Submitted on May 4, 2007
Accepted on July 31, 2007
Effect of exercise with and without a thermal clamp on the plasma heat shock protein 72 response
Martin Whitham1*, Stewart J. Laing2, Anna Jackson2, Norbert Maassen3, and Neil Peter Walsh1
1 School of Sport, Health and Exercise Sciences, University of Wales Bangor, Bangor, United Kingdom
2 Olympic medical institute, Northwick Park Hospital, London, United Kingdom
3 Medical School Hannover, Sports and Exercise Physiology, Hannover, Germany
* To whom correspondence should be addressed. E-mail: m.whitham{at}bangor.ac.uk.
The contribution of heat and exercise related stress to the release of heat shock protein 72 (HSP72) is currently unknown. The purpose of the present study was to determine the combined and independent effects of heat and exercise on the extracellular (e)HSP72 response. Eleven moderately trained male volunteers (mean ±SD: age 21 ± 4 yr; body mass 75.7 ± 7.7 kg; maximal oxygen uptake (VO2max) 57.8 ± 3.3 ml/kg/min) completed four 2 h, heat manipulated, water immersion trials. Trials were exercise induced heat (EIH: rectal temperature change +2.2°C), clamped exercise (CEX: 0°C), passive heating (PHT: +2.3°C), and control (CON: 0°C). Exercise trials (EIH and CEX) comprised deep water running at 58.5 ± 2.4 and 59.1 ± 1.7 % (VO2max). eHSP72 and catecholamine concentrations were determined by ELISA and HPLC respectively, pre and post immersion. All trials induced an eHSP72 response (P<0.05) with post immersion values significantly greater on EIH compared with other trials (6.0 ± 3.4; CEX 3.8 ± 2.6; PHT 2.7 ± 2.1; CON 2.2 ± 1.9 ng/ml). Exercising with a thermal clamp blunted the eHSP72 response, but post immersion values were also greater than CON. PHT induced a large catecholamine response but post immersion eHsp72 values did not reach significance versus CON. Given that exercising with a thermal clamp evoked a significant increase in plasma eHsp72 concentration, exercise related stressors other than heat appeared influential in stimulating Hsp72 release. Moreover, the catecholamine data from PHT suggest neither epinephrine nor norepinephrine were solely responsible for eHsp72 release.
