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Effect of Permissive Dehydration on Induction and Decay of Heat Acclimation, and Temperate Exercise Performance.

ABSTRACT: Purpose: It has been suggested that dehydration is an independent stimulus for heat acclimation (HA), possibly through influencing fluid-regulation mechanisms and increasing plasma volume (PV) expansion. There is also some evidence that HA may be ergogenic in temperate conditions and that this may be linked to PV expansion. We investigated: (i) the influence of dehydration on the time-course of acquisition and decay of HA; (ii) whether dehydration augmented any ergogenic benefits in temperate conditions, particularly those related to PV expansion. Methods: Eight males [VO2max: 56.9(7.2) mL·kg-1·min-1] undertook two HA programmes (balanced cross-over design), once drinking to maintain euhydration (HAEu) and once with restricted fluid-intake (HADe). Days 1, 6, 11, and 18 were 60 min exercise-heat stress tests [HST (40°C; 50% RH)], days 2-5 and 7-10 were 90 min, isothermal-strain (Tre ~ 38.5°C), exercise-heat sessions. Performance parameters [VO2max, lactate threshold, efficiency, peak power output (PPO)] were determined pre and post HA by graded exercise test (22°C; 55%RH). Results: During isothermal-strain sessions hypohydration was achieved in HADe and euhydration maintained in HAEu [average body mass loss -2.71(0.82)% vs. -0.56(0.73)%, P < 0.001], but aldosterone concentration, power output, and cardiovascular strain were unaffected by dehydration. HA was evident on day 6 {reduced end-exercise Tre [-0.30(0.27)°C] and exercise heart rate [-12(15) beats.min-1], increased PV [+7.2(6.4)%] and sweat-loss [+0.25(0.22) L.h-1], P < 0.05} with some further adaptations on day 11 {further reduced end-exercise Tre [-0.25(0.19)°C] and exercise heart rate [-3(9) beats.min-1], P < 0.05}. These adaptations were not notably affected by dehydration and were generally maintained 7-days post HA. Performance parameters were unchanged, apart from increased PPO (+16(20) W, irrespective of condition). Conclusions: When thermal-strain is matched, permissive dehydration which induces a mild, transient, hypohydration does not affect the acquisition and decay of HA, or endurance performance parameters. Irrespective of hydration, trained individuals require >5 days to optimize HA.

SUBMITTER: Neal RA

PROVIDER: S-EPMC5120118 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

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Effect of Permissive Dehydration on Induction and Decay of Heat Acclimation, and Temperate Exercise Performance.

Neal Rebecca A RA Massey Heather C HC Tipton Michael J MJ Young John S JS Corbett Jo J

Frontiers in physiology 20161123

<b>Purpose:</b> It has been suggested that dehydration is an independent stimulus for heat acclimation (HA), possibly through influencing fluid-regulation mechanisms and increasing plasma volume (PV) expansion. There is also some evidence that HA may be ergogenic in temperate conditions and that this may be linked to PV expansion. We investigated: (i) the influence of dehydration on the time-course of acquisition and decay of HA; (ii) whether dehydration augmented any ergogenic benefits in tempe ...[more]

