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1 Altitude Research Center, University of Colorado, Aurora & Colorado Springs, Colorado, United States
* To whom correspondence should be addressed. E-mail: asubudhi{at}uccs.edu.
To determine if fatigue at maximal aerobic power output was associated with a critical decrease in cerebral oxygenation, thirteen male cyclists performed incremental maximal exercise tests (25 W*min-1 ramp) under normoxic (NORM: 21% FIO2) and acute hypoxic (HYPOX: 12% FIO2)) conditions. Near infrared spectroscopy (NIRS) was used to monitor concentration (µM) changes of oxy- and deoxy-hemoglobin (
[O2Hb], HHb]) in the left vastus lateralis muscle and frontal cerebral cortex. Changes in total Hb were calculated ([THb] = [O2Hb] + [HHb]) and used as an index of change in regional blood volume. Repeated measures ANOVA analyses were performed across treatments and workrates (
=0.05). During NORM, cerebral oxygenation rose between 25 and 75% peak power output (Powerpeak) (increased [O2Hb], inc. [HHb], inc. [THb]), but fell from 75 to 100% Powerpeak (decreased [O2Hb], inc. [HHb], no change [THb]). In contrast, during HYPOX, cerebral oxygenation dropped progressively across all workrates (dec. [O2Hb], inc. [HHb]), while [THb] again rose up to 75% Powerpeak and remained constant thereafter. Changes in cerebral oxygenation during HYPOX were larger than NORM. In muscle, oxygenation decreased progressively throughout exercise in both NORM and HYPOX (dec. [O2Hb], inc. [HHb], inc. [THb]), although [O2Hb] was unchanged between 75 and 100% Powerpeak. Changes in muscle oxygenation were also greater in HYPOX compared to NORM. Based on these findings, it is unlikely that changes in cerebral oxygenation limit incremental exercise performance in normoxia, yet it is possible that such changes play a more pivotal role in hypoxia.
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