Local hypoxia will yield mitochondrial biogenesis in the myocardium; yet destroy these same structures in the skeletal fibers. (read zhelyazkov and Dasheva)
Ministry of Education of the Russian FederationWhen insufficient flow of oxygen for normal aerobic cellular metabolism of hydrogen ions are formed. The resulting acidosis rapidly destroys the cells and stops just in metabolism, if only a certain amount of hydrogen ions does not appear in the conversion of lactate piruvata, and then to lactic acid. Thus, although an excess of lactic acid is considered to be dangerous, it represents an important compensatory mechanism in preventing cellular damage due to acidosis.
Understand that there is an enormous amount of research on this subject from overseas sources. You merely have to search for it via the proper channels.
Some more from a friend and colleague of mine from the National Sports Academy in Sofia Bulgaria:mitochondrial damage or/and dysfunction is caused by : i) high acidosis ii), Moderate work (medium intensity) - Should not exceed anaerobic threshold. Doing so leads to hypoxia and destruction of mitochondria.
Hi James! What date are the quotes above? I am not sure of the mechanism described here (i.e., hydrogen ions) and the definition of hypoxia…
Just to clarify, I meant that 4 mmol.l-1 is most probably a small value for a sprinter, i.e., produced easily/quickly. Pfaff has mentioned much higher values for sprinters and anyway, it’s not rocket science to figure that out vs. (some) endurance runners.