Jessica Mee

Isothermic and fixed intensity heat acclimation methods induce similar heat adaptation following short and long-term timescales

Heat acclimation requires the interaction between hot environments and exercise to elicit thermoregulatory adaptations. Optimal synergism between these parameters is unknown. Common practise involves utilising a fixed workload model where exercise prescription is controlled and core temperature is uncontrolled, or an isothermic model where core temperature is controlled and work rate is manipulated to control core temperature. Following a baseline heat stress test; 24 males performed a between groups experimental design performing short term heat acclimation (STHA; five 90 min sessions) and long term heat acclimation (LTHA; STHA plus further five 90 min sessions) utilising either fixed intensity (50% VO2peak), continuous isothermic (target rectal temperature 38.5 °C for STHA and LTHA), or progressive isothermic heat acclimation (target rectal temperature 38.5 °C for STHA, and 39.0 °C for LTHA). Identical heat stress tests followed STHA and LTHA to determine the magnitude of adaptation. All methods induced equal adaptation from baseline however isothermic methods induced adaptation and reduced exercise durations (STHA = -66% and LTHA = -72%) and mean session intensity (STHA = -13% VO2peak and LTHA = -9% VO2peak) in comparison to fixed (p < 0.05). STHA decreased exercising heart rate (-10 b min(-1)), core (-0.2 °C) and skin temperature (-0.51 °C), with sweat losses increasing (+0.36 Lh(-1)) (p<0.05). No difference between heat acclimation methods, and no further benefit of LTHA was observed (p > 0.05). Only thermal sensation improved from baseline to STHA (-0.2), and then between STHA and LTHA (-0.5) (p<0.05). Both the continuous and progressive isothermic methods elicited exercise duration, mean session intensity, and mean T(rec) analogous to more efficient administration for maximising adaptation. Short term isothermic methods are therefore optimal for individuals aiming to achieve heat adaptation most economically, i.e. when integrating heat acclimation into a pre-competition taper. Fixed methods may be optimal for military and occupational applications due to lower exercise intensity and simplified administration.

Isothermic and fixed-intensity heat acclimation methods elicit equal increases in Hsp72 mRNA

Thermotolerance, to which heat shock protein‐72 (Hsp72) contributes, is an acquired state achieved following heat acclimation (HA), eliciting cellular adaption and protection against thermal stress. Optimal HA methods achieving the greatest heat shock response (HSR) are equivocal; therefore, investigation of methods provoking the greatest sustained HSR is required to optimize cellular adaptation. Twenty‐four males performed short‐term HA (STHA; five sessions) and long‐term HA (LTHA; STHA plus further five sessions) utilizing fixed‐intensity (FIXED; workload = 50% V ˙ O 2 p e a k ), continuous isothermic HA [ISOCONT; target rectal temperature (Trec) = 38.5 °C], or progressive isothermic HA (ISOPROG; target Trec = 38.5 °C for STHA then target Trec = 39.0 °C for LTHA). Leukocyte Hsp72 mRNA was measured pre‐ and post day 1, day 5, and day 10 of HA via reverse transcription quantitative polymerase chain reaction to determine the HSR. Hsp72 mRNA increased (P < 0.05) pre‐ to post day 1, pre‐ to post day 5, and pre to post day 10 in FIXED, ISOCONT, and ISOPROG, but no differences were observed between methods (P > 0.05). The equal Hsp72 mRNA increases occurring from consistent, reduced, or increased endogenous strain following STHA and LTHA suggest that transcription occurs following attainment of sufficient endogenous criteria. These data give confidence that all reported HA methods increase Hsp72 mRNA and are capable of eliciting adaptations toward thermotolerance.

A comparison of males and females' temporal patterning to short- and long-term heat acclimation

