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Ventilatory response to exercise does not evidence electroencephalographical respiratory‐related activation of the cortical premotor circuitry in healthy humans
Author(s) -
Jutand L.,
Tremoureux L.,
Pichon A.,
Delpech N.,
Denjean A.,
Raux M.,
Straus C.,
Similowski T.
Publication year - 2012
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2012.02427.x
Subject(s) - hyperpnea , respiratory compensation , physical medicine and rehabilitation , control of respiration , respiratory system , medicine , physical exercise , psychology , physical therapy , neuroscience , anaerobic exercise
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 (i PPM ) 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 i PPM s. 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 i PPM s, 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.