Exercise training from late middle age until senescence does not attenuate the declines in skeletal muscle aerobic function

Abstract

We previously showed that 7 wk of treadmill exercise training in late-middle-aged rats can reverse the modest reductions in skeletal muscle aerobic function and enzyme activity relative to values in young adult rats (Exp Physiol 93: 863-871, 2008). The purpose of the present study was to determine whether extending this training program into senescence would attenuate the accelerated decline in the muscle aerobic machinery normally seen at this advanced age. For this purpose, 29-mo-old Fisher 344 Brown-Norway rats underwent 5 or 7 mo of treadmill exercise training. Training resulted in greater exercise capacity during an incremental treadmill exercise test and reduced percent body fat in 34- and 36-mo-old rats and improved survival. Despite these benefits at the whole body level, in situ muscle aerobic capacity and muscle mass were not greater in the trained groups at 34 mo or 36 mo of age. Similarly, the trained groups did not have higher activities of citrate synthase (CS) or Complex IV in homogenates of either the plantaris (fast twitch) or the soleus (slow twitch) muscles at either age. Finally, protein expression of CS (a marker of mitochondrial content) and peroxisome proliferator-activated receptor-gamma coactivator-1 (relating to the drive on mitochondrial biogenesis) were not higher in the trained groups. Therefore, although treadmill training from late middle age into senescence had significant benefits on running capacity, survival, and body fat, it did not prevent the declines in muscle mass, muscle aerobic capacity, or mitochondrial enzyme activities normally seen across this age, revealing a markedly diminished plasticity of the aerobic machinery in response to endurance exercise at advanced age.

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

“…However, there is also evidence that the plasticity of the NMJ to physical activity is attenuated with ageing and denervation may become exacerbated by exercise training in very old age 7. Specifically, aged rats subjected to long‐term exercise training exhibited greater muscle atrophy and myocyte oxidative damage compared with aged‐matched sedentary controls 295, 296. The potential for physical activity to induce adverse effects when initiated in old age has not been addressed in humans.…”

PGC-1α and Myokines in the Aging Muscle – A Mini-Review

“…In any case, recent advances imply that a modulation of PGC-1 ␣ levels in muscle might be beneficial for sarcopenia patients. First, old rats with a blunted induction of PGC-1 ␣ expression subsequent to exercise are also resistant to exercise-mediated improvement of sarcopenia [54] . Similarly, PGC-1 ␣ is required for exercise-mediated prevention of the functional decline of mitochondrial enzymes in aging in mice [ 60 ].…”

Initiating treadmill training in late middle age offers modest adaptations in Ca2+handling but enhances oxidative damage in senescent rat skeletal muscle

“…The training protocol is described in detail in a previous publication from our laboratory (3). Briefly, the rats were trained on a treadmill as described in our previous study (2) over the first 2 mo (60 min, 5 days/wk), as this was shown to yield significant benefits for skeletal muscle and whole body function in late-middle-aged animals.…”