The extent to which the sympathetic nervous system and other neuroendocrine transmitters regulate adipose tissue lipolysis during basal and stimulated conditions is unclear. Individuals with a spinal cord injury (SCI) lack direct sympathetic innervation to tissues below the level of lesion. This disruption of neural pathways affects both direct stimulation of abdominal fat tissue as well as indirect stimulation by hormones (i.e., catecholamines) of the adrenal medulla. Because of the lack of direct neural and circulating catecholamine input to lower-body fat tissue, persons with SCI represent a model for examining lipolysis in the absence of major sympathetic drive. This protocol examines the effects of exercise and isoproterenol stimulation on adipose tissue lipolysis in persons with and without sympathetic innervation of the adrenal medulla and adipose tissue. To test the role of direct sympathetic innervation and circulating catecholamines in regulating fat breakdown in adipose tissue, lipolysis (i.e., glycerol production) will be measured in situ in able-bodied subjects and those with a spinal cord injury, at rest and during arm exercise, using the technique of microdialysis. We hypothesize that SCI will have a reduced lipolytic rate, due to lower direct and circulating catecholamine levels, compared to AB subjects. Furthermore, the degree of disruption of lipolysis in SCI will vary according to lesion level, such that subjects with high thoracic (T1- T4) or cervical spinal cord lesions will show the greatest reduction in lipolytic rate, because of loss of both direct and adrenally- mediated sympathetic stimulation.
