Acute and adaptive responses in humans to exercise in a warm, humid environment

Abstract

Acute and repeated exposure for 8-13 consecutive days to exercise in humid heat was studied. Twelve fit subjects exercised at 150 W [45% of maximum O2 uptake (V.O2,max)] in ambient conditions of 35 degrees C and 87% relative humidity which resulted in exhaustion after 45 min. Average core temperature reached 39.9 +/- 0.1 degrees C, mean skin temperature (T-sk) was 37.9 +/- 0.1 degrees C and heart rate (HR) 152 +/- 6 beats min-1 at this stage. No effect of the increasing core temperature was seen on cardiac output and leg blood flow (LBF) during acute heat stress. LBF was 5.2 +/- 0.3 l min-1 at 10 min and 5.3 +/- 0.4 l min-1 at exhaustion (n = 6). After acclimation the subjects reached exhaustion after 52 min with a core temperature of 39.9 +/- 0.1 degrees C, T-sk 37.7 +/- 0.2 degrees C, HR 146 +/- 4 beats min-1. Acclimation induced physiological adaptations, as shown by an increased resting plasma volume (3918 +/- 168 to 4256 +/- 270 ml), the lower exercise heart rate at exhaustion, a 26% increase in sweating rate, lower sweat sodium concentration and a 6% reduction in exercise V.O2. Neither in acute exposure nor after acclimation did the rise of core temperature to near 40 degrees C affect metabolism and substrate utilization. The physiological adaptations were similar to those induced by dry heat acclimation. However, in humid heat the effect of acclimation on performance was small due to physical limitations for evaporative heat loss.

Impact of mild dehydration on wellness and on exercise performance

“…There appears to be a critical body temperature above which humans and other mammals will not continue to exercise voluntarily. A consistent finding in the published literature is that voluntary fatigue occurs at a core temperature of about 401C (Gisolfi & Copping, 1974;Nielsen et al, 1993Nielsen et al, , 1997). An inability of the central temperature control mechanism, or of the effector mechanisms that respond to input from the hypothalamus, to compensate for orthostatic simultaneously, metabolic and thermoregulatory demands may result in heat syncope, characterised by extreme peripheral vasodilation and a fall in arterial blood pressure (Werner, 1993).…”

“…Important among these is the cessation of physical activity that results in a marked reduction in the rate of metabolic heat production. Nielsen et al (1993Nielsen et al ( , 1997 have speculated that at a critical core temperature (about 401C in humans) there may be a negative effect on the brain's motor control centres. Such effects are consistent with the loss of motor coordination, reduction in motor drive and increased perception of effort that typically occur in the later stages of prolonged exercise in the heat.…”

An evaluation of salt intake and iodine nutrition in a rural and urban area of the Côte d’Ivoire

“…However, because the sodium intake data from the weighed food records was similar to the sodium data from the 24 h collections, it appears that in this study population losses of sodium in sweat were low. Previous studies have shown that one of the physiological adaptations to hot, humid conditions is lowered concentrations of sodium in sweat (Nielson, 1997), and this mechanism may help explain why sweat sodium losses were minimal in this study.…”

Extracellular Hsp72 concentration relates to a minimum endogenous criteria during acute exercise-heat exposure

“…Whitham et al (2006) demonstrated increased eHsp72 was associated with higher plasma levels of catecholamines and heart rate, whilst it has also been observed that following passive heating, neither epinephrine nor norepinephrine was solely responsible for eHsp72 release (Whitham et al 2007). Johnson and Fleshner (2006) identified α-adrenergic stimulation, notably through norepinephrine elevation (Nielsen et al 1997;Ortega et al 2006;Whitham et al 2006;Giraldo et al 2010;Iguchi et al 2012) as responsible for Hsp72 release into the circulation, this alongside the work of Whitham et al (2006Whitham et al ( , 2007 suggest a requirement for individuals to be presented with sustained physiological challenge during exercise-heat stress (Johnson and Fleshner 2006). Exercise intensity, or α-adrenergic stimulation via norepinephrine is likely required to be above an intensity threshold to elicit significant eHsp72 response with the greater exercise intensity data from Périard et al (2012) leading to data contrasting that of Marshall et al (2006).…”