Published Online
on June 1, 2004

A more recent version of this article appeared on June 15, 2004

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Submitted on December 11, 2003
Revised on March 9, 2004
Accepted on March 9, 2004

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

Ole Johan Kemi MSc, Per Magnus Haram BSc, Ulrik Wisløff PhD, and yvind Ellingsen MD, PhD^*

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

^* To whom correspondence should be addressed. E-mail: oyvind.ellingsen{at}medisin.ntnu.no.

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 A regimen of regular intensity-controlled treadmill exercise was implemented and withdrawn to identify cellular mechanisms associated with exercise capacity and maximal oxygen uptake (VO₂max).

Methods and Results--Time-dependent associations between cardiomyocyte dimensions, contractile capacity, and VO₂max 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 VO₂max (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 VO₂max (R²=0.87, P<0.02). When training stopped, exercise-gained VO₂max decreased 50% within 2 weeks and stabilized at 5% above sedentary controls after 4 weeks. Cardiomyocyte size regressed in parallel with VO₂max and remained (9%) above sedentary after 4 weeks, whereas cardiomyocyte shortening, contraction/relaxation- and Ca²⁺-transient 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 VO₂max (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 VO₂max 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.

Key words: exercise • myocytes • hypertrophy • contractility • endothelium

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