Mark J. Patterson

Induction and Decay of Short-Term Heat Acclimation in Moderately and Highly Trained Athletes

A rethinking of current heat-acclimation strategies is required as most research and advice for improving physiological strain in the heat includes maintaining hydration using long-term acclimation protocols (>10 days). Furthermore, these strategies have tended to use untrained and moderately trained participants. Therefore, the aims of this review were to (i) investigate the effectiveness of short-term heat acclimation (STHA) with moderately and highly trained athletes; (ii) determine the importance of fluid regulatory strain, which has a thermally independent role in heat adaptation; (iii) assess the impact of STHA on a marker of thermotolerance (inducible heat-shock protein 70 [HSP70]); and (iv) provide further information on the decay of acclimation to heat. The review suggests that 5-day STHA is effective, and adaptations may be more pronounced after fluid regulatory strain from a dehydration-acclimation regimen. Furthermore, highly trained athletes may have similar physiological gains to those who are less trained using STHA. However, research has tended to focus on untrained or moderately trained participants and more information is required for highly trained populations. HSP70 response is upregulated across STHA. This indicates increased thermotolerance and protective adaptive change that may indicate HSP70 response as a useful marker of heat acclimation. Physiological adaptations after heat acclimation are relatively short term and may vanish only a few days or weeks after removal from heat exposure. From a practical perspective 5-day STHA may be the preferred acclimation regimen for moderately and highly trained athletes as it has been shown to be effective, less expensive and less likely to disrupt the tapering for competition in elite performers. Furthermore, updated information on the time course of acclimation decay may allow a reliable estimate of how long individuals can be free from heat exposure before reacclimation is required. This is particularly pertinent in present times as many athletes, civilians andmilitary personnel increasingly have to relocate to different climates of the world, often within a short period of time.

The topography of eccrine sweating in humans during exercise

The purpose of this study was to investigate the distribution of steady-state sweating rates (msw), during stressful exercise and heat exposures. Six men completed 42-min trials: 2-min rest and 40-min cycling at 40% peak power in 36.6° C (relative humidity 46.0%). The msw, was monitored using ventilated capsules at the forehead, and at three additional sites. Repeat trials allowed monitoring from eleven skin surfaces. Auditory canal temperature (Tac) and 11 skin temperatures were measured. After normalising msw to the forehead response within subjects, differences in Tac and onset time thresholds, and transient and steady-state msw were examined. The pooled, lower torso msw onset [mean 45.5 (SEM 42.0) s] preceded that of the head [mean 126.5 (SEM 34.8) s, P<0.05], but was not significantly different from the legs [mean 66.6 (SEM 25.7) s], upper torso [mean 80.2 (SEM 36.8) s] or arms [mean 108.6 (SEM 31.2) s]. Transient msw did not differ among regions (P=0.16). Mean, steady-state forehead msw [3.20 (SEM 0.51) mg · cm−2 · min−1]was not significantly greater than the scapula, forearm, hand, stomach and lower back msw (in descending order), but was greater than the chest [1.6 (SEM 0.2)], upperarm [1.6 (SEM 0.2)], calf [1.5 (SEM 0.3)] and thigh msw [1.0 (SEM 0.2), P<0.05 for all comparisons]. The results did not support the caudal-to-rostral sweat onset evident during supine, resting heat stress. Equivalent Tac sweat thresholds existed between sites, while steady-state msw topography varied among subjects and was not dominated by central regions.

Sustained and generalized extracellular fluid expansion following heat acclimation

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 ± 14.2versus 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.

To Cool, But Not Too Cool : That Is the Question-Immersion Cooling for Hyperthermia

