Finally, the team turned their attention to the acidosis seen in the MRI muscle work. But first they had to find a way to measure acid within the cells. To do this they developed a pioneering system of nanosensors, tiny molecules that could be inserted inside the muscle cells, and light up at different acidity (pH).
Early results show that acidosis – too much acid – occurs in M.E. patients’ muscle in the lab, just as it did in the muscles of the same M.E. patients when they exercised in MRI studies. Now that is an exciting result. But there’s more.
At this point I’m afraid we need to look in a little more detail at how cells generate energy. As some will remember from biology at school (I didn’t!), glucose is first converted to a molecule called pyruvate, which is centre-stage in this story.
Normally, pyruvate is used by the mitochondria (the dynamos of the cell) to produce energy as well as carbon dioxide, burning up oxygen in the process: this is why we breathe in oxygen and breathe out carbon dioxide. Not only does this ‘aerobic’ activity generate a lot of energy, it also doesn’t generate acid.
However, the other possibility is for pyruvate to be converted to lactic acid – and too much lactic acid leads to acidosis. You also get very little energy out of the lactic acid route, and oxygen isn’t needed: it is called anaerobic energy production.
Not much energy
Prof Newton’s team think that in M.E., too much pyruvate gets turned to lactic acid and not enough gets burned cleanly by mitochondria. The result is not much energy, acidosis and consequent fatigue – which could explain a lot about M.E.
But why is this happening? It seems that in M.E. muscles, a key molecule (called PDK [Pyruvate dehydrogenase kinase]) is too active, which sends more pyruvate down the lactic acid pathway leading to acidosis and muscle dysfunction.
