Effect of Activated Sweat Glands on the Intensity-Dependent Sweating Response to Sustained Static Exercise in Mildly Heated Humans

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1 Short Communication Japanese Journal of Physiology, 52, , 2002 Effect of Activated Sweat Glands on the Intensity-Dependent Sweating Response to Sustained Static Exercise in Mildly Heated Humans Narihiko KONDO, Shuji YANAGIMOTO, Ken AOKI, Shunsaku KOGA*, and Yoshimitsu INOUE Laboratory for Applied Human Physiology, Faculty of Human Development, Kobe University, Kobe, Japan; * Kobe Design University, Kobe, , Japan; and Osaka International University, Osaka, Japan Abstract: Changes in the number of activated sweat glands (ASGs) and sweat output per gland (SGO) with increased exercise intensity during sustained static exercise were investigated. Fourteen male subjects performed 20, 35, and 50% maximal voluntary contraction (MVC) for 60 s with the right hand (exercised arm) at an ambient temperature of 35 C and 50% relative humidity. Although sublingual, local skin, and mean skin temperatures remained essentially constant throughout the exercise at each intensity, the sweating rate (SR) of nonglabrous skin on the nonexercised left forearm increased significantly with a rise in exercise intensity (p 0.05). Changes in the number of ASGs with rising exercise intensity paralleled changes in the SR, but the SGO did not change markedly with altered exercise intensity. These results suggest that in mildly heated humans, at less than 50% MVC, the increase in the SR from nonglabrous skin with rising exercise intensity during sustained static exercise is dependent on changes in the number of ASGs and not on SGO. [Japanese Journal of Physiology, 52, , 2002] Key words: isometric handgrip exercise, internal temperature, sudomotor center. Humans have a capacity greater than other mammals to sweat during exercise, especially when physical activity is performed in hot climates. The sweating rate (SR) from nonglabrous skin during dynamic exercise is modulated by thermal factors (internal and skin temperatures) [1 3] and by nonthermal factors [4, 5]. Moreover, the sweating response during sustained static exercise is modulated only by nonthermal factors when the sudomotor center has been activated [6 11] because internal and skin temperatures (thermal factors) do not change during exercise. During a sustained handgrip exercise, the SR from nonglabrous skin is reported to increase with exercise intensity, indicating that the magnitude of nonthermal factors affects the magnitude of the SR during exercise [8]. An increased SR could be due to an increased density of activated sweat glands (ASGs), increased sweat output per gland (SGO), or a combination of both factors. We recently reported that during dynamic exercise, increases in the SR from nonglabrous skin depend on the number of ASGs and the SGO when exercise intensity is elevated from low- (35% maximal oxygen uptake: V O2 max ) to moderate- (50% V O2 max ) intensity exercise, and on SGO alone with a change from moderate- to higher-intensity exercise (65% V O2 max ) [12]. However, the contribution of ASGs and SGO in elevating the SR with rising exercise intensity during sustained static exercise (a change in the magnitude of nonthermal factors only) remains unclear. This study investigated the dependence of ASGs and SGO on changes in the SR from nonglabrous skin with rising exercise intensity during sustained static exercise in mildly heated humans. The subjects were 14 healthy males aged Received on February 5, 2002; accepted on March 19, 2002 Correspondence should be addressed to: Narihiko Kondo, Laboratory for Applied Human Physiology, Faculty of Human Development, Kobe University, 3 11 Tsurukabuto, Nada-ku, Kobe, Japan. Tel: ; Fax: , kondo@kobe-u.ac.jp Japanese Journal of Physiology Vol. 52, No. 2,

