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Abstract

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 (V02pea0, 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.
V02peak 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 (V02peab P = .005; MAPR, P = .03). There was a strong correlation between
the change in MAPR and the change in peak total body oxygen consumption (V02peak) over the study (r =
0.875; P < .0001), the change in MAPR accounting for 70% of the change in V02peak'
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. (J Cardiac
Fail 2007;13:79-85)

Item Type:	Article
Authors/Creators:	Williams, AD and Carey, MF and Selig, S and Krum, H and Hayes, A and Patterson, J and Toia, D and Hare, DL
Journal or Publication Title:	Journal of Cardiac Failure
Publisher:	Elsevier
ISSN:	1071-9164
DOI / ID Number:	10.1016/j.cardfail.2006.10.017
Additional Information:	The definitive version is available at http://www.sciencedirect.com
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