Here another great study , which shows the same reaction.
What as well is missing is the respiratory respond to the sprints. and the CO2 reaction including the reaction of H + accumulation.
In our different case information we see in sprints very often a 2 directional respiration. Very fast and shallow, which initial leads in a capnometer to a hypocapnic reaction in sprints at the mouth piece, but due to the delay in CO2 arterial an what we can measure, we see rather a higher CO2 arterial , which shifts the O2 Diss curve to the right and therefor creates a deoxygenation with the central ( brain reacting the fastest due to the need of O2.)
The question here is as we discuss since a while.
A drop in O2 saturation does not mean hypoxia , it means the opposite as long we see a drop the organ takes O2 out and can still take it out ( bio availability ) So a drop in Brain O2 is a sign of using O2 not of being hypoxic. Once oxygenation reaches a plateau and stays there, than we reached a zero bio availability in the at area, despite O2 still there but can't be released and now we have a hypoxic situation.
The drop in O2 in the brain shows, that this is the most vital team ember , who needs O2 to function properly and will take it first and if enough left the rest can get it and we see a drop in the extremity system.
Just a critical thought to some of the conclusion we can read in many studies. What do you think?.
Integrative Physiology Unit,
University of Lethbridge
Dynamic Physiotherapy, Lifemark Health Inc.
The study examined the influence of cerebral (prefrontal cortex) and muscle (vastus lateralis)
oxygenation on the ability to perform repeated, cycling sprints. Thirteen team-sport athletes
performed ten, 10-s sprints (with 30 s of rest) under normoxic (F
IO2 0.21) and acute hypoxic
IO2 0.13) conditions in a randomised, single-blind fashion and crossover design. Mechanical
work was calculated and arterial O
2 saturation (SpO2) was estimated via pulse oximetry for every
sprint. Cerebral and muscle oxy-(O
2Hb), deoxy-(HHb), and total haemoglobin (THb) were
monitored continuously by near-infrared spectroscopy. Compared with normoxia, hypoxia
induced larger decrements in S
pO2 and work (11.6% and 7.6%, respectively; P<0.05). In the
muscle, we observed a fairly constant level of deoxygenation across sprints, with no effect of the
condition. In normoxia, regional cerebral oxygenation increased during the first two sprints and
slightly fluctuated thereafter. In contrast, this initial cerebral hyper-oxygenation was attenuated
in hypoxia. Changes in [O
2Hb] and [HHb] occurred earlier and were larger in hypoxia compared
with normoxia (
P<0.05), while regional blood volume (Δ[THb]) remained unaffected by the
condition. Changes in cerebral [HHb] and mechanical work were strongly correlated in normoxia
and hypoxia (R
2=0.81 and R2=0.85, respectively; P<0.05), although the slope of this relationship
differed (normoxia: -351.3 ± 183.3 vs. hypoxia: -442.4 ± 227.2;
P<0.05). The results of this
NIRS study show that O
2 availability influences oxygenation of the prefrontal cortex during
repeated, short sprints. By using a hypoxia paradigm, the study suggests that cerebral
oxygenation may impose a limitation to repeated-sprint ability.
intermittent sprints, brain oxygenation, NIRS, hypoxia, altitude