21 - Deconditioning and energy expenditure

Summary

Introduction

The relative contributions of restoration of basic physiologic processes, neuroplasticity, and behavioral compensation to functional recovery after neurologic insult are unknown. Traditionally, the extent of recovery was viewed as being almost exclusively dependent on the state of the neuromuscular system. As a consequence, intervention strategies have focused primarily on improving the capacity of that system – an approach that has met with limited success in terms of restoring functional independence. It is now becoming clear that recovery cannot be explained solely on the basis of improved neuromuscular function. For example, Roth and colleagues (1998) determined that less than a third of the variance in disability following stroke can be explained by the extent of neurologic impairment. Recently, attention has turned to multi-system approaches to neurorehabilitation that address the interaction of neuromuscular, cardiorespiratory, and musculoskeletal systems and the environment. With growing evidence of a high prevalence of deconditioning among individuals with neurologic involvement, the interaction between the neuromuscular and cardiorespiratory systems is of particular interest.

Both primary effects of upper motor neuron damage (e.g., paralysis, spasticity, sensory-perceptual impairments) and secondary effects (e.g., contractures, inactivity, disuse muscle atrophy, fatigue) contribute to the deconditioned state of individuals with neurologic lesions. Frequently, these effects are superimposed on an already compromised cardiorespiratory system resulting from co-morbid cardiovascular disease (Kennedy, 1986; Roth, 1993) as well as lifestyle- and age-related declines in cardiorespiratory fitness (Bouchard et al., 1990).