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I have a 56 yo insulin dependant type 2 diabetic patient who has recently taken up triathlon. Has had minor musculoskeletal injuries which have responded well to treatment, but now complains of severe muscle fatigue following events and longer training sessions which seem to correspond to elevated BSL's. Does anyone know of a sports endo or physiologist in the Brisbane region who could offer advice for this chap?
Diabetes can cause an aching muscle pain that is not unlike fibromyalgia. There is also diabetic myopathy, which is probably an end stage of the aching muscles. There is also a diabetes muscle infarct type problem which is mroe serious but it does not sound like that.
OR it could simply be that he is unable to get enough glucose into the muscles due to the diabetes and in the longer sessions, is just accumulating more lactate ... maybe thats creating high than normal tissue damage.
__________________ Craig Payne
__________________________________________________ ___________________________________ Follow me on Twitter | Run Junkie God put me on this earth to accomplish a certain number of things - right now I am so far behind, I will never die.
Thanks for that Craig. My impression is that it would be in the latter of your suggested diagnoses - low muscle glycogen levels or something. Here on the Sunshine Coast we have only one endo and no sports physicians. Thought more expert advice may be of benefit if referred to Brisbane.
Heres an article about team type 1 Diabetic pro cyclists. Might be of interst to your patient, But maybe you can contact the team they will have some of the most upto date info on recovery, training etc for people with Diabetes. They are also trying to promote diabetic people increasing activity levels so maybe more open to share info.
Type 2 diabetes mellitus (T2DM) and aging are characterized by insulin resistance and impaired mitochondrial energetics. In lower organisms, remodeling by the protease pcp1 (PARL ortholog) maintains the function and lifecycle of mitochondria. We examined whether variation in PARL protein content is associated with mitochondrial abnormalities and insulin resistance. PARL mRNA and mitochondrial mass were both reduced in elderly subjects and in subjects with T2DM. Muscle knockdown of PARL in mice resulted in malformed mitochondrial cristae, lower mitochondrial content, decreased PGC1α protein levels, and impaired insulin signaling. Suppression of PARL protein in healthy myotubes lowered mitochondrial mass and insulin-stimulated glycogen synthesis and increased reactive oxygen species production. We propose that lower PARL expression may contribute to the mitochondrial abnormalities seen in aging and T2DM.
Press Release: New Culprit In Muscle Defects, Insulin Resistance That Come With Age
Type 2 diabetes is a widespread problem for many people these days, and our risk for insulin resistance and diabetes only grows as we age. Now, a new report in the May issue of Cell Metabolism, a Cell Press publication, reveals a new contributor to the problem: The muscles of elderly people and of people with type 2 diabetes contain lower concentrations of a protein known as PARL (short for "presenilin-associated rhomboid-like").
PARL plays an important role within cells in remodeling power-generating mitochondria. It's PARL's job to oversee mitochondria's quality control, specifically by maintaining their integrity as the cellular components undergo normal processes of fission and fusion.
The findings provide yet another link between insulin resistance and the function of mitochondria, the researchers say.
When mitochondria aren't functioning properly, food doesn't get metabolized to the level that it should, explained Anthony Civitarese of Pennington Biomedical Research Center. Instead of getting burned, fats accumulate in cells where they impair insulin's action. As mitochondria fail to work efficiently, they also produce more damaging free radicals.
In the new study, Civitarese's team wanted to follow up on previous clues that PARL might play a role in mitochondrial abnormalities and insulin resistance. To do that, they examined PARL expression levels in the muscles of healthy young people compared to elderly people. Importantly, they specifically compared young and elderly people who were similar to one another in other respects, including their body composition, fatty acid and glucose levels, and physical activity levels.
Relative to younger people, older people showed signs of insulin resistance. They also had fewer numbers of mitochondria and lower expression of the PARL gene.
Follow-up studies in mice showed that treatments designed to lower PARL levels in muscle led to fewer mitochondria, reductions in other important mitochondrial proteins, and reduced insulin sensitivity. Studies in human muscle cells showed essentially the same thing, the researchers report.
"These overlapping answers point to a common mechanism for insulin resistance and the defects that come with aging," Civitarese said.
Together with earlier evidence, the findings show "that lower PARL expression is an early defect altering mitochondrial function and insulin resistance in response to a metabolic challenge," the researchers wrote. "We hypothesize that impaired PARL function is an important risk factor for the development of insulin resistance in skeletal muscle by decreasing mitochondrial mass and energetics and increasing oxidative stress, thus contributing to impaired glucose metabolism. As insulin resistance continues to develop, mitochondrial function, oxidative damage, and PARL activity may decline further, leading to a vicious cycle that eventually contributes to the development of T2DM or other age-associated diseases, including sarcopenia," a loss of muscle mass and strength.
Civitarese said it's not clear why PARL levels decline with age, but the findings suggest that increasing PARL levels may bring metabolic benefits. There is some possibility that PARL could be used as a drug or drug target, but he cautions that such a path would likely be difficult. That's because PARL does its work in a hard-to-reach place -- inside mitochondria, which are encapsulated in a double membrane.