Abstract
1231 PURPOSE: Maximal oxygen uptake (VO2max) is linked to cardiovascular health. However, the contribution of cardiomyocyte dimension and contractility and endothelial function to increased and decreased VO2max has yet to be defined. Thus, we investigated the relationship between VO2max and the cellular features of the heart and artery. METHODS: Time-dependent relationships between VO2max and cardiomyocyte hypertrophy and contractility were investigated after high-intensitycontrolled treadmill-running for 2–13 weeks, detraining for 2 and 4 weeks, or sedentary controls. Endothelial-dependent carotid artery relaxation was also determined in detraining. RESULTS: With training, cardiomyocyte length, relaxation, shortening, Ca2+ decay and volume correlated with increased VO2max (r = 0.92, −0.92, 0.88, −0.84, 0.73; p<0.01); multiple regression identifying cell length, relaxation and Ca2+ decay as the main explanatory variables (87%) for VO2max. With detraining, exercise-gained VO2max decreased 50% within 2 weeks, and stabilized 5% above sedentary after 4 weeks. Multiple regression identified cardiomyocyte length and vasorelaxation as the main determinants (76%) for regressed VO2max. However, cardiomyocyte length, volume, width, shortening and Ca2+ decay, and vasorelaxation all correlated with VO2max (r = 0.85, 0.84, 0.75, 0.63, −0.54, −0.37; p<0.01). Cardiomyocyte size regressed in line with VO2max with detraining; thus remained above sedentary after 4 weeks, whereas cardiomyocyte shortening, contraction/relaxation- and Ca2+-transient timecourses, and endothelial-dependent vasorelaxation regressed completely within 2 weeks of detraining. CONCLUSIONS: This is the first study clarifying the cellular contributions for altered VO2max during training and detraining. Furthermore, cardiomyocyte size, contractility, Ca2+ handling, and arterial endothelial function need 1–2 months of exercise to plateau, but only 2–4 weeks to vanish.
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