Humans can program and control movements, including breathing-related movements. On the electroencephalogram (EEG), this preparation is accompanied by a low-amplitude negativity starting approximately 2.5 s before inspiration that is best known as a Bereitschaftspotential (BP). The presence of BPs has been described during the compensation of mechanical inspiratory loading, thus identifying a cortical involvement in the corresponding ventilatory behavior. The pathophysiological interpretation of this cortical involvement depends on its transient or enduring nature. This study addressed this issue by looking for BPs during sustained inspiratory loading (1 h). Nine healthy male volunteers were studied during unloaded quiet breathing and inspiratory threshold loading (with unloaded expiration). Analyses of EEG signal and ventilatory variables were used to compare beginning and end of sessions. Inspiratory threshold loading caused ventilatory modifications that persisted, unchanged, for an hour. The presence of a BP at the beginning and end of a session was the most frequent occurrence (6 of 9 cases with a 17-cmH2O threshold load; 8 of 9 cases with a 23-cmH2O load). These observations support the hypothesis that the cerebral cortex is involved in the compensation of sustained experimental inspiratory loading. How this translates to respiratory disease involving acute changes in respiratory mechanics remains to be determined.

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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.

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.