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      Heat Acclimation Decay and Re-Induction: A Systematic Review and Meta-Analysis

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          Abstract

          Background

          Although the acquisition of heat acclimation (HA) is well-documented, less is known about HA decay (HAD) and heat re-acclimation (HRA). The available literature suggests 1 day of HA is lost following 2 days of HAD. Understanding this relationship has the potential to impact upon the manner in which athletes prepare for major competitions, as a HA regimen may be disruptive during final preparations (i.e., taper).

          Objective

          The aim of this systematic review and meta-analysis was to determine the rate of HAD and HRA in three of the main physiological adaptations occurring during HA: heart rate (HR), core temperature ( T c), and sweat rate (SR).

          Data Sources

          Data for this systematic review were retrieved from Scopus and critical review of the cited references.

          Study Selection

          Studies were included when they met the following criteria: HA, HAD, and HRA (when available) were quantified in terms of exposure and duration. HA had to be for at least 5 days and HAD for at least 7 days for longitudinal studies. HR, T c, or SR had to be monitored in human participants.

          Study Appraisal

          The level of bias in each study was assessed using the McMaster critical review form. Multiple linear regression techniques were used to determine the dependency of HAD in HR, T c, and SR from the number of HA and HAD days, daily HA exposure duration, and intensity.

          Results

          Twelve studies met the criteria and were systematically reviewed. HAD was quantified as a percentage change relative to HA (0% = HA, 100% = unacclimated state). Adaptations in end-exercise HR decreased by 2.3% ( P < 0.001) for every day of HAD. For end-exercise T c, the daily decrease was 2.6% ( P < 0.01). The adaptations in T c during the HA period were more sustainable when the daily heat exposure duration was increased and heat exposure intensity decreased. The decay in SR was not related to the number of decay days. However, protracted HA-regimens seem to induce longer-lasting adaptations in SR. High heat exposure intensities during HA seem to evoke more sustained adaptations in SR than lower heat stress. Only eight studies investigated HRA. HRA was 8–12 times faster than HAD at inducing adaptations in HR and T c, but no differences could be established for SR.

          Limitations

          The available studies lacked standardization in the protocols for HA and HAD.

          Conclusions

          HAD and HRA differ considerably between physiological systems. Five or more HA days are sufficient to cause adaptations in HR and T c; however, extending the daily heat exposure duration enhances T c adaptations. For every decay day, ~ 2.5% of the adaptations in HR and T c are lost. For SR, longer HA periods are related to better adaptations. High heat exposure intensities seem beneficial for adaptations in SR, but not in T c. HRA induces adaptations in HR and T c at a faster rate than HA. HRA may thus provide a practical and less disruptive means of maintaining and optimizing HA prior to competition.

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          Most cited references116

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          Heat acclimation improves exercise performance.

          This study examined the impact of heat acclimation on improving exercise performance in cool and hot environments. Twelve trained cyclists performed tests of maximal aerobic power (VO2max), time-trial performance, and lactate threshold, in both cool [13°C, 30% relative humidity (RH)] and hot (38°C, 30% RH) environments before and after a 10-day heat acclimation (∼50% VO2max in 40°C) program. The hot and cool condition VO2max and lactate threshold tests were both preceded by either warm (41°C) water or thermoneutral (34°C) water immersion to induce hyperthermia (0.8-1.0°C) or sustain normothermia, respectively. Eight matched control subjects completed the same exercise tests in the same environments before and after 10 days of identical exercise in a cool (13°C) environment. Heat acclimation increased VO2max by 5% in cool (66.8 ± 2.1 vs. 70.2 ± 2.3 ml·kg(-1)·min(-1), P = 0.004) and by 8% in hot (55.1 ± 2.5 vs. 59.6 ± 2.0 ml·kg(-1)·min(-1), P = 0.007) conditions. Heat acclimation improved time-trial performance by 6% in cool (879.8 ± 48.5 vs. 934.7 ± 50.9 kJ, P = 0.005) and by 8% in hot (718.7 ± 42.3 vs. 776.2 ± 50.9 kJ, P = 0.014) conditions. Heat acclimation increased power output at lactate threshold by 5% in cool (3.88 ± 0.82 vs. 4.09 ± 0.76 W/kg, P = 0.002) and by 5% in hot (3.45 ± 0.80 vs. 3.60 ± 0.79 W/kg, P < 0.001) conditions. Heat acclimation increased plasma volume (6.5 ± 1.5%) and maximal cardiac output in cool and hot conditions (9.1 ± 3.4% and 4.5 ± 4.6%, respectively). The control group had no changes in VO2max, time-trial performance, lactate threshold, or any physiological parameters. These data demonstrate that heat acclimation improves aerobic exercise performance in temperate-cool conditions and provide the scientific basis for employing heat acclimation to augment physical training programs.
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            Integrated physiological mechanisms of exercise performance, adaptation, and maladaptation to heat stress.

