Animal studies have shown that heat acclimation (HA) is neuro-protective against traumatic brain injury, and provide cardio-protection, following an ischaemic attack. The pathways associated with HA and its protective nature, have been found to be linked in animals with the induction of hypoxia inducible factor 1a(HIF-1a) and heat shock protein 72(Hsp72). HA has also been shown to upregulate Epo receptor (EpoR), a target gene for HIF-1a, providing neuron and myocardium protection in animals. However, whether similar protective adaptations to HA occur in humans is yet to be confirmed. The aim of this study was to investigate the impact of HA on HIF-1a and Hsp72 induction and their effect on EpoR regulation in human subjects. We hypothesise that HA will upregulate HIF-1a and Hsp72 and this upregulation will increase EpoR expression. To test this hypothesis, healthy, highly trained male cyclists/triathletes, with a mean age of 30.26±7.49 yrs and a VO2max of 58.55±5.91 ml/kg/min, were randomly assigned to a heat group (HG = 10 subjects) or a neutral group (NG = 11 subjects). Aerobic fitness and acute exercise have been shown to impact on Hsp72 and HIF-1 regulation. In an effort to limit the impact of these potentially confounding factors, only highly fit subjects were recruited and maintained the same level of training during the HA. Subjects in HG trained for 6 consecutive days on a bike for 1 hour per day at 70% of their VO2max, in 35º C and 40% humidity. Subjects in NG performed the same training sessions at 22º C and 40% humidity. Venous blood samples were collected at rest, and 60 minutes into recovery following the 1h exercise. Flow cytometry was used to assess levels of HIF-1a, Hsp72 and EpoR expression in monocytes at the various time points. There was no significant difference between the 2 groups before HA in terms of anthropometric data or on proteins expression. Following the intervention, HG showed an average drop in core body temperature of 0.3º C post-exercise, a hallmark of acclimation to heat. Post intervention, no significant increase in HIF-1a, Hsp72 or EpoR levels was observed in the NG. In contrast, , a significant increase in resting HIF-1a, Hsp72 and EpoR expression (average upregulation of 111%, 29% and 13% respectively) was observed in the HG. HIF-1a targeted pathways are activated by HA in animal studies, and contribute to various tissue protection. HA in human subjects also involves an upregulation of HIF-1a, Hsp72 and EpoR potentially implicating these proteins in the protective pathways associated with HA. Further work is required to investigate these proteins and their protective nature in human tissue.
© Copyright 2009 14th annual Congress of the European College of Sport Science, Oslo/Norway, June 24-27, 2009, Book of Abstracts. Published by The Norwegian School of Sport Sciences. All rights reserved.