Ben J. Lee,1 Richard W. A. Mackenzie, Valerie Cox, Rob S. James, and Charles D. Thake
Exercise Science Applied Research Group, Coventry University, Priory Street, Coventry CV1 5FB, UK. Inflammation and Infection Group, School of Science and Technology, University of Westminster, New Cavendish Street, London W1W 6UW, UK.
The aim of this study was to determine whether short-term heat acclimation (STHA) could confer increased cellular tolerance to acute hypoxic exercise in humans as determined via monocyte HSP72 (mHSP72) expression. Sixteen males were separated into two matched groups. The STHA group completed 3 days of exercise heat acclimation; 60 minutes cycling at 50% VȮ 2peak in 40∘C 20% relative humidity (RH). The control group (CON) completed 3 days of exercise training in 20∘C, 40% RH. Each group completed a hypoxic stress test (HST) one week before and 48 hours following the final day of CON or STHA. Percentage changes in HSP72 concentrations were similar between STHA and CON following HST1 (P = 0.97). STHA induced an increase in basal HSP72 (P = 0.03) with no change observed in CON (P = 0.218). Basal mHSP72 remained elevated before HST2 for the STHA group (P < 0.05) and was unchanged from HST1 in CON (P > 0.05). Percent change in mHSP72 was lower after HST2 in STHA compared to CON (P = 0.02). The mHSP72 response to hypoxic exercise was attenuated following 3 days of heat acclimation. This is indicative of improved tolerance and ability to cope with the hypoxic insult, potentially mediated in part by increased basal reserves of HSP72.
Heat acclimation induces an increase in basal stores of the evolutionarily conserved molecular chaperone heat shock protein 72 (HSP72) [1, 2]. Additionally, HSP72 is induced by exposure to hypoxia at rest in humans . These data demonstrate a degree of commonality in stress adaption and thus the potential to exploit cross acclimation in humans in preparation for exposures to different physiological stressors. An increase in the basal stores of HSP72 represents an improvement in a cell’s ability to tolerate stress without the need for de novo protein synthesis  and is an accepted marker in an organism’s adaptation to stress . It is possible that invoking the heat shock response (HSR) via exposure to one stress may induce a degree of tolerance to a second, different stressor . This cross acclimation is well documented in vivo and in vitro in animal models (for a review see Horowitz, 2007 ). For example, hemodynamic recovery is enhanced in heat acclimated animals exposed to a hypoxic stressor (such as ischemia reperfusion) compared to control animals . However, to date very little is known about the evocation of acclimation in vivo in humans. Taylor et al.  indicated that increased basal stores of monocyte HSP72 (mHSP72) during 5 daily resting hypoxic exposures were associated with reduced oxidative stress after submaximal exercise in normoxia. However the absence of normoxic or normothermic  controls in human in vivo studies often makes it difficult to determine whether the intervention alone led to the increase in mHSP72.