Circulation, Vol 80, 1338-1346, Copyright © 1989 by American Heart Association
DM Mancini, E Coyle, A Coggan, J Beltz, N Ferraro, S Montain and JR Wilson
Patients with heart failure frequently exhibit abnormal skeletal muscle
metabolic responses to exercise, as assessed with 31P NMR. To investigate
whether these metabolic abnormalities are due to intrinsic skeletal muscle
changes, we performed gastrocnemius muscle biopsies on 22 patients with
heart failure (peak VO2, 15.4 +/- 4.7 ml/kg/min; ejection fraction, 20 +/-
7%) and on eight normal subjects. Biopsies were analyzed for fiber type and
area, capillarity, citrate synthase, phosphofructokinase, lactate
dehydrogenase, and beta-hydroxyacyl CoA dehydrogenase activity. All
patients with heart failure also underwent 31P NMR studies of their calf
muscle during plantarflexion at three workloads. Muscle pH responses and
the relation of the ratio of inorganic phosphate to phosphocreatine
(Pi/PCr) to systemic VO2 were then evaluated. Compared with normal
subjects, patients with heart failure exhibited a shift in fiber
distribution with increased percentage of the fast twitch, glycolytic,
easily fatigable type IIb fibers (normal subjects, 22.7 +/- 10.1; heart
failure, 33.1 +/- 11.1%; p less than 0.05), atrophy of type IIa (normal
subjects, 5,477 +/- 1,109; heart failure, 4,239 +/- 1,247 microns 2; p less
than 0.05) and type IIb fibers (normal subjects, 5,957 +/- 1,388; heart
failure, 4,144 +/- 945 microns 2; p less than 0.01), and decreased activity
of beta- hydroxyacyl CoA dehydrogenase (normal subjects, 5.17 +/- 1.44;
heart failure, 3.67 +/- 1.68 mol/kg protein/hr; p less than 0.05). No
significant linear correlation could be identified between the slope of the
Pi/PCr to VO2 relation and muscle histochemistry or enzyme activities.
Similarly, no linear relation was found between intracellular pH at peak
exercise and any muscle variable.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Contribution of intrinsic skeletal muscle changes to 31P NMR skeletal muscle metabolic abnormalities in patients with chronic heart failure
Department of Medicine, University of Pennsylvania, Philadelphia 19104.
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