INTRODUCTION Patient cooling time can impact upon the prognosis of heat illness. Although ice-cold-water immersion will rapidly extract heat, access to ice or cold water may be limited in hot climates. Indeed, some have concerns regarding the sudden cold-water immersion of hyperthermic individuals, whereas others believe that cutaneous vasoconstriction may reduce convective heat transfer from the core. It was hypothesized that warmer immersion temperatures, which induce less powerful vasoconstriction, may still facilitate rapid cooling in hyperthermic individuals. METHODS Eight males participated in three trials and were heated to an esophageal temperature of 39.5 degrees C by exercising in the heat (36 degrees C, 50% relative humidity) while wearing a water-perfusion garment (40 degrees C). Subjects were cooled using each of the following methods: air (20-22 degrees C), cold-water immersion (14 degrees C), and temperate-water immersion (26 degrees C). RESULTS The time to reach an esophageal temperature of 37.5 degrees C averaged 22.81 min (air), 2.16 min (cold), and 2.91 min (temperate). Whereas each of the between-trial comparisons was statistically significant (P < 0.05), cooling in temperate water took only marginally longer than that in cold water, and one cannot imagine that the 45-s cooling time difference would have any meaningful physiological or clinical implications. CONCLUSION It is assumed that this rapid heat loss was due to a less powerful peripheral vasoconstrictor response, with central heat being more rapidly transported to the skin surface for dissipation. Although the core-to-water thermal gradient was much smaller with temperate-water cooling, greater skin and deeper tissue blood flows would support a superior convective heat delivery. Thus, a sustained physiological mechanism (blood flow) appears to have countered a less powerful thermal gradient, resulting in clinically insignificant differences in heat extraction between the cold and temperate cooling trials.

Sweat distribution before and after repeated heat exposure

Abstract We investigated the impact of short-term, moderate humidity heat acclimation upon sweat distribution. Eight males completed six daily heat exposures [cycling: ambient temperature 39.5 (0.2)°C, relative humidity 59.2 (0.8)%], during which auditory canal temperature (Tac) was maintained 1.4°C above pre-exposure levels for 70 min by manipulating the work rate. On days 1 and 6, Tac and local sweat rates (m˙sw: eight sites) were monitored. The pre-exposure, resting Tac and the Tac sweat threshold decreased from day 1 to day 6 [36.83 (0.05)°C vs 36.62 (0.05)°C, and 36.90 (0.05)°C vs 36.75 (0.05)°C, respectively; both P<0.05]. However, the sweat-onset time, sweat sensitivity (Δm˙sw/ΔTac) and established m˙sw were unaltered (P > 0.05). There was also no evidence of a post-acclimation redistribution in established m˙sw between the eight skin regions, though both the sweat sensitivity and established m˙sw for the forehead and hand were significantly greater than at the remaining sites (P<0.05). It is concluded that the 5-day heat acclimation regimen provided only a minimal stimulus for sudomotor adaptation.

The Interaction of Body Armor, Low-Intensity Exercise, and Hot-Humid Conditions on Physiological Strain and Cognitive Function

OBJECTIVE This project was aimed at evaluating the impact of combat armor on physiological and cognitive functions during low-intensity exercise in hot-humid conditions (36 degrees C and 60% relative humidity). METHODS Nine males participated in three trials (2.5 hours), walking at two speeds and wearing different protective equipment: control (combat uniform and cloth hat); torso armor with uniform and cloth hat; and full armor (uniform, torso armor, and helmet). RESULTS As time progressed, core temperatures increased and deviated significantly among trials, rising at 0.37 degrees C h(-1) (control), 0.41 degrees C h(-1) (torso armor), and 0.51 degrees C h(-1) (full armor). Heart rates also progressively diverged, and subjects lost significantly more sweat during the two armored trials. However, cognitive-function tests revealed neither significant main effects nor time by treatment interactions. CONCLUSION The combat armor and helmet significantly increased thermal and cardiovascular strain, but these were unlikely to lead to either exertional heat illness or impaired cognitive function during uneventful urban, military patrols in hot-humid conditions.

Short-term heat acclimation is effective and may be enhanced rather than impaired by dehydration

Most heat acclimation data are from regimes longer than 1 week, and acclimation advice is to prevent dehydration. Objectives: We hypothesized that (i) short‐term (5‐day) heat acclimation would substantially improve physiological strain and exercise tolerance under heat stress, and (ii) dehydration would provide a thermally independent stimulus for adaptation. Methods: Nine aerobically fit males heat acclimated using controlled‐hyperthermia (rectal temperature 38.5°C) for 90 min on 5 days; once euhydrated (EUH) and once dehydrated (DEH) during acclimation bouts. Exercising heat stress tests (HSTs) were completed before and after acclimations (90‐min cycling in Ta 35°C, 60% RH). Results: During acclimation bouts, [aldosterone]plasma rose more across DEH than EUH (95%CI for difference between regimes: 40–411 pg ml−1; P = 0.03; n = 5) and was positively related to plasma volume expansion (r = 0.65; P = 0.05), which tended to be larger in DEH (CI: −1 to 10%; P = 0.06; n = 9). In HSTs, resting forearm perfusion increased more in DEH (by 5.9 ml 100 tissue ml−1 min−1: −11.5 to −1.0; P = 0.04) and end‐exercise cardiac frequency fell to a greater extent (by 11 b min−1: −1 to 22; P = 0.05). Hydration‐related effects on other endocrine, cardiovascular, and psychophysical responses to HSTs were unclear. Rectal temperature was unchanged at rest but was 0.3°C lower at end exercise (P < 0.01; interaction: P = 0.52). Conclusions: Short‐term (5‐day) heat acclimation induced effective adaptations, some of which were more pronounced after fluid‐regulatory strain from permissive dehydration, and not attributable to dehydration effects on body temperature. Am. J. Hum. Biol. 26:311–320, 2014.

