Prolonged high-intensity ventilation is associated with the development of rapid shallow breathing with decreased end-inspiratory volumes of all chest wall compartments. During respiratory muscle endurance training using normocapnic hyperpnoea, tidal volume (V(T)) is normally kept constant. The aim of this study was to investigate possible changes in muscle recruitment during constant-V(T) hyperpnoea, to assess potential mechanisms related to rapid shallow breathing. Ten healthy subjects performed 1h of normocapnic hyperpnoea at 70% of maximal voluntary ventilation. Chest wall volume changes were assessed by optoelectronic plethysmography. End-inspiratory (1.08 ± 0.18 versus 0.96 ± 0.27 l, p=0.017) and end-expiratory volumes (-0.13 ± 0.15 versus -0.31 ± 0.19 l, p=0.007) of the pulmonary ribcage decreased significantly and lung function and respiratory muscle strength were reduced (all p<0.05). Since with forced, constant V(T) only the inspiratory rib cage muscles were unable to sustain end-inspiratory volume of their compartment, inspiratory rib cage muscles are the most likely candidate responsible for the development of rapid shallow breathing.