In:
Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 100, No. 7 ( 2007-04-13), p. 1079-1088
Kurzfassung:
The extent and mechanism of the cardiac benefit of early exercise training following myocardial infarction (MI) is incompletely understood, but may involve blunting of abnormalities in Ca 2+ -handling and myofilament function. Consequently, we investigated the effects of 8-weeks of voluntary exercise, started early after a large MI, on left ventricular (LV) remodeling and dysfunction in the mouse. Exercise had no effect on survival, MI size or LV dimensions, but improved LV fractional shortening from 8±1 to 12±1%, and LVdP/dt P30 from 5295±207 to 5794±207 mm Hg/s (both P 〈 0.05), and reduced pulmonary congestion. These global effects of exercise were associated with normalization of the MI-induced increase in myofilament Ca 2+ -sensitivity (ΔpCa 50 =0.037). This effect of exercise was PKA-mediated and likely because of improved β 1 -adrenergic signaling, as suggested by the increased β 1 -adrenoceptor protein (48%) and cAMP levels (36%; all P 〈 0.05). Exercise prevented the MI-induced decreased maximum force generating capacity of skinned cardiomyocytes (F max increased from 14.3±0.7 to 18.3±0.8 kN/m 2 P 〈 0.05), which was associated with enhanced shortening of unloaded intact cardiomyocytes (from 4.1±0.3 to 7.0±0.6%; P 〈 0.05). Furthermore, exercise reduced diastolic Ca 2+ -concentrations (by ∼30%, P 〈 0.05) despite the unchanged SERCA2a and PLB expression and PLB phosphorylation status. Importantly, exercise had no effect on Ca 2+ -transient amplitude, indicating that the improved LV and cardiomyocyte shortening were principally because of improved myofilament function. In conclusion, early exercise in mice after a large MI has no effect on LV remodeling, but attenuates global LV dysfunction. The latter can be explained by the exercise-induced improvement of myofilament function.
Materialart:
Online-Ressource
ISSN:
0009-7330
,
1524-4571
DOI:
10.1161/01.RES.0000262655.16373.37
Sprache:
Englisch
Verlag:
Ovid Technologies (Wolters Kluwer Health)
Publikationsdatum:
2007
ZDB Id:
1467838-X