Ok, apparently I could be bothered (a bit).
I think I detect either foul play or at least a conclusion being altered for some reason.
If you look at the quote in my last post, it seems (in poor English) to say that there was a difference in L-lactate levels in cells either at rest or post-EPS, or possibly both (as I said, it is very poorly written).
But when you go to the relevant chapter of the thesis, you find this:
´5.3.1.2 Myoblast L-lactate measurement
L-lactate concentration was measured in CFS/ME (n=5) and control (n=4) myoblast samples. At baseline (0μM DCA) CFS/ME and control myoblasts, samples did not exhibit significantly different L-lactate concentrations. Similarly, DCA treatment (40μm) did not induce any significant effect on either group. Displayed in Figure 5.6.´
and this:
´5.3.1.3 Myotube L-lactate measurement at rest and post-EPS
L-lactate concentration was measured in CFS/ME (n=4) and control myotubes (n=3) at rest and following 24-hours EPS. When CFS/ME myotubes were compared to controls at rest and following EPS there was no significant difference in L-lactate concentration at baseline (0μM) or following DCA (40μM) treatment. Similarly, EPS stimulation exhibited no significant alteration in L-lactate concentration when compared to resting levels in both samples at baseline and following DCA treatment. See figure 5.7.´
Again, the second paragraph is not written well at all. This opaqueness may be intentional, though. If you look at the graph, there does seem to my untrained eye to be a difference between cases and controls after exercise. I am statistically-illiterate, but if you look at the graph, cases go from approx 1.6-7 to 2.5 pmols/well after exercise, whilst controls go from approx 1.8 to 1.9 (the same trend is observed in samples treated with DCA). How is this not a significant difference? Perhaps the author does not think that it is a significant (or politically savvy) comparison, but then why do they seem to mention it in abstract?
Another interesting difference:
´Although, lactic acidification work did not impact upon O2.- generation, a cytotoxicity assay revealed CFS/ME myoblasts to exhibit greater viability than control cells following treatment with lactic acid. This was an interesting finding as it suggests the CFS/ME patient cells to tolerate substantial acidification, although it is difficult to determine the mechanism behind this occurrence. However, as previously described several studies have revealed profound 112
intramuscular acidosis in CFS/ME patients [Jones et al. 2012; 2010], it is possible as a consequence that cells have developed an improved buffering capacity to cope with excessive acidification.´
Finally, this gem:
´It is important to note that contrasting patient bio-energetic responses to exercise exhibited with in vivo studies may be due to the level of patient engagement, which is a key limitation of that mode of investigation. For example, Jones et al. [2012] reported CFS/ME patients to fall into 2 distinct categories in relation to Phosphocreatine (PCr) depletion in response to exercise. The first group demonstrated normal bio-energetic dysfunction, exhibiting PCr depletion to a comparable level to controls when exercising at the same level of MVC. Conversely, the second group exhibited low-level PCr depletion and no exercise induced acidosis as a consequence. The authors postulated this effect to be evidence of some form of exercise avoidance behaviour. In contrast, the in vitro exercise model utilised in the present study eliminates the need for patient compliance in the exercise protocol and enables the bio-energetic function of all patient muscle samples to be examined equally following the same EPS strategy.´
In the context of that last paragraph, I have no qualms about summarising most of the conclusions that can be drawn from the paper as ´it´s in the blood, stupid!´