Older people should undertake resistance exercise, as it has been shown to reduce risk of mortality and age-related disease. Most older people do not do this, and are therefore living with unnecessarily poor health and prospects. In this context, it is interesting to see the data presented here, in which researchers show that overall level of fitness and training in older people has no effect on the ability of resistance training to produce added muscle in a previously untrained part of the body. Yes, there are all sorts of declines relating to muscle tissue function that take place during aging, but a sedentary individual is no worse off than a fit individual in this particular aspect of muscle physiology. Thus it is is never too late to start a program of resistance exercise in order to obtain benefits to health, even if one has been sedentary throughout life.
Skeletal muscle is vital for the maintenance of physical function, nutrient deposition, and basal metabolism. Aging leads to a progressive loss of skeletal muscle, termed sarcopenia, which progresses at a rate of 0.5-1% per annum from the 5th decade, alongside 3-5-fold greater reductions in strength. Accordingly, sarcopenia may drive the development, and progression, of many adverse age-related health events and force a dependence on external healthcare services. Sarcopenia progression is thought to be underpinned by inherent aging factors (i.e., hormonal changes) and aggravated by environmental and lifestyle factors (i.e., poor nutrition, obesity, and reduced activity), that blunt the muscle protein synthesis (MPS) response to normally robust anabolic stimuli, such as hyperaminoacidemia and resistance exercise.
This age-related muscle "anabolic resistance" may be underpinned by impairments in translational efficiency in the mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway. Whilst resistance exercise (RE) is effective at enhancing muscle anabolic sensitivity and augmenting muscle mass and strength in older individuals, myofibrillar adaptive remodeling responses are attenuated compared with younger individuals. However, chronic structured exercise training is known to alter acute muscle protein turnover rates in young and older individuals. Therefore, commencing exercise training in early adulthood, and continuing this practice through middle-to-older age, may offset or delay the onset of muscle anabolic resistance, with implications for age-related muscle loss.
Highly active older individuals who have maintained structured exercise training habits, Master Athletes (MA), display superior indices of physiological function (VO2max and strength), muscle morphology and, typically, a more favorable body composition than their untrained age-matched counterparts (OC). The only study to date to investigate MPS in MA, reported that highly trained master triathletes (older than 50 years) displayed lower MPS rates following a bout of downhill running than younger triathletes. However, rested-state MPS was not measured, preventing firm conclusions regarding the net MPS response to the exercise stimulus. The aim of the present study was to compare 48 hour rested-state and RE-induced integrated myofibrillar protein synthesis (iMyoPS) rates between MA and age-matched untrained individuals and to establish the acute intramuscular signaling response to an acute bout of RE contraction.
Our findings demonstrate no discernible difference in rested-state or exercise-induced iMyoPS rates between MA and OC. Furthermore, we observed no clear difference in the mTORC1-mediated signaling response to exercise between MA and OC. Taken together, these data suggest that despite divergent long-term exercise habits in MA, OC possess a similar capacity to upregulate intramuscular signaling and iMyoPS in response to unaccustomed exercise contraction.