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

Williams, Andrew D., Carey, Michael F., Selig, Steve, Hayes, Alan, Krum, Henry, Patterson, Jeremy, Toia, Deidre and Hare, David L. 2007, Circuit resistance training in chronic heart failure improves skeletal muscle mitochondrial ATP production rate—A randomized controlled trial, Journal of cardiac failure, vol. 13, no. 2, pp. 79-85, doi: 10.1016/j.cardfail.2006.10.017.

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Title Circuit resistance training in chronic heart failure improves skeletal muscle mitochondrial ATP production rate—A randomized controlled trial
Author(s) Williams, Andrew D.
Carey, Michael F.
Selig, Steve
Hayes, Alan
Krum, Henry
Patterson, Jeremy
Toia, Deidre
Hare, David L.
Journal name Journal of cardiac failure
Volume number 13
Issue number 2
Start page 79
End page 85
Publisher Elsevier
Place of publication Amsterdam, The Netherlands
Publication date 2007-03
ISSN 1071-9164
1532-8414
Keyword(s) exercise
oxidative capacity
skeletal muscle
Summary 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.
Language eng
DOI 10.1016/j.cardfail.2006.10.017
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2007, Elsevier Inc.
Persistent URL http://hdl.handle.net/10536/DRO/DU:30033449

Document type: Journal Article
Collection: School of Exercise and Nutrition Sciences
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