Circulation, Vol 78, 320-326, Copyright © 1988 by American Heart Association
BM Massie, M Conway, B Rajagopalan, R Yonge, S Frostick, J Ledingham, P Sleight and G Radda
Previous studies with 31P nuclear magnetic resonance have demonstrated that
patients with chronic congestive heart failure often exhibit increased
glycolytic metabolism and impaired oxidative phosphorylation in exercising
skeletal muscle, but the mechanism for these changes remains unresolved.
This study was conducted to determine whether these abnormalities result
from impaired blood flow or oxygen delivery. Nine patients with
mild-to-moderate congestive heart failure and nine age- and size-matched,
healthy control volunteers were studied during repetitive submaximal finger
flexion exercise under aerobic and ischemic conditions. Skeletal muscle
metabolism was assessed by 31P nuclear magnetic resonance of the flexor
digitorum superficialis muscle. During steady-state aerobic exercise at 33%
of each subject's predetermined maximum workload, the patients with
congestive heart failure exhibited significantly lower pH values (6.65 +/-
0.22 vs. 6.97 +/- 0.09, p less than 0.002) and phosphocreatine
concentrations, expressed as [phosphocreatine]/([phosphocreatine] +
[inorganic phosphate]) (0.59 +/- 0.14 vs. 0.79 +/- 0.08, p less than
0.002). Similar differences were also present throughout ischemic exercise
at the same workload. Based upon these measurements, calculated lactate
production and adenosine 5'-triphosphate consumption rates were
significantly higher in the patients with congestive heart failure. These
results indicate that in many patients with congestive heart failure
exercising muscle exhibits increased glycolytic metabolism and appears to
be metabolically less efficient in relation to external work performed.
These changes cannot be explained by impaired blood flow or oxygen delivery
alone.
ARTICLES
Skeletal muscle metabolism during exercise under ischemic conditions in congestive heart failure. Evidence for abnormalities unrelated to blood flow
Department of Biochemistry, Nuffield Department of Medicine, Oxford, United Kingdom.
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