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1 Groupe Hospitalier Pitie-Salpetriere, Laboratoire de Physiopathologie Respiratoire et Unite de Reanimation, Service de Pneumologie, PARIS, France; CHU de Rouen, Service de Physiologie, ROUEN, France
2 Royal Brompton Hospital, Respiratory Muscle Laboratory, LONDON, United Kingdom
3 Groupe Hospitalier Pitie-Salpetriere, Laboratoire de Physiopathologie Respiratoire et Unite de Reanimation, Service de Pneumologie, PARIS, France; Universite Paris VI Pierre et Marie Curie, UPRES EA 2397, PARIS, France
4 Hopital Armand Trousseau, Service de Pneumologie Pediatrique, Unite INSERM E 0213, PARIS, France
5 Guys Kings & St Thomas School of Medicine, Respiratory Muscle Laboratory, Kings College Hospital, LONDON, United Kingdom
* To whom correspondence should be addressed. E-mail: m.polkey{at}rbh.nthames.nhs.uk.
It is unknown whether changes in corticomotor excitability follow exercise in healthy humans. The present study was designed to test the hypothesis that a fall in the motor evoked potential amplitude elicited by transcranial magnetic stimulation of the diaphragm motor area would occur following an incremental exercise task, and if so whether such changes would be more or less marked in the area of the cortex representing a locomotor muscle, the quadriceps. Eleven healthy subjects (3 F, 33±3, weight 77±5 kg, height 177±7 cm, BMI = 25.6 ± 1.6 kg/m2) volunteered to participate in the study. Force was measured as transdiaphragmatic pressure and isometric tension in response to supramaximal peripheral magnetic nerve stimulation (Tw Pdi and Tw Q respectively). Motor evoked potentials (MEP) were recorded from these muscles in response to transcranial magnetic stimulation (TMS) and peripheral stimulation. Following baseline force measurements and TMS subjects performed a period of sub maximal exercise (gentle walking). Measurements were repeated 5 and 20 minutes after this. They then exercised on a treadmill with an incremental protocol to exhaustion. TMS was performed at baseline and at 5, 20, 40 and 60 minutes after exhaustive exercise and force measurements were obtained at baseline, 20 minutes and 60 minutes. The mean duration of exercise was 18±4 minutes and subjects achieved a mean maximum heart rate of 172±10 bpm. Tw Pdi and Tw Q were not different from baseline after exercise but a significant decrease was observed in diaphragm MEP amplitude 5 minutes after the end of the exercise that reached a nadir at 20 minutes (respectively 60±38% and 45±24%, of baseline, p=0.0001). At the same times the mean quadriceps MEP were 59±39% and 74±32 % of baseline (respectively p<0.0001 and p<0.01). The reduction in diaphragm MEP amplitude was significantly greater than the reduction in quadriceps MEP amplitude at 20 minutes (p<0.001). Studies using paired stimuli and using esophageal diaphragmatic electrode confirmed a likely intracortical mechanism for this depression. Our data confirm significant depression of both diaphragm and quadriceps motor evoked potentials following incremental treadmill exercise.
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