Exercise training reverses adiponectin resistance in skeletal muscle of patients with chronic heart failure. Issue 17 (16th June 2011)

• Record Type: Journal Article
• Authors: Van Berendoncks, An M; Garnier, Anne; Beckers, Paul; Hoymans, Vicky Y; Possemiers, Nadine; Fortin, Dominique; Van Hoof, Viviane; Dewilde, Sylvia; Vrints, Christiaan J; Ventura-Clapier, Renée; Conraads, Viviane M
• Is Part Of: Heart. Volume 97:Issue 17(2011)
• Page Start: 1403
• Page End: 1409
• Publication Date: 2011-06-16
• Subjects: Adiponectin -- energy metabolism -- heart failure -- exercise training; Heart -- Diseases -- Treatment -- Periodicals; Cardiology -- Periodicals; 616.12
• DOI: 10.1136/hrt.2011.226373
• Languages: English
• ISSNs: 1355-6037

Abstract

Abstract : Background: Resistance to the insulin-sensitising adipocytokine, adiponectin, has been described at the level of the skeletal muscle in patients with chronic heart failure (CHF). Objective: To investigate whether exercise training (ET) would improve skeletal muscle energy metabolism and adiponectin signalling. Methods: In a prospective cohort study, patients with CHF were recruited from the Cardiac Rehabilitation Centre, Antwerp University Hospital. They underwent 4 months' combined endurance–resistance ET. Skeletal muscle mRNA and protein expression of adiponectin, AdipoR1 and downstream metabolic genes were measured. Results: Adiponectin mRNA expression in the nine CHF patients was higher than that in 10 matched healthy subjects (p=0.007), whereas AdipoR1 and downstream-located genes involved in lipid (PPAR-α, ACADM) and glucose metabolism (AMPK, hexokinase2) were down-regulated. Skeletal muscle AdipoR1 correlated with VO2 peak (r=0.900; p=0.001), maximal workload (r=0.753; p=0.019) and steady state workload (r=0.928; p<0.001). ET increased maximal workload and muscle strength. In addition, ET lowered adiponectin mRNA expression (p=0.017), whereas the expression of AdipoR1 (p=0.011) and downstream metabolic genes was increased to levels comparable to those in healthy subjects. ELISA confirmed the normalisation of skeletal muscle adiponectin expression at the protein level (p=0.047). Conclusion: At the level of the skeletal muscle, CHF patients are characterised by increased adiponectin expression and decreased expression of AdipoR1 and downstream metabolic genes. ET normalises the mRNA expression of adiponectin and AdipoR1 and reverses disorders in lipid and glucose metabolism in skeletal muscle. These alterations in metabolic gene expression may help to understand the beneficial effects of ET in CHF.