Chronic low-intensity interval exercise training attenuated diastolic impairment and preserved myocardial oxygen balance in a swine model of heart failure with preserved ejection fraction.
Does chronic low-intensity interval exercise training improve myocardial oxygen balance and diastolic function in a swine model of HFpEF?
Chronic low-intensity interval exercise training preserves myocardial oxygen balance and improves diastolic function in a large animal model of HFpEF.
Absolute Event Rate: 70% vs 82%
p-value: p=<0.05
We have previously reported chronic low-intensity interval exercise training attenuates fibrosis, impaired cardiac mitochondrial function, and coronary vascular dysfunction in miniature swine with left ventricular (LV) hypertrophy (Emter CA, Baines CP. Am J Physiol Heart Circ Physiol 299: H1348-H1356, 2010; Emter CA, et al. Am J Physiol Heart Circ Physiol 301: H1687-H1694, 2011). The purpose of this study was to test two hypotheses: 1) chronic low-intensity interval training preserves normal myocardial oxygen supply/demand balance; and 2) training-dependent attenuation of LV fibrotic remodeling improves diastolic function in aortic-banded sedentary, exercise-trained (HF-TR), and control sedentary male Yucatan miniature swine displaying symptoms of heart failure with preserved ejection fraction. Pressure-volume loops, coronary blood flow, and two-dimensional speckle tracking ultrasound were utilized in vivo under conditions of increasing peripheral mean arterial pressure and β-adrenergic stimulation 6 mo postsurgery to evaluate cardiac function. Normal diastolic function in HF-TR animals was characterized by prevention of increased time constant of isovolumic relaxation, normal LV untwisting rate, and enhanced apical circumferential and radial strain rate. Reduced fibrosis, normal matrix metalloproteinase-2 and tissue inhibitors of metalloproteinase-4 mRNA expression, and increased collagen III isoform mRNA levels (P < 0.05) accompanied improved diastolic function following chronic training. Exercise-dependent improvements in coronary blood flow for a given myocardial oxygen consumption (P < 0.05) and cardiac efficiency (stroke work to myocardial oxygen consumption, P < 0.05) were associated with preserved contractile reserve. LV hypertrophy in HF-TR animals was associated with increased activation of Akt and preservation of activated JNK/SAPK. In conclusion, chronic low-intensity interval exercise training attenuates diastolic impairment by promoting compliant extracellular matrix fibrotic components and preserving extracellular matrix regulatory mechanisms, preserves myocardial oxygen balance, and promotes a physiological molecular hypertrophic signaling phenotype in a large animal model resembling heart failure with preserved ejection fraction.
Marshall et al. (Sat,) conducted a other in Heart failure with preserved ejection fraction (HFpEF) (n=14). Chronic low-intensity interval exercise training vs. Sedentary heart failure (HF) and sedentary control (Con) was evaluated on Time constant of left ventricular pressure decay (tau, ms) (p=<0.05). Chronic low-intensity interval exercise training attenuated diastolic impairment and preserved myocardial oxygen balance in a swine model of heart failure with preserved ejection fraction.