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[Engadin]

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F U L L   T I T L E :    No effect of the endurance training status on senescence despite reduced inflammation in skeletal muscle of older individuals.

 

 

 

P A Y W A L L E D   S O U R C E :   American Journal of Physiology - Endocrinology and Metabolism

 

 

 

 

 

 

Abstract

 

The aim of the present study was to determine if the training status decreases inflammation, slows down senescence and preserves telomeres health in skeletal muscle in older compared to younger subjects, with a specific focus on satellite cells. Analyses were conducted on skeletal muscle and cultured satellite cells from vastus lateralis biopsies (n=34) of male volunteers divided into four groups: young sedentary (YS), young trained cyclists (YT), old sedentary (OS) and old trained cyclists (OT).

 

The senescence state and inflammatory profile were evaluated by telomere dysfunction-induced foci (TIF) quantification, senescence associated b-gal (SA-b-Gal) staining and qRT-PCR. Independently of the endurance training status, TIF levels (+35%, P < 0.001) and the percentage of SA-b-Gal positive cells (+30%, P < 0.05) were higher in cultured satellite cells of older compared to younger subjects. p16 (4-5 fold) and p21 (2-fold) mRNA levels in skeletal muscle were higher with age but unchanged by the training status. Aging induced higher CD68 mRNA levels in human skeletal muscle (+102%, P = 0.009).

 

Independently of age, both trained groups had lower IL-8 mRNA levels (-70%, P = 0.011) and tended to have lower TNFa mRNA levels (-40%, P = 0.10) compared with the sedentary subjects. All together, we found that the endurance training status did not slow down senescence in skeletal muscle and satellite cells in older compared to younger subjects despite reduced inflammation in skeletal muscle. These findings highlight that the link between senescence and inflammation can be disrupted in skeletal muscle.

 

 

 

 

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Edited by Engadin, 04 August 2020 - 12:20 PM.

[Engadin]

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Another source: NewAtlas (Anti-aging enzyme discovery raises prospect of lifespan extension)

 

 

 

 

 

 

A study from researchers at KAIST (Korea Advanced Institute of Science and Technology) is providing new insights into a cellular energy pathway that has been linked to longer lifespan. The research, conducted in human cells and roundworms, raises the prospect of anti-aging therapeutics that can extend lifespan by activating this pathway.

 

AMPK (adenosine monophosphate-activated protein kinase) is an enzyme that acts as a metabolic master switch. It has been described as a “magic bullet” protein, conferring broad beneficial health effects, from improving cardiovascular health to extending lifespan. It is activated in response to low cellular energy levels, as is often seen during exercise or periods of caloric restriction.

 

An increasing volume of study has found activating AMPK in animal models leads to notable increases in lifespan, prompting a surge in research investigating this enzyme.

 

The new KAIST study focused on this pathway in a tiny roundworm, caenorhabditis elegans (C. elegans), often used by researchers as a model to investigate lifespan. The researchers discovered an enzyme called VRK-1 works in tandem with AMPK to regulate cellular energy processes.

 

Boosting VRK-1 activity in the roundworms extended the organism’s lifespan by stimulating AMPK activity, and inhibiting the enzyme reduced its lifespan. Moving to laboratory cell tests the researchers verified this VRK-1 to AMPK mechanism does seem to occur in human cells, suggesting it is possible the lifespan-extending results may be replicated in human subjects.

 

“This raises the intriguing possibility that VRK-1 also functions as a factor in governing human longevity, and so perhaps we can start developing longevity-promoting drugs that alter the activity of VRK-1,” explains Seung-Jae V. Lee, who lead the new research.

 

It is still extraordinarily early days for the research, and the next steps will be to explore the effects of modulating VRK-1 activity in more complex animal models such as rodents. Lee says the success in replicating this VRK-1 to AMPK mechanism in human cells suggests the pathway may be relevant in a number of complex organisms, but it is still unclear how this could be harnessed for therapeutic outcomes.

 

 

 

 

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