**3. Effects of exercise training on thermoregulation in warm and hot conditions**

Thermoregulatory responses are improved by aerobic and endurance exercise training, resulting in reduced physiological strain and therefore enhanced cardiovascular and exercise capacities during exercise in warm and hot conditions. These adaptations are remarkable when exercise training is performed in the heat [1]. After a 10-day training period in a cool condition (Ta , 20°C), SkBF and sweat rate responses to increased Tes during exercise (Ta , 25°C) are enhanced. After a subsequent 10-day training period in a hot condition (T<sup>a</sup> , 35°C), these responses improved further [27]. The increased SkBF and sweating responses are characterized by the early start of cutaneous vasodilation and sweating responses to increased Tes [28, 29] and the increased sensitivity to increase SkBF and sweat rate in response to an increased Tes compared with before exercise training [28, 29]. It is suggested that the mechanisms of the increase in thermoregulatory responses with exercise training are similar to those following acclimations to repeated heat exposures, including adaptations of the thermoregulatory center and thermoregulatory effectors [1, 12] as well as an increase in VO2max [30] and PV [28, 31, 32].

It is suggested that the exercise-induced PV expansion is primarily associated with an increase in total volume of extracellular fluid [33]. An increase in plasma protein (mainly albumin content) also contributes by drawing fluids into the intravascular space from the interstitium [33–35]. Facilitated Na<sup>+</sup> and water reabsorption [33, 36] and an enhancement of voluntary fluid intake with increased thirst sensation [37] (associated with an activated renin-angiotensin-aldosterone system and vasopressin release) during and after exercise or dehydration are suggested as mechanisms of training-induced increases in extracellular fluid volume [38]. Increases in plasma protein may be due to activated hepatic plasma protein synthesis [39, 40] and enhanced translocation of protein to the intravascular space from the interstitium [41] coincide with a restricted transcapillary escape ratio of protein [42].

duct induced by an enhanced sensitivity to aldosterone [45]. To maintain PV during exercise, hypotonic sweat is advantageous because hypotonic sweat loss causes a greater increase in osmolality of extracellular fluid. It promotes the shift of water from intracellular to extracellular fluid space according to the osmotic gradient between the spaces [45]. This therefore attenuates the decreased PV and venous return to the heart. As a result, the decreased thermoregulatory responses with a sweating loss at a given volume are attenuated with low Na<sup>+</sup>

Body Temperature Regulation During Exercise and Hyperthermia in Diabetics

http://dx.doi.org/10.5772/intechopen.74063

centration in sweat [46]. Moreover, the delayed onset of cutaneous vasodilation and sweating responses to increased Tes at a given increase in Posm was attenuated in heat-acclimated individuals in whom an increased Posm by sweating loss at a given volume was enhanced due to

The susceptibility to heat related-illnesses in the elderly [6] is caused by a deterioration in thermoregulatory responses with aging [47, 48]. Previous studies have indicated that even healthy elderly individuals have an impaired thermal perception [49] and impaired autonomic [50, 51] and behavioral [52, 53] thermoregulatory responses. A recent study indicated that skin warmth detection thresholds in the extremities and the whole-body thermal sensation deteriorated with normal aging under both normothermic conditions and under passive heat-induced mild hyperthermic conditions [54]. Decreased VO2max and cardiovascular capacity associate with the deteriorated thermoregulation with aging [51]. Nevertheless, elderly individuals with a similar level of VO2max to young individuals are known to show an attenuated response of SkBF both during passive heat stress in whole-body or local-body parts and during exercise under a hot environment compared to young individuals [55, 56]. Specifically, Kenney et al. [56] used bretylium tosylate to block the local release of norepinephrine on the forearm skin. They suggested that the attenuated SkBF response to hyperthermia during exercise in a hot condition was caused not by an enhanced vasoconstrictor system but mainly by a decreased sensitivity of the active vasodilator system to increased Tes. In addition, the whole-body and local sweat rate in response to passive heat stress or exercise are attenuated in the elderly compared to young adults [57]. Several physiological changes with advancing age, for example, such as decreased PV and increased Posm at baseline [58], diminished thirst sensation [58], and responses in antidiuretic hormone and aldosterone after thermal dehydration [38], are suggested to be associated with the decreased thermoregulatory responses in the elderly. Decreased renal concentrating ability [59] and lower reabsorptive ability of sweat gland ducts [59] with advancing age are also suggested to be associated with the deteriorated thermoregulatory responses with aging. Vasoconstriction of splanchnic organs during exercise, which enhances the redistribution of cardiac output to the skin vasculature, is associated with increased cutaneous vasodilation in youth, which is also attenuated with aging [60]. Furthermore, elderly individuals commonly take a variety of prescription drugs that may affect thermoregulatory responses and body fluid regulation [1]. Exercise training and heat acclimation can improve the blunted body fluid regulation and thermoregulation with aging, although generally the improvement of

