Rationale:

Muscular power output during heavy exercise is regulated in a complex way. Several factors including a pre-determined template based on past experience & receptors which sense disturbances in homeostasis caused by exercise and feed back to the central nervous system help regulate power output. The rapidity with which these receptors sense derangements in the mileau internal is not established.

Objectives:

To evaluate the rapidity with which physiological disturbances caused by the inhalation of a hypoxic gas mixture are sensed & lead to changes in power output.

Methods:

Well-trained, task habituated, cyclists (n = 7) (VO₂max = 54.9 +/- 7.0 ml*min^-1*kg^-1, Peak Power = 343 +/- 55 Watts) performed two 5-km time trials. In the interval between 3.0-3.5 km (~45s), they were switched (double blind) from breathing room air (RA) to breathing from a bag containing either RA or a hypoxic gas mixture (HYPO) (~15%O₂; equivalent to ~2500-m altitude). After 3.5 km they switched back to RA. Power output (Watts), velocity and distance were measured using a strain gauge based dynamometer (SRM). Arterial O₂ saturation was measured by pulse oximetry.

Results:

There was a significant decrease in arterial O₂ saturation between 3.0 km to 3.5 km in HYPO (94 +/- 4 to 84 +/- 2%) but not during RA (95 +/- 2 to 95 +/- 2%). During the same interval, there was no change in Watts (256 +/- 57 to 258 +/- 49 vs 268 +/- 44 to 264 +/- 50 W), velocity (35 +/- 3 ot 35 +/- 4 vs 35 +/- 3 to 35 +/- 3 km*hr^-1), or heart rate (159 +/- 30 to 160 +/- 33 vs 174 +/- 17 to 176 +/- 16 bpm) in HYPO vs RA, respectively. Following HYPO, O₂ saturation returned to baseline quickly (<30s).

Conclusions:

Despite the significant arterial hypoxemia induced by HYPO, there was no evidence that muscular power output decreased in response to the change in the mileau internal. This suggests that muscular power output may be insensitive to arterial desaturation (which is unlikely) or that the sensor for hypoxemia is relatively slow responding.