As we get older changes occur in all the structures we normally use to challenge the forces of gravity. At first, I would like to describe the effect of aging in our musculoskeletal system starting with our bones and then moving on to our muscles and joints. Our skeletal structure is a model of internal rigidity that allows us mobility and which protects our vital organs. Bone is made of mineral deposits principally calcium that takes up to about 45% of its volume, soft tissue that accounts for 30% of its volume and water (Medina,1996). Human bones can withstand pressures of about 24.000 pounds per square inch; yet, if you removed the mineral deposits what is left would be flexible enough to tie it into knots (Medina,1996). There are compact long bones in our thighs and arms, spongy short bones in our wrists and ankles, flat bones in our ribs and irregularly shaped bones that can either be compact or spongy. The adult body is continually resculpting and replacing older structures with newer bone, and the cells responsible for that are the osteoblasts while the osteoclasts are the ones that reabsorb the solid bone material. The inability to keep up this work in later years accounts for much of the skeleton’s aging process. Eventually, there is a progressive loss of bone mineral content as the years go by. In addition, the rate of reabsorbsion by the osteoclasts exceeds the rate of replacement meaning that there is an overall reduction in bone mass. Hence, the bone become weaker and as we get older they begin to fail. Besides, there appears to be age related delivery problems in the ability of the small intestine to continue to absorb some basic building blocks such as calcium (Medina, 1996). The failure may be due to a reduction in vitamin D, which is the one involved in snatching calcium out of the food by giving it to the systems that feed our bones. Without an adequate supply of these raw materials, new bone minerals would not be laid down; thus, the bone would get weaker and weaker. There may also be an increase in the overall porosity of a given bone’s internal structure, which would have the same weakening effect. When we are young, our bones break in the same way a young branch does when it is snapped from a tree, a great deal of bending must occur before it breaks, and when it does, many energy-absorbing fracture lines are created (Medina,1996). When we are older, the change in mineralization makes our bones not only weaker, but also more brittle making them harder to repair because our ability to fix them lessens with age.
Moreover, age-related gender differences exist in the aging process. There are two ways to measure the difference. First, in a measure of total skeletal mass, men lose 3% of their skeletal weight per decade, while women lose 8% per decade. As a measure of total mineral density throughout adult life, the total reduction in women is about 30%, while in men is about 15% (Brooks, 2004). Women eventually achieve a rate of loss that is double that of men. Post-menopausal women are affected the most, due to estrogen loss. I will address the effect of personal habits such as exercise on slowing down such processes, but we need to keep in mind that The Clock of Ages ticks irreversibly inside our bones.
The primary factor contributing to our loss of mobility as we get older has to do with how the aging process affects our joints. Joints can be subdivided into many categories, based on certain common characteristics. One way is to organize them according to their ability to move and in so doing we find three overall classes: diarthrotic joints are joints that are freely movable (knees and shoulders); amphiarthrotic joints are joints that can move slightly (the discs lying between bones in the back); and synarthrotic joints are joints that do not move (the human skull) (Hamill, 1995). As we age, tiny but very important internal molecular interactions within collagen and elastin fibers begin to change. This causes contiguous fibrous structures in our ligaments and tendons to fragment meaning that the ligaments and tendons are not able to handle the stressful forces placed upon them (Hamill, 1995). As a result, they become more prone to injury. Besides, as we get older, the arterial cartilage, that transparent friction-reducing coating on the edges of our bones, begin to change and the cells that normally manufacture these cartilagenous layers change their molecular output (Medina, 1996). Consequently, the structure becomes thinner and less springy causing a restriction in mobility.
To understand how muscles are affected by the passage of years, it is important to understand that between our 40s and 50s the loss is fairly minimal. By the time we reach our 60s and 70s, there is a 10–20% reduction in total strength (Brooks, 2004). When we really experience loss is in our 70s and 80s, typically 30–40% of the total. This loss is more severe in the muscles of the legs than in the hands and arms (Brooks, 2004).
Muscles are some of the most age-resistant tissues we possess. Our muscular abilities decline with age, primarily because they lose some of their mass. It appears that, after a period of time, certain muscle fibers start to atrophy. They don’t all do it at the same rate (hence the differences seen in our fast- and slow-twitch capabilities), and different muscle groups show different levels of destruction (Brooks, 2004). However, myofibers eventually die, and the more fibers that are destroyed, the less mass exists within the muscle. The cells are eventually replaced with connective tissue and, later, with fat. This reduction in mass means a loss of cells and an overall decrease in strength. Because this loss is measured at the cellular level, the next question is: why do the cells die? The first idea takes its cue from what happens to muscle when it is unused. When these tissues no longer receive neural input, there is pronounced atrophy and reabsorption of left-over muscle molecules. When these nerves die, the muscles no longer contract. Another theory has to do with a loss of blood flow to a particular area. As we age, it is increasingly difficult for the blood supply to nourish and cleanse some of our deeper tissues (Medina, 1996). If this happens to a muscle, the muscle cells will die. This has the obvious effect of weakening the overall muscle tissue in which such degeneration occurs. The second idea has less to do with communication than with energy sources. The mitochondria’s are responsible for giving muscles their energy. There is some evidence that they have less of an ability to pump energy into the tissues as we increase in age. This lack of energy would render some of the fibers inactive, that would possibly lead to atrophy and cell death (Medina, 1996).
There is a great deal of evidence suggesting that this deterioration of our skeletal muscles can be slowed down through exercise. If the muscle remains active, it will not atrophy as quickly. The tissue can maintain or even increase its overall strength, regardless of the age at which it is tested. In fact, aging adults can benefit from exercise, relative to their previous capabilities, at the same rate younger people do. For example, I teach elderly people thought the “Silver Sneakers” program twice a week and we do cardio as well as strength training, and I can definitely say that they greatly benefit from exercise. Regardless their age and or fitness level their range of motion and strength levels has increased amazingly. 
On the other hand, our bones age primarily because of a loss of minerals. The ability to keep minerals stuck to our bones is a complex task, requiring efficient absorption from the intestine and a ready supply of cellular re-modelers (Medina, 1996). The effect of exercise on these processes has not been greatly studied, yet research still needs to be done.
Therefore, if muscles can be greatly improved with exercise, and bones may not be improved at all, how are the joints affected by increased activity? No amount of exercise can eliminate or reverse the damage that has accumulated over a lifetime of use (Brooks, 2004). The greatest benefit to keeping our joints as flexible as comes from exercising muscles. If the various muscle groups that support the joints can be strengthened, less stress will be placed upon the weakened tendons, ligaments and joint structures (Brooks, 2004). However, the verdict from the passage of years is clear. The tendons and ligaments will break down, the cartilage will change molecular composition and the fluid between bones will get too thin that even exercise cannot reverse these processes (Medina, 1996). Elevated physical activity only serves to increase the likelihood of injury.As a result, the aging process cannot be reversed but we need to learn how to live and cope with it. I would like to quote Amiel “To know how to grow old is the master work of wisdom, and one of the most difficult chapters in the great art of living”. 

References 
Brooks, Douglas. (2004). The Complete Book of Personal Training. Campaign: IL, Human Kinetics.

Hamill, Joseph,. Knutzen, Kathleen. (1995). Biomechanics: Basis of the Human Movement. Lippincott William and Wilkins.

Medina, John. (1996). The Clock of Ages: Why we age, How we age, Winding Back the Clock.Cambridge NY:New YorkCambridgeUniversity Press.