OBESITY @ 110 POUNDS
If you've ever had a hunch that rates of obesity are severely under-represented in society, your suspicions are probably not incorrect. Disuse muscular atrophy occurs as early as 5 days after the onset of immobilization, so it's not hard to imagine the havoc 10 or 15 or 40 years of low/no activity could wreak upon your muscular system.
The image on the right is a typical representation of what happens with muscular denervation & the loss of higher threshold motor units. Muscular function in those areas may not be completely lost if activity levels remain above a certain low level threshold, but with 40% fewer muscle fibers, fat (adipose) tissue will begin its marbling journey into your tissue, gradually causing greater rates of physical dysfunction.
This is precisely why it's possible to be obese at 110 pounds. As contractile tissue is gradually replaced with adipose tissue - within & between muscles, lean body mass plummets - by 40% in the example above. As your lean mass craters, your ability to store glycogen diminishes in concert with your lowered capacity for the higher intensity work which would be required to utilize said glycogen, & maintain the higher threshold motor units; fast-twitch fibers.
Instead, dietary consumption of carbohydrate is almost immediately & exclusively stored in visceral or muscular fat deposits, and as such, your lean mass decreases at the same time as your fat mass goes through the roof. This makes it possible to see a body fat percentage north of 40% or 50%, even in somebody who doesn't remotely appear to have a weight problem. (think skinny-fat)
Needless to say, this problem is exacerbated by the ravages of time, in conjunction with a poor diet and a complete lack of higher intensity physical activity. The potential upside - or silver lining - is that the loss of motor units in muscle, and motor neurons in the spinal cord, may be attenuated by the reinnervation of 'rescue' neuron branches, which give the remaining motor units in muscle an increased density of muscle fibers. This, in turn, may help to preserve some amount of overall muscle mass, as well as the muscles' capacity to generate meaningful force.
The authors of this study speculate - quite reasonably in my opinion - that losses in motor units should therefore precede clinically relevant muscle loss, such as that found in degenerative processes such as Sarcopenia. Of further interest is the idea that reinnervated motor units such as those found in the elderly, tend to be less controllable due to instability in the neuromuscular junction, potentially leading to issues with fine motor control, or more 'complex' motor control.
As neurons in the spinal cord can never be recovered once they're lost, it becomes increasingly important to PREVENT the loss of motor neurons and the motor units they supply. Research has shown that neuromuscular adaptations to higher intensity exercise are very favorable throughout middle age, and in the elderly as well. Even with the reduced movement control as described above, resistance training has been demonstrated to improve movement control and stability in the elderly, thus providing a direction for future research and early detection preventative care.