Abstract
Previous studies have shown that acute exercise preconditions the myocardium from ischemic injury. The purpose of this study was to test whether acute exercise protects the hypertensive myocardium from ischemia-induced diastolic rigor, and to compare the response between normotensive and uncompensated hypertensive hearts. Hearts harvested from female Wistar-Kyoto (WKY; n = 24) and spontaneously hypertensive rats (SHR; n = 27) (age:10–12 weeks) were exposed to ischemia (Langendorff isovolumic preparation; 22 minutes of no flow ischemia and studied following prior conditions of: 1) no exercise (WKY-CON, n=8; SHR-CON, n=8); 2) ischemia initiated one hour post-acute exercise (WKY-1HR, n = 8; SHR-1HR, n = 11); and 3) ischemia initiated 24 hours post-acute exercise (WKY-24HR; n = 8; SHR-24HR, n = 8). Acute exercise consisted of one bout of treadmill running at 25 m/min for 60 minutes. Heart weight was similar between WKY and SHR despite elevated in vivo resting systolic blood pressure and rate pressure product in SHR (P<0.05). During normoxic perfusion, left ventricular (LV) Langendorff performance was similar between WKY and SHR over the post-exercise time course. However, during ischemia, LV diastolic rigor was less in WKY vs. SHR (P<0.05). Acute exercise augmented ischemia-induced LV dysfunction one hour post-exercise in SHR (P<0.05), with gradual recovery by 24 hours post-exercise. These data suggest that acute exercise promotes ischemic diastolic rigor in SHR, even prior to the development of cardiac hypertrophy.
Highlights
There are numerous cardiovascular health benefits associated with regular participation in exercise and physical activity
After 60 minutes of exercise, systolic blood pressures (SBP) in SHR remained significantly greater compared to WKY (P
Heart weight (HW), HW/body weight (BW) ratio, tibial length (TL) and HW/TL were similar between groups
Summary
There are numerous cardiovascular health benefits associated with regular participation in exercise and physical activity. Strenuous exercise in humans has been shown to promote cardiac fatigue (Oxbourough et al 2010; Starnes and Bowles 1995; Scharag et al 2008) and tissue damage in the heart (George et al 2004) with several studies showing transient cardiac functional decrements (Dawson et al 2007) and increased plasma concentrations of cardiac-specific troponins following exercise (George et al 2004; Urhausen et al 2004; Trivax et al 2010). The literature suggests that acute aerobic exercise elicits various reponses, with cardioprotection juxtaposed to temporal periods of cardiac dysfunction/damage
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