Metformin hämmar muskeltillväxten

[King Grub]

Studie på äldre. Den negativa effekten av inflammationshämmande på muskeltillväxten är mycket större hos unga.

Progressive resistance exercise training (PRT) is the most effective known intervention for combating aging skeletal muscle atrophy. However, the hypertrophic response to PRT is variable, and this may be due to muscle inflammation susceptibility. Metformin reduces inflammation, so we hypothesized that metformin would augment the muscle response to PRT in healthy women and men aged 65 and older. In a randomized, double-blind trial, participants received 1,700 mg/day metformin (N = 46) or placebo (N = 48) throughout the study, and all subjects performed 14 weeks of supervised PRT. Although responses to PRT varied, placebo gained more lean body mass (p = .003) and thigh muscle mass (p < .001) than metformin. CT scan showed that increases in thigh muscle area (p = .005) and density (p = .020) were greater in placebo versus metformin. There was a trend for blunted strength gains in metformin that did not reach statistical significance. Analyses of vastus lateralis muscle biopsies showed that metformin did not affect fiber hypertrophy, or increases in satellite cell or macrophage abundance with PRT. However, placebo had decreased type I fiber percentage while metformin did not (p = .007). Metformin led to an increase in AMPK signaling, and a trend for blunted increases in mTORC1 signaling in response to PRT. These results underscore the benefits of PRT in older adults, but metformin negatively impacts the hypertrophic response to resistance training in healthy older individuals.

Aging Cell. 2019 Sep 26:e13039. Metformin blunts muscle hypertrophy in response to progressive resistance exercise training in older adults: A randomized, double-blind, placebo-controlled, multicenter trial: The MASTERS trial.

[Frustrator]

Någon som sett någon studie på hur mycket antiinflammatorisk effekt metformin har jmf med diklofenak och Ipren?

[axeln]

Är metmorfin något läkemedel? Jag äter etoricoxib och plaquenil dagligen och märker att kvaliteten på träningen är enormt sämre jämfört med innan och framstegen går extremt mycket långsammare

[King Grub]

Det är en diabetesmedicin.

[Frustrator]

Det är en diabetesmedicin.

Som också har antiinflammatorisk effekt har det visat sig på senare år.

[Brofessorn]

Det är en diabetesmedicin.

Som marknadsförs som ett livselixir. Jag fattade först inte varför, men tydligen är det ganska populärt bara för att "få bättre insulinkänslighet" och bygga mer muckler. Några som är besatta av det är Ben Greenfield och Jay Campbell.

[Ahlnold]

Är metmorfin något läkemedel?



Snygg felstavning :d

[Anders The Peak]

Det är en diabetesmedicin.

Används även vid behandling av PCOS (https://sv.wikipedia.org/wiki/Polycystiskt_ovariesyndrom)

Undrar om inte flertalet läkare som arbetar med den här patientgruppen redan har sett hos sina patienter att muskelmassan försvinner sakteliga hos de flesta som behandlas.
Jag har observerat det och jag tror att det är något som är allmänt känt.

[King Grub]

Metformin förstör celler och förkortar livet.

The diabetes drug metformin is to be clinically tested in aged humans to achieve health span extension, but little is known about responses of old non-diabetic individuals to this drug. By in vitro and in vivo tests we found that metformin shortens life span and limits cell survival when provided in late life, contrary to its positive early life effects. Mechanistically, metformin exacerbates aging-associated mitochondrial dysfunction towards respiratory failure, aggravated by the inability of old cells to upregulate glycolysis in response to metformin, leading to ATP exhaustion. The beneficial dietary restriction effect of metformin on lipid reserves is abrogated in old animals, contributing to metabolic failure, while ectopic stabilization of cellular ATP levels alleviates late life metformin toxicity in vitro and in vivo. The toxicity is also suspended in nematodes carrying diabetes-like insulin receptor insufficiency and showing prolonged resilience to metabolic stress induced by metformin. In sum, we uncovered an alarming metabolic decay triggered by metformin in late life which may limit its benefits for non-diabetic elderly patients. Novel regulators of life extension by metformin are also presented.

https://www.biorxiv.org/content/10.1101/863357v1?fbclid=IwAR3Sa33eei4NUr42FMMlN_cRxPNyZMF4 DUdZV53a2ub0KjxZH8qluzNHvQ8

[Baha]

Som diabetiker borde man avstå metformin till förmån för annan medicin?

[King Grub]

Evidence from clinical trials and observational studies suggests that both progressive resistance exercise training (PRT) and metformin delay a variety of age-related morbidities. Previously, we completed a clinical trial testing the effects of 14 weeks of PRT + metformin (metPRT) compared to PRT with placebo (plaPRT) on muscle hypertrophy in older adults. We found that metformin blunted PRT-induced muscle hypertrophic response. To understand potential mechanisms underlying the inhibitory effect of metformin on PRT, we analyzed the muscle transcriptome in 23 metPRT and 24 plaPRT participants. PRT significantly increased expression of genes involved in extracellular matrix remodeling pathways, and downregulated RNA processing pathways in both groups, however, metformin attenuated the number of differentially expressed genes within these pathways compared to plaPRT. Pathway analysis showed that genes unique to metPRT modulated aging-relevant pathways, such as cellular senescence and autophagy. Differentially expressed genes from baseline biopsies in older adults compared to resting muscle from young volunteers were reduced following PRT in plaPRT and were further reduced in metPRT. We suggest that although metformin may blunt pathways induced by PRT to promote muscle hypertrophy, adjunctive metformin during PRT may have beneficial effects on aging-associated pathways in muscle from older adults.

Aging. 2020 Oct 18;12. Metformin alters skeletal muscle transcriptome adaptations to resistance training in older adults.