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plundstam

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 #1 

In the pursuit of understanding more of how the oxygen fluctuates in the frontal cortex during exercise, Near-infrared spectroscopy (NIRS) based cerebral oximetry was investigated on 6 elite athletes. This was investigated during sub-maximal as well as maximal exercise in a hypoxic environment at 9400ft. It is believed in parts of the exercise and scientific community that oxygen saturation in the brain have effect on the Extended Central Governor Model (ECGM). In this case, it was brought to our attention through specialists in the field who were interested to attain more data to understand this complex issue to a higher degree. The coaching group included in this testing were interested in getting more insight into brain perfusion and oxygenation dynamics. Here (attached graphs) are examples of three athletes involved in this testing episode.

During these trials Cerebral oximeters from Coviden invos were used. These devices (Cerebral oximeters) use near infrared light of various wavelengths to determine regional hemoglobin oxygen saturation (rSO2) in the frontal cortex. The measurements were accomplished with adhesive pads applied over the frontal cortex (both right and left side) that both emit and capture reflected near-infrared light passing through the cranial bone to and from the underlying cerebral tissue. Beyond providing continuous insight into regional oxygenation of the brain, NIRS cerebral oximetry may allow coaches and physiologists to use the brain as an index organ which represents the adequacy of tissue perfusion and oxygenation of other vital organs, hence the interest in the timing and structure of the ECGM. This is a concept that is supported by some coaches in the field, or at least very interesting to some coaches in the field of how this effects elite athletic performance. It is identified that some coaches are interested in the timing of oxygen saturation between the working musculature and the frontal cortex. The understanding how the circulatory system mobilize oxygen in the blood during exercise could give more insight to how the ECGM impact physiological output. Investigative trials in this field could give more insight data, related to rSOmonitoring, that the well-protected brain may act as a indexorgan of how well all of the vital organs are perfused.
The topic of deoxygenation and it's effect on central motor drive is interesting for the coaches in this field. How does the reductions of oxygen in the prefrontal cortex impact performance at near maximal exercise or at maximal exercise. Does this function signal central systems to decrease the exercise intensity?? Does this impair executive functions that influence the decision to stop exercising or reduce the intensity of exercise? In this case 6 elite endurance subjects performed three different cycle tests, the first test was an incremental cycle tests (25W/5min ramp), the second test was a VO2 max test (25W/1min ramp), the third test was a Critical Power (CP) test at 125% of max VO2 corresponding load. This was done for max time, all tests were executed during acute hypoxia. The attached graphs present the trend data during this testing episode. (see graphs attached).  

 Results usually show that prefrontal oxygenation is maintained or increased slightly during light- to moderate-intensity exercise but decreases near maximal exercise intensity. We did not see this in all the athletes during the test at a hypoxic environment (9400ft), in some cases we did see the oxygen directly decrease during the augment of exercise. This was particularly prevalent during the 2nd and 3d set of exercises. Prior to the first incremental stage test we had the athletes do baseline respiratory resting measurements for 8min. The Cerebral oxidative data collected during this hypoxic testing tended to show a decrease in rSO2 during moderate to intensive exercise in the prefrontal cortex. The rSO2 did spike directly post exercise, this scenario seem to stress oxygen transport systems and amplifie changes in cerebral oxygenation to reach homeostasis and a re-balance of such.
 Although it appears that the trend among these athletes are pretty consistent, there needs to be further investigative applications using the NIRS systems available to understand this very interesting topic further. This testing was not focused only on the cerebral oxygenation and therefore only one part of many aspects of  performance. Therefore this topic needs more continuous NIRS recordings spanning normoxic and hypoxic exposures going forward.
   
  

Juerg Feldmann

Fortiori Design LLC
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 #2 
This is super great  Thanks P for that great summary.
 Here some add on questions and  we may in fact see some answers  based on the above study , when looking at the full data's, which where connected.
 When manipulating  respiration to change O2 Diss curve in a high intensity  you can see  Brain  oxygenation   changing   before we see a change in the  extremity.
 CO2  increase  creates a vasodilatation and  CO2 decreases ( Hypocapnia a vasoconstriction  in the  circulation in the brain.
 So   when using brain O2  testing like with the equipment mentioned above and or Portamon light you  can assess this incredible interesting reactions.
I use this idea in some cases of chronic migraine people, where the current m=medical groups simply give up.  I manipulate the CO2 levels over the Spiro Tiger and test with Capnometer. Than  I  do a RRA and basically do the opposite from what they do when they have a Migraine.
 I let the patient come in spontaneous , when he has a  full blown migraine and than test again RRA look at the shift in O2 Diss curve and than adjust the Spiro Tiger   to the  opposite situation. Meaning If a client  has a hypocapnic respiration during  his headache I let him  work hypercapnic and visa versa  and in  some cases the headache basically disappears in a bout 2 minutes.
 ( Not all but  as it seems the once, who create this problem over a respiratory reaction. In  all the cases, where it worked  all of them had a hypocapnic respiration during their . headache  and EtCO2  below 30.  I than increase the EtCO2  to 45 - 50  by using the Spiro Tiger and let   them breath slightly of  normocapnic with 2 arrows down , check with the Capnometer and  balance it out than  to 45 - 50 Et CO2 . Just a spontaneous  feedback here and I am sure P has more info on the situation during the shift  they saw in  the oxygenation.
 Altitude has an interesting reaction n respiration. The majority of people will increase  the RF an d if not optimal trained with the respiration the TV   often drops but the overall VE is up  at night and at rest and even under work and the drift towards  a hypocapnia and misconstruction of the blood vessels   in the brain. Fun  would be to see the RRA  on sea level an than at the altitude and see, whether   one or more of the athletes alone due to the  altitude may have shifted the O2 Diss curve and as such the brain oxygenation trend. Than   in the lower intensity, where there was  little or no challenge the RF and VT increase both  with VE and the CO2  goes up as such but under higher load and limitation of respiration  the trend of RF and TV and CO2 may have shifted.
 All speculation in this cases  but the data's may   give us more info's.
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 

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?.

 

Kurt Smith

 

MSc(c),BSc. RK.

 

Integrative Physiology Unit,

 

University of Lethbridge

 

Dynamic Physiotherapy, Lifemark Health Inc.

 

2

Abstract

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

 

(F

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.

Key words:

intermittent sprints, brain oxygenation, NIRS, hypoxia, altitude

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