PMID: 27932993

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Project description:The purpose of this study was to investigate the alterations in serum heat shock protein (Hsp) 70 levels during a 15-consecutive-day intermittent heat-exercise protocol in a 29-year-old male ultra marathon runner. Heat acclimation, for the purpose of physical activities in elevated ambient temperatures, has numerous physiological benefits including mechanisms such as improved cardiac output, increased plasma volume and a decreased core temperature (T (c)). In addition to the central adaptations, the role of Hsp during heat acclimation has received an increasing amount of attention. The acclimation protocol applied was designed to correspond with the athlete's tapering period for the 2007 Marathon Des Sables. The subject (VO(2)max = 50.7 ml.kg(-1).min(-1), peak power output [PPO] = 376 W) cycled daily for 90 min at a workload corresponding to 50% of VO(2)max in a temperature-controlled room (average WBGT = 31.9 +/- 0.9 degrees C). Venous blood was sampled before and after each session for measurement of serum osmolality and serum Hsp70. In addition, T (c), heart rate (HR) and power output (PO) was measured throughout the 90 min to ensure that heat acclimation was achieved during the 15-day period. The results show that the subject was successfully heat acclimated as seen by the lowered HR at rest and during exercise, decreased resting and exercising T (c) and an increased PO. The heat exercise resulted in an initial increase in Hsp70 concentrations, known as thermotolerance, and the increase in Hsp70 after exercise was inversely correlated to the resting values of Hsp70 (Spearman's rank correlation = -0.81, p < 0.01). Furthermore, the 15-day heat-exercise protocol also increased the basal levels of Hsp70, a response different from that of thermotolerance. This is, as far as we are aware, the first report showing Hsp70 levels during consecutive days of intermittent heat exposure giving rise to heat acclimation. In conclusion, a relatively longer heat acclimation protocol is suggested to obtain maximum benefit of heat acclimation inclusive of both cellular and systemic adaptations.

Project description:Exercise and exogenous heat each stimulate multiple adaptations, but their roles are not well delineated, and that of the related stressor, dehydration, is largely unknown. While severe and prolonged hypohydration potentially "silences" the long-term heat acclimated phenotype, mild and transient dehydration may enhance cardiovascular and fluid-regulatory adaptations. We tested the hypothesis that exogenous heat stress and dehydration additively potentiate acute (24 h) cardiovascular and hematological outcomes following exercise. In a randomized crossover study, 10 physically-active volunteers (mean ± SD: 173 ± 11 cm; 72.1 ± 11.5 kg; 24 ± 3 year; 6 females) completed three trials of 90-min orthostatically-stressful calisthenics, in: (i) temperate conditions (22°C, 50% rh, no airflow; CON); (ii) heat (40°C, 60% rh) whilst euhydrated (HEAT), and (iii) heat with dehydration (no fluid ~16 h before and during exercise; HEAT+DEHY). Using linear mixed effects model analyses, core temperature (TCORE) rose 0.7°C more in HEAT than CON (95% CL: [0.5, 0.9]; p < 0.001), and another 0.4°C in HEAT+DEHY ([0.2, 0.5]; p < 0.001, vs. HEAT). Skin temperature also rose 1.2°C more in HEAT than CON ([0.6, 1.8]; p < 0.001), and similarly to HEAT+DEHY (p = 0.922 vs. HEAT). Peak heart rate was 40 b·min-1 higher in HEAT than in CON ([28, 51]; p < 0.001), and another 15 b·min-1 higher in HEAT+DEHY ([3, 27]; p = 0.011, vs. HEAT). Mean arterial pressure at 24-h recovery was not consistently below baseline after CON or HEAT (p ≥ 0.452), but was reduced 4 ± 1 mm Hg after HEAT+DEHY ([0, 8]; p = 0.020 vs. baseline). Plasma volume at 24 h after exercise increased in all trials; the 7% increase in HEAT was not reliably more than in CON (5%; p = 0.335), but was an additional 4% larger after HEAT+DEHY ([1, 8]; p = 0.005 vs. HEAT). Pooled-trial correlational analysis showed the rise in TCORE predicted the hypotension (r = -0.4) and plasma volume expansion (r = 0.6) at 24 h, with more hypotension reflecting more plasma expansion (r = -0.5). In conclusion, transient dehydration with heat potentiates short-term (24-h) hematological (hypervolemic) and cardiovascular (hypotensive) outcomes following calisthenics.

