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J Appl Physiol (January 31, 2003). doi:10.1152/japplphysiol.00279.2002
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Submitted on April 1, 2002
Accepted on January 24, 2003

Training Induced Changes in Skeletal Muscle Na+ -K+ Pump Number and Isoform Expression in Rats with Chronic Heart Failure

Bryan Helwig1, Katherine M Schreurs1, Joslyn Hansen1, K. S Hageman1, Michael G Zbreski1, Richard M McAllister1, Kathy E Mitchell1, and Timothy I Musch1*

1 Anatomy & Physiology, Kansas State University, Manhattan, KS, USA

* To whom correspondence should be addressed. E-mail: musch{at}vet.ksu.edu.

The mechanisms responsible for the decrements in exercise performance in chronic heart failure (CHF) remain poorly understood, but it has been suggested that sarcolemmal alterations could contribute to the early onset of muscular fatigue. Previously, we demonstrated that the maximal number of ouabain binding sites (Bmax) is reduced in the skeletal muscle of rats with CHF (Musch TI, Wolfram S, Hageman KS, and Pickar JG. J Appl Physiol 92: 2326-2334, 2002). These reductions may coincide with changes in Na+-K+-ATPase isoform ({alpha}and {beta})expression. In the present study, we tested the hypothesis that the reductions in Bmax would coincide with alterations in the {alpha}and {beta}subunit expression of the sarcolemmal Na+-K+-ATPase of rats with CHF. Moreover, we tested the hypothesis that exercise training would increase Bmax along with producing significant changes in {alpha}and {beta}subunit expression. Rats underwent a sham operation (Sham, n=10) or a surgically-induced myocardial infarction followed by random assignment to either a control (MI, n=16) or exercise training group (MI-T, n=16). The MI-T rats performed exercise training (ET) for 6-8 weeks. Hemodynamic indices demonstrated that the MI and MI-T rats suffered from severe left ventricular dysfunction and chronic congestive heart failure. Maximal oxygen uptake (VO2max) and endurance capacity (run time to fatigue) were reduced in MI rats when compared to Sham. Bmax in the soleus and plantaris muscles and the expression of the {alpha}2 isoform of the Na+-K+-ATPase in the red portion of the gastrocnemius (gastrocnemiusred) muscle were reduced in MI rats. In contrast, the expression of the {beta}1 isoform was increased. After ET, VO2max and run time to fatigue were increased in the MI-T group of rats. This coincided with increases in soleus and plantaris Bmax and the expression of the {alpha}2 isoform in the gastrocnemiusred muscle. In addition, the expression of the {beta}2 isoform of the gastrocnemiusred muscle was increased in the MI-T rats when compared to their sedentary counterparts. This study demonstrates that CHF-induced alterations in skeletal muscle Na+-K+-ATPase including Bmax and isoform expression can be partially reversed by ET.




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