The current study assessed sex differences in thermoregulatory and physiological adaptation to short‐term (STHA) and long‐term heat acclimation (LTHA). Sixteen (eight males; eight females) participants performed three running heat tolerance tests (RHTT), preceding HA (RHTT1), following 5 days HA (RHTT2) and 10 days HA (RHTT3). The RHTT involved 30‐min running (9 km/h, 2% gradient) in 40 °C, 40% relative humidity. Following STHA, resting rectal temperature (Trrest) (males: −0.24 ± 0.16 °C, P ≤ 0.001; females: −0.02 ± 0.08 °C, P = 0.597), peak rectal temperature (Trpeak) (males: −0.39 ± 0.36 °C, P ≤ 0.001; females −0.07 ± 0.18 °C, P = 0.504), and peak heart rate (males: −14 ± 12 beats/min, P ≤ 0.001; females: −5 ± 3 beats/min, P = 0.164) reduced in males, but not females. Following STHA, sweat rate relative to body surface area (SRBSA) increased (428 ± 269 g/h/m2, P = 0.029) in females, but not males (−11 ± 286 g/h/m2, P = 0.029). Following LTHA, Trrest (males: −0.04 ± 0.15 °C, P = 0.459; females: −0.22 ± 0.12 °C, P ≤ 0.01) and Trpeak (males: −0.05 ± 0.26 °C, P = 0.590; females: −0.41 ± 0.24 °C, P ≤ 0.01) reduced in females, but not males. Following LTHA, SRBSA increased in males (308 ± 346 g/h/m2, P = 0.029), but not females (44 ± 373 g/h/m2, P = 0.733). Males and females responded to STHA; however, females required LTHA to establish thermoregulatory and cardiovascular stability. HA protocols should be designed to target sex differences in thermoregulation for optimal adaptation.

Repeatability of a running heat tolerance test

At present there is no standardised heat tolerance test (HTT) procedure adopting a running mode of exercise. Current HTTs may misdiagnose a runners susceptibility to a hyperthermic state due to differences in exercise intensity. The current study aimed to establish the repeatability of a practical running test to evaluate individuals ability to tolerate exercise heat stress. Sixteen (8M, 8F) participants performed the running HTT (RHTT) (30 min, 9 km h(-1), 2% elevation) on two separate occasions in a hot environment (40 °C and 40% relative humidity). There were no differences in peak rectal temperature (RHTT1: 38.82 ± 0.47 °C, RHTT2: 38.86 ± 0.49 °C, Intra-class correlation coefficient (ICC)=0.93, typical error of measure (TEM) = 0.13 °C), peak skin temperature (RHTT1: 38.12 ± 0.45, RHTT2: 38.11 ± 0.45 °C, ICC = 0.79, TEM = 0.30 °C), peak heart rate (RHTT1: 182 ± 15 beats min(-1), RHTT2: 183 ± 15 beats min(-1), ICC = 0.99, TEM = 2 beats min(-1)), nor sweat rate (1721 ± 675 g h(-1), 1716 ± 745 g h(-1), ICC = 0.95, TEM = 162 g h(-1)) between RHTT1 and RHTT2 (p>0.05). Results demonstrate good agreement, strong correlations and small differences between repeated trials, and the TEM values suggest low within-participant variability. The RHTT was effective in differentiating between individuals physiological responses; supporting a heat tolerance continuum. The findings suggest the RHTT is a repeatable measure of physiological strain in the heat and may be used to assess the effectiveness of acute and chronic heat alleviating procedures.

Leukocyte Hsp72 mRNA transcription does not differ between males and females during heat acclimation

ABSTRACT Purpose: Thermotolerance is an acquired state of increased cytoprotection achieved following single or repeated exposures to heat stress, in part characterized by changes in the intracellular 72 kda heat shock protein (HSP72; HSPA1A). Females have demonstrated reduced exercise induced HSP72 in comparison to males. This study examined sex differences in heat shock protein 72 messenger ribonucleic acid (Hsp72 mRNA) transcription during heat acclimation (HA) to identify whether sex differences were a result of differential gene transcription. Methods: Ten participants (5M, 5F) performed 10, 90 min controlled hyperthermia [rectal temperature (Tre) ≥ 38.5°C] HA sessions over 12 d. Leukocyte Hsp72 mRNA was measured pre and post D1, D5, and D10, via Reverse transcription polymerase chain reaction (RT-QPCR). Results: HA was evidenced by a reduction in resting Tre (−0.4 ± 0.5°C) and resting heart rate [(HR); −13 ± 7 beats.min−1] following HA (p ≤ 0.05). During HA no difference (p > 0.05) was observed in ΔTre between males (D1 = 1.5 ± 0.2°C; D5 = 1.6 ± 0.4°C; D10 = 1.8 ± 0.3°C) and females (D1 = 1.5 ± 0.5°C; D5 = 1.4 ± 0.2°C; D10 = 1.8 ± 0.3°C). This was also true of mean Tre demonstrating equality of thermal stimuli for mRNA transcription and HA. There were no differences (p > 0.05) in Hsp72 mRNA expression between HA sessions or between males (D1 = +1.8 ± 1.5-fold; D5 = +2.0 ± 1.0 fold; D10 = +1.1 ± 0.4-fold) and females (D1 = +2.6 ± 1.8-fold; D5 = +1.8 ± 1.4-fold; D10 = +0.9 ± 1.9-fold). Conclusions: This experiment demonstrates that there is no difference in Hsp72 mRNA increases during HA between sexes when controlled hyperthermia HA is utilised. Gender specific differences in exercise-induced HSP72 reported elsewhere likely result from post-transcriptional events.

