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 (P), 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 aged-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 < .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. Circulation 73, No. 6, 1127-1136, 1986 PATIENTS with chronic heart failure are frequently limited by exertional fatigue.",2 This fatigue is typically associated with abnormally elevated blood lactate levels, suggesting that altered muscle metabolism may be responsible." 2 Therefore, we recently sought to investigate muscle metabolism in patients with heart failure using phosphorous nuclear magnetic resonance (NMR)

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Blood flow to working skeletal muscle is frequently reduced in patients with heart failure or peripheral vascular disease. To determine if phosphorus nuclear magnetic resonance (NMR) can noninvasively detect such muscle underperfusion, gated phosphorus-31 NMR spectroscopy was used to compare muscle inorganic phosphate, phosphocreatine and pH during mild wrist flexion exercise at 0.2, 0.4 and 0.6 W in eight normal men, before and after reduction of forearm blood flow. Forearm flow was reduced by cuff inflation to a pressure determined by Doppler ultrasound to bring flow to 40 to 60% of control. Attention was focused on the inorganic phosphate to phosphocreatine (Pi/PCr) ratio and pH, two variables potentially sensitive to muscle oxygen delivery. At rest with normal flow, Pi/PCr averaged 0.12 +/- 0.03 and pH averaged 7.02 +/- 0.04. Exercise produced a progressive increase in Pi/PCr (0.2 W = 0.43 +/- 0.12; 0.4 W = 0.75 +/- 0.31; 0.6 W = 1.04 +/- 0.47) and a modest decrease in pH (0.2 W = 6.94 +/- 0.04; 0.4 W = 6.86 +/- 0.18; 0.6 W = 6.85 +/- 0.06). Flow reduction had no effect on Pi/PCr or pH at rest. In contrast, flow reduction during exercise was associated with higher Pi/PCr at all three work loads (0.2 W = 0.60 +/- 0.27; 0.4 W = 0.99 +/- 0.50; 0.6 W = 2.00 +/- 1.26 [all p less than 0.05 versus normal flow]) and lower pH (0.2 W = 6.78 +/- 0.12; 0.4 W = 6.69 +/- 0.23; 0.6 W = 6.65 +/- 0.30 [p less than 0.01 versus normal flow at 0.2 and 0.4 W; p = 0.05 at 0.6 W]).(ABSTRACT TRUNCATED AT 250 WORDS)