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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #153442
Title: EXERCISE TRAINING ALTERS SKELETAL MUSCLE MITOCHONDRIAL MORPHOMETRY IN HEART FAILURE PATIENTS

Author
item SANTORO, CHERYL - UNIVERSITY OF CONNECTICUT
item COSMAS, ARTHUR - UNIVERSITY OF CONNECTICUT
item FROMAN, DANIEL - BOSTON UNIV MED CENTER
item MORGHAN, ALIA - UNIV OF RHODE ISLAND
item BAIROS, LYNN - TUFTS-HNRCA
item LEVESQUE, SEBRINA - UNIV OF RHODE ISLAND
item ROUBENOFF, RONENN - TUFTS-HNRCA
item HENNESSEY, JAMES - RHODE ISLAND HOSPITAL
item LAMONT, LINDA - UNIV OF RHODE ISLAND
item MANFREDI, THOMAS - UNIV OF RHODE ISLAND

Submitted to: Journal of Cardiovascular Risk
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/16/2002
Publication Date: 9/1/2002
Citation: SANTORO, C., COSMAS, A., FROMAN, D., MORGHAN, A., BAIROS, L., LEVESQUE, S., ROUBENOFF, R., HENNESSEY, J., LAMONT, L., MANFREDI, T. EXERCISE TRAINING ALTERS SKELETAL MUSCLE MITOCHONDRIAL MORPHOMETRY IN HEART FAILURE PATIENTS. JOURNAL OF CARDIOVASCULAR RISK. 2002;9:377-381.

Interpretive Summary: Congestive heart failure is the fastest growing heart disease in the elderly. For many years, it was thought that exercise worsened heart failure by increasing demands on the heart, and that dietary treatment was limited to sodium restriction. We now know that heart failure leads to loss of skeletal muscle ('cardiac cachexia'), and have shown that exercise can improve muscle strength and function, and thus improve the well-being of patients with heart failure and their ability to remain independent. In addition, we have shown that strength training (progressive resistance exercise) can be done by patients with heart failure without any deleterious effects on the heart. In this study, we examined the effect of exercise on skeletal muscle energy metabolism using electron microscopic analysis to determine the effect of exercise on mitochondria. Mitochondria are the cell's energy factories, and an increase in their size suggests that exercise training leads to better muscle function by providing more energy to the muscle cells. Six patients with heart failure were trained for 16 weeks, and showed significant imporovement in exercise capacity and strength. We found 23% increase in average mitochondrial size after 16 weeks of strength training, suggesting that resistance training can increase muscle endurance by enhancing mitochondial size. These results show that even with heart failure, the skeletal muscle can still respond to the positive stimulus of exercise and improve the functional capacity of patients. Exercise treatment should be considered part of the treatment of all patients with heart failure.

Technical Abstract: BACKGROUND: Previous research has demonstrated that exercise intolerance in heart failure patients is associated with significant alterations in skeletal muscle ultrastructure and oxidative metabolism that may be more consequential than cardiac output. DESIGN: To examine the effect of exercise training on skeletal muscle mitochondrial size in chronic heart failure patients. METHODS: Six heart failure patients participated in 16-weeks of supervised upper and lower extremity exercise training. At the conclusion of training, percutaneous needle biopsies of the vastus lateralis were taken and electron microscopy was used to assess mitochondrial sizes. RESULTS: The exercise programme resulted in a significant increase in peak maximal oxygen consumption (P < 0.05) and anaerobic threshold (P < 0.04). Knee extension muscle force increased following training (P < 0.02). After exercise training, the average size of the mitochondria increased by 23.4% (0.036 to 0.046 mu(2), (P < 0.015) and the average shape was unaltered. CONCLUSION: Exercise training with heart failure patients alters skeletal muscle morphology by increasing mitochondrial size, with no change in shape. This may enhance oxidative metabolism resulting in an increased exercise tolerance.