The response of transverse (T)‐tubules to exercise training in health and disease remains unclear. Therefore, we studied the effect of exercise training on the density and spacing of left ventricle cardiomyocyte T‐tubules in normal and remodeled hearts that associate with detubulation, by confocal laser scanning microscopy. First, exercise training in normal rats increased cardiomyocyte volume by 16% ( P < 0.01), with preserved T‐tubule density. Thus, the T‐tubules adapted to the physiologic hypertrophy. Next, we studied T‐tubules in a rat model of metabolic syndrome with pressure overload‐induced concentric left ventricle hypertrophy, evidenced by 15% ( P < 0.01) increased cardiomyocyte size. These rats had only 85% ( P < 0.01) of the T‐tubule density of control rats. Exercise training further increased cardiomyocyte volume by 8% ( P < 0.01); half to that in control rats, but the T‐tubule density remained unchanged. Finally, post‐myocardial infarction heart failure induced severe cardiac pathology, with a 70% ( P < 0.01) increased cardiomyocyte volume that included both eccentric and concentric hypertrophy and 55% ( P < 0.01) reduced T‐tubule density. Exercise training reversed 50% ( P < 0.01) of the pathologic hypertrophy, whereas the T‐tubule density increased by 40% ( P < 0.05) compared to sedentary heart failure, but remained at 60% of normal hearts ( P < 0.01). Physiologic hypertrophy associated with conserved T‐tubule spacing (∼1.8–1.9 µm), whereas in pathologic hypertrophy, T‐tubules appeared disorganized without regular spacing. In conclusion, cardiomyocytes maintain the relative T‐tubule density during physiologic hypertrophy and after mild concentric pathologic hypertrophy, whereas after severe pathologic remodeling with a substantial loss of T‐tubules; exercise training reverses the remodeling and partly corrects the T‐tubule density. J. Cell. Physiol. 226: 2235–2243, 2011. © 2010 Wiley‐Liss, Inc
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