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...

We measured intra-and extravascular body-fluid compartments in 12 resting males before (day 1; control), during (day 8) and after (day 22) a 3-week, exercise-heat acclimation protocol to investigate plasma volume (PV) changes. Our specific focus was upon the selective nature of the acclimation-induced PV expansion, and the possibility that this expansion could be sustained during prolonged acclimation. Acclimation was induced by cycling in the heat, and involved 16 treatment days (controlled hyperthermia (90 min); core temperature = 38.5• C) and three experimental exposures (40 min rest, 96.9 min (S.D. 9.5 min) cycling), each preceded by a rest day. The environmental conditions were a temperature of 39.8• C (S.D. 0.5 • C) and relative humidity of 59.2% (S.D. 0.8%). On days 8 and 22, PV was expanded and maintained relative to control values (day 1: 44.0 ± 1.8; day 8: 48.8 ± 1.7; day 22: 48.8 ± 2.0 ml kg −1 ; P < 0.05). The extracellular fluid compartment (ECF) was equivalently expanded from control values on days 8 (279.6 ± 14.2 versus 318.6 ± 14.3 ml kg −1 ; n = 8; P < 0.05) and 22 (287.5 ± 10.6 versus 308.4 ± 14.8 ml kg −1 ; n = 12; P < 0.05). Plasma electrolyte, total protein and albumin concentrations were unaltered following heat acclimation (P > 0.05), although the total plasma content of these constituents was elevated (P < 0.05). The PV and interstitial fluid (ISF) compartments exhibited similar relative expansions on days 8 (15.0 ± 2.2% versus 14.7 ± 4.1%; P > 0.05) and 22 (14.4 ± 3.6% versus 6.4 ± 2.2%; P = 0.10). It is concluded that the acclimation-induced PV expansion can be maintained following prolonged heat acclimation. In addition, this PV expansion was not selective, but represented a ubiquitous expansion of the extracellular compartment.

It is concluded that the plasma volume was not defended more vigorously following humid-heat acclimation. Indeed, a greater fluid loss may well underlie the mechanisms for enhancing plasma volume recovery when heat acclimation is induced using the controlled-hyperthermia technique.

These observations have two implications. First, one cannot assume that PV changes reflect those of the entire extracellular compartment. Second, since immersion also increases interstitial fluid pressure, fluid leaving the interstitium must have been rapidly replaced by intracellular water.

Gradual conversion to raloxifene from low-dose estrogen, with a progression from 60 mg every alternate day to 60 mg/day, is a viable option in potentially symptomatic, postmenopausal women.