Exertional Fatigue Due to Skeletal Muscle Dysfunction in Patients With Heart Failure

BackgroundExertional fatigue in patients with chronic heart failure is usually attributed to skeletal muscle underperfusion. Recently, skeletal muscle atrophy, abnormal muscle metabolic responses, and reduced muscle enzyme levels have been noted in such patients, raising the possibility that some patients may develop muscle fatigue due to intrinsic muscle abnormalities. The present study was undertaken to determine if a subpopulation of patients with heart failure develops exertional fatigue due to skeletal muscle dysfunction rather than to reduced muscle flow. Methods and ResultsAll exercise hemodynamic studies performed in our laboratory on patients with heart failure were reviewed to identify those who exhibited peak exercise V02 levels .18 ml min--1 kg-1 due to leg fatigue and who underwent insertion of a Swan-Ganz catheter and leg blood flow catheter. Thirty-four patients were identified. Six normal subjects were also studied to define normal leg flow and femoral venous lactate responses to exercise. Patients with peak exercise leg flow levels within the normal mean flow level ±2 SEM were considered to have normal skeletal muscle flow during exercise. Nine of the 34 patients with heart failure were found to have normal leg blood flow during exercise. All of these patients terminated exercise due to leg fatigue, and all exhibited abnormal increases in femoral venous lactate concentrations (slope of work load versus femoral venous lactate: normal, 0.33±0.07 mg/W; heart failure with normal flow, 0.81±0.08 mg/W;p<0.002). There was no significant difference between patients with normal leg flows and those with reduced flow in age, ejection fraction, and resting hemodynamic measurements. However, patients with normal flows exhibited more normal cardiac output responses to exercise and tended to have higher peak exercise Vo2 (14.1±0.9 versus 11.5±0.7 ml - min-1 kg-1 p< 0.05). ConclusionA substantial percentage of patients with chronic heart failure develop exertional fatigue due to skeletal muscle dysfunction rather than to reduced skeletal muscle blood flow. In such patients, therapeutic interventions probably should be directed at improving the skeletal muscle abnormalities rather than at improving skeletal muscle flow.

[1]  H. Drexler,et al.  Alterations of Skeletal Muscle in Chronic Heart Failure , 1992, Circulation.

[2]  R. Lenkinski,et al.  Contribution of Skeletal Muscle Atrophy to Exercise Intolerance and Altered Muscle Metabolism in Heart Failure , 1992, Circulation.

[3]  F. Cobb,et al.  Altered Skeletal Muscle Metabolic Response to Exercise in Chronic Heart Failure: Relation to Skeletal Muscle Aerobic Enzyme Activity , 1991, Circulation.

[4]  F. Cobb,et al.  Skeletal muscle biochemistry and histology in ambulatory patients with long-term heart failure. , 1990, Circulation.

[5]  S. Adamopoulos,et al.  Effects of physical training in chronic heart failure , 1990, The Lancet.

[6]  B Chance,et al.  Noninvasive detection of skeletal muscle underperfusion with near-infrared spectroscopy in patients with heart failure. , 1989, Circulation.

[7]  E. Coyle,et al.  Contribution of intrinsic skeletal muscle changes to 31P NMR skeletal muscle metabolic abnormalities in patients with chronic heart failure. , 1989, Circulation.

[8]  M. Higginbotham,et al.  Relation between central and peripheral hemodynamics during exercise in patients with chronic heart failure. Muscle blood flow is reduced with maintenance of arterial perfusion pressure. , 1989, Circulation.

[9]  L. Stevenson,et al.  Prevalence and hemodynamic correlates of malnutrition in severe congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. , 1989, The American journal of cardiology.

[10]  M. Higginbotham,et al.  Exercise training in patients with severe left ventricular dysfunction. Hemodynamic and metabolic effects. , 1988, Circulation.

[11]  S. Frostick,et al.  Skeletal muscle metabolism during exercise under ischemic conditions in congestive heart failure. Evidence for abnormalities unrelated to blood flow. , 1988, Circulation.

[12]  S. Frostick,et al.  Skeletal muscle metabolism in patients with congestive heart failure: relation to clinical severity and blood flow. , 1987, Circulation.

[13]  S. Frostick,et al.  31P nuclear magnetic resonance evidence of abnormal skeletal muscle metabolism in patients with congestive heart failure. , 1987, The American journal of cardiology.

[14]  B. Chance,et al.  Abnormal skeletal muscle bioenergetics during exercise in patients with heart failure: role of reduced muscle blood flow. , 1986, Circulation.

[15]  B. Chance,et al.  Evaluation of energy metabolism in skeletal muscle of patients with heart failure with gated phosphorus-31 nuclear magnetic resonance. , 1985, Circulation.

[16]  J. Wilson,et al.  Exercise intolerance in patients with chronic heart failure: role of impaired nutritive flow to skeletal muscle. , 1984, Circulation.

[17]  C. Honig,et al.  Lactate accumulation in fully aerobic, working, dog gracilis muscle. , 1984, The American journal of physiology.

[18]  P D Gollnick,et al.  Effects of disuse on the structure and function of skeletal muscle. , 1983, Medicine and science in sports and exercise.

[19]  A. Fishman,et al.  Oxygen Utilization and Ventilation During Exercise in Patients with Chronic Cardiac Failure , 1982, Circulation.