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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Question  one :
 If  I take an athlete, lets
' say a runner.  And I test   him on a treadmill for a VO2  max . Than I test him on a hand ergo meter   for VO2 max.
 What is the result. ?
So  could we argue:
  It is not the VO2  max, which predicts the performance, but the  performance  who asks for a certain  VO2. ?

Question 2.
 Here the classical idea of energy production at the start of a load  see pic  1.
 Why do we see in SmO2  a severe drop in SmO2  at the start, if we do not use  O2 ? Pic  2
And look at pic  3   O2  deficit  due to the lag of  O2 .
 What about the O2  which is  stored  in Mb  and the one which is in the blood  on Hb. 
Any  answers  are welcome.

Attached Images
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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Some  ? answers  or  more confusion?
a)T.D. Noakes

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 :
  T.D. Noakes

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.



Posts: 266
Here's a study using a different NIRS device that attempts to quantify the relative contributions of myoglobin and hemoglobin.  We need to be careful not to directly apply these results to Moxy because we typically measure on a different site and the Moxy uses a multiple send to receive spacing algorithm.  It's still good information to consider.
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