**4. Effects of biological aging on thermoregulation in warm and hot** 

these is lower or limited relative to their younger counterparts.

low Na<sup>+</sup>

**conditions**

concentration in sweat [46].

con-

95

PV expansion by exercise training results in a reduction in lactic acid concentration in the blood at the same absolute intensity of exercise (an enhanced lactate threshold), which contributes to a suppression of increase in Posm during exercise. This mechanism contributes to the downward shift of the body core temperature threshold for cutaneous vasodilation and sweating after training. Moreover, expanded PV increases venous return to the heart and cardiac filling pressure and therefore enhances cardiac stroke volume. It also improves the responses of SkBF and sweat rate to increased core body temperature during exercise [11, 16, 17]. Indeed, an increase in cardiac stroke volume and also the sensitivity of increase in SkBF to increased Tes during exercise in a warm condition (T<sup>a</sup> , 30°C) was closely correlated to a PV expansion by a 10-day endurance training (60% VO2max for 1 h/day at 30°C) [28]. Additionally, Goto et al. [43] reported the influences of protein and carbohydrate (CHO) supplementation just after exercise (Pro-CHO; 0.36 g protein/kg and 3.6 kcal) during the 5-day training period (70% VO2max for 30 min/day) in a warm environment (T<sup>a</sup> , 30°C) on PV and thermoregulatory responses. They suggested that, in the Pro-CHO group, plasma albumin content (Albcont) and therefore PV increased by ~10% and ~8%, respectively. These were significantly higher than the increase of ~4% in the placebo intake control group (CNT; 0.9 kcal and 0 g protein/kg body weight). They attributed the increase in Albcont to activated hepatic albumin synthesis following exercise due to the increased substance bioavailability [39, 40] and also the effects of insulin on protein synthesis in hepatocytes [44]. Most notably, the sensitivity of an increase in SkBF and sweat rate to increased Tes enhanced after training more in the Pro-CHO group compared with the CNT group. Additionally, both groups showed a significant decrease in heart rate and Tes during exercise after training period. However, these adaptations were more prominent in the Pro-CHO group than in the CNT group, indicating decreased cardiovascular and thermal strains after the training period with PV expansion.

In addition, Ikegawa et al. [31] supported the observations by Goto et al. [43] by presenting an increased PV with an early shift of the onset of the cutaneous vasodilation and sweating responses to an increased Tes after the same training protocol. Further, the early shift of the onset of the cutaneous vasodilation and sweating responses was wholly or partly diminished after the expanded PV by training was reduced to the pre-training level by using the diuretics. Furthermore, Ichinose et al. [28] showed that 10 days of exercise training (60% VO2max for 60 min/day at 30°C) attenuated the sensitivity of the upward shift of Tes threshold for cutaneous vasodilation with the increased Posm by hypertonic saline infusion, though the threshold for sweating was not changed. Furthermore, they suggested that increased PV after training correlated with the attenuated sensitivity to hyperosmolality in each individual, suggesting that the attenuation is associated with the stretch of cardiopulmonary baroreceptors induced by PV expansion. Thus, the enhanced thermoregulation and cardiovascular capacities after exercise training are closely associated with PV expansion in addition to the neural adaptation of the thermoregulatory center and thermoregulatory effectors [1, 12].

