Some ? answers or more confusion?
Hill could not have known that ATP depletion, rather than lactic acid accumulation, causes skeletal muscle rigor.
If correct, this classical theory in which lactic acid acts as the peripheral regulator or ‘‘poison’’21 of muscle contraction would adequately explain why skeletal muscle rigor has never been reported during exercise in healthy persons.
However, this mechanism is unable to explain why skeletal muscle rigor, as opposed to muscle cramps, has also never been observed in persons with those disorders of metabolism that prevent normal rates of skeletal muscle lactate and glycolytic ATP production because of defined enzymatic defects in either the glycogenolytic or glycolytic metabolic pathways, for example, patients with McArdle’s syndrome. 18 22 Even more interesting is the finding, known for more than 38 years23 and confirmed more recently,24 that fatigue and abnormal skeletal muscle function during exercise in McArdle’s syndrome occurs without significant reductions in skeletal muscle ATP oncentrations,23 as is also the case in other skeletal muscle glycolytic or glycogenolytic isorders.18 As the defining characteristic of some of these disorders is the inability to generate lactate and hydrogen ions (lactic acid),25 neither elevated muscle lactate concentrations nor increased intracellular acidosis can be the peripheral ‘‘governor’’ or ‘‘poison’’ that prevents the development
of skeletal muscle rigor in these disorders. Hence, another theory26 must be found that will also explain the protection of ATP homeostasis in scles that lack a crucial pathway for ATP generation.
And how about a posible answer :
One possibility is the recent proposal of Shulman and Rothman27 that muscle glycogenolysis makes the major contribution to the rapid ATP requirements during millisecond muscle contractions, and that glycogen resynthesis then occurs from metabolic intermediaries that contain carbon, including lactate, and from oxygen provided in the blood. Thus the lactate produced by rapid glycogenolysis during millisecond muscle contractions can then contribute to oxidative metabolism and the resynthesis of glycogen, hence the ‘‘glycogen shunt’’.27 The absence of the glycogen shunt in some patients with McArdle’s syndrome would then explain their reduced exercise capacity.27
Furthermore, Vissing and Haller28 have recently shown that the exercise performance of patients with McArdle’s syndrome increases when they ingest 75 g of sucrose prior to exercise and that, following sucrose ingestion, they terminate exercise with higher blood lactate concentrations than when exercise follows the ingestion of a placebo. Thus, the inability to generate lactate, rather than the overproduction of this supposedly poisonous metabolite, limits the exercise capacity of some patients with this condition.