Aim: Previous data have reported increases in HSP72 expression in skeletal muscles after endurance training but the physiological and biochemical signals that induce HSP72 accumulation remain largely unknown. In this study, we tested the hypothesis that energy status is a key regulatory event for HSP72 accumulation in skeletal muscles.
Methods: Reduction of high-energy phosphate levels was induced by supplementation with a creatine analogue, beta-guanidinopropionic acid (GPA) for 3 weeks while control rats received distilled water in the same conditions. Half of the animals were kept sedentary while the others were submitted to a short-term (2 weeks) training program on a treadmill (30 m min-1, 0% slope; 50-70 min day-1).
Results: GPA supplementation resulted in a large drop ( approximately 50%) in adenosine triphosphate (ATP) level in both fast and slow muscles whether the animals were trained or remained sedentary. HSP72 level did not change with GPA alone, but the training-induced increase in HSP72 level was strongly enhanced by superimposition of GPA diet in fast but not in slow skeletal muscles. The changes in HSP72 level were not linked to changes in fibre typology and/or mitochondrial capacities.
Conclusions: The results of the present investigation indicate that levels of high-energy phosphate per se do not play a direct role in determining HSP72 level in skeletal muscles. However, during superimposition of training to GPA, then the adaptive strategy of fast-twitch muscle (e.g. plantaris) seems to be directed towards appearance of some properties of red, oxidative fibres (increase in oxidative capacities and HSP72 level).