Circulation, Vol 73, 1127-1136, Copyright © 1986 by American Heart Association
DH Wiener, LI Fink, J Maris, RA Jones, B Chance and JR Wilson
Using phosphorous nuclear magnetic resonance, we have previously
demonstrated that patients with heart failure often exhibit abnormal
forearm muscle metabolism during forearm exercise. To determine if this
altered metabolism is due to reduced muscle flow, we measured forearm blood
flow with plethysmography and forearm muscle inorganic phosphate (Pi),
phosphocreatine (PCr), and pH with 31P nuclear magnetic resonance
spectroscopy at rest and during mild forearm exercise (0.2, 0.4, and 0.6 W)
in 21 men with heart failure and in 12 age-matched normal male subjects.
The Pi/PCr ratio was correlated with power output and the slope of this
relationship was used as an index of forearm metabolism. At rest, both
groups had similar Pi/PCr ratios (normal subjects 0.11 +/- 0.05; patients
with heart failure 0.11 +/- 0.03; p = NS) and forearm blood flows (normal
subjects 2.9 +/- 1.4 ml/min/100 ml; patients with heart failure 2.6 +/- 1.2
ml/min/100 ml; p = NS). In both groups, exercise resulted in a progressive
increase in both Pi/PCr and forearm blood flow as power output increased.
However, the patients exhibited a steeper slope of the Pi/PCr-to-power
output relationship than did the normal subjects (normal subjects 1.4 +/-
0.6 Pi/PCr U/W; patients with heart failure 3.0 +/- 2.4 Pi/PCr U/W; p less
than .03). In contrast, forearm blood flow was similar in both groups
during exercise (at 0.2 W, 6.3 +/- 3.3 and 6.8 +/- 3.2 ml/min/100 ml in
normal subjects and patients with heart failure, respectively; at 0.4 W,
8.7 +/- 6.5 and 8.3 +/- 3.3; at 0.6 W, 12.8 +/- 7.9 and 12.0 +/- 4.6; all p
= NS). Nine of the 21 patients with heart failure had slopes of the
Pi/PCr-to-power output relationship above the normal range. These nine
patients also had forearm blood flows comparable to flows observed in the
normal subjects. These data indicate that forearm muscle metabolism during
forearm exercise is altered in a subpopulation of patients with heart
failure. This metabolic alteration does not appear to be due to decreased
muscle blood flow, suggesting that other mechanisms, such as alterations in
mitochondrial population or substrate utilization, may be responsible.
ARTICLES
Abnormal skeletal muscle bioenergetics during exercise in patients with heart failure: role of reduced muscle blood flow
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