Sauna exposure immediately prior to short-term heat acclimation accelerates phenotypic adaptation in females

OBJECTIVES Investigate whether a sauna exposure prior to short-term heat acclimation (HA) accelerates phenotypic adaptation in females. DESIGN Randomised, repeated measures, cross-over trial. METHODS Nine females performed two 5-d HA interventions (controlled hyperthermia Tre≥38.5°C), separated by 7-wk, during the follicular phase of the menstrual cycle confirmed by plasma concentrations of 17-β estradiol and progesterone. Prior to each 90-min HA session participants sat for 20-min in either a temperate environment (20°C, 40% RH; HAtemp) wearing shorts and sports bra or a hot environment (50°C, 30% RH) wearing a sauna suit to replicate sauna conditions (HAsauna). Participants performed a running heat tolerance test (RHTT) 24-h pre and 24-h post HA. RESULTS Mean heart rate (HR) (85±4 vs. 68±5 bpm, p≤0.001), sweat rate (0.4±0.2 vs. 0.0±0.0Lh-1, p≤0.001), and thermal sensation (6±0 vs. 5±1, p=0.050) were higher during the sauna compared to temperate exposure. Resting rectal temperature (Tre) (-0.28±0.16°C), peak Tre (-0.42±0.22°C), resting HR (-10±4 bpm), peak HR (-12±7 bpm), Tre at sweating onset (-0.29±0.17°C) (p≤0.001), thermal sensation (-0.5±0.5; p=0.002), and perceived exertion (-3±2; p≤0.001) reduced during the RHTT, following HAsauna; but not HAtemp. Plasma volume expansion was greater following HAsauna (HAsauna, 9±7%; HAtemp, 1±5%; p=0.013). Sweat rate (p≤0.001) increased and sweat NaCl (p=0.006) reduced during the RHTT following HAsauna and HAtemp. CONCLUSIONS This novel strategy initiated HA with an attenuation of thermoregulatory, cardiovascular, and perceptual strain in females due to a measurably greater strain in the sauna compared to temperate exposure when adopted prior to STHA.

Restricted sweat evaporation preceding short term heat acclimation accelerates adaption in females

Short term heat acclimation (STHA) is a preferred regime for athletes, since it is easier to adopt when sustaining quality training and tapering performance in the weeks prior to competition. Females have been reported to establish an enhance sudomotor function following STHA; however, they require long term HA to establish cardiovascular and thermoregulatory adaptation [1]. The current study, assessed the effectiveness of five days of controlled hyperthermia HA, combined with a restricted sweat evaporation exposure, to elicit thermoregulatory, cardiovascular and sudomotor adaptation.

Females exposed to 24 h of sleep deprivation do not experience greater physiological strain, but do perceive heat illness symptoms more severely, during exercise-heat stress

ABSTRACT There is limited and inconclusive evidence surrounding the physiological and perceptual responses to heat stress while sleep deprived, especially for females. This study aimed to quantify the effect of 24 h sleep deprivation on physiological strain and perceptual markers of heat-related illness in females. Nine females completed two 30-min heat stress tests (HST) separated by 48 h in 39°C, 41% relative humidity at a metabolic heat production of 10 W · kg−1. The non-sleep deprived HST was followed by the sleep deprivation (SDHST) trial for all participants during the follicular phase of the menstrual cycle. Physiological and perceptual measures were recorded at 5 min intervals during the HSTs. On the cessation of the HSTs, heat illness symptom index (HISI) was completed. HISI scores increased after sleep deprivation by 28 ± 16 versus 20 ± 16 (P = 0.01). Peak (39.40 ± 0.35°C vs. 39.35 ± 0.33°C) and change in rectal temperature (1.91 ± 0.21 vs. 1.93 ± 0.34°C), and whole body sweat rate (1.08 ± 0.31 vs. 1.15 ± 0.36 L · h−1) did not differ (P > 0.05) between tests. No difference was observed in peak, nor rise in: heart rate, mean skin temperature, perceived exertion or thermal sensation during the HSTs. Twenty-four hours sleep deprivation increased perceptual symptoms associated with heat-related illness; however, no thermoregulatory alterations were observed.