Heat Acclimation and Performance in Hypoxic Conditions

Heled, Yuval; Peled, Amir; Yanovich, Ran; Shargal, Eyal; Pilz-Burstein, Rutie; Epstein, Yoram; Moran, Daniel S.

doi:10.3357/asem.3241.2012

Cited by 38 publications

(42 citation statements)

References 18 publications

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“…Individuals using this approach would also have the option of working at higher work intensities than are possible under hypoxic conditions due to the increased reductions in aerobic capacity experienced in hypoxia. Heat acclimation regimens that elevate plasma volume have been shown to improve physical performance (VO 2 peak and time trial performance) at sea level in well-trained participants [36,41] and cognitive function during acute hypoxia [18]. Thus, those looking for an adjunct to training may consider the potential benefits of acute and repeated heat training sessions over the more commonly applied altitude model of training.…”

Section: Discussionmentioning

confidence: 99%

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The impact of submaximal exercise during heat and/or hypoxia on the cardiovascular and monocyte HSP72 responses to subsequent (post 24 h) exercise in hypoxia

et al. 2014

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BackgroundThe aims of this study were to describe the cellular stress response to prolonged endurance exercise in acute heat, hypoxia and the combination of heat and hypoxia and to determine whether prior acute exposure to these stressors improved cellular tolerance to a subsequent exercise bout in hypoxia 24 h later.MethodsTwelve males (age 22 ± 4 years, height 1.77 ± 0.05 m, mass 79 ± 12.9 kg, VO2 max 3.57 ± 0.7 L · min-1) completed four trials (30-min rest, 90-min cycling at 50% normoxic VO2 max) in normothermic normoxia (NORM; 18°C, FIO2 = 0.21), heat (HEAT; 40°C, 20% RH), hypoxia (HYP; FIO2 = 0.14) or a combination of heat and hypoxia (COM; 40°C, 20% RH, FIO2 = 0.14) separated by at least 7 days. Twenty-four hours after each trial, participants completed a hypoxic stress test (HST; 15-min rest, 60-min cycling at 50% normoxic VO2 max, FIO2 = 0.14). Monocyte heat shock protein 72 (mHSP72) was assessed immediately before and after each exercise bout.ResultsmHSP72 increased post exercise in NORM (107% ± 5.5%, p > 0.05), HYP (126% ± 16%, p < 0.01), HEAT (153% ± 14%, p < 0.01) and COM (161% ± 32%, p < 0.01). mHSP72 had returned to near-resting values 24 h after NORM (97% ± 8.6%) but was elevated after HEAT (130% ± 19%), HYP (118% ± 17%) and COM (131% ± 19%) (p < 0.05). mHSP72 increased from baseline after HSTNORM (118% ± 12%, p < 0.05), but did not increase further in HSTHEAT, HSTHYP and HSTCOM.ConclusionsThe prior induction of mHSP72 as a result of COM, HEAT and HYP attenuated further mHSP72 induction after HST and was indicative of conferred cellular tolerance.

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Section: Discussionmentioning

confidence: 99%

“…military personnel) between different environmental settings. For example, individuals who are physiologically adapted to heat may tolerate moderately hypoxic environments better than non-acclimated individuals [18]. …”

Section: Introductionmentioning

confidence: 99%

The impact of submaximal exercise during heat and/or hypoxia on the cardiovascular and monocyte HSP72 responses to subsequent (post 24 h) exercise in hypoxia

et al. 2014

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“…There was a long gap between the 1955 study of Hiestand et al (66) where mice acclimated for 14 days survived anoxia better than the nonacclimated ones and 1993 when data on heat acclimation mediated cross-tolerance began to accumulate (119). We have evidence that heat acclimation induces cross tolerance against several environmental stressors associated with oxygen supply-oxygen demand mismatching such as ischemia/reperfusion, hypoxia (64,77,119,242) hyperoxia (4,42) ionizing radiation (176) TBI (211), and noise induced hearing loss (167).…”

