This study investigated alterations of heart rate (HR) and sympathovagal balance during lower body negative pressure (LBNP) in 7 males with tetraplegia(T; spinal cord lesions from C5-C7) and 7 able-bodied men (C). HR was continuously monitored during graded LBNP at -15, -30, -45 and -60 mmHg. Parasympathetic (PNS) and sympathetic (SNS) control of HR were derived using coarse grained spectral analysis. Compared to resting values, HR at -15 mmHg did not change significantly in either group. However, at -30, -45 and -60 mmHg LBNP, HR increased significantly (p<0.05) in T (by 18, 30, and 36 b·min-1, respectively) and in C (by 7, 14, 26 b·min-1, respectively), but markedly less in C compared to T(p<0.05). PNS was significantly reduced (p<0.05) in T at -15, -30 and-45 mmHg (by -0.01, -0.17, -0.20, respectively) and in C during -15, -45 and-60 mmHg (by -0.09,-0.10,-0.17, respectively). No significant differences in PNS were observed between T and C. SNS activity did not change significantly in T or C at any level of LBNP, except for a significant increase in C at -30 mmHg (p<0.05). This study demonstrates that exposure to high levels of orthostatic stress (above -15 mmHg LBNP) elicit a significantly greater cardioacceleration in individuals with tetraplegia compared to able-bodied subjects. Remarkably, these results suggest that in people with tetraplegia as well as in able-bodied cohorts the increase in HR during LBNP is primarily elicited by vagal withdrawal and not by increased sympathetic activity.
B-12 SLIDE SPINAL CORD INJURY