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Adaptations to Exercise Training

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Coronary Vasculature

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Abstract

Repeated bouts of exercise are widely recognized as a factor that reduces the risk of ischemic heart disease [1–5]. Exercise training (ET) cardiovascular benefits include improved cardiac function and O2 utilization and greater cardiac efficiency associated with a reduced resting heart rate. In patients with coronary heart disease, a 3-month program of exercise conditioning significantly reduced the exercise angina threshold, suggesting an increased myocardial O2 supply [6]. Meta-analysis of 51 studies involving 8,440 patients who participated in exercise-based cardiac rehabilitation programs revealed a 31 % reduction in cardiovascular mortality [7]. Cardiac responses to increased O2 demands depend on both adequate myocardial perfusion and transcapillary exchange at the cellular level [8]. Accordingly, improved O2 delivery to myocardial cells resulting from exercise training could result from biochemical/physiological and/or structural adaptations, which could occur at various levels of the coronary hierarchy. Such adaptations can include several levels of control, e.g. endothelial, neurohumoral, metabolic, and myogenic, as well as at several levels of the coronary hierarchy, i.e. conduit arteries, arterioles, and the capillary bed. This chapter reviews the adaptations that occur in healthy as well as diseased hearts.

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Abbreviations

EC:

Endothelial cell

ET:

Exercise training

LV:

Left ventricle

MI:

Myocardial infarction

NO:

Nitric oxide

RV:

Right ventricle

VEGF:

Vascular endothelial growth factor

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Tomanek, R.J. (2013). Adaptations to Exercise Training. In: Coronary Vasculature. Springer, Boston, MA. https://doi.org/10.1007/978-1-4614-4887-7_8

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