In this overview, human morphological and functional adaptations during naturally and artificially induced heat adaptation are explored. Through discussions of adaptation theory and practice, a theoretical basis is constructed for evaluating heat adaptation. It will be argued that some adaptations are specific to the treatment used, while others are generalized. Regarding ethnic differences in heat tolerance, the case is put that reported differences in heat tolerance are not due to natural selection, but can be explained on the basis of variations in adaptation opportunity. These concepts are expanded to illustrate how traditional heat adaptation and acclimatization represent forms of habituation, and thermal clamping (controlled hyperthermia) is proposed as a superior model for mechanistic research. Indeed, this technique has led to questioning the perceived wisdom of body-fluid changes, such as the expansion and subsequent decay of plasma volume, and sudomotor function, including sweat habituation and redistribution. Throughout, this contribution was aimed at taking another step toward understanding the phenomenon of heat adaptation and stimulating future research. In this regard, research questions are posed concerning the influence that variations in morphological configuration may exert upon adaptation, the determinants of postexercise plasma volume recovery, and the physiological mechanisms that modify the cholinergic sensitivity of sweat glands, and changes in basal metabolic rate and body core temperature following adaptation.
Literature from the past 168 years has been filtered to provide a unified summary of the regional distribution of cutaneous water and electrolyte losses. The former occurs via transepidermal water vapour diffusion and secretion from the eccrine sweat glands. Daily insensible water losses for a standardised individual (surface area 1.8 m2) will be 0.6–2.3 L, with the hands (80–160 g.h−1) and feet (50–150 g.h−1) losing the most, the head and neck losing intermediate amounts (40–75 g.h−1) and all remaining sites losing 15–60 g.h−1. Whilst sweat gland densities vary widely across the skin surface, this same individual would possess some 2.03 million functional glands, with the highest density on the volar surfaces of the fingers (530 glands.cm−2) and the lowest on the upper lip (16 glands.cm−2). During passive heating that results in a resting whole-body sweat rate of approximately 0.4 L.min−1, the forehead (0.99 mg.cm−2.min−1), dorsal fingers (0.62 mg.cm−2.min−1) and upper back (0.59 mg.cm−2.min−1) would display the highest sweat flows, whilst the medial thighs and anterior legs will secrete the least (both 0.12 mg.cm−2.min−1). Since sweat glands selectively reabsorb electrolytes, the sodium and chloride composition of discharged sweat varies with secretion rate. Across whole-body sweat rates from 0.72 to 3.65 mg.cm−2.min−1, sodium losses of 26.5–49.7 mmol.L−1 could be expected, with the corresponding chloride loss being 26.8–36.7 mmol.L−1. Nevertheless, there can be threefold differences in electrolyte losses across skin regions. When exercising in the heat, local sweat rates increase dramatically, with regional glandular flows becoming more homogeneous. However, intra-regional evaporative potential remains proportional to each local surface area. Thus, there is little evidence that regional sudomotor variations reflect an hierarchical distribution of sweating either at rest or during exercise.
The distribution of cutaneous thermosensitivity has not been determined in humans for the control of autonomic or behavioural thermoregulation under open-loop conditions. We therefore examined local cutaneous warm and cool sensitivities for sweating and whole-body thermal discomfort (as a measure of alliesthesia). Thirteen males rested supine during warming (+4• C), and mild (−4 • C) and moderate (−11 • C) cooling of ten skin sites (274 cm 2 ), whilst the core and remaining skin temperatures were clamped above the sweat threshold using a water-perfusion suit and climate chamber. Local thermosensitivities were calculated from changes in sweat rates (pooled from sweat capsules on all limbs) and thermal discomfort, relative to the changes in local skin temperature. Thermosensitivities were examined across local sites and body segments (e.g. torso, limbs). The face displayed stronger cold (−11• C) sensitivity than the forearm, thigh, leg and foot (P = 0.01), and was 2-5 times more thermosensitive than any other segment for both sudomotor and discomfort responses (P = 0.01). The face also showed greater warmth sensitivity than the limbs for sudomotor control and discomfort (P = 0.01). The limb extremities ranked as the least thermosensitive segment for both responses during warming, and for discomfort responses during moderate cooling (−11• C). Approximately 70% of the local variance in sudomotor sensitivity was common to the alliesthesial sensitivity. We believe these open-loop methods have provided the first clear evidence for a greater facial thermosensitivity for sweating and whole-body thermal discomfort.
We tested the hypothesis that local sweat rates would not display a systematic postadaptation redistribution toward the limbs after humid heat acclimation. Eleven nonadapted males were acclimated over 3 wk (16 exposures), cycling 90 min/day, 6 days/wk (40°C, 60% relative humidity), using the controlled-hyperthermia acclimation technique, in which work rate was modified to achieve and maintain a target core temperature (38.5°C). Local sudomotor adaptation (forehead, chest, scapula, forearm, thigh) and onset thresholds were studied during constant work intensity heat stress tests (39.8°C, 59.2% relative humidity) conducted on days 1, 8, and 22 of acclimation. The mean body temperature (T b) at which sweating commenced (threshold) was reduced on days 8 and 22 (P Ͻ 0.05), and these displacements paralleled the resting thermoneutral T b shift, such that the T b change to elicit sweating remained constant from days 1 to 22. Whole body sweat rate increased significantly from 0.87 Ϯ 0.06 l/h on day 1 to 1.09 Ϯ 0.08 and 1.16 Ϯ 0.11 l/h on days 8 and 22, respectively. However, not all skin regions exhibited equivalent relative sweat rate elevations from day 1 to day 22. The relative increase in forearm sweat rate (117 Ϯ 31%) exceeded that at the forehead (47 Ϯ 18%; P Ͻ 0.05) and thigh (42 Ϯ 16%; P Ͻ 0.05), while the chest sweat rate elevation (106 Ϯ 29%) also exceeded the thigh (P Ͻ 0.05). Two unique postacclimation observations arose from this project. First, reduced sweat thresholds appeared to be primarily related to a lower resting T b, and more dependent on T b change. Second, our data did not support the hypothesis of a generalized and preferential trunk-to-limb sweat redistribution after heat acclimation.body core temperature; sweating; sweat threshold THE PRINCIPAL AVENUE for heat dissipation in hot environments is via evaporative cooling, with sudomotor enhancement accompanying endurance training and heat adaptation. The latter can elicit a reduced core temperature (T c ) threshold for sweating onset (6,8,24,37), a greater sensitivity to changes in T c (13,32,40), an elevated steady-state expulsion rate (24-26, 37), eccrine gland hypertrophy (33), and an apparent redistribution of sweating toward the limbs (15, 31, 37), representing our potentially most potent adaptive responses to chronic heat stress. In this paper, we focus on sudomotor threshold and local sweat rate (ṁ sw ) changes accompanying humid heat acclimation.Höfler (15) and Shvartz et al. (37) first reported heat acclimation induced a peripheral redistribution of sweating, such that postacclimation limb ṁ sw appeared to be elevated more than at central body sites. This apparent peripheral shift in secretion could facilitate greater heat dissipation, if lower preacclimation limb ṁ sw (5, 12, 19) was also associated with less than optimal local evaporation rates. Because limbs have a relatively large surface area:mass ratio, an elevation in sweating and evaporation could enhance thermal homeostasis. However, while data from Höfler (15) First, these obs...
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