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We conclude that healthy older adults show evidence of mitochondrial impairment and muscle weakness, but that this can be partially reversed at the phenotypic level, and substantially reversed at the transcriptome level, following six months of resistance exercise training.
#science #aging #exercise #physiology #biology #pathology #muscles #training #health
journals.plos.org/plosone/arti

journals.plos.orgResistance Exercise Reverses Aging in Human Skeletal MuscleHuman aging is associated with skeletal muscle atrophy and functional impairment (sarcopenia). Multiple lines of evidence suggest that mitochondrial dysfunction is a major contributor to sarcopenia. We evaluated whether healthy aging was associated with a transcriptional profile reflecting mitochondrial impairment and whether resistance exercise could reverse this signature to that approximating a younger physiological age. Skeletal muscle biopsies from healthy older (N = 25) and younger (N = 26) adult men and women were compared using gene expression profiling, and a subset of these were related to measurements of muscle strength. 14 of the older adults had muscle samples taken before and after a six-month resistance exercise-training program. Before exercise training, older adults were 59% weaker than younger, but after six months of training in older adults, strength improved significantly (P<0.001) such that they were only 38% lower than young adults. As a consequence of age, we found 596 genes differentially expressed using a false discovery rate cut-off of 5%. Prior to the exercise training, the transcriptome profile showed a dramatic enrichment of genes associated with mitochondrial function with age. However, following exercise training the transcriptional signature of aging was markedly reversed back to that of younger levels for most genes that were affected by both age and exercise. We conclude that healthy older adults show evidence of mitochondrial impairment and muscle weakness, but that this can be partially reversed at the phenotypic level, and substantially reversed at the transcriptome level, following six months of resistance exercise training.

There is strong evidence of brain-related abnormalities in COVID-19.

However, it remains unknown whether the impact of #SARS-#CoV-2 infection can be detected in milder cases,
and whether this can reveal possible mechanisms contributing to brain #pathology.

Here we investigated #brain #changes in 785 participants of UK Biobank (aged 51–81 years) who were imaged twice using magnetic resonance imaging,

including 401 cases who tested positive for infection with SARS-CoV-2 between their two scans
—with 141 days on average separating their diagnosis and the second scan
—as well as 384 controls.

The availability of pre-infection imaging data reduces the likelihood of pre-existing risk factors being misinterpreted as disease effects.

We identified significant longitudinal effects when comparing the two groups, including

(1) a greater reduction in grey matter thickness and tissue contrast in the orbitofrontal cortex and parahippocampal gyrus;

(2) greater changes in markers of tissue damage in regions that are functionally connected to the primary olfactory cortex; and

(3) a greater reduction in global brain size in the SARS-CoV-2 cases.

The participants who were infected with SARS-CoV-2 also showed on average a greater cognitive decline between the two time points.

Importantly, these imaging and cognitive longitudinal effects were still observed after excluding the 15 patients who had been hospitalised.

These mainly limbic brain imaging results may be the in vivo hallmarks of a degenerative spread of the disease through olfactory pathways,
of neuroinflammatory events,
or of the loss of sensory input due to anosmia.

Whether this deleterious effect can be partially reversed, or whether these effects will persist in the long term, remains to be investigated with additional follow-up.

nature.com/articles/s41586-022

NatureSARS-CoV-2 is associated with changes in brain structure in UK Biobank - NatureAfter infection with SARS-CoV-2, individuals show a greater reduction in grey matter thickness and tissue contrast in the orbitofrontal cortex and parahippocampal gyrus; greater changes in markers of tissue damage in regions that are functionally connected to the primary olfactory cortex; and a greater reduction in global brain size.

The gut knows: "Stress can make people feel sick, and bacteria in the gut might be to blame, according to a study1 in mice. The research suggests that a stressed brain directly shuts down specific glands in the gut, affecting gut bacteria and the body’s broader immune system."
#science #immunology #pathology #neurobiology #microbiology #health #stress
nature.com/articles/d41586-024

www.nature.comHow the stressed-out brain can weaken the immune systemStress leads to disarray of the gut microbiome, which in turn causes inflammation and a drop in the body’s ability to fend off infection.