Effects of reduced ambient temperature on fat utilization during submaximal exercise.

PURPOSE The influence of cold air exposure on fuel utilization during prolonged cycle exercise was investigated. METHODS Nine male subjects cycled for 90 min in ambient temperatures of -10 degrees C, 0 degrees C, 10 degrees C, and 20 degrees C. External work performed between conditions was constant. Mean oxygen consumption (VO2) over the 90 min in the 20 degrees C trial corresponded to 64 +/- 5.8% VO2peak. RESULTS Although mean skin temperature was different between trials (P < 0.05), rectal temperatures were not different. At -10 degrees C and 0 degrees C, the respiratory exchange ratio was higher compared with 10 degrees C and 20 degrees C (0.98 +/- 0.01 and 0.97 +/- 0.01 vs 0.92 +/- 0.01 and 0.91 +/- 0.01; P < 0.05). The associated rates of fat oxidation were lower at -10 degrees C and 0 degrees C compared with 10 degrees C and 20 degrees C (0.15 +/- 0.06 and 0.17 +/- 0.06 vs 0.35 +/- 0.06 and 0.40 +/- 0.04 g.min-1; P < 0.05). Blood glycerol was lower at -10 degrees C and 0 degrees C compared with 20 degrees C (P < 0.05); mean values were 0.13 +/- 0.0, 0.13 +/- 0.0, and 0.18 +/- 0.0 mmol.L-1 for the -10 degrees C, 0 degrees C, and 20 degrees C trials, respectively. Mean VO2 was lower in the -10 degrees C trial than the 20 degrees C trial (2.53 +/- 0.06 vs 2.77 +/- 0.09. L.min-1; P < 0.05). Mean blood glucose concentrations were lower at -10 degrees C than 20 degrees C (4.9 +/- 0.2 vs 5.3 +/- 0.1 mmol.L-1; P < 0.05). Although plasma epinephrine concentrations were greater during the 20 degrees C trial compared with all other trials (P < 0.05), plasma norepinephrine did not differ between trials. CONCLUSION The diminished fat oxidation at colder temperatures potentially reflects a reduction in lipolysis and/or mobilization of FFA or impairment in the oxidative capacity of the muscle.

Effects of artificially-induced anaemia on sudomotor and cutaneous blood flow responses to heat stress

Abstract The influence of artificially induced anaemia on thermal strain was evaluated in trained males. Heat stress trials (38.6°C, water vapour pressure 2.74 kPa) performed at the same absolute work rates [20 min of seated rest, 20 min of cycling at 30% peak aerobic power (V˙O2peak), and 20 min cycling at 45% V˙O2peak] were completed before (HST1) and 3–5 days after 3 units of whole blood were withdrawn (HST2). Mild anaemia did not elevate thermal strain between trials, with auditory canal temperatures terminating at 38.5°C [(0.16), HST1] and 38.6°C [(0.13), HST2; P > 0.05]. Given that blood withdrawal reduced aerobic power by 16%, this observation deviates from the close association often observed between core temperature and relative exercise intensity. During HST2, the absolute and integrated forearm sweat rate (m˙sw) exceeded control levels during exercise (P < 0.05), while a suppression of forehead m˙sw occurred (P < 0.05). These observations are consistent with a possible peripheral redistribution of sweat secretion. It was concluded that this level of artificially induced anaemia did not impact upon heat strain during a 60-min heat stress test.

Whole-body fluid distribution in humans during dehydration and recovery, before and after humid-heat acclimation induced using controlled hyperthermia

This experiment was designed to test the hypothesis that the plasma volume is not selectively defended during exercise‐ and heat‐induced dehydration following humid‐heat acclimation.