Aerobic Fitness Is Associated With Cardiomyocyte Contractile Capacity and Endothelial Function in Exercise Training and Detraining

Author:

Kemi Ole Johan1,Haram Per Magnus1,Wisløff Ulrik1,Ellingsen Øyvind1

Affiliation:

1. From the Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway (O.J.K., P.M.H., U.W., Ø.E.), and the Department of Cardiology, St Olav’s Hospital, Trondheim, Norway (U.W., Ø.E.).

Abstract

Background— 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 A regimen of regular intensity-controlled treadmill exercise was implemented and withdrawn to identify cellular mechanisms associated with exercise capacity and maximal oxygen uptake (V̇ o 2 max). Methods and Results— Time-dependent associations between cardiomyocyte dimensions, contractile capacity, and V̇ o 2 max 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, Ca 2+ decay, and estimated cell volume correlated with increased V̇ o 2 max ( r =0.92, −0.92, 0.88, −0.84, 0.73; P <0.01). Multiple regression analysis identified cell length, relaxation, and Ca 2+ decay as the main explanatory variables for V̇ o 2 max ( R 2 =0.87, P <0.02). When training stopped, exercise-gained V̇ o 2 max decreased 50% within 2 weeks and stabilized at 5% above sedentary controls after 4 weeks. Cardiomyocyte size regressed in parallel with V̇ o 2 max and remained (9%) above sedentary after 4 weeks, whereas cardiomyocyte shortening, contraction/relaxation- and Ca 2+ -transient time courses, and endothelium-dependent vasorelaxation regressed completely within 2 to 4 weeks of detraining. Cardiomyocyte length, estimated cell volume, width, shortening, and Ca 2+ decay and endothelium-dependent arterial relaxation all correlated with V̇ o 2 max ( r =0.85, 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 V̇ o 2 max during detraining ( R 2 =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.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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