|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Sports Science, University of Innsbruck, Innsbruck, Austria
2 Department of Neurology, Innsbruck Medical University, Innsbruck, Austria
* To whom correspondence should be addressed. E-mail: wolfgang.loescher{at}uibk.ac.at.
The effects of acute hypoxia on motor cortex excitability, force production and voluntary activation were studied using single and double-pulse transcranial magnetic stimulation techniques in fourteen healthy male subjects. Electrical supramaximal stimulations of the right ulnar nerve were performed and transcranial magnetic stimulations (TMS) were delivered to the first dorsal interosseus (FDI) motor cortex area during short-term hypoxic (HX) and normoxic (NX) condition. M-waves voluntary activation, F-waves, resting motor threshold (rMT), recruitment curves (100-140% of rMT), and short interval intracortical inhibition (SICI) and intracortical facilitation (ICF) were measured. Moreover, motor-evoked potentials (MEP) and cortical silent periods (CSP) were determined during brief isometric maximum right index finger abductions (MVC). Hypoxia was induced by breathing a fraction of inspired oxygen of 12% via a face mask. M-waves, voluntary activation and F-waves did not differ between NR and HX. The rMT was significantly lower in HX (55.79 ± 9.40 %) than in NX (57.50 ± 10.48 %), P < 0.01) while MEP recruitment curve, SICI, ICF, MVC and MEP were unaffected by HX. In contrast, the SP in HX (158.21 ± 33.96 ms) was significantly shortened compared to NX (169.42 ± 39.69ms) (P < 0.05). These data demonstrate that acute hypoxia results in increased cortical excitability and suggest that acute hypoxia alters motor cortical ion channel function and GABAergic transmission.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |