Circulation, Vol 86, 903-908, Copyright © 1992 by American Heart Association
JR Minotti, P Pillay, L Chang, L Wells and BM Massie
BACKGROUND. Recent research has demonstrated that patients with congestive
heart failure (CHF) exhibit significant functional impairment of skeletal
muscle and that these changes may be important determinants of exercise
capacity. Although muscle strength may be mildly reduced, the most
significant abnormality is markedly enhanced muscle fatigue. The goal of
the present study is to determine whether accelerated fatigue is caused by
impaired muscle activation, as a result of inadequate central motor drive
or neuromuscular transmission, or by a change in the muscle itself. METHODS
AND RESULTS. The study population consisted of nine patients with New York
Heart Association class I-III CHF and eight sedentary, age- and sex-matched
control subjects. Maximal voluntary contraction force of the foot
dorsiflexors (primarily the tibialis anterior) was quantified as a measure
of muscle strength, isometric endurance was quantified by the time required
for force to decline to 60% of maximal during a sustained maximal
contraction, and dynamic endurance was defined as the number of maximal
contractions required for force to decline to 60% of maximal under a
protocol of six repetitions per minute with an incremental duty cycle. The
degree of central motor drive failure was quantified by the degree of force
augmentation produced by a superimposed tetanic stimulus delivered to the
peroneal nerve during the initial maximal voluntary contraction and at the
time when force during the sustained isometric contraction declined to 60%
of maximal. Neuromuscular junction transmission was examined by quantifying
the amplitude of the compound muscle action potential (M wave) in response
to a single nerve stimulus during fatiguing exercise. Muscle strength was
relatively preserved in the CHF patients versus the control subjects (93
+/- 41 versus 105 +/- 34 lb; p = NS), but isometric endurance (time to
decline to 60%, 34 +/- 15 versus 54 +/- 19 seconds; p less than 0.02) and
dynamic endurance (number of repetitions before decline to 60%, 30 +/- 6
versus 43 +/- 7 contractions; p less than 0.001) were both impaired.
Tetanic nerve stimulation increased force by similar degrees in the two
groups, and the amplitude of the M wave did not decline in either group
during exercise. CONCLUSIONS. These findings indicate that enhanced muscle
fatigue in patients with CHF is not caused by impaired central motor drive
or an abnormality of neuromuscular junction transmission but rather by an
abnormality in the muscle itself.
ARTICLES
Neurophysiological assessment of skeletal muscle fatigue in patients with congestive heart failure
Department of Medicine, University of California San Francisco.
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