Static exercise-induced increase in blood pressure in individuals with cervical spinal cord injury.

Abstract

To compare the pressor response to static exercise in subjects with cervical spinal cord injury (SCI) at the C6 to C8 level with that in able-bodied control subjects. In these SCI subjects, the descending supraspinal sympathetic neurons and afferent pathways from the contracting muscles to peripheral vessels via the medullary cardiovascular center are damaged. Mean arterial blood pressure, heart rate, and plasma concentrations of norepinephrine, epinephrine, renin activity, vasopressin, aldosterone, and human atrial natriuretic peptide were measured during a 2-minute period of sustained contraction of elbow flexor group muscle in 7 SCI subjects and 7 age-matched able-bodied control subjects. Static exercise resulted in a significant increase in mean blood pressure (p<.05) in both SCI subjects (pre-exercise. 74.7+/-2.2 mm Hg; static exercise, 81.9+/-4.1 mm Hg) and control subjects (pre-exercise, 101.0+/-4.2 mm Hg; static exercise, 117.0+/-4.9 mm Hg). In SCI subjects, there was no change in heart rate during exercise, whereas in control subjects heart rate increased during exercise (p<.05) (pre-exercise, 8.7+/-3.8 beats/min: static exercise, 76.0+/-3.1 beats/min). There were no significant changes in the hormone levels in the SCI subjects throughout the experiment. The significant increase in mean blood pressure observed in the present study indicates the presence of peripheral control from muscle receptors and evoked pressor response during static exercise in SCI subjects.