ridecamp@endurance.net: Re: tying up

Re: tying up

Tivers (Tivers@aol.com)
Sun, 7 Dec 1997 15:22:45 EST

Here's an abstract of an interesting paper that plays upon similar observation
of the results of the tying up syndrome..

Adenine nucleotides and glycogen are degraded in skeletal muscle during no-
flow ischaemia. Past investigations have ascribed these metabolic changes to
the severe energetic stress which arises with the removal oi exogenous
substrates (principally oxygen). We tested this hypothesis by measuring the
high-energy phosphagen and glycogen contents of stimulated rat hindlimb
muscles (1 twitch s(-1)) prior to and following 40 min of no-flow ischaemia or
hypoxic perfusion without glucose (PaO2 = 4.6 +/- 0.1 torr, plasma glucose =
0.3 +/- 0.1 mmol L-1). Both experimental protocols eliminated exogenous
substrate supply, however, the maintenance of flow during hypoxic perfusion
ensured the removal of metabolic by-products. A period oi forty minutes of
skeletal muscle ischaemia was characterized by reductions in the total adenine
nucleotide pool, phosphocreatine and glycogen in the slow oxidative soleus,
fast oxidative-glycolytic plantaris and the fast glycolytic while
gastrocnemius. Compared to ischaemia, the total adenine nucleotide pool was
higher (by 7.2-13.3 mu mol g(-1) dry wt) and the glycogen content lower (by
10.0-16.6 mu mol g(-1) dry wt) in skeletal muscle exposed to hypoxic perfusion
without glucose. The ability of hypoxic perfusion to attenuate TAN degradation
and augment glycogenolysis can be attributed to metabolic by-product removal.
By limiting muscle lactate and PCO2 accumulation, hypoxic perfusion without
glucose attenuates cellular acidification; this could in turn limit AMP
deaminase activation and glycogen phosphorylase inhibition. We conclude that
the ischaemia-induced alterations in adenine nucleotide and glycogen
metabolism arise in response to the elimination of exogenous substrates and to
the accumulation of metabolic by-products.

Note that the altered glycogen metabolism is the result of a cascade of
problems, not the cause of them. I believe something similar is occurring in
tying up. Those papers studying muscle glycogen breakdown as a cause of tying
up may be studying the result of the syndrome instead. One way to develop
ishcaemia within a muscle is to have that muscle grow large with fuel and
water too quickly, expanding it against the fascia, and squeezing it down so
that the servicing blood vessels are occluded. This cuts oxygen delivery to
the muscle cells--and would result in "cramps".

ti

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