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

• Published in: Journal of cardiac failure Vol. 13; no. 2; pp. 79 - 85
• Main Authors: Williams, Andrew D., PhD, Carey, Michael F., PhD, Selig, Steve, PhD, Hayes, Alan, PhD, Krum, Henry, MB, BS, PhD, FRACP, Patterson, Jeremy, PhD, Toia, Deidre, BSc, Hare, David L., MB, BS, DPM, FRACP
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.03.2007
• Subjects: Adenosine Triphosphate - biosynthesis; Aged; Biopsy; Cardiovascular; Exercise; Exercise Test; Exercise Therapy - methods; Female; Heart Failure - metabolism; Heart Failure - physiopathology; Humans; Male; Middle Aged; Mitochondria, Muscle - metabolism; Mitochondria, Muscle - pathology; Muscle, Skeletal - metabolism; Muscle, Skeletal - pathology; Muscle, Skeletal - physiopathology; Oxidative capacity; Oxidative Stress; Patient Compliance; Skeletal muscle; Treatment Outcome; Skeletal muscle; Exercise; Oxidative capacity
• ISSN: 1071-9164; 1532-8414
• DOI: 10.1016/j.cardfail.2006.10.017

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 (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.