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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