Circuit resistance training in chronic heart failure improves skeletal muscle mitochondrial ATP production rate - A randomized controlled trial

Background: We aimed to determine the role of skeletal muscle mitochondrial ATP production rate (MAPR) in relation to exercise tolerance after resistance training (RT) in chronic heart failure (CHF). Methods and Results: Thirteen CHF patients (New York Heart Association functional class 2.3 +/- 0.5 Left ventricular ejection fraction 26 +/- 8%; age 70 +/- 8 years) underwent testing for peak total body oxygen consumption (VO2peak), and testing vastus lateralis muscle biopsy. Patients were then randomly allocated to I I weeks of RT (n = 7), or continuance of usual care (C; n = 6), after which testing was repeated. Muscle samples were analyzed for MAPR, metabolic enzyme activity, and capillary density. VO2peak and MAPR in the presence of the pyruvate and malate (P+M) substrate combination, representing carbohydrate metabolism, increased in RT (P < .05) and decreased in C (P < .05), with a significant difference between groups (VO2peak, P = .005; MAPR, P = .03). There was a strong correlation between the change in MAPR and the change in peak total body oxygen consumption (VO2peak) over the study (r = 0.875; P < .0001), the change in MAPR accounting for 70% of the change in VO2peak. Conclusions: These findings suggest that mitochondrial ATP production is a major determinant of aerobic capacity in CHF patients and can be favorably altered by muscle strengthening exercise.