AIM:The neural structures responsible for the coupling between ventilatory control and pulmonary gas exchange during exercise have not been fully identified. Suprapontine mechanisms have been hypothesized but not formally evidenced. Because the involvement of a premotor circuitry in the compensation of inspiratory mechanical loads has recently been described, we looked for its implication in exercise-induced hyperpnea.METHODS:Electroencephalographical recordings were performed to identify inspiratory premotor potentials (iPPM) in eight physically fit normal men during cycling at 40 and 70% of their maximal oxygen consumption ((V)·O(2max) ). Relaxed pedalling (0 W) and voluntary sniff manoeuvres were used as negative and positive controls respectively.RESULTS:Voluntary sniffs were consistently associated with iPPMs. This was also the case with voluntarily augmented breathing at rest (in three subjects tested). During the exercise protocol, no respiratory-related activity was observed whilst performing bouts of relaxed pedalling. Exercise-induced hyperpnea was also not associated with iPPMs, except in one subject.CONCLUSION:We conclude that if there are cortical mechanisms involved in the ventilatory adaptation to exercise in physically fit humans, they are distinct from the premotor mechanisms activated by inspiratory load compensation.

The present investigation was intended to assess the consequences of an inspiratory load on the diaphragm central component of fatigue during exercise. We recorded the motor potential evoked (MEP) by transcranial magnetic stimulation of the motor cortex in 10 subjects. The diaphragm and rectus femoris were studied before and 10, 20, and 40 min after two 16-min cycling exercise (E) trials requiring 55% of maximal oxygen uptake: 1) one with an inspiratory threshold load (E + ITL), corresponding to 10% of maximal inspiratory pressure; and 2) the other without the load (E). Dyspnea, heart rate, electromyographic activity of the sternocleidomastoid, and diaphragm work were significantly higher in E + ITL than in E. Neither trial affected the response to phrenic magnetic stimulation, which was performed 15 and 25 min postexercise, or the maximal inspiratory pressure (116 and 120 cm H(2)O before E and E + ITL, respectively, and 110 and 114 cm H(2)O at 30 min postexercise). Whereas the amplitude of the diaphragm MEP was unaffected by E + ITL (+2.1 +/- 29.4%), a significant decrease was observed 10 min after E compared with baseline (-37.1 +/- 22.3%) and compared with E + ITL. The MEP amplitude of rectus femoris remained unchanged with E and E + ITL. The recruitment of synergistic agonists during E + ITL may have normalized the major ventilatory stress and reset up the excitability of the diaphragm pathway.