BACKGROUND: Exercise intolerance is the primary chronic symptom in patients with heart failure and preserved ejection fraction (HFPEF), the most common form of heart failure in older persons, and can result from abnormalities in cardiac, vascular, and skeletal muscle, which can be further worsened by physical deconditioning. However, it is unknown whether skeletal muscle abnormalities contribute to exercise intolerance in HFPEF patients. METHODS: This study evaluated lean body mass, peak exercise oxygen consumption (VO2), and the short physical performance battery in 60 older (69 ± 7 years) HFPEF patients and 40 age-matched healthy controls. RESULTS: In HFPEF versus healthy controls, peak percent total lean mass (60.1 ± 0.8% vs. 66.6 ± 1.0%, p < .0001) and leg lean mass (57.9 ± 0.9% vs. 63.7 ± 1.1%, p = .0001) were significantly reduced. Peak VO2 was severely reduced including when indexed to leg lean mass (79.3 ± 18.5 vs. 104.3 ± 20.4 ml/kg/min, p < .0001). Peak VO2 was correlated with percent total (r = .51) and leg lean mass (.52, both p < .0001). The slope of the relationship of peak VO2 with percent leg lean mass was markedly reduced in HFPEF (11 ± 5 ml/min) versus healthy controls (36 ± 5 ml/min; p < .001). Short physical performance battery was reduced (9.9 ± 1.4 vs. 11.3 ± 0.8) and correlated with peak VO2 and total and leg lean mass (all p < .001). CONCLUSION: Older HFPEF patients have significantly reduced percent total and leg lean mass and physical functional performance compared with healthy controls. The markedly decreased peak VO2 indexed to lean body mass in HFPEF versus healthy controls suggests that abnormalities in skeletal muscle perfusion and/or metabolism contribute to the severe exercise intolerance in older HFPEF patients.
BACKGROUND: Exercise intolerance is the primary chronic symptom in patients with heart failure and preserved ejection fraction (HFPEF), the most common form of heart failure in older persons, and can result from abnormalities in cardiac, vascular, and skeletal muscle, which can be further worsened by physical deconditioning. However, it is unknown whether skeletal muscle abnormalities contribute to exercise intolerance in HFPEF patients. METHODS: This study evaluated lean body mass, peak exercise oxygen consumption (VO2), and the short physical performance battery in 60 older (69 ± 7 years) HFPEF patients and 40 age-matched healthy controls. RESULTS: In HFPEF versus healthy controls, peak percent total lean mass (60.1 ± 0.8% vs. 66.6 ± 1.0%, p < .0001) and leg lean mass (57.9 ± 0.9% vs. 63.7 ± 1.1%, p = .0001) were significantly reduced. Peak VO2 was severely reduced including when indexed to leg lean mass (79.3 ± 18.5 vs. 104.3 ± 20.4 ml/kg/min, p < .0001). Peak VO2 was correlated with percent total (r = .51) and leg lean mass (.52, both p < .0001). The slope of the relationship of peak VO2 with percent leg lean mass was markedly reduced in HFPEF (11 ± 5 ml/min) versus healthy controls (36 ± 5 ml/min; p < .001). Short physical performance battery was reduced (9.9 ± 1.4 vs. 11.3 ± 0.8) and correlated with peak VO2 and total and leg lean mass (all p < .001). CONCLUSION: Older HFPEF patients have significantly reduced percent total and leg lean mass and physical functional performance compared with healthy controls. The markedly decreased peak VO2 indexed to lean body mass in HFPEF versus healthy controls suggests that abnormalities in skeletal muscle perfusion and/or metabolism contribute to the severe exercise intolerance in older HFPEF patients.
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