Purpose: Patients with chronic heart failure (CHF) typically complain about skeletal muscle fatigue. In rat experiments, reduced intracellular calcium release seems to be related to fatigue development in normal skeletal muscle but not in muscle from rats with CHF. We therefore hypothesize that training may not improve intracellular calcium cycling to the same extent in muscles from patients with CHF compared with healthy controls (HC).
Methods: Thirteen HC and 11 CHF patients performed 6 wk of unilateral knee extensor endurance training. Computed tomographic examinations of the thigh and biopsies of vastus lateralis were obtained bilaterally before and after the training period.
Results: Peak power of the trained leg was 10% and 14% greater than that in the untrained leg in HC and CHF, respectively. For the HC, training resulted in a higher Ca2+ release rate and a lower leak in the trained leg associated with a tendency of increased ryanodine receptor (RyR) content with reduced phosphorylation level. In the trained leg of CHF patients, RyR content was reduced without associated changes of either Ca2+ leak or release rate.
Conclusions: Training in HC has an effect on Ca2+ leak and release of the sarcoplasmic reticulum, but in CHF patients, training is achieved without such changes. Thus, calcium handling seems not to be the site of decreased exercise tolerance in CHF.
1Institute for Experimental Medical Research, Oslo University Hospital, Ullevål, NORWAY; 2Center for Heart Failure Research, University of Oslo, Oslo, NORWAY; 3Norwegian School of Sport Sciences, Oslo, NORWAY; and 4Department of Cardiology, Oslo University Hospital, Oslo, NORWAY
Address for correspondence: Morten Munkvik, M.D., Oslo University Hospital, Ullevål, Kirkeveien 166, N-0407 Oslo, Norway; E-mail: email@example.com.
Submitted for publication June 2009.
Accepted for publication September 2009.
Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.acsm-msse.org).