Autonomic Alterations After SCI: Implications for Exercise Performance

Abstract

The disruption of autonomic pathways after spinal cord injury (SCI) leads to a highly unstable cardiovascular system, with impaired blood pressure and heart rate regulation. In addition to low resting blood pressure, on a daily basis the majority of those with SCI suffer from transient episodes of aberrantly low and high blood pressure (termed orthostatic hypotension and autonomic dysreflexia, respectively). Due to a combination of these autonomic disturbances and a myriad of lifestyle factors, the pernicious process of cardiovascular disease is accelerated after SCI, resulting in increased risk of stroke and heart disease. Unfortunately, these secondary consequences of SCI are only beginning to receive appropriate clinical attention. Immediately after high-level SCI, major cardiovascular abnormalities present in the form of neurogenic shock. After subsiding, new issues related to blood pressure instability arise, including orthostatic hypotension and autonomic dysreflexia. Disruption of autonomic function leads to inappropriate exercise responses often resulting in blunted cardiovascular capacity. After high thoracic or cervical SCI, blood pressure responses to exercise are reduced or absent, while often heart rate cannot rise above that set by the sinoatrial node, which together reduce aerobic performance. Some athletes choose to induce potentially life-threatening episodes of autonomic dysreflexia in order increase blood