Abstract
Respiratory muscles are essential to alveolar ventilation. These muscles work against increased mechanical loads due to airflow limitation and geometrical changes of the thorax derived from pulmonary hyperinflation. Respiratory muscle fibres show several degrees of impairment in cellular and subcellular structures which, in many cases, are proportional to the severity of the disease and accompanying conditions (ageing, deconditioning, starvation, comorbidity). This structural impairment translates, from the functional point of view, to a loss of strength (capacity to generate tension) and an increased susceptibility to failure in the face of a particular load (early onset of fatigue).