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 T₁₂ and L₄ (n=7); T₅ and T₁₁ (n=9); and C₆ and T₄ (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-L₄ group (0.92+0.04, 0.94+0.05 and 0.94+0.04, respectively), while it increased significantly in the T₅-T ₁₁ group (0.88+0.07, 0.94+0.05, 1.00+0.08) and increased even more in the C₆-T₄ 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.