In addition, numerous studies describe the natural loss of muscle mass in the aged. Mayer et al. note that muscle strength decreases gradually between the third and fifth decade of life (Mayer et al., 2011: 359). They describe an ‘accelerated, non-linear decrease of muscle mass up to 15% that has been shown to increase to as much as 30% by the 8th decade in sedentary geriatric patients’. Other studies (Watson, 2000; Brennan, 2002) report the rate of muscle mass loss to be more gradual, stating that losses of 3–5% are seen following the sixth decade of life. In their studies, Watson (2000) and Brennan (2002) also reported strength loss as high as 30% per decade after age 60.

Strength loss studies suggest that traditional aerobic and endurance training activities employed in rehabilitation, while effective in the reduction of coronary heart disease, may also contribute to positive changes in both muscle strength and bone density (Wallace & Cumming, 2000; Kean et al., 2004).

Mayer et al. (2011) cite several studies supporting these findings, suggesting that muscle mass may be increased with training intensities ranging from 60% to 85% of a patient’s maximum voluntary strength (Mayer et al., 2011). In their research, Mayer et al. cite training effects having a positive effect on the maintenance of muscle strength through gains in muscle mass. Unfortunately, they also report compliance as clinicians’ greatest obstacle, noting that current studies show that only 10–15% of the elderly participate in regular training sessions.

The decrease in ground substance creates a loss of critical interfiber distance which restricts the ability of the fibers to move smoothly over each other. With intervertebral disc disease of the spine, decreased collagen mobility may compromise not only spinal mobility, but also spine length. Changes in the length of the spine may also impair breathing patterns in the geriatric patient (Wilson, 2004).

Contractures, frequently the result of tight joint capsules, fibrotic or short muscles, or other scar tissues, are part fibrous adhesions and part collagenous shortening. Newly developed contractures have a greater portion of fibrinous adhesions, whereas chronic contractures are more collagenous. Normal activity may break down fibrinous adhesions, but collagenous shortening often requires heat, prolonged low-load progressive stretching and possible surgical manipulation.

Hyaluronic acid is secreted from the hyaline (articular) cartilage that covers the surface of synovial joints. Compression of the joint enhances this secretion which entraps the synovial fluid among the hyaluronic acid molecules and lubricates the joint during movement. Secretion of hylauronic acid decreases with age, thus causing a diminution in the effectiveness of joint lubrication (Pickles, 1983). Another source of joint stiffness is said to occur as a result of ‘articular gelling’. In healthy joints surface-active phospholipids (SAPL) inhibit the ‘gelling’ process (Hills & Thomas, 1998). What triggers the ‘deactivation’ of SAPL in the joint is not known.

Cartilage, having no direct blood supply of its own, receives its nutrients from the blood flow in adjacent bones and the synovial fluid in the joint cavity. Chondroblasts secrete a glycoprotein (chondroitin sulfate) into the surrounding matrix and, through osmosis, attract water containing dissolved gases, inorganic salts and other organic materials necessary for normal cartilage cell metabolism. Dehydration of the cartilage occurs with increasing age due to decreased secretion of chondroitin sulfate (Pickles, 1983). Normal loading and unloading of cartilage is necessary for the movement of nutrients in and out of the chondrocytes. Without joint compression, metabolites remain in the matrix and oxygen content is lowered, causing a reduction in glycoprotein secretion and an increase in the collagen precursor, procollagen. This process may convert hyaline cartilage to fibrocartilage. Degeneration of the cartilage is not reversible. However, further deleterious changes in the cartilage can be avoided through initiation of regular activities that promote alternating compression and expansion (relaxation) of the joint resulting in increased nutrition to the cartilaginous tissue.