Physical fitness and level of regular exercise are closely related to cardiovascular health. A regimen of regular intensity-controlled treadmill exercise was implemented and withdrawn to identify cellular mechanisms associated with exercise capacity and maximal oxygen uptake (V̇2max).Methods and Results—
Time-dependent associations between cardiomyocyte dimensions, contractile capacity, and V̇2max were assessed in adult rats after high-level intensity-controlled treadmill running for 2, 4, 8, and 13 weeks and detraining for 2 and 4 weeks. With training, cardiomyocyte length, relaxation, shortening, Ca2+ decay, and estimated cell volume correlated with increased V̇2max (r =0.92, −0.92, 0.88, −0.84, 0.73; P <0.01). Multiple regression analysis identified cell length, relaxation, and Ca2+ decay as the main explanatory variables for V O2max (R2 =0.87, P <0.02). When training stopped, exercise-gained V̇2max decreased 50% within 2 weeks and stabilized at 5% above sedentary controls after 4 weeks. Cardiomyocyte size regressed in parallel with V̇2max and remained (9%) above sedentary after 4 weeks, whereas cardiomyocyte shortening, contraction/relaxation- and Ca2+ ransient time courses, and endothelium-dependent vasorelaxation regressed completely within 2 to 4 weeks of detraining. Cardiomyocyte length, estimated cell volume, width, shortening, and Ca2+decay and endothelium-dependent arterial relaxation all correlated with V̇2max (r =.85, 0.84, 0.75, 0.63, −0.54, −0.37; P <0.01). Multiple regression identified cardiomyocyte length and vasorelaxation as the main determinants for regressed V̇2max during detraining (R2 =0.76, P =0.02).Conclusions—
Cardiovascular adaptation to regular exercise is highly dynamic. On detraining, most of the exercise-gained aerobic fitness acquired over 2 to 3 months is lost within 2 to 4 weeks. The close association between cardiomyocyte dimensions, contractile capacity, arterial relaxation, and aerobic fitness suggests cellular mechanisms underlying these changes.