title: Atrial myocyte function and Ca2+ handling is associated with inborn aerobic capacity.
abstract: BACKGROUND
  Although high aerobic capacity is associated with effective cardiac function, the effect of aerobic capacity on atrial function, especially in terms of cellular mechanisms, is not known. We aimed to investigate whether rats with low inborn maximal oxygen uptake (VO2 max) had impaired atrial myocyte contractile function when compared to rats with high inborn VO2 max.
  
  
  RESULTS
  Atrial myocyte function was depressed in Low Capacity Runners (LCR) relative to High Capacity Runners (HCR) which was associated with impaired Ca(2+) handling. Fractional shortening was 52% lower at 2 Hz and 60% lower at 5 Hz stimulation while time to 50% relengthening was 43% prolonged and 55% prolonged, respectively. Differences in Ca(2+) amplitude and diastolic Ca(2+) level were observed at 5 Hz stimulation where Ca(2+) amplitude was 70% lower and diastolic Ca(2+) level was 11% higher in LCR rats. Prolonged time to 50% Ca(2+) decay was associated with reduced sarcoplasmic reticulum (SR) Ca(2+) ATPase function in LCR (39%). Na(+)/Ca(2+) exchanger activity was comparable between the groups. Diastolic SR Ca(2+) leak was increased by 109%. This could be partly explained by increased ryanodine receptors phosphorylation at the Ca(2+)-calmodulin-dependent protein kinase-II specific Ser-2814 site in LCR rats. T-tubules were present in 68% of HCR cells whereas only 33% LCR cells had these structures. In HCR, the significantly higher numbers of cells with T-tubules were combined with greater numbers of myocytes where Ca(2+) release in the cell occurred simultaneously in central and peripheral regions, giving rise to faster and more spatial homogenous Ca(2+)-signal onset.
  
  
  CONCLUSIONS
  This data demonstrates that contrasting for low or high aerobic capacity leads to diverse functional and structural remodelling of atrial myocytes, with impaired contractile function in LCR compared to HCR rats.
authors.affiliation: K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
authors.forename: Anne Berit
authors.initials: AB
authors.lastname: Johnsen
authors.forename: Natale P L
authors.initials: NP
authors.lastname: Rolim
authors.forename: Tomas
authors.initials: T
authors.lastname: Stølen
authors.forename: Marcia
authors.initials: M
authors.lastname: Alves
authors.forename: Mirta M L
authors.initials: MM
authors.lastname: Sousa
authors.forename: Geir
authors.initials: G
authors.lastname: Slupphaug
authors.forename: Steven L
authors.initials: SL
authors.lastname: Britton
authors.forename: Lauren G
authors.initials: LG
authors.lastname: Koch
authors.forename: Godfrey L
authors.initials: GL
authors.lastname: Smith
authors.forename: Ulrik
authors.initials: U
authors.lastname: Wisløff
authors.forename: Morten A
authors.initials: MA
authors.lastname: Høydal
mesh_terms: D000332:Aerobiosis; D000818:Animals; D020013:Calcium Signaling; D002469:Cell Separation; D003971:Diastole; D006325:Heart Atria / Q000166:cytology*; D009200:Myocardial Contraction / Q000502:physiology; D032383:Myocytes, Cardiac / Q000502:physiology*; D010101:Oxygen Consumption / Q000502:physiology; D010805:Physical Conditioning, Animal; D051381:Rats; D012508:Sarcolemma / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000378:metabolism