Ehte Orlova

ABSTRACT Endurance training is a widely practised physical exercise modality aimed at increasing the aerobic working capacity. This review discusses the current state-of-the-art in research on the mechanisms of the exercise-induced quantitative and qualitative alterations in mitochondrial biogenesis and intracellular energy transfer in cardiac and skeletal muscle cells. The data show that endurance training exerts a permissive effect on biogenesis of mitochondria through stimulating multiple pathways converging at activation of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). These pathways are mediated by stress hormones (glucocorticoids and catecholamines), p38 mitogen-activated protein kinase (MAPK), class III histone deacylases (SIRT1 and SIRT3), cyclic nucleotide regulatory binding protein (CREB), p53 tumor suppressor protein, and AMP-activated protein kinase (AMPK). As a result, oxidative capacity of cardiac and skeletal muscle cells increases to cope with enhanced ATP turnover. In parallel, exercise induces significant changes in intrinsic properties of mitochondria expressed as suppressed capacity to produce ROS and resistance to permeability transition and apoptotic signals. These effects of training enable to protect myocardium by attenuating the decay in cardiac function in conditions of ischemic heart disease, heart failure, diabetes, and obesity. The beneficial effects of endurance training disappear in conditions of application of excessive training volumes which results in overtraining syndrome (OTS) characterized by skeletal and cardiac muscle damage and suppression of oxidative energy metabolism. Therefore, establishing criteria for early detection of development of OTS to avoid associated harmful impact on organism is of ultimate importance.

The present study was undertaken to characterize and review the changes in energy metabolism in rat myocardium in response to chronic exhaustive exercise. It was shown that a treadmill exercise program applied for six weeks led the rats into a state characterized by decreased performance, loss of body weight and enhanced muscle catabolism, indicating development of overtraining syndrome. Electron microscopy revealed disintegration of the cardiomyocyte structure, cellular swelling and appearance of peroxisomes. Respirometric assessment of mitochondria in saponin-permeabilized cells in situ revealed a decreased rate of oxidative phosphorylation (OXPHOS) due to diminished control over it by ADP and impaired functional coupling of adenylate kinase to OXPHOS. In parallel, reduced tissue content of cytochrome c was observed, which could limit the maximal rate of OXPHOS. The results are discussed with respect to relationships between the volume of work and corresponding energy metabolism. ...