[Skeletal musculature modifications and mechanisms of fatigue in chronic heart failure]

The majority of patients with chronic heart failure (CHF) have a decreased exercise tolerance. It has not been well established if muscle fatigue is related to a peripheral myopathy with specific metabolic, histologic and biochemical abnormalities. CHF patients demonstrate depressed oxidative capacity and activation of anaerobic glycolysis, leading to a reduction in the energy substrates. In addition, the skeletal muscles of the lower limbs demonstrate a shift toward type IIb fibers. Many factors, such as prolonged immobilization, reduced blood flow and neuroendocrine activation, can be cited in order to explain the origin of this myopathy. Recent studies show that immobilization is not the only reason for modifications in skeletal muscle composition, since patients with disuse atrophy show an increased percentage in myosin heavy chain I, while IIb is decreased. The opposite pattern is observed in CHF. It would appear that several factors such as deconditioning, prolonged immobilization and reduced blood flow, may produce muscular atrophy. The reasons behind specific changes in fibre composition may be found in metabolic factors such as insulin resistance, TNF levels and dysfunction of the ergo-metabolo muscle receptors.