analysis of variance was performed by using Sheffé's test when F values were significant to compare the data across rest and exercise intensity. The P value for significance was set at 0.05.

	RESULTS

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION REFERENCES

Changes in body temperature (T_es and skin temperature), HR, MAP, SkBF on the forearm, and SR on the forearm and palm during a handgrip exercise at 30% MVC for 60 s are shown in Fig. 1; responses were similar for 45 and 60% MVC bouts. T_es and were essentially constant throughout all exercise bouts. The T_es during each handgrip exercise was 37.16 ± 0.06, 37.14 ± 0.06, 37.14 ± 0.05, and 37.15 ± 0.04°C at 15, 30, 45, and 60% MVC, respectively. HR, MAP, SkBF, and SR all increased progressively during the handgrip exercise at 30, 45, and 65% MVC but not at 15% MVC (Fig. 2).

View larger version (18K): [in this window] [in a new window]   Fig. 1.   Typical changes in esophageal temperature (Tes), mean skin temperature (sk), heart rate (HR), mean arterial pressure (MAP), skin blood flow (SkBF) on forearm, and sweating rate (SR) on forearm and palm during handgrip exercise for 60 s at 30% maximal voluntary contraction (MVC). Values are means ± SE for 8 subjects.

View larger version (29K): [in this window] [in a new window]   Fig. 2.   Responses in SR on forearm and palm at 4 exercise intensities (15, 30, 45, and 60% MVC) for 60 s. Values are means ± SE for 8 subjects.

SR on the palm increased abruptly just after the onset of exercise and then reached a steady state (Fig. 2). In contrast, above 30% MVC the SR on the forearm tended to increase progressively after the onset of sweating at each exercise intensity (Fig. 2). The delay before the onset of sweating on the forearm was 15.5 ± 3.4 s at 30% MVC, 10.8 ± 3.2 s at 45% MVC, and 8.8 ± 4.2 s at 60% MVC. There were significant differences (P < 0.05) in the delay between all the exercise intensities except 45 and 60% MVC. At 15% MVC no parameters changed markedly during the exercise (Fig. 3). The increases in SR on the forearm at 30, 45, and 60% MVC were significantly different from baseline levels, and there were significant differences between exercise intensities (P < 0.05; Fig. 3), except between 45 and 60% MVC. The increase in SR on the forearm was 0.05 ± 0.023, 0.121 ± 0.023, 0.242 ± 0.051, and 0.290 ± 0.056 mg · cm² · min¹ at 15, 30, 45, and 60% MVC, respectively. SR on the palm above 45% MVC increased significantly from baseline. The pattern of the change in SR on the forearm with the rise in intensity was similar to that of RPE (Fig. 3), and there was a significant relationship between SR and the RPE throughout the experiments (r = 0.728, P < 0.05). T_es and were similar across exercise intensities (Fig. 3). The change in HR (Fig. 3) increased significantly with a rise in exercise intensity above 30% MVC, whereas RPE increased significantly with each rise in exercise intensity. MAP increased significantly with a rise in exercise intensity (P < 0.05; Fig. 3).

View larger version (26K): [in this window] [in a new window]   Fig. 3.   Changes in HR (HR), rating of perceived effort (RPE), MAP (MAP), Tes, sk, and SR on forearm and palm with a rise in exercise intensity (15, 30, 45, and 60% MVC). Values are means ± SE for 8 subjects. * Significant difference between the exercise intensities, P < 0.05. ** Significant difference between exercise intensities, P < 0.01. # Significant difference from preexercise level, P < 0.05. ## Significant difference from preexercise level, P < 0.01.

Table 1 shows the percent changes in SkBF and CVC on the forearm during each experiment. SkBF tended to increase with a rise in intensity, but there was no significant increase from baseline at 15 or 30% MVC. At all exercise intensities, CVC was not significantly different from baseline, although it tended to increase with intensity.

	DISCUSSION

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION REFERENCES

It has been reported that a sustained handgrip exercise in mild hyperthermia does not change body temperatures (T_es and skin temperature) (13). In this study, there were no significant differences in T_es and during each exercise or across the exercise intensities (Figs. 1 and 3). Thus we could separate the effect of nonthermal factors from the effect of changes in internal temperature and on the sweating response during all exercise intensities. On the other hand, SR on the forearm increased with exercise intensity (Fig. 3), suggesting that the increase in SR is associated with nonthermal factors. In this study, we investigated the relationship between sweating responses to a sustained handgrip exercise and exercise intensity (magnitude of nonthermal factors). Van Beaumont and Bullard (28) did not show how the nonthermal SR changed with exercise intensity. In addition, Vissing et al. (33) indicated that skin sympathetic nerve and electrodermal activity increased only with a rise in static exercise intensity in normothermia, when thermoregulatory sudomotor activity is absent. Therefore, from these studies, it is impossible to conclude how the sweating response depends on a change in static exercise intensity. In contrast, in this study, the SR on the forearm at 30, 45, and 60% MVC, but not at 15% MVC, increased significantly from baseline in mild hyperthermic conditions. This indicates that 15% MVC is not sufficiently intense for nonthermal factors to induce a sweating response. Thus we believe that this study is the first to show how the sweating response to sustained static exercise changes with a rise in exercise intensity when the sudomotor system is already activated. The discussion focuses on these findings and examines possible mechanisms by which the SR on the forearm shows handgrip-intensity-dependent responses.

