title: Aerobic fitness is associated with cardiomyocyte contractile capacity and endothelial function in exercise training and detraining.
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 A regimen of regular intensity-controlled treadmill exercise was implemented and withdrawn to identify cellular mechanisms associated with exercise capacity and maximal oxygen uptake (VO2max).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.
authors.affiliation: Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway.
authors.forename: Ole Johan
authors.initials: OJ
authors.lastname: Kemi
authors.forename: Per Magnus
authors.initials: PM
authors.lastname: Haram
authors.forename: Ulrik
authors.initials: U
authors.lastname: Wisløff
authors.forename: Øyvind
authors.initials: Ø
authors.lastname: Ellingsen
mesh_terms: 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
chemical_list: D009599:Nitroprusside; D010656:Phenylephrine; D000109:Acetylcholine; D002118:Calcium; D019331:NG-Nitroarginine Methyl Ester