title: Endurance exercise alters the contractile responsiveness of rat heart to extracellular Na+ and Ca2+.
abstract: OBJECTIVE
  The isovolumic contractile responsiveness of left ventricular (LV) myocardium to altered extracellular [Ca2+], [Na+], and pacing frequency was examined using perfused hearts (37 degrees C) isolated from sedentary (SED) and treadmill-trained (TR) adult female rats.
  
  
  RESULTS
  The suppressive effect of reducing perfusate free [Ca2+] to 0.7 mM on LV developed pressure (delta LVP) was greater in the TR hearts compared with SED hearts (P < 0.05). When perfusate [Na+] was reduced to 120 mM ([Ca2+] = 0.7 mM), delta LVP augmentation was greatest in the TR hearts (P < 0.05). The negative force-frequency relationship observed at physiologic [Ca2+] and [Na+] was progressively altered toward a positive force-frequency relationship with each subsequent change in perfusate [Ca2+] and [Na+] although the effect was greatest in TR hearts (P < 0.05).
  
  
  CONCLUSIONS
  Training elicited a small but significant (P < 0.05) prolongation in the pressure development phase of contraction. Under the physiological [Ca2+], [Na+] perfusion condition, training produced an increase in the magnitude of extrasystolic potentiation of LV pressure, whereas the time constant of mechanical restitution was unaffected. Training affected neither the Ca(2+)-dependence nor the maximal capacity of [3H] ryanodine binding to LV myocardial homogenates. The simplest interpretation of [Na+] and [Ca2+] reduction experiments is that myocardial Ca2+ efflux was augmented by exercise training.
authors.affiliation: Department of Kinesiology and Applied Physiology, University of Colorado, Boulder 80309-0354, USA.
authors.forename: E B
authors.initials: EB
authors.lastname: Lankford
authors.forename: D H
authors.initials: DH
authors.lastname: Korzick
authors.forename: B M
authors.initials: BM
authors.lastname: Palmer
authors.forename: B L
authors.initials: BL
authors.lastname: Stauffer
authors.forename: J Y
authors.initials: JY
authors.lastname: Cheung
authors.forename: R L
authors.initials: RL
authors.lastname: Moore
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology*; D002304:Cardiac Pacing, Artificial; D005260:Female; D006321:Heart / Q000187:drug effects*; D006339:Heart Rate / Q000502:physiology; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology*; D010807:Physical Endurance / Q000502:physiology*; D019275:Radiopharmaceuticals; D051381:Rats; D017207:Rats, Sprague-Dawley; D012433:Ryanodine / Q000378:metabolism; D012964:Sodium / Q000378:metabolism / Q000494:pharmacology*; D013997:Time Factors; D014316:Tritium; D016277:Ventricular Function, Left / Q000187:drug effects; D018879:Ventricular Premature Complexes / Q000503:physiopathology; D017725:Ventricular Pressure / Q000187:drug effects
chemical_list: D019275:Radiopharmaceuticals; D014316:Tritium; D012433:Ryanodine; D012964:Sodium; D002118:Calcium