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J Physiol Volume 575, Number 3, 937-952, September 15, 2006 DOI: 10.1113/jphysiol.2006.113936
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INTEGRATIVE

Arterial oxygenation influences central motor output and exercise performance via effects on peripheral locomotor muscle fatigue in humans

Markus Amann1, Marlowe W. Eldridge1, Andrew T. Lovering1, Michael K. Stickland1, David F. Pegelow1 and Jerome A. Dempsey1

1 University of Wisconsin Medical School, The John Rankin Laboratory of Pulmonary Medicine, Madison, WI, USA

Changing arterial oxygen content (CaO2) has a highly sensitive influence on the rate of peripheral locomotor muscle fatigue development. We examined the effects of CaO2 on 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 CaO2 (17.6–24.4 ml O2 dl–1), induced by variations in inspired O2 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 ({Delta}Qtw; 1–100 Hz). Central neural drive during the time trials was estimated via quadriceps electromyogram. Increased CaO2 from 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 {Delta}Qtw (–33 to –35%) induced by the exercise was not different among the four time trials (P > 0.2). These effects of CaO2 on time trial performance and {Delta}Qtw were reproducible (coefficient of variation = 1–6%) over repeated trials at each FIO2 on separate days. In the same subjects, changing CaO2 also affected performance time to exhaustion at a fixed work rate, but similarly there was no effect of {Delta} CaO2 on peripheral fatigue. Based on these results, we hypothesize that the effect of CaO2 on 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.

(Received 22 May 2006; accepted after revision 21 June 2006; first published online 22 June 2006)
Corresponding author M. Amann: The John Rankin Laboratory of Pulmonary Medicine, 4245 Medical Science Center, 1300 University Avenue, Madison, WI 53706, USA. Email: amann{at}wisc.edu




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