Aerobic fitness is associated with cardiomyocyte contractile capacity and endothelial function in exercise training and detraining.
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 A regimen of regular intensity-controlled treadmill exercise was implemented and withdrawn to identify cellular mechanisms associated with exercise capacity and maximal oxygen uptake (VO2max).


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.
Kemi
Ole Johan
OJ
Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway.
Haram
Per Magnus
PM
Wisløff
Ulrik
U
Ellingsen
Øyvind
Ø
D000109:Acetylcholine / Q000494:pharmacology; D000332:Aerobiosis; D000818:Animals; D001835:Body Weight; D002118:Calcium / Q000378:metabolism; D002339:Carotid Arteries / Q000187:drug effects / Q000502:physiology; D048429:Cell Size; D004730:Endothelium, Vascular / Q000502:physiology*; D005260:Female; D006321:Heart / Q000033:anatomy & histology; D009200:Myocardial Contraction; D032383:Myocytes, Cardiac / Q000502:physiology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D009929:Organ Size; D010101:Oxygen Consumption; D010656:Phenylephrine / Q000494:pharmacology; D010805:Physical Conditioning, Animal; D011897:Random Allocation; D051381:Rats; D012420:Running; D014664:Vasodilation / Q000187:drug effects
D009599:Nitroprusside; D010656:Phenylephrine; D000109:Acetylcholine; D002118:Calcium; D019331:NG-Nitroarginine Methyl Ester