27 mars 2014

Triathlon and Lactate Revisited



We know many triathletes who are unable to run fast after being the best competing Ironman.  “Maca” and Natasha Badmann are examples.  Simon Lessing was the world champion for five years in a row before he faded.  They all had distance training without speed.  This is an observation that needs research to know what happened.  I said to know what happened because I believe that research should follow what we see.  I had a friend who was Professor at SUNY Potsdam, Vilma Mazetti, who ones came to Mexico on Mexicana Airline, but refused to get back on the plane because she thought that the plane was too small and was not the one offered by Mexicana when she bought the ticket.  She was convinced by a friend that it was the same plane.  She started to laugh after being convinced and told me: “I thought it was a joke what they say about Argentines.” Doubts about theories and doubts about our own theories should be present all the time and one need a Mendelian approach to continue working.  I have been doing this work my whole life that goes beyond 50 years:

Between 1856 and 1863 Mendel cultivated and tested some 29,000 pea plants (i.e., Pisum sativum). This study showed that one in four pea plants had purebred recessive alleles, two out of four were hybrid and one out of four were purebred dominant. His experiments led him to make two generalizations, the Law of Segregation and the Law of Independent Assortment, which later came to be known as Mendel's Laws of Inheritance.

The following article helps to understand what plasticity is; how one cell is differentiated and how once it is differentiated, the cell cannot return to be a stem cell or something different.  Once a neuron is differentiated into olfactory cell it cannot be something different.  The same thing for a neuron that differentiated into slow signaling neuron, it cannot come back to be a fast signaling neuron. These changes are not seen in any athlete.  The runners evolve from short distance to long distance because they are unable to keep the same speed after years of training.  EVERYTHING IS IN OUR HEAD.

The energy requirements of the brain are amazingly high; indeed, while representing only 2% of the body mass, its oxygen and glucose utilization account for approximately 20% of those of the whole organism, almost ten times more than those predicted on a mass basis (Magistretti, 1999). A similar mismatch is observed for blood flow destined to the brain, which represents over 10% of cardiac output. In addition to these quantitative aspects, brain metabolism has other distinctive features, in particular its regional variability and the nature of its cellular determinants. At the macroscopic level, one regional variability is manifested by the difference in energy metabolism between grey and white matter (Clarke and Sokoloff, 1994). But a much finer feature of brain metabolism is that its regional variability is strongly determined by the ever-changing spatially and temporally specified levels of synaptic activity.


The coupling between synaptic activity and glucose utilization (neurometabolic coupling) is a central physiological principle of brain function that has provided the basis for 2-deoxyglucose-based functional imaging with positron emission tomography (PET). Astrocytes play a central role in neurometabolic coupling, and the basic mechanism involves glutamate-stimulated aerobic glycolysis; the sodium-coupled reuptake of glutamate by astrocytes and the ensuing activation of the Na-K-ATPase triggers glucose uptake and processing via glycolysis, resulting in the release of lactate from astrocytes. Lactate can then contribute to the activity-dependent fuelling of the neuronal energy demands associated with synaptic transmission. An operational model, the ‘astrocyte–neuron lactate shuttle’, is supported experimentally by a large body of evidence, which provides a molecular and cellular basis for interpreting data obtained from functional brain imaging studies.
The Journal of Experimental Biology 209, 2304-2311


We have mentioned on previous posts that lactate is good and the way we “word,” the grammar we use regarding lactate changes the utility of lactate.

When speaking about lactate, I have to show you a different way of looking at it.  Another language so we can see something else helpful; like Hinojosa when speaking English.  In Medicine there are many monuments left for our heroes and at the end it is difficult to see “the real.” Lactate is the most effective transport of energy for our body in the “fight or flight” situation; when the body has an emergency, lactate is produced.  OUR BRAIN NEURONS USE LACTATE AS THE ONLY FUEL to do our daily task. I assume that neurons use it in general as the main fuel. So, lactate is “good.”  We have to produce lactate to get the neuro-fibers firing.  Around 4millimols per cc of blood allows us to finish an Olympic Distance Triathlon at our best pace.  The more tolerance we acquired to lactate the better we are.  Here, it is important to point out that sometimes the cybernetic equilibrium is lost and lactate continues to increase without being used by neurons or other cells (not in the case of Lance Armstrong as you will see below).  Anecdotally, we can say that even if we finish a marathon in “the sweet spot,” our lactate goes up above 10. It means, we have a tolerance to lactate above 4. Dr. Cheung in his article writes regarding the subject.

When stressing the body the muscles suffer change according to the amount of Growth Hormone (GH) released by the body, which also depends on the amount of cortisol released by the body.  At a certain limit cortisol inhibits the release of growth hormone but cortisol is necessary to release GH.  Too much cortisol knocks out the growth hormone production and as a consequence the changes we are looking for do not take place.  That is why the stress should be according to our objectives and level of training.  If one wants to run 30 minutes-10k; one need to increase the time on the stress zone progressively until being able to run five minutes at the same speed, in the scale of 1-10, 7-8 effort makes the trick.  Keeping technique and cadence is very important (please, read previous 1, 2 and 3 parts); as I said, training is very specific and the improvements made would be according to the training cadence and technique.   At the same time neurological training should take place.  Neurons do not use fat or proteins as fuels.  They depend on glucose. In order to keep firing as a “plug” for the muscles, neurons need training which can be gotten at the regular muscular training, but one needs specific training to increase the firing rate if one pursues a different performance level.  How can the neurons keep firing if one does no train neurons to fire at high speed for a long period of time?  If one´s pulse is high or low depends on the neurological training and this is the main player in our speed, not so much the muscles.  When one trains and the pulse remains low even when we try to increase it by increasing speed; it means that the neurons are tired, and the muscles could be o.k.


LIFE IS SPECIFIC AS WELL AS OUR TRAINING AND WE DECIDE WHAT WE WANT: “We cannot have our cake and eat it.”  The point to know here is whether or not we are informed about our training!

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