            This article emphasizes significant recent advances regarding heat stress and its impact on exercise performance, adaptations, fluid electrolyte imbalances, and pathophysiology. During exercise-heat stress, the physiological burden of supporting high skin blood flow and high sweating rates can impose considerable cardiovascular strain and initiate a cascade of pathophysiological events leading to heat stroke. We examine the association between heat stress, particularly high skin temperature, on diminishing cardiovascular/aerobic reserves as well as increasing relative intensity and perceptual cues that degrade aerobic exercise performance. We discuss novel systemic (heat acclimation) and cellular (acquired thermal tolerance) adaptations that improve performance in hot and temperate environments and protect organs from heat stroke as well as other dissimilar stresses. We delineate how heat stroke evolves from gut underperfusion/ischemia causing endotoxin release or the release of mitochondrial DNA fragments in response to cell necrosis, to mediate a systemic inflammatory syndrome inducing coagulopathies, immune dysfunction, cytokine modulation, and multiorgan damage and failure. We discuss how an inflammatory response that induces simultaneous fever and/or prior exposure to a pathogen (e.g., viral infection) that deactivates molecular protective mechanisms interacts synergistically with the hyperthermia of exercise to perhaps explain heat stroke cases reported in low-risk populations performing routine activities. Importantly, we question the "traditional" notion that high core temperature is the critical mediator of exercise performance degradation and heat stroke. Published 2011. This article is a U.S. Government work and is in the public domain in the USA.
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              The Effects of Heat Adaptation on Physiology, Perception and Exercise Performance in the Heat: A Meta-Analysis.

              Exercise performance and capacity are impaired in hot, compared to temperate, conditions. Heat adaptation (HA) is one intervention commonly adopted to reduce this impairment because it may induce beneficial exercise performance and physiological and perceptual adaptations. A number of investigations have been conducted on HA but, due to large methodological differences, the effectiveness of different HA regimens remain unclear.
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                Author and article information

                Contributors
                h.a.m.daanen@vu.nl
                Journal
                Sports Med
                Sports Med
                Sports Medicine (Auckland, N.z.)
                Springer International Publishing (Cham )
                0112-1642
                1179-2035
                11 November 2017
                11 November 2017
                2018
                : 48
                : 2
                : 409-430
                Affiliations
                [1 ]ISNI 0000 0004 1754 9227, GRID grid.12380.38, Department of Human Movement Sciences, Faculty of Behavioural and Movement Sciences, Amsterdam Movement Sciences, , Vrije Universiteit Amsterdam, ; Van der Boechorststraat 7, 1081BT Amsterdam, The Netherlands
                [2 ]Athlete Health and Performance Research Centre, Aspetar Orthopaedic and Sports Medicine Hospital, Doha, Qatar
                [3 ]ISNI 0000 0004 0385 7472, GRID grid.1039.b, Research Institute for Sport and Exercise, , University of Canberra, ; Canberra, ACT Australia
                Author information
                http://orcid.org/0000-0002-7459-0678
                Article
                808
                10.1007/s40279-017-0808-x
                5775394
                29129022
                5f22cef8-be25-43bd-bb85-1c75805bac8c
                © The Author(s) 2017

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100010677, H2020 Health;
                Award ID: 668786
                Award Recipient :
                Categories
                Systematic Review
                Custom metadata
                © Springer International Publishing AG, part of Springer Nature 2018

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