Level 8 Valued Member
I'm not sure what to make of it. When I read it it looks like the SS group was more reliant on glycolysis than the LS group:Are we reading the results the same way?
To me it seems to line up with the AGT style of training:
The SS group had the less acidic pH overall.
The SS group also had lower "markers" (if that's the right word)for glycolysis: lower pyruvate and lactate levels.
The SS group had a lower reduction in muscle ATP as well.
Also, the G-6-P is interesting. If I'm not mistaken that's a molecule which is part of glycolysis.
"Rate of muscle glycolysis was similar in SS and LS during the first sprint, but twofold higher in SS than LS during the last sprint (P < 0.05)."
"Muscle [phosphocreatine] before the last sprint was 1.5-fold lower in SS than LS (P < 0.001). "
"PCr utilization during a single sprint was smaller in SS than LS, but PCr availability before the last sprint was lower in SS than LS....suggests that limitations in PCr availability may have played a more prominent role in peripheral fatigue development during the multiple short- than the long-sprint protocol." - this statement doesn't maybe make sense compared to the next observation
"Thus, even though intracellular [Pi] was not measured in the present study, it is conceivable that Pi-dependent alterations in sarcoplasmic reticulum Ca2+ cycling contributed to the larger degree of peripheral fatigue observed in LS."
Which is consistent with other studies linking accumulation of Pi to reduced contractile forces independent of lactate and hydrogen ion accumulation.
And again maybe playing devil's advocate, is this just showing a logical pattern of fatigue? The longer you sustain an effort the greater the accumulation of PhosphoCreatine byproduct. This study seems to show the duality of increased glycolysis magnitude in LS also increasing PCr stores, but the inorganic phosphate from using it reduced contractile force anyway. So maybe supporting the SS as a training approach for increasing output, but this study didn't last long enough to measure adaptive response over time to the different protocols. Reading it, it doesn't seem to support the metabolic aspect although I certainly could be missing a great deal - much of the chemistry is WAY over my head.
This research does a good job of isolating the effect in mice:
"Even after 100 fatiguing tetani, force was not significantly affected in CK–/– fibers (lacking creatine kinase), whereas by this time force was reduced to <30% of the original in wild-type fibers"