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Arterial oxygenation influences central motor output and exercise performance via effects on peripheral locomotor muscle fatigue in humans
Author(s) -
Amann Markus,
Eldridge Marlowe W.,
Lovering Andrew T.,
Stickland Michael K.,
Pegelow David F.,
Dempsey Jerome A.
Publication year - 2006
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2006.113936
Subject(s) - hyperoxia , peripheral , femoral nerve , muscle fatigue , medicine , oxygenation , physical medicine and rehabilitation , hypoxia (environmental) , stimulation , cycling , cardiology , anesthesia , electromyography , chemistry , oxygen , organic chemistry , archaeology , lung , history
Changing arterial oxygen content ( C aO 2) has a highly sensitive influence on the rate of peripheral locomotor muscle fatigue development. We examined the effects of C aO 2on exercise performance and its interaction with peripheral quadriceps fatigue. Eight trained males performed four 5 km cycling time trials (power output voluntarily adjustable) at four levels of C aO 2(17.6–24.4 ml O 2 dl −1 ), induced by variations in inspired O 2 fraction (0.15–1.0). Peripheral quadriceps fatigue was assessed via changes in force output pre‐ versus post‐exercise in response to supra‐maximal magnetic femoral nerve stimulation (Δ Q tw ; 1–100 Hz). Central neural drive during the time trials was estimated via quadriceps electromyogram. Increased C aO 2from hypoxia to hyperoxia resulted in parallel increases in central neural output (43%) and power output (30%) during cycling and improved time trial performance (12%); however, the magnitude of Δ Q tw (−33 to −35%) induced by the exercise was not different among the four time trials ( P > 0.2). These effects of C aO 2on time trial performance and Δ Q tw were reproducible (coefficient of variation = 1–6%) over repeated trials at each F IO 2on separate days. In the same subjects, changing C aO 2also affected performance time to exhaustion at a fixed work rate, but similarly there was no effect of Δ C aO 2on peripheral fatigue. Based on these results, we hypothesize that the effect of C aO 2on locomotor muscle power output and exercise performance time is determined to a significant extent by the regulation of central motor output to the working muscle in order that peripheral muscle fatigue does not exceed a critical threshold.