Circulation, Vol 84, 2034-2039, Copyright © 1991 by American Heart Association
DA Sterns, SM Ettinger, KS Gray, SK Whisler, TJ Mosher, MB Smith and LI Sinoway
BACKGROUND. Resting sympathetic nervous system activity is increased in
heart failure. Whether sympathetic nervous system responses during exercise
are increased is controversial. Furthermore, the role of muscle
metaboreceptors and central command in regulating sympathetic outflow has
been largely unexplored. METHODS AND RESULTS. Muscle sympathetic nerve
activity (MSNA, peroneal nerve) was measured in nine heart failure subjects
and eight age-matched control subjects during static exercise (30% maximal
voluntary contraction) for 2 minutes and during a period of posthandgrip
regional circulatory arrest. This maneuver isolates the metaboreceptor
contribution to sympathetic nervous system responses. MSNA responses were
similar during static exercise in the two groups. During posthandgrip
regional circulatory arrest we observed a marked attenuation in MSNA
responses in the heart failure subjects (15% increase in heart failure
versus 57% increase in control subjects). A cold pressor test demonstrated
a normal MSNA response to a potent nonspecific stimulus in the heart
failure subjects (heart failure subjects, 141% increase; control subjects,
215% increase; NS). Nuclear magnetic resonance spectroscopy studies in five
separate heart failure subjects and five control subjects suggested that
the attenuated metaboreceptor response in heart failure was not due to
reduced H+ production. CONCLUSIONS. Skeletal muscle metaboreceptor
responses are impaired in heart failure. Because MSNA responses during
static exercise are similar in the two groups, mechanisms aside from
metaboreceptor stimulation must be important in increasing sympathetic
nervous system activity.
ARTICLES
Skeletal muscle metaboreceptor exercise responses are attenuated in heart failure
Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.
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