AUTHOR=Torres-Peralta Rafael , Losa-Reyna José , Morales-Alamo David , González-Izal Miriam , Pérez-Suárez Ismael , Ponce-González Jesús G. , Izquierdo Mikel , Calbet José A. L. TITLE=Increased PIO2 at Exhaustion in Hypoxia Enhances Muscle Activation and Swiftly Relieves Fatigue: A Placebo or a PIO2 Dependent Effect? JOURNAL=Frontiers in Physiology VOLUME=7 YEAR=2016 URL=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00333 DOI=10.3389/fphys.2016.00333 ISSN=1664-042X ABSTRACT=

To determine the level of hypoxia from which muscle activation (MA) is reduced during incremental exercise to exhaustion (IE), and the role played by P_IO₂ in this process, ten volunteers (21 ± 2 years) performed four IE in severe acute hypoxia (SAH) (P_IO₂ = 73 mmHg). Upon exhaustion, subjects were asked to continue exercising while the breathing gas mixture was swiftly changed to a placebo (73 mmHg) or to a higher P_IO₂ (82, 92, 99, and 142 mmHg), and the IE continued until a new exhaustion. At the second exhaustion, the breathing gas was changed to room air (normoxia) and the IE continued until the final exhaustion. MA, as reflected by the vastus medialis (VM) and lateralis (VL) EMG raw and normalized root mean square (RMSraw, and RMSNz, respectively), normalized total activation index (TAINz), and burst duration were 8–20% lower at exhaustion in SAH than in normoxia (P < 0.05). The switch to a placebo or higher P_IO₂ allowed for the continuation of exercise in all instances. RMSraw, RMSNz, and TAINz were increased by 5–11% when the P_IO₂ was raised from 73 to 92, or 99 mmHg, and VL and VM averaged RMSraw by 7% when the P_IO₂ was elevated from 73 to 142 mmHg (P < 0.05). The increase of VM-VL average RMSraw was linearly related to the increase in P_IO₂, during the transition from SAH to higher P_IO₂ (R² = 0.915, P < 0.05). In conclusion, increased P_IO₂ at exhaustion reduces fatigue and allows for the continuation of exercise in moderate and SAH, regardless of the effects of P_IO₂ on MA. At task failure, MA is increased during the first 10 s of increased P_IO₂ when the IE is performed at a P_IO₂ close to 73 mmHg and the P_IO₂ is increased to 92 mmHg or higher. Overall, these findings indicate that one of the central mechanisms by which severe hypoxia may cause central fatigue and task failure is by reducing the capacity for reaching the appropriate level of MA to sustain the task. The fact that at exhaustion in severe hypoxia the exercise was continued with the placebo-gas mixture demonstrates that this central mechanism has a cognitive component.