I was interested to read this article on high-intensity exercise. It's about healthy people rather than people with ME, but it's about abnormal responses to very small amounts of exercise. Can anyone extrapolate anything useful from this?
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Very interesting ... I wonder if there's different approaches that work better for people who won't improve at all from high-intensity exercise. Or at least approaches that are more effective and efficient compared to other approaches.
Similar genetic predispositions could also account for why some people improve with GET, on the off-chance that they all aren't misdiagnosed or spontaneously recovering to start with.
In the programme they explained that peopel with the low response gene dont respond well to any exercise not just high intensity. The most interesting part for me was about HIT changing the way the body processes glucose, so that risk of diabetes dropped substantially after just 3 mins of HIT a week over a 6 week period - even in the non exercise responders, they were still getting this major benefit. It was their lung and cardiac capacity that didnt increase. I often worry about diabetes as i have a terrible sugar addiction and sugar can make me feel very very strange - I also have gained weight since being ill and am quite high risk for diabetes.
I wonder if PWME who are still relatively sick could handle HIT? i know its a crazy question really - i just wonder what effect it would have on us. So frustrated with not being able to be more physical and fitter
I was interested to read this article on high-intensity exercise. It's about healthy people rather than people with ME, but it's about abnormal responses to very small amounts of exercise. Can anyone extrapolate anything useful from this?
Ah thanks, that is interesting. Yes, the insulin sensitivity is interesting. Did they say in the program whether people got the same change in insulin sensitivity from normal intensity exercise?
Perhaps this is of interest?
MCT1 genetic polymorphism influence in high intensity circuit training: a pilot study.
Cupeiro R, Benito PJ, Maffulli N, Caldern FJ, Gonzlez-Lamuo D.
Source
Mutations in MCT1 cDNA in patients with symptomatic deficiency in lactate transport.
N Merezhinskaya, W N Fishbein, J I Davis, J W Foellmer
Biochemical Pathology Division, Environmental Pathology Department, Room M093C, Armed Forces Institute of Pathology, Washington, DC 20306-6000, USA.
We identified 5 patients with subnormal erythrocyte lactate transport plus symptoms and signs of muscle injury on exercise and heat exposure. All had transport rates below the 95% envelope for normals. Three cases had rates 40-50% of mean normal. One was found to have a missense mutation in monocarboxylate transporter 1 (MCT1), the gene for the red cell lactate transporter (also expressed in skeletal muscle), at a conserved site, which was not mutated in a cohort of 90 normal humans. The other 2 cases had a different missense mutation (at a nonconserved site), which was also not mutated in the normal cohort. All 3 patients were heterozygotes. We presume that these mutations are responsible for their subnormal lactate transport, and hence their muscle injury under environmental stress; homozygous patients should be more seriously compromised. The other 2 cases had lactate transport rates 60-65% of mean normal, and their MCT1 revealed a third mutation, which proved to be a common polymorphism in the normal cohort. These 2 patients may be physiologic outliers in lactate transport, with their muscle damage arising from some other genetic defect.