The Na+ concentration of sweat is important to maintain PV during exercise. It decreases after exercise training or heat acclimation due to an enhanced Na+ reabsorption at the sweat gland duct induced by an enhanced sensitivity to aldosterone [45]. To maintain PV during exercise, hypotonic sweat is advantageous because hypotonic sweat loss causes a greater increase in osmolality of extracellular fluid. It promotes the shift of water from intracellular to extracellular fluid space according to the osmotic gradient between the spaces [45]. This therefore attenuates the decreased PV and venous return to the heart. As a result, the decreased thermoregulatory responses with a sweating loss at a given volume are attenuated with low Na<sup>+</sup> concentration in sweat [46]. Moreover, the delayed onset of cutaneous vasodilation and sweating responses to increased Tes at a given increase in Posm was attenuated in heat-acclimated individuals in whom an increased Posm by sweating loss at a given volume was enhanced due to low Na<sup>+</sup> concentration in sweat [46].

Increases in plasma protein may be due to activated hepatic plasma protein synthesis [39, 40] and enhanced translocation of protein to the intravascular space from the interstitium [41]

PV expansion by exercise training results in a reduction in lactic acid concentration in the blood at the same absolute intensity of exercise (an enhanced lactate threshold), which contributes to a suppression of increase in Posm during exercise. This mechanism contributes to the downward shift of the body core temperature threshold for cutaneous vasodilation and sweating after training. Moreover, expanded PV increases venous return to the heart and cardiac filling pressure and therefore enhances cardiac stroke volume. It also improves the responses of SkBF and sweat rate to increased core body temperature during exercise [11, 16, 17]. Indeed, an increase in cardiac stroke volume and also the sensitivity of increase in SkBF to

expansion by a 10-day endurance training (60% VO2max for 1 h/day at 30°C) [28]. Additionally, Goto et al. [43] reported the influences of protein and carbohydrate (CHO) supplementation just after exercise (Pro-CHO; 0.36 g protein/kg and 3.6 kcal) during the 5-day training period

responses. They suggested that, in the Pro-CHO group, plasma albumin content (Albcont) and therefore PV increased by ~10% and ~8%, respectively. These were significantly higher than the increase of ~4% in the placebo intake control group (CNT; 0.9 kcal and 0 g protein/kg body weight). They attributed the increase in Albcont to activated hepatic albumin synthesis following exercise due to the increased substance bioavailability [39, 40] and also the effects of insulin on protein synthesis in hepatocytes [44]. Most notably, the sensitivity of an increase in SkBF and sweat rate to increased Tes enhanced after training more in the Pro-CHO group compared with the CNT group. Additionally, both groups showed a significant decrease in heart rate and Tes during exercise after training period. However, these adaptations were more prominent in the Pro-CHO group than in the CNT group, indicating decreased cardiovascu-

In addition, Ikegawa et al. [31] supported the observations by Goto et al. [43] by presenting an increased PV with an early shift of the onset of the cutaneous vasodilation and sweating responses to an increased Tes after the same training protocol. Further, the early shift of the onset of the cutaneous vasodilation and sweating responses was wholly or partly diminished after the expanded PV by training was reduced to the pre-training level by using the diuretics. Furthermore, Ichinose et al. [28] showed that 10 days of exercise training (60% VO2max for 60 min/day at 30°C) attenuated the sensitivity of the upward shift of Tes threshold for cutaneous vasodilation with the increased Posm by hypertonic saline infusion, though the threshold for sweating was not changed. Furthermore, they suggested that increased PV after training correlated with the attenuated sensitivity to hyperosmolality in each individual, suggesting that the attenuation is associated with the stretch of cardiopulmonary baroreceptors induced by PV expansion. Thus, the enhanced thermoregulation and cardiovascular capacities after exercise training are closely associated with PV expansion in addition to the neural adapta-

concentration of sweat is important to maintain PV during exercise. It decreases after

, 30°C) was closely correlated to a PV

, 30°C) on PV and thermoregulatory

reabsorption at the sweat gland

coincide with a restricted transcapillary escape ratio of protein [42].

increased Tes during exercise in a warm condition (T<sup>a</sup>

94 Diabetes and Its Complications

(70% VO2max for 30 min/day) in a warm environment (T<sup>a</sup>

lar and thermal strains after the training period with PV expansion.

tion of the thermoregulatory center and thermoregulatory effectors [1, 12].

exercise training or heat acclimation due to an enhanced Na+

The Na+
