Influence of sympathetic vascular regulation on heart-rate scaling structure: spinal cord lesion as a model of progressively impaired autonomic control.

Estimation of self-similarity is a promising tool for quantifying alterations in cardiovascular dynamics. To evaluate the as yet unexplored influence of sympathetic vascular regulation on the scaling exponent, namely on the parameter characterizing self-similarity, we studied patients with a spinal cord injury as a model of progressively impaired vascular control. We considered 24 able-bodied subjects (AB) and 23 paraplegics with increasing lesion levels: between T(12) and L(4) (n=7); T(5) and T(11) (n=9); and C(6) and T(4) (n=7). We recorded the heart rate in three conditions characterized by increasing sympathetic activation: supine (SUP), sitting (SIT) and exercise (EXE). We calculated the scaling exponent by detrended fluctuation analysis (H(DFA)). Sympathetic activation had different effects on H(DFA), depending on the lesion level. H(DFA) tended to decrease in AB from SUP (0.85+0.02; mean+SEM) and SIT (0.84+0.02) to EXE (0.79+0.02). It remained constant in the T(12)-L(4) group (0.92+0.04, 0.94+0.05 and 0.94+0.04, respectively), while it increased significantly in the T(5)-T(11) group (0.88+0.07, 0.94+0.05, 1.00+0.08) and increased even more in the C(6)-T(4) group (0.83+0.07, 0.91+0.05, 1.06+0.06). Results suggest that heart-rate self-similarity depends on vascular sympathetic control, because it is altered by spinal-cord lesions, even when cardiac neural control is intact.