Abstract
Reduced cardiorespiratory fitness or cardiorespiratory deconditioning is a secondary physical impairment commonly reported to affect people after traumatic brain injury (TBI), both in the short- and long-term. Eleven studies have measured peak oxygen uptake${\rm ({\dot V}O}_{{\rm 2peak}} )$to evaluate fitness in this population. The mean (SD)${\rm \dot VO}_{{\rm 2peak}}$from these studies was 27.2 (6.7) mL.kg−1·min−1, which is markedly below the average fitness level of age-matched healthy individuals. The aetiology of cardiorespiratory deconditioning has not been well evaluated among people with TBI; however, studies on prolonged bed rest and studies on the acute consequences of TBI inform our current understanding. The primary aim of this paper is to present a model to describe the physiological factors contributing to the development of cardiorespiratory deconditioning among people with severe TBI. We propose that both central and peripheral factors contribute to reduced fitness, and that these changes occur because of both the initial brain damage and trauma sustained and the prolonged and initially extreme physical inactivity that is commonly experienced after this type of injury. Reduced fitness can significantly affect the ability to return to pre-injury activities. Given that reintegration into the community is a key goal of rehabilitation among people with TBI, interventions that can prevent or reverse reduced fitness need to be implemented.
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