It has been shown that central command during static handgrip exercise is the main mechanism that stimulates sympathetic outflow (including vasoconstrictor, vasodilator, and sudomotor) to skin (32). RPE is reported to be an index of central command during exercise (32, 33). In this study, there was a significant relationship between the two parameters. Therefore, these results suggest that central command may be one of the mechanisms that shows the intensity-dependent sweating response during handgrip exercise.

In cats, mechanoreceptor activity increases rapidly within a few seconds of the onset of tension development (11). In this study, the onset of the sweating response was at 15.5, 10.8, and 8.8 s at 30, 45, and 60% MVC, respectively. However, it is suggested that there is some delay before sweat appears on the skin surface if the mechanoreceptors activate a sympathetic efferent signal to sweat glands. In addition, Kondo et al. (14) indicated that the increase in SR was not great during passive limb movement compared with during active limb movement, which means that mechanoreceptors in working muscle were stimulated predominately. Therefore, from these results we cannot exclude the possibility that afferent signals from mechanoreceptors affect the sweating responses and suggest that a detailed study of the effect of these receptors on the sweating response in humans is needed.

It was reported that the SR on the forearm and chest, but not the SR on the palm, during postexercise ischemia was significantly higher than the baseline rate in mild hyperthermic conditions (13). In addition, although the internal temperature measured sublingually increased significantly during muscle ischemia, the SR during the ischemia was significantly higher than baseline (4). MAP did not differ from baseline during postexercise ischemia after a 60-s handgrip at 30% MVC (13, 26). This suggests that this intensity of exercise is not of sufficient magnitude to trigger the muscle metaboreflex, because the input stimulus for the muscle metaboreflex is thought to be the effect of intramuscular pH changes (11, 20, 22, 30). In contrast, Nishiyasu et al. (20) showed that muscle pH decreased significantly during postexercise ischemia after 45- and 60-s handgrip exercises at 50% MVC. In addition, Kondo et al. (13) showed that during postexercise ischemia after a handgrip exercise at 45% MVC for 60 s, MAP was significantly different from baseline. These results indicate that the increase in SR on the forearm at 45 and 60% MVC may, in part, be attributed to the afferent signals from muscle metaboreceptors.

There is a regional difference in the nonthermal sweating response between the forearm and palm. Palm sweating (hairless region) is different from the thermal sweating that occurs on the forearm (hairy region) and is strongly influenced by mental and emotional stress (15, 21, 24). In addition, it has been reported that during static contraction changes in skin sympathetic nerve activity supplying the sole of the foot (hairless regions), which is suggested to consist mainly of sudomotor nerves, may be influenced by central command and input from peripheral mechanoreceptors (23). In this study, although the exercise-intensity-dependent sweating response was similar at both these sites (Fig. 3), there was a difference in the time courses of the SR (Fig. 2). SR on the palm increased abruptly just after the handgrip exercise was started and then reached an essentially steady state during the exercise. In contrast, the SR on the forearm increased progressively once a threshold was reached after the subjects started to exercise (30, 45, and 60% MVC). This indicates that the nonthermal factors associated with the sweating response may differ in the palm and forearm.

In this study, the increase in SR on the forearm was not significantly different at 45 and 60% MVC (Fig. 3). This may be due to two factors. It is possible that the sweating response to nonthermal factors reaches a plateau around these exercise intensities, because RPE as an index of central command differed between the two intensities. Skin sympathetic nervous activity is reported to be influenced by baroreceptors (6, 7, 31). Because the sympathetic pathways are thought to mediate the basic sweating response, the effect of the baroreflex on the sweating response cannot be denied. However, more detailed study of the sweating response with sustained handgrips at higher intensities is needed.

Taylor et al. (27) showed that SkBF and CVC on the forearm and chest during handgrip exercise at 30% MVC did not change during the first 60 s of exercise at normothermia and in local heating at 39°C. In this study, SkBF at 15 and 30% MVC did not increase significantly from baseline (Table 1). In contrast, there was significant increase from baseline with handgrip exercise at 45% MVC and above. In contrast, CVC did not change significantly from baseline at all exercise intensities, because SkBF and the change in MAP increased progressively with the rise in intensity (Fig. 3, Table 1).

In conclusion, handgrip exercise at 15% MVC did not evoke a marked change from baseline in SR on the forearm, whereas the increased SR at 30, 45, and 60% MVC was significantly different from baseline. The SR on the palm above 45% MVC increased significantly from baseline. Although the SR on the forearm and palm tended to increase with a rise in handgrip exercise intensity, there was a difference in the time course for the SR at the two sites. The SR on the palm plateaued after an abrupt increase, whereas the SR on the forearm increased progressively with a given threshold. Furthermore, the body temperatures (T_es and ) were similar at all exercise intensities. These results indicate that increases in SR on the forearm with the intensity of sustained handgrip exercise are due to nonthermal factors and that the magnitude of these factors is responsible for the magnitude of the SR during the exercise.