Project description:The aim of the present study was to investigate the effect of one week dehydration heat exposure on thoracic aorta reactivity in rats. Eighteen Male Sprague-Dawley rats were randomly divided into 3 groups (n=6 each group): Control group (CN), heat exposure group (HE), dehydration heat exposure group (DHE). The CN group was exposed to a room temperature of 24°C, while the HE and DHE groups were exposed to a heat temperature of 32°C. After 7 days of heat exposure, the heart rate and blood pressure of the rats were measured, and the noradrenaline (NA)-induced contraction on the aorta rings was measured by tension recording. The average contents of malondialdehyde (MDA) and superoxide dismutase (SOD) in serum were detected using ELISA. The expression of apoptotic genes in the thoracic aorta was measured using RT-PCR. Compared with CN, the heart rate in the HE and DHE groups had a tendency to become retarded, but there was no significant difference (P>0.05). In the HE group, the systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) of the rats were significantly higher than that of the CN (P<0.05). In the DHE group, the SBP of rats was significantly higher than that of the CN (P<0.05), while the SBP, DBP, and MAP of the rats were decreased compared to the rats in the HE group, although there was no statistical significance (P>0.05). In the HE and DHE groups, the NA-induced contraction on the rats thoracic aorta ring was larger than that of the CN (P<0.05), albeit there was no significant difference between the HE and DHE groups (P>0.05). The serum SOD content decreased in the HE and DHE groups, however, the reduction was significant only in the DHE group (P<0.05). The content of MDA in serum was significantly increased in the DHE group (P<0.05). The expression of BAX was significantly upregulated whereas Bcl2 expression was decreased in the DHE group (P<0.05). The results showed that a high temperature was harmful to the body, especially in the case of lack of food and water. Additionally, the heat exposure elevated blood pressure, and increased arterial reactivity, which were related to the elevated production of MDA, led to the impaired production of SOD, and an increase of cell apoptosis. These findings are useful to understand the influence of dehydrated heat exposure on the vascular function, and they provide certain theoretical and experimental guidance for protection under high temperature.

Project description:Heat acclimation by post-exercise hot water immersion (HWI) on six consecutive days reduces thermal strain and improves exercise performance during heat stress. However, the retention of adaptations by this method remains unknown. Typically, adaptations to short-term, exercise-heat-acclimation (<7 heat exposures) decay rapidly and are lost within 2 weeks. Short-term protocols should therefore be completed within 2 weeks of relocating to the heat; potentially compromising pre-competition/deployment training. To establish whether adaptations from post-exercise HWI are retained for up to 2 weeks, participants completed a 40-min treadmill run at 65% max in the heat (33°C, 40% RH) before (PRE) and 24 h after (POST) the HWI intervention (n = 13) and then at 1 week (WK 1) and 2 weeks (WK 2) after the HWI intervention (n = 9). Heat acclimation involved a 40-min treadmill run (65% max) on six consecutive days in temperate conditions (20°C), followed by ≤40 min HWI (40°C). Post-exercise HWI induced heat acclimation adaptations that were retained for at least 2 weeks, evidenced by reductions from PRE to WK 2 in: resting rectal core temperature (T re, -0.36 ± 0.25°C), T re at sweating onset (-0.26 ± 0.24°C), and end-exercise T re (-0.36 ± 0.37°C). Furthermore, mean skin temperature (T sk) (-0.77 ± 0.70°C), heart rate (-14 ± 10 beats⋅min-1), rating of perceived exertion (-1 ± 2), and thermal sensation (-1 ± 1) were reduced from PRE to WK 2 (P < 0.05). However, PRE to POST changes in total hemoglobin mass, blood volume, plasma volume, the drive for sweating onset, sweating sensitivity and whole body sweating rate did not reach significance (P > 0.05). As such, the reduction in thermal strain during exercise-heat stress appears likely due to the reduction in resting T re evident at POST, WK 1, and WK 2. In summary, 6 days of post-exercise HWI is an effective, practical and accessible heat acclimation strategy that induces adaptations, which are retained for at least 2 weeks. Therefore, post-exercise HWI can be completed during an athlete's pre-taper phase and does not suffer from the same practical limitations as short-term, exercise-heat-acclimation.

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Effect of Permissive Dehydration on Induction and Decay of Heat Acclimation, and Temperate Exercise Performance.

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Effect of Permissive Dehydration on Induction and Decay of Heat Acclimation, and Temperate Exercise Performance.

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