How much of age-related degeneration stems from lifestyle (secondary aging) versus inherent processes derived from the operation of metabolism (primary aging)? If you become sedentary with age, or pile on the visceral fat, then both of those are going to harm you in ways that overlap with the inherent mechanisms of aging - accelerating the accumulation of damage and dysfunction in and between the cells of your tissues.
The balance of primary versus secondary aging is likely to be different in different tissues. I noticed a few recent papers that look at narrow aspects of muscle aging and find a surprising lack of primary aging, for example. This suggests that many of the observed changes that occur in muscle early in the aging process are driven as much by a lack of exercise - and related matters of lifestyle that have a negative impact on health - as by the known forms of biological damage down at the level of cells and tissues.
Repair of skeletal muscle after injury is a key aspect of maintaining proper musculoskeletal function. Studies have suggested that regenerative processes - including myogenesis and angiogenesis - are impaired during advanced age, but evidence from humans is limited. This study aimed to compare active muscle regeneration between healthy young and older adults. We evaluated changes [in] muscle regeneration at precisely two (T2) and seven (T3) days following acute muscle injury [in] men and women aged 18-30 and ≥ 70 years, matched for gender and body mass index.
Following muscle injury, force production declined 16% and 14% in young and older adults, respectively, by T2 and in each group returned to 93% of baseline strength by T3. Despite modest differences in the pattern of response, post-injury changes in intramuscular concentrations of myogenic growth factors and number of myonuclear cells were largely similar between groups. Likewise, post-injury changes [in] indices of inflammation [and] angiogenesis did not significantly differ between groups. These findings suggest that declines in physical activity and increased co-morbidity may contribute to age-related impairments in active muscle regeneration rather than aging per se.
Aging is associated with a progressive decline in skeletal muscle mass. It has been hypothesized that an attenuated muscle protein synthetic response to the main anabolic stimuli may contribute to the age-related loss of muscle tissue. The aim of the present study was to compare the muscle protein synthetic response following ingestion of a meal-like amount of dietary protein plus carbohydrate between healthy young and older men.
Twelve young (21 ± 1 years) and 12 older (75 ± 1 years) men [consumed labeled protein, allowing] us to assess the subsequent incorporation of casein-derived amino acids into muscle protein. [There were] no differences between groups. We conclude that the use of dietary protein-derived amino acids for muscle protein synthesis is not impaired in healthy older men following intake of protein plus carbohydrate.
You can't exercise your way out of aging to death, but you can certainly make life harder for yourself (and shorter, and more expensive) by failing to remain trim and fit. On the flip side of the coin, there is this recent research below: it suggests that the intrinsic primary aging of muscle isn't something that you can do much about through exercise, even while exercise is enormously beneficial for other reasons.
A fundamental challenge for modern medicine is to generate new strategies to cope with the rising proportion of older people within society, as unaddressed it will make many health care systems financially unviable. Ageing impacts both quality of life and longevity through reduced musculoskeletal function. What is unknown in humans is whether the decline with age, referred to as "sarcopenia," represents a molecular ageing process or whether it is primarily driven by alterations in lifestyle, e.g. reduced physical activity and poor nutrition.
Because the details of such interactions will be uniquely human, we aimed to produce the first reproducible global molecular profile of human muscle age, one that could be validated across independent clinical cohorts to ensure its general applicability. We combined this analysis with extensive data on the impact of exercise training on human muscle phenotype to then identify the processes predominately associated with age and not environment.
We were able to identify unique gene pathways associated with human muscle growth and age and were able to conclude that human muscle age-related molecular processes appear distinct from the processes directly regulated by those of physical activity.