MUSCLE EFFLUX OF GLUTAMINE
IN ORAL CREATINE OVERSUPPLIED SPORTSMEN
CAN MIMIC STRESS CONDITIONS
WITH INCREASED RISKS OF ATHLETIC TRAUMAS
By Renato COCCHI MD, neurologist and medical
psychologist.
Key words: sport, glutamine, creatine,
stress, glutamate, acethylcholine, athletic traumas.
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During the 2nd World Congress on Stress (Melbourne, 1998) Dr G. Tassani and I asserted
that stress, even the first phase of overtraining syndrome, induces an
increased supply of peripheral Acetylcholine (ACh) for increased availability
of its precursor, the choline. This happens because brain reduced turnover of
ACh reduces the blood-barrier transport into the brain of choline, but also by
an increased efflux of choline from the brain. As for the vagal district, an
increasing of ACh during stress had experimental evidence (Hata et al. 1986;
Kita et al., 1986).
The vagal stimulation grows because the direct link
between hypothalamic glutamate hyperfunction, and stimulation of some vagal
brain nuclei like Nucleus Dorsalis Vagi and Nucleus Tracti Solitarii. (Kunos et
al., 1995; Pluzhnichenko, 1997; Yoneda and Tache', 1995).
Since many physicians have a poor understanding of the dynamic of that
mechanism, often we erroneously heard about heart infarcts in such cases.
Luckily these are rare events as spontaneous ones.
That drives to postures unbalance and to a power magnification of the
athletic gesture. This is the result of a magnified but wrong setting of
postures, when they usually set according to their brain kinetic memory
mirroring normal conditions.
So postures can play at their excursion's limits, with reduced margins
for recovery. In that state a provoked athletic trauma could be heavier, because
the postures do not easily allow the balance to reset, being at work with poor
compensating margins.
Which role could play a creatine excess diet in this mechanism?
Creatine's function is to favour the resynthesis of phospho-creatine,
and so the muscular ATP production. The increasing of the body muscular mass
could be due to the extra work the larger amount of ATP lets doing, since
physical fatigue appears later.
Glutamine is the main precursor of the brain glutamate (Baxter, 1975;
Ward, Thanki and Bradford, 1983; Laake et al., 1995; Shuplakow et al., 1977). In
all stress conditions at all origin they have, there is growing of the brain
glutamate, the more spread excitatory neurotransmitter that produces cascade
negative reactions when in excess. (See: Friedman MJ, Charney DS and Deutch AY.
Neurobiologcal and clinical consequences of stress, Philadelphia,
Lippicott-Raven 1995).
Sometimes athletes tried to increase their own athletic performances
with high doses' creatine diet (up to 20-30 g daily = 5.0-7.5 kg of red meat).
If so they set off also an up efflux of muscular glutamine into blood,
according to the increased muscular synthesis of glutamine.
Blood glutamine easily crosses the blood-brain barrier and so makes the
brain glutamate increasing. In absence of stress this fact could be not
neurochemically relevant although some symptoms of the increased brain
glutamate could arise, like in stress.
When in a stressed condition, the oversupply of creatine diet in
athletes could increase the harmful followings of the stress itself.
Daily doses do not reach more than 2g for creatine-phosphate and 500mg
for glutamine.
References.
Cocchi R.
Antidepressive properties of l-glutamine. Preliminary report. Acta psychiat
belg 1976, 76: 658-666.
Hata T,
Kita T, Higashiguchi T, Ichida S. Total Ach content, and activities of choline
acetyltransferase and acetylcholinesterase in brain and duodenum of
SART-stressed (repeated cold-stressed) rat. Japan. J Pharmacol 1986, 41:
475-485.
Horger
BA, Roth RH. Stress and central amino acid system. In: Friedman MJ, Charney DS,
Deutch AJ. (eds). Neurobiological and clinical consequences of stress: From
normal adaptation to PTSD. Philadelphia, Lippincott-Raven 1995: 61-81.
Kita T,
Hata T, Higashiguchi T, Itoh E., Kavabata A. Changes of total acetylcholine and
the activity of related enzymes in SART-(repeated cold)-stressed rat brain and
duodenum. Japan.
J Pharmacol 1986, 40: 174-177.
Laake
J.H. et al.: Glutamine from glial cells is essential for the maintenance of the
nerve terminal pool of glutamate: Immunogold evidence from hippocampal slice
cultures. J.
Neurochem. 1995, 65: 871-881.
Meister
A. Metabolism of l-glutamine. Physiol Rev 1956, 36: 103-126.
Meister
A. On the synthesis and utilisation of l-glutamine. Harvey Lect. 1969, 63:
139-168.
Pluzhnichenko
EB. Spatial organization of hypothalamic neurons projecting to the
"gastric region" of the vagosolitary complex. Neurosci Behav Physiol 1997, 27:
688-691.
Rowbottom
DG, Keast D, Morton AR. The emerging role of glutamine as an indicator of
exercise stress and overtraining. Sports Med 1996, 21: 80-97.
Shuplakow
O. et al.: Glial and neuronal glutamine pools at glutamergic synapses with
distinct properties. Neuroscience 1977, 77: 1201-1212.
Yoo S.S.,
Field C.J., McBurney M.I.: Glutamine supplementation maintains intramuscular
glutamine concentrations and normalizes lymphocyte function in infected early weaned
pigs. J. Nutr. 1997, 127: 2253-2259.
Author's address: dr Renato COCCHI, via
Rabbeno, 3
42100 Reggio Emilia (Italy)
renatococchi@libero.it
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