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The effect of hyperoxia on cortical activation following maximal whole body exercise in humans
Author(s) -
Volianitis Stefanos,
Bjarrum Mille,
Carlson Christine,
Rasmussen Peter,
Overgaard Anders,
Fabricius-Bjerre Anders,
Secher Niels H,
Nielsen Henning B,
Petersen Nicolas C
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb747
Subject(s) - hyperoxia , biceps , brachioradialis , medicine , rowing , elbow , cardiology , physical medicine and rehabilitation , electromyography , anesthesia , motor cortex , hypoxemia , anatomy , lung , stimulation , archaeology , history
During maximal whole body exercise arterial hypoxemia may reduce cerebral oxygenation and provoke central fatigue, defined as an inability of the central nervous system to fully recruit the involved muscles. This study evaluated the effect of hyperoxia on central fatigue indices, i.e., reduction in maximal voluntary contraction (MVC) and transcranial magnetic stimulated (TMS) force generation. Six competitive rowers performed 2000 m all‐out exercise on a rowing ergometer in normoxia and hyperoxia (30% O 2 ). Arm MVC was assessed with electromyography (EMG) of the m. biceps brachii and the m. brachioradialis. Voluntary activation of the elbow flexor muscles was assessed with TMS single pulses that were delivered to the motor cortex and evoked motor potential in the biceps brachii. Arterial hemoglobin O 2 saturation was 92.5 +/− 0.2% during exercise in normoxia, while it was maintained at 98.9 +/− 0.2% in hyperoxia. Maximal rowing in normoxia resulted in a significant reduction (7.4 +/−5.1 %) in MVC, while there was no difference in the extra force produced by TMS. Following hyperoxic exercise the MVC and TMS were not different. These data indicate that following maximal rowing the force generating capacity of the elbow flexor muscles is attenuated but, even though TMS could not confirm a role of central fatigue for the force deficit, hyperoxia may prevent the development of such force deficit.

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