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 resting vastus lateralis muscle biopsy. Patients were then randomly allocated to 11 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. © 2007 Elsevier Inc. All rights reserved.

Item Type:	Refereed Article
Research Division:	Biomedical and Clinical Sciences
Research Group:	Cardiovascular medicine and haematology
Research Field:	Cardiology (incl. cardiovascular diseases)
Objective Division:	Health
Objective Group:	Clinical health
Objective Field:	Clinical health not elsewhere classified
UTAS Author:	Williams, AD (Associate Professor Andrew Williams)
ID Code:	41198
Year Published:	2007
Web of Science® Times Cited:	55
Deposited By:	Health Sciences A
Deposited On:	2007-08-01
Last Modified:	2009-08-25
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