Intrinsic changes in skeletal muscle are being increasingly suspected as pa
rt of the underlying cause of exercise intolerance in patients with chronic
heart failure (CHF). The objective of the present study was to determine w
hether differences existed between CHF patients and age-matched healthy con
trols in the concentration of skeletal muscle Na+-K+-ATPase (adenosine trip
hosphatase), a cation pump that functions to restore Na+-K+ gradients and p
rotect membrane excitability. Moreover, given the potency for physical acti
vity in altering long-term regulation of the pump, an additional objective
was to examine the role of activity level in pump expression in CHF patient
s. Na+-K+-ATPase concentration (pmol/g wet wt) determined in the vastus lat
eralis muscle of 27 CHF mates (ejection fraction, 23 +/-1.6%), using the va
nadate facilitated [H-3] ouabain binding technique, was not different (264
+/- 10) from 10 sedentary controls (268 +/-: 19, P > 0.05). Similarly, no d
ifferences (P > 0.05) could be found between female patients (228 +/- 16, n
= 7) and controls (243 +/- 13, n = 9). Differences between untrained contr
ol (294 +/- 20, n = 7), chronically active (251 +/- 20, n = 9), and trained
(252 +/- 16, n = 6) CHF groups in Na+-K+ pump expression were also insigni
ficant. This study indicates that long-term regulation of Na+-K+-ATPase con
centration is not altered in moderate CHF patients, regardless of the histo
ry of regular activity. However, the positive correlations (P < 0.05) that
were observed between peak aerobic power ((V) over dot O-2 peak) and Na+-K-ATPase (r = 0.422) and (V) over dot O-2 peak and maximal citrate synthase
activity (r= 0.404) suggests a role for the skeletal muscle in explaining e
xercise intolerance in CHF patients. (C) 2001 John Wiley & Sons, Inc.