Section: Heat Acclimation Mediated Cross-tolerancementioning

confidence: 99%

Heat Acclimation, Epigenetics, and Cytoprotection Memory

Horowitz

2014

Comprehensive Physiology

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Heat acclimation is a within-life phenotypic adaptation to heat. Plasticity of the thermoregulatory system is crucial for the induction of heat acclimation. In the last two decades, it has become clear that heat causes adaptive shifts in gene expression which adjust the protein balance. These changes are part of the evolvement of the acclimated phenotype. The molecular-cellular aspects of some acclimatory mechanisms that have only been explained by physiological-effectorial mechanisms have been discovered. This review attempts to bridge the gap between the classic physiological heat acclimation profile and the molecular/cellular mechanisms underlying the evolvement of the acclimated phenotype. Heat acclimation leads to leftward and rightward shifts in temperature thresholds of heat dissipation organs and thermal injury, respectively, thereby expanding the acclimated dynamic thermoregulatory range. Interactions between ambient temperature and afferent drives from effector organs to the hypothalamic thermoregulatory center with modifications in warm/cold sensitive neuron ratio and excitability contribute to the threshold changes. The altered threshold for thermal injury is associated with progressive enhancement of inducible cytoprotective networks, including HSP70, HSF1, and HIF-1ɑ. These molecules are also important in acclimatory kinetics. Aspects of cross-adaption, cross-tolerance and interference with heat acclimation are explained using molecular-cellular physiological interactions, with the heart, skeletal muscles, and water secretory glands as models. Lastly, the roles of epigenetic mechanisms in transcriptional regulation during induction of the acclimated phenotype, its decay, and reinduction are discussed. Posttranslational histone modifications in the promoters of hsp70 and hsp90 form part of our prototype model of heat-acclimation-mediated cytoprotective memory.

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“…Equates to ∼1.9% faster—Lorenzo et al 90 12 Cyclists (2 female), Mixed design; 10 btwn, 2 wthn∼446716.6 (10*100)Matched abs workrate (50% V̇O2peak temperate)40°C, 30%?Seated Cycling↑ 6.5 ±4 .5V̇O 2 peak ↑5% 60-min WT ↑6% PO@LT ↑5%V̇O 2 peak ↑8% 60-min WT ↑8% PO@LT ↑5%Garrett et al 91 8 male rowers,?668T c @ 38.540°C,Drank 0.1 L,Seated↑ 4.5 ±4 .5—2-km TT ↑ 1% No control (1*0.5+ 60%−2.50%Cycling(0.7 – 8.3) (0.2 – 1.6) 5*90) Buchheit et al 93 ; Racinais et al 124 15-19 high-fit male soccer No control??∼8.5 (6*60-95)Normal training practices39-43°C, 12-30%? (Ad lib)Upright SoccerRest: ↑ ∼7 Ex: ↑ ∼4 ±7 Range: −10 to +20YoYo IR1 f ↑7%Total and fast run distance related to ΔPVHeled et al 130 8 mod fit males No control?57∼9 and 24 (5 and13 * ∼1.85 h p/d)Matched abs workrate (Walk @ 30% V̇O2max temperate)40˚C 40% RH?…”

Section: Introductionmentioning

confidence: 98%

Heat stress and dehydration in adapting for performance: Good, bad, both, or neither?

et al. 2016

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Physiological systems respond acutely to stress to minimize homeostatic disturbance, and typically adapt to chronic stress to enhance tolerance to that or a related stressor. It is legitimate to ask whether dehydration is a valuable stressor in stimulating adaptation per se. While hypoxia has had long-standing interest by athletes and researchers as an ergogenic aid, heat and nutritional stressors have had little interest until the past decade. Heat and dehydration are highly interlinked in their causation and the physiological strain they induce, so their individual roles in adaptation are difficult to delineate. The effectiveness of heat acclimation as an ergogenic aid remains unclear for team sport and endurance athletes despite several recent studies on this topic. Very few studies have examined the potential ergogenic (or ergolytic) adaptations to ecologically-valid dehydration as a stressor in its own right, despite longstanding evidence of relevant fluid-regulatory adaptations from short-term hypohydration. Transient and self-limiting dehydration (e.g., as constrained by thirst), as with most forms of stress, might have a time and a place in physiological or behavioral adaptations independently or by exacerbating other stressors (esp. heat); it cannot be dismissed without the appropriate evidence. The present review did not identify such evidence. Future research should identify how the magnitude and timing of dehydration might augment or interfere with the adaptive processes in behaviorally constrained versus unconstrained humans.

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Heat Acclimation and Performance in Hypoxic Conditions

Abstract: Prior heat acclimation may reduce physiological strain and improve cognitive performance in moderate hypoxia. Further studies are required in order to evaluate the possibility of implementing this method as an operational preconditioning tool.

Cited by 38 publications

References 18 publications

The impact of submaximal exercise during heat and/or hypoxia on the cardiovascular and monocyte HSP72 responses to subsequent (post 24 h) exercise in hypoxia

The impact of submaximal exercise during heat and/or hypoxia on the cardiovascular and monocyte HSP72 responses to subsequent (post 24 h) exercise in hypoxia

Heat Acclimation, Epigenetics, and Cytoprotection Memory

Heat stress and dehydration in adapting for performance: Good, bad, both, or neither?

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