Circuit Resistance Training in Chronic Heart Failure Improves Skeletal Muscle Mitochondrial ATP Production Rate-A Randomized Controlled Trial

Andrew D Williams, Michael F Carey, Steven Selig, Alan Hayes, Henry Krum, Jeremy Patterson, Deidre Toia, David Hare

Research output: Contribution to journalArticleResearchpeer-review

50 Citations (Scopus)


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.
Original languageEnglish
Pages (from-to)79 - 85
Number of pages7
JournalJournal of Cardiac Failure
Issue number2
Publication statusPublished - 2007

Cite this