2 N. KONDO et al. ( SD) years (height, cm; weight, kg). All subjects were nonsmokers and medication-free. Each subject was informed in advance about the procedures and purpose of the study and provided written consent. Experimental protocols were approved by the institutional committee on human investigation. The experiments were conducted in an environmental chamber (SR-3000, Nagano Science Co. Ltd., Osaka, Japan) that was maintained at an ambient temperature of 35 C and 50% humidity with minimal air movement. We selected these environmental conditions to cause sudomotor activation by increasing skin temperature without a marked change in internal temperature. Following a 30-min rest period, each subject performed two maximal voluntary contractions (MVC) of the right arm (exercised arm) by using a handgrip dynamometer the higher value of the two was used to determine the relative workload (% MVC). Subsequently, subjects were rested again for about 30 min, after which baseline data were recorded for 5 min (at rest) before performing the isometric handgrip exercise with their right arms. Each subject performed a 60-s handgrip exercise at 20, 35, and 50% MVC in random order. All subjects used a visual feedback system to maintain handgrip force. Respiratory frequency was controlled at 12 cycles/min, and a rest of at least 10 min was allowed between performance. During this rest, the thermoregulatory variables (SR, sublingual temperature [T or ] and skin temperatures) returned to preexercise levels. In all experiments, the T or, local skin temperature (T sl ) at eight body sites (chest, forearm, palm, forehead, abdomen, thigh, lower leg, and foot), SR on the forearm (nonglabrous skin), heart rate (HR), arterial blood pressure (systolic and diastolic), and rating of perceived effort (RPE) were measured. T or and T sl were measured with a copper constantan thermocouple. The mean skin temperature (T sk ) was calculated by the method reported by Hardy and DuBois [13]. The SR on the nonexercised left forearm was measured continuously by the ventilated capsule (0.95 cm 2 ) method with a capacitance hygrometer (HMP 133Y, Vaisala, Helsinki, Finland). The temperatures and SR were recorded every second, and the data were stored in a personal computer (PC9801RA, NEC Co. Ltd., Tokyo, Japan) with a data logger (HR2300, Yokogawa Co. Ltd., Tokyo, Japan). ASGs and SGO were identified during a 10-s window, and the number of ASGs was measured at a site adjacent to the sweat capsule by the starch-iodide technique [12, 14]. SGO was calculated by dividing the SR over the same period by the number of ASGs recorded. HR was measured continuously with an electrocardiogram. Arterial blood pressure was measured from the left finger with the Penaz method (Finapres, Ohmeda Co. Ltd., Madison, USA). Mean arterial pressure (MAP) was calculated as the diastolic pressure plus one third of the pulse pressure. At the end of each trial, each subject was asked to rate his RPE on a scale from 6 to 20 [15] as an index of central command [11]. Data were analyzed for a 60 s preexercise period and the final 30 s of each handgrip exercise. For a comparison of data across rest and exercise intensities, a one-way analysis of variance (ANOVA) was performed with Scheffe s test when the F-values were significant. The p-value for significance was set at All data are expressed as the mean SEM. Figure 1 shows changes in HR, RPE, MAP, T or, and T sl on the forearm, and in T sk during isometric handgrip exercises at 20, 35, and 50% MVC. The intensity at 20% MVC induced no marked changes in HR and MAP from baseline values. Changes in RPE and MAP with a rise in exercise intensity differed significantly between exercise intensities, and HR at 50% MVC increased significantly compared with 20% MVC. For each exercise intensity, changes in T or, T sl on the forearm, and T sk remained constant (Fig. 1). Figure 2 shows changes in the SR on the forearm, the number of ASGs, and SGO during isometric handgrip exercise at 20, 35, and 50% MVC. The SR at 35 and 50% MVC increased significantly from baseline. The SR increased with rising exercise intensity, and the SR at 50% MVC was significantly greater than the SR at 20 or 35% MVC. The change in the number of ASGs with increased exercise intensity paralleled changes in the SR, but SGO did not change markedly with increased exercise intensity. This study investigated how the number of ASGs and the SGO affect the SR from the nonexercised arm during increased handgrip exercise intensity. During the exercises, the SR increased with a rise in exercise intensity this increase in intensity caused a similar change in the number of ASGs, but not in the SGO. Body temperature variables did not differ between exercise intensities (Fig. 1). These results indicate that in hot climates, the increase in the SR from nonglabrous skin with increased exercise intensity during sustained static exercise is dependent on the number of ASGs and not on the SGO. It has been suggested that sweating from nonglabrous skin during isometric handgrip exercise in a hot climate is controlled by nonthermal factors [7, 8, 10]. The results of the present study have supported this postulate. Nonthermal inputs are perhaps a combination of central command [4, 10, 11], and 230 Japanese Journal of Physiology Vol. 52, No. 2, 2002

