[Clinical investigation of diaphragmatic function. Relationships with the biology of muscle]

Diaphragmatic strength, which can be roughly estimated by non invasive techniques such as maximal inspiratory pressure or sniff nasal pressure, is specifically assessed by the measurement of transdiaphragmatic pressure during electric or magnetic phrenic nerve stimulation. However, muscle endurance is probably a more relevant parameter in pulmonary disease. Recent progress in the field of diaphragm biology were mainly obtained in animal models. Data in human disease are currently restricted to COPD and steroid induced myopathy. In COPD patients, recent studies demonstrated significant adaptations of diaphragm fibers susceptible to counterbalance the mechanical disadvantage due to hyperinflation. These changes include an increased proportion of fatigue resistant type I fibers, a decrease in sarcomere length and an increase in mitochondrial density. Regarding corticosteroid induced myopathy, numerous experimental studies are available whereas data are scarce in human disease. Respiratory corticosteroid myopathy is characterized by markedly decreased strength and endurance of inspiratory muscles. Histologic data obtained by quadriceps biopsies in COPD patients demonstrated diffuse fiber atrophy, increased variation in diameter of fibers and diffuse necrotic fibers. Recent data in rats suggest that decreased IGF expression induced by corticosteroids might contribute to diaphragmatic changes.