10 déc. 2014

Triathlon and Speed II



I am not a fan of Eisenhower but there are things related to our task that should be taken into consideration:
“Don't join the book burners. Don't think you are going to conceal faults by concealing evidence that they ever existed. Don't be afraid to go in your library and read every book…”
When we see evidence, we should not hide it if we want to improve.  There is a limit to generalize evidence, and it will depend on the stage of our knowledge.  We have to know better in order to improve.

There is research regarding neurons under low oxygen pressure.  We have an electronic device called oximetry which can measure oxygen saturation in blood indirectly, and it is non-invasive.  Normal people can tolerate 95% of oxygen saturation pressure measured by oximetry without getting short of breath. Below 93%, it precipitates shortness of breath indirectly because it corresponds to high CO2 in blood.  When working at the VA hospital we had Vets having 60% of oxigen saturation at rest without using oxygen at home; 55% was needed for the insurance to give oxygen at home.  By walking 50 meters and taking the blood gas sample standing, the Vets were able to score below 55%.  What is happening to our neurons when we do not have enough oxygen pressure?  There are studies done on animal (reptiles) and mammals to understand this phenomenon in order to help patients with strokes.  We are generalizing evidence because this kind of studies are related to speed training.
Is Exercise-Induced Arterial Hypoxemia in Triathletes Dependent on Exercise Modality?

We concluded that Exercise Induce Arterial Hypoxemia was greater during running than cycling for a similar metabolic rate corresponding to training intensity and that EIAH could thus be considered dependent on exercise modality.

There are generalizations in the above statement that needs to be addressed:
1)   The VO2 max is not the same for the different disciplines in these athletes; the CO2 drive and O2 drive would be trigger differently.  In other words, the metabolic rate is the same but the training fitness is not the same for the two disciplines; lactate threshold is not the same.
2)   The hypoxic drive is not that important; breathing drive:
Normal respiration is driven mostly by the levels of carbon dioxide in the arteries, which are detected indirectly by central chemoreceptors when carbon dioxide crosses the blood brain barrier, forming detectable Hydrogen ions, and directly by peripheral chemoreceptors, and very little by the oxygen levels. An increase in carbon dioxide will cause chemoreceptor reflexes to trigger an increase in ventilation. Hypoxic drive accounts normally for 10% of the total drive to breathe. This increases as the PaO2 goes to 70 torr and below, while hypoxic drive is no longer active when PaO2 exceeds 170 torr.
Please read the article written by French researchers to follow me. 
 
3)   Are the French training more and more efficiently cycling than running?  As a coach, this would be my guess.  The CO2 diffusion is 20 time faster than the O2 diffusion, breathing more rapidly helps to lose CO2 instead of increasing O2 to the same degree.
4)   What we see is that hypoxemia is present when we are expecting the oxygen saturation not to drop more than 4% from baseline.
5)   Hypoxemia installs even when changing from running to cycling and stays there until the end of the exercise period.
6)   Transitioning appears to be necessary as training to improve our ability to cope with low oxygen pressure.  Swimmers sometimes train 400 meters running (all out) before sprinting swimming.
Let’s go back to our subject of how the neurons adapt to hypoxemia.  The subject of neurons adapting to low oxygen pressure is what gives SPEED.  Studies were done and sponsored to help patients with strokes when the O2 saturation decreases significantly.
First, oxygen signaling is well developed in hypoxia-tolerant neurons, making them ideal models for studying signal transduction processes during adaptations to hypoxia. Second, hypoxia-tolerant neurons are useful models for distinguishing between injury and adaptation induced by hypoxia. This is of obvious interest in determining the relevance of proposed therapeutic interventions for patients with hypoxic or ischemic diseases. Third, these neurons may help in the identification of entirely new targets for treating diseases that involve hypoxia

This makes fartlek the training of choice.  Without the hypoxic episodes, short in duration and recovery al 60% with high cadence, the neurological changes to go fast does not exist:
Hypoxia Boosts Walking Ability in Spinal Cord Patients
Experimental models demonstrating that hypoxia therapy induces cellular and physiological changes in the nervous system that translate into beneficial plasticity and strength laid the groundwork for this new work, said Dr. Trumbower.
www.medscape.org

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