[Molecular mechanisms of exercise-induced cardiovascular adaptations. Influence of epigenetics, mechanotransduction and free radicals].

The description of mechanisms underlying exercise-induced heart and vascular bed adaptations reveals and highlights the significance of different mechanical and metabolic stimuli that possibly evoke various short-term and long-term regulations and adaptations of these tissues. In this brief review the molecular mechanisms mediated by free radicals and/or mechanical stimulation and, are therefore involved in the modulation of the extracellular matrix and epigenetics-based regulation of the functional genome will be discussed. In the heart and the vascular bed free radicals play important roles in physiological and pathophysiological processes. Exercise leads on the one hand to increased free radicals but on the other hand improves the antioxidative capacity. This phenomenon shifts the cellular oxidative stress balance and also a variety of signal cascades that mediate physiological and pathophysiological heart and vascular bed adaptations. A similar great significance can be attributed to mechanical stimulation which directly or indirectly influences a variety of signaling cascades. It was demonstrated that exercise alters the molecular composition and architecture of the extracellular matrix which in turn plays an important role in the regulation of different mechanical stimuli-mediating signaling cascades. These alterations in the molecular composition and architecture of the extracellular matrix are of high significance for cellular adaptation processes, possibly also in the sense of epigenetic modulations that are actually only indirectly linked to exercise in cardiovascular tissues. However, there is growing evidence that epigenetic modulations mediated by exercise and physical activity can provoke modifications of the functional genome in heart and vascular beds, comparable to already well-described phenomena, e.g. diet or inflammation.