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Metformin Inhibits Mitochondrial Adaptations To Aerobic Exercise Training In Older Adults

re: COVID
re: ethics in medicine
re: Metformin

Real science is never settled, and anyone who has certainty on such things is not qualified to discuss it.

I was listening to Brain Energy: A Revolutionary Breakthrough in Understanding Mental Health @AMAZON recently, stemming from interest in mitochondrial function.

IMO, the #1 issue with all health is the health and productivity of mitochondria, which not only produce energy, but control genetic expression—far more than what was once thought.

Hence, a drug that impairs improvements in mitochondrial function should be treated with extreme concern and skepticism.

Metformin Inhibits Mitochondrial Adaptations To Aerobic Exercise Training In Older Adults

2018-12-11

Metformin and exercise independently improve insulin sensitivity and decrease the risk of diabetes. Metformin was also recently proposed as a potential therapy to slow aging. However, recent evidence indicates that adding metformin to exercise antagonizes the exercise-induced improvement in insulin sensitivity and cardiorespiratory fitness.

The purpose of this study was to test the hypothesis that metformin diminishes the improvement in insulin sensitivity and cardiorespiratory fitness after aerobic exercise training (AET) by inhibiting skeletal muscle mitochondrial respiration and protein synthesis in older adults (62 ± 1 years). In a double-blinded fashion, participants were randomized to placebo (n = 26) or metformin (n = 27) treatment during 12 weeks of AET.

Independent of treatment, AET decreased fat mass, HbA1c, fasting plasma insulin, 24-hr ambulant mean glucose, and glycemic variability. However, metformin attenuated the increase in whole-body insulin sensitivity and VO2 max after AET.

In the metformin group, there was no overall change in whole-body insulin sensitivity after AET due to positive and negative responders. Metformin also abrogated the exercise-mediated increase in skeletal muscle mitochondrial respiration. The change in whole-body insulin sensitivity was correlated to the change in mitochondrial respiration. Mitochondrial protein synthesis rates assessed during AET were not different between treatments.The influence of metformin on AET-induced improvements in physiological function was highly variable and associated with the effect of metformin on the mitochondria

These data suggest that prior to prescribing metformin to slow aging, additional studies are needed to understand the mechanisms that elicit positive and negative responses to metformin with and without exercise.

...

CONCLUSION

...metformin inhibits the increase in skeletal muscle mitochondrial respiration after 12 weeks of moderate to vigorous AET despite no differences between placebo and metformin on mitochondrial protein synthesis.

Metformin also attenuated the increase in whole‐body insulin sensitivity and CRF after AET. However, metformin did not inhibit other AET improvements, including telomere elongation, fasting insulin, 24‐hr mean glucose, and body composition.

Our findings suggest that combining two healthspan extending treatments, metformin and exercise, may interfere with the improvement in some parameters of physiological function and do not interact synergistically. This study indicates that further research is needed before broadly prescribing metformin as a treatment to slow aging.

WIND: the perfect assembly-line medicine drug: hook 'em so that self improvement is slow to comne, have 'em take it for life. Next patient please!

Exercise is a drug-free approach with numerous benefits with no side effects. Here we have a drug that narrowly targets one issue, but BLOCKS the “feel good” positive feedback loop that ought to result from excercise. Is there a worse idea than taking a drug that makes exercise seem futile, by blocking the positive feedback loop of steady improvement?

N = 1: My wife has been taking Metformin, but also walking 3 miles or so daily for two years now, as well as swimming. There are small improvements, but I’ve been puzzled as to why such a nil gain in fitness. Has Metformin been sabotaging her efforts, muting what should be very significant gains in fitness? I’m trying to persuade her to stop the Metformin since a CGM she’s using should immediately indicate if there is any surge in blood glucose.

To accept that tradeoff without very serious concern equates to a serious ethical lapse on the part of any prescribing physician unless that physician FIRST at least attempts to gain patient compliance with an exercise regimen. If the patient declines, then Metformin is maybe better than nothing.

How many physicians have the time or patience to do the right thing first, other than perhaps giving it 30 seconds of lip service? Physicians do not get paid for improving health, particularly those in institutions (the vast majority)—they get paid for following the Standard of Care guidelines, that is, bandaid approaches aka “treatment” in which little to nothing is fundamentally improved. That’s the system we have, and while it is indeed an ethical lapse on the part of physicians, this systemic corruption is not the fault of any particular physician, nor is it fixable without some cataclysmic disruption of the health care system. As with everything, personal responsibility comes to bear.

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