Exercise intolerance in patients with chronic heart failure: role of impaired nutritive flow to skeletal muscle.

John R. Wilson, Jack L. Martin, David E. Schwartz, Nancy Ferraro

Circulation · 1984 · 451 citations · 20 references

Concepts

TL;DR

Patients with chronic heart failure frequently have reduced maximal exercise capacity. The study sought to determine whether impaired nutritive flow to skeletal muscle causes exercise intolerance by comparing cardiac output, leg blood flow, and leg metabolism during maximal bicycle exercise in patients with normal, moderately reduced, and markedly reduced VO₂. Researchers measured cardiac output, leg blood flow, and leg metabolism during maximal bicycle exercise in seven patients with normal VO₂, eight with moderate reduction, and eight with marked reduction. They observed that worsening exercise intolerance was associated with progressive declines in cardiac output, leg blood flow, and maximal leg VO₂, all patients stopped due to leg fatigue, and similar high leg O₂ extraction and lactate gradients suggested that exercise was limited by critical muscle underperfusion, confirming that impaired nutritive flow to skeletal muscle underlies reduced maximal exercise capacity in chronic heart failure.

Abstract

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.

References

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