Chronic Exercise Effects: The Therapeutic Outcome

Abstract

Electrical stimulation causes muscle to contract by the generation of action potentials on nerve and muscle following the application of electrical current to the skin, motor nerve, or the muscle directly (see, e.g. Peckham, 1976; Petrofsky et al., 1976; Solomonow et al., 1978; Thoma et al., 1978). Current design of microprocessors allows multichannel control through standard feedback control techniques for movement in muscle (Petrofsky and Phillips, 1979, 1980, 1981; Phillips and Petrofsky, 1980). Using these techniques, it is now possible to control movement in muscle. However, one problem that may not be apparent is the deconditioning of the body that follows spinal cord injury. After SCI, muscle is not used and atrophies. This so-called disuse atrophy is similar to the atrophy that occurs in muscles after prolonged hospital stays or when a leg or arm is immobilized in a cast for a few months. Associated with disuse atrophy is demineralization of bones. This is analogous to the demineralization that occurs with prolonged bed rest and with prolonged stays outside the earth’s gravity. When bone is not stressed in a normal manner, calcium leaves the bone and is excreted by the body. This makes the bone fragile and predisposes it to injury. The fragility of bones creates a long-term medical problem for people who have been in wheelchairs for many years. The lack of use of part of the body also results in deconditioning of the heart and the cardiovascular and pulmonary systems. This predisposes SCI individuals to cardiovascular disease, renal disease, and pulmonary disease (such as pneumonia). Consequently, before wide-scale computer-controlled technology can be applied to wheelchair-bound individuals or before any successful reversal of SCI can be attempted, the patient needs to be reconditioned to normal physical fitness or as near to normal as possible.