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Mechanisms of exercise‐induced improvements in the contractile apparatus of the mammalian myocardium
Author(s) -
Kemi O. J.,
Wisløff U.
Publication year - 2010
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2010.02132.x
Subject(s) - endurance training , cardiology , heart failure , medicine , myocardial infarction , vo2 max , aerobic exercise , cardiac function curve , training effect , physical exercise , heart disease , cardiovascular physiology , physical medicine and rehabilitation , physical therapy , training (meteorology) , heart rate , physics , meteorology , blood pressure
One of the main outcomes of aerobic endurance exercise training is the improved maximal oxygen uptake, and this is pivotal to the improved work capacity that follows the exercise training. Improved maximal oxygen uptake in turn is at least partly achieved because exercise training increases the ability of the myocardium to produce a greater cardiac output. In healthy subjects, this has been demonstrated repeatedly over many decades. It has recently emerged that this scenario may also be true under conditions of an initial myocardial dysfunction. For instance, myocardial improvements may still be observed after exercise training in post‐myocardial infarction heart failure. In both health and disease, it is the changes that occur in the individual cardiomyocytes with respect to their ability to contract that by and large drive the exercise training‐induced adaptation to the heart. Here, we review the evidence and the mechanisms by which exercise training induces beneficial changes in the mammalian myocardium, as obtained by means of experimental and clinical studies, and argue that these changes ultimately alter the function of the whole heart and contribute to the changes in whole‐body function.