3 Activated Sweat Glands during Static Exercise Fig. 1. Changes in heart rate (HR), rating of perceived effort (RPE), mean arterial pressure (MAP), sublingual temperature (T or ), local skin temperature on the forearm (T sl ), and mean skin temperature (T sk ) relative to 20, 35, and 50% maximal voluntary contraction (MVC) during isometric handgrip exercise. Values are expressed as the mean SEM. #: significantly different from the rest (p 0.05); *: significantly different from exercise intensity (p 0.05). mechano- [4, 7, 8, 10, 16] and metabosensitive [7, 9] receptors in the exercising muscle. These nonthermal factors affect the increase in the SR following a rise in exercise intensity. But although baroreflexes are thought to influence the sweating response from nonglabrous skin during dynamic exercise [17] and MAP increases with exercise intensity (Fig. 1), we recently reported that blood pressure elevation during postisometric exercise ischemia does not modify sweating responses [9]. This suggests that MAP is not very likely to affect the exercise-intensity dependent sweating response from nonglabrous skin during isometric handgrip exercises. During graded dynamic exercise (i.e., 35 to 50% V O2 max ), the increase in the SR from nonglabrous skin is initially due to a combination of an increased number of ASGs and increased SGO [12]. Further increases in the SR when exercise intensity is elevated from 50 to 65% V O2 max, are solely due to increases in SGO, and the SR increases almost steadily with exercise intensity. In contrast, as shown in this study the increased SR from nonglabrous skin with a rise in exercise intensity during isometric exercise is due to changes in the number of ASGs rather than to changes in the SGO. During this type of isometric exercise, the internal temperature does not change markedly from rest values, whereas during dynamic exercise the internal temperature increases significantly from rest values. This indicates that the activation of the sudomotor center is greater during dynamic exercise than during isometric exercise because the effect of internal temperature on the sudomotor center is predomi- Japanese Journal of Physiology Vol. 52, No. 2,

4 N. KONDO et al. glands. In summary, although body temperature (sublingual, local skin, and mean skin temperatures) remained constant throughout isometric handgrip exercises of varying intensity, the SR of nonglabrous skin on the nonexercised forearm significantly increased with a rise in exercise intensity. The changes in the number of ASGs with rising exercise intensity paralleled changes in the SR, but the SGO did not change markedly with exercise intensity. These results suggest that in mildly heated humans, at less than 50% MVC, increases in the SR with exercise intensity during sustained static exercise are dependent on the number of ASGs and not on the SGO. We sincerely thank our volunteer subjects. REFERENCES Fig. 2. Changes in sweating rate (SR) on the forearm, density of activated sweat glands (ASGs), and sweat output per gland (SGO) relative to 20, 35, and 50% maximal voluntary contraction (MVC) during isometric handgrip exercise. Values are expressed as the mean SEM. #: significantly different from the rest (p 0.05); *: significantly different from exercise intensity (p 0.05). nant compared with skin temperature [2]. In this study, the increase in the number of ASGs paralleled the increase in the SR with a rise in exercise intensity, but the SGO did not change (Fig. 2). These results suggest that the set-point excitability of eccrine sweat glands contributed to the intensity-dependent sweating responses following increased exercise intensity during isometric exercise, and that the effect of nonthermal factors on changes in the SR from nonglabrous skin might affect the recruitment of activated sweat 1. Johnson JM and Park MK: Effect of upright exercise on threshold for cutaneous vasodilation and sweating. J Appl Physiol 50: , Nadel ER, Mitchell JM, Saltin B, and Stolwijk JAJ: Peripheral modifications to the central drive for sweating. J Appl Physiol 31: , Nielsen B: Thermoregulation in rest and exercise. Acta Physiol Scand 323 (Suppl): Van Beaumont W and Bullard RW: Sweating: its rapid response to muscular work. Science 141: , Yamazaki F, Sone R, and Ikagami H: Responses of sweating and body temperature to sinusoidal exercise. J Appl Physiol 76: , Crandall CG, Musick J, Hatch JP, Kellogg DR Jr, and Johnson JM: Cutaneous vascular and sudomotor responses to isometric exercise in humans. J Appl Physiol 79: , Kondo N, Tominaga, H, Shibasaki M, Aoki K, Koga S, and Nishiyasu T: Modulation of the thermoregulatory sweating response to mild hyperthermia during activation of the muscle metaboreflex in humans. J Physiol (Lond) 515: , Kondo N, Tominaga, H, Shibasaki M, Aoki K, Okada S, and Nishiyasu T: Effects of exercise intensity on the sweating response to a sustained static exercise. J Appl Physiol 88: , Shibasaki M, Kondo N, and Crandall CG: Evidence for metaboreceptor stimulation of sweating in normothermia and heat-stressed humans. J Physiol (Lond) 534: , Van Beaumont W and Bullard RW: Sweating: exercise stimulation during circulatory arrest. Science 152: , Vissing SF: Differential activation of sympathetic discharge to skin and skeletal muscle in humans. Acta Physiol Scand 161(Suppl): 639, Kondo N, Takano S, Aoki K, Shibasaki M, Tominaga, H, and Inoue Y: Regional differences in the effect of exercise intensity on thermoregulatory sweating and cutaneous vasodilation. Acta Physiol Scand 164: 71 78, 232 Japanese Journal of Physiology Vol. 52, No. 2, 2002

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