Circulation, Vol 69, 1079-1087, Copyright © 1984 by American Heart Association
JR Wilson, JL Martin, D Schwartz and N Ferraro
The maximal exercise capacity of patients with chronic heart failure is
frequently reduced. To investigate whether this exercise intolerance is
caused by inadequate nutritive flow to skeletal muscle, we compared cardiac
outputs, leg blood flow, and leg metabolism during maximal bicycle exercise
in seven patients with normal maximal oxygen uptake (VO2) (greater than 20
ml/min/kg; group A), eight patients with heart failure and moderately
reduced maximal VO2 (15 to 18 ml/min/kg; group B), and eight patients with
heart failure and markedly reduced maximal VO2 (less than 14 ml/min/kg;
group C). As the severity of exercise intolerance increased from group A to
group C there was a progressive decline in cardiac output and leg blood
flow at any given workload accompanied by a progressive decline in maximal
cardiac output (liters/min) (A, 12.4 +/- 1.0; B, 8.7 +/- 0.9; C, 5.5 +/-
0.7), maximal leg flow (liters/min) (A, 4.0 +/- 0.3; B, 2.6 +/- 0.4; C, 1.4
+/- 0.2), and maximal leg VO2 (ml/min) (A, 564 +/- 49; B, 403 +/- 41; C,
213 +/- 35 ml/min). All patients terminated exercise because of severe leg
fatigue. At termination of exercise, all three groups exhibited similar
marked levels of leg O2 extraction (%) (A, 80 +/- 2; B, 83 +/- 3; C, 89 +/-
1) and high femoral-arterial lactate gradients (mg/dl) (A, 15.4 +/- 2.6; B,
18.3 +/- 3.5; C, 19.2 +/- 3.6), suggesting that exercise was limited when a
critical level of muscle underperfusion was reached. These data suggest
that the reduced maximal exercise capacity of patients with chronic heart
failure is primarily due to impaired nutritive flow to skeletal muscle and
resultant muscular fatigue.
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Exercise intolerance in patients with chronic heart failure: role of impaired nutritive flow to skeletal muscle
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