Thanks
@Bebo321, very interesting article. It does suggest that Glycogenolysis is impaired in T1s due to reduced glucagon function, and that T1s make up for the deficit by increasing gluconeogenesis during exercise, which non-diabetics don't do at all.
Some caveats I have about this study though:
- 5 T1 subjects only and all quite young
- subjects in a low insulin state, which will upregulate gluconeogenesis
- (also subjects all on NPH basal insulin which is rather ancient)
- [Edit: continuous constant infusion of (isotopic tracer) glucose - insignificant quantities, <5mg/min]
- internal contradiction in the paper as to whether plasma glucagon did or didn't change in the T1 subjects
- uncertainties in the range of 5% - 10% in the measurements used to estimate glycogen usage, when glycogen usage was said to be less than 1% of total reserves
- the results are seriously inconsistent with the previous studies (though the argument is the measurement was better in this study)
Despite all this the likelihood is that this study is right and T1s respond to exercise very differently from non diabetics in where they mobilise the extra glucose from. That because our ability to upregulate Glycogenolysis via glucagon is impaired (by around two thirds in the study group), we compensate by upregulating gluconeogenesis, apparently via norepinephrine.
It slightly doesn't match with my life experience though. It doesn't explain the reality of post exercise hypos very well, if glycogen depletion is only one third of the excess glucose supply. Doesn't it suggest you would have a raging protein hunger after exercise? Or actually lose muscle mass after exercising?
I guess I'm not totally convinced but it's still a really useful and helpful article, thank you.
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