Circulation, Vol 87, 470-475, Copyright © 1993 by American Heart Association
JR Wilson, DM Mancini and WB Dunkman
BACKGROUND. Exertional 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 RESULTS. All exercise hemodynamic studies performed in our
laboratory on patients with heart failure were reviewed to identify those
who exhibited peak exercise VO2 levels < or = 18 ml.min-1 x 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 x kg-1, p <
0.05). CONCLUSIONS. A 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.
ARTICLES
Exertional fatigue due to skeletal muscle dysfunction in patients with heart failure
Cardiology Division, Hospital of the University of Pennsylvania, Philadelphia 19104-4283.
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