Patients with chronic heart failure (CHF) report difficulty performing activities of daily living. To our knowledge, however, no study has directly measured performance in activities of daily living in these patients to systematically assess their level of physical disability. Moreover, the contribution of skeletal muscle weakness to physical disability in CHF remains unclear. Thus, we measured performance in activities of daily living in CHF patients and controls, its relationship to aerobic capacity and muscle strength, and the effect of resistance exercise training to improve muscle strength and physical disability.
Patients and controls were assessed for performance in activities of daily living, self-reported physical function, peak aerobic capacity, body composition, and muscle strength before and after an 18-wk resistance training program. To remove the confounding effects of several disease-related factors (muscle disuse, hospitalization, acute illness), we recruited controls with similar activity levels as CHF patients and tested patients >6 months after any disease exacerbation/hospitalization.
Performance in activities of daily living was 30% lower (P < 0.05) in CHF patients versus controls and was related to both reduced aerobic capacity (P < 0.001) and muscle strength (P < 0.01). Moreover, resistance training improved (P < 0.05 to P < 0.001) physical function and muscle strength in patients and controls similarly, without altering aerobic capacity.
CHF patients are characterized by marked physical disability compared with age- and physical activity-matched controls, which is related to reduced aerobic capacity and muscle strength. CHF patients respond to resistance training with normal strength/functional adaptations. Our results support muscle weakness as a determinant of physical disability in CHF and show that interventions that increase muscle strength (resistance training) reduce physical disability.
1Department of Medicine, College of Medicine, University of Vermont, Burlington, VT; and 2Department of Molecular Physiology and Biophysics, College of Medicine, University of Vermont, Burlington, VT
Address for correspondence: Michael J. Toth, Ph.D., Health Science Research Facility 126B, 149 Beaumont Ave., University of Vermont, Burlington, VT 05405; E-mail: email@example.com.
Submitted for publication December 2010.
Accepted for publication January 2011.