Thought Of The Day – Metabolism in PH, Heart v. Skeletal Muscle

Fatty acid oxidation is a slower but more energy producing process than glycolysis, but glycolysis is a much faster process. In slow twitch muscle fibers (predominantly present in marathon runners, for example), complete glucose and fatty acid oxidation occurs, but in fast twitch muscle fibers (predominantly present in sprinters, for example), glycolysis predominates. 

Glycolysis is upregulated and present in the heart (myocardium), pulmonary vasculature, immune cells, and bone marrow progenitor cells in PH. Is the heart (which primarily relies on fatty acid oxidation) in PH switching to glycolysis to compensate (i.e. to build muscle to compensate for increased afterload)? 

Or does the heart not need to do this, but is in glycolysis mode anyway, perhaps because of the sick lung circulation? Or perhaps it just due to the fact that the heart is receiving blood with a lower oxygenation than normal, due to pulmonary arterial resistance (glycolysis is seen in tissues that are not well perfused with blood or during hypoxic conditions). Conversely, is there a fundamental signaling flaw in pulmonary arteries telling arterial cells to proliferate in order to reduce blood flow through an area that it thinks is damaged in order to match and optimize ventilation/perfusion? Or is the only means of V/Q matching pulmonary vasoconstriction, leading one to believe that the proliferative nature in pulmonary arteries is not for V/Q but because of something else (like cancer)?

Perhaps what would help here, in order to determine if heart in a glycolytic metabolic state is compensating for increased pulmonary pressures, is a comparison calculation between 1) the size and amount of fast twitch muscle fiber needed for a maximal physical impulse (for example, the sum of all of the fast twitch muscle fiber mass of a sprinter and the sprinters fastest feasible sprint for x amount of time capable of carrying out this sprint) and 2) the size and amount of myocardium tissue compared to the maximal pulmonary artery pressure during systole. In essence, we would be comparing the relative muscle capacity between fast twitch skeletal muscle fiber and the myocardium to see if they match in their ability to carry out high energy tasks. It might make sense since in severe PH, the RV has to deal with up to a 7 fold increase in pressure (which is WAY more than the increase that the LV encounters when you have elevated systemic blood pressure issues).


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