Résumé
Intense physical practices like marathon or triathlon result in transient left ventricular (LV) dysfunction, characterized by transient reduction of LV diastolic relaxation without changes in systolic function by unknown mechanisms. Our study aimed to investigate in vivo and in vitro the involvement of known regulators of diastolic function such as eNOS and oxidative stress signalling pathways in a rat model. Wistar rats experienced prolonged exhaustive exercise (PEE) (3 hours; 65% of maximal aerobic velocity), in association or not with an antioxidant treatment (N-acetylcysteine, 50mg.kg-1, i.p.). Systolic cardiac function evaluated in vivo by echocardiography and ex vivo in Langendorff isolated heart was unchanged by PEE, while parameters of diastolic function were severely altered. At the cellular level, PEE had no effect on myofilament calcium sensitivity, TnI expression and phosphorylation. However, PEE was associated with marked alteration of calcium handling during contraction. The amplitude of calcium transient was reduced in PEE hearts when compared to Ctrl ones and both Tau and time to baseline50 (TTBl50), two indexes reflecting the kinetic of Ca2+ reuptake by the SR were increased by PEE. Finally, an interesting point is that antioxidant treatment with NAC during PEE totally prevents the alteration of the diastolic function. To conclude, the present results show that PEE induced oxidative stress that targeted preferentially calcium handling rather than myofilaments, and may be responsible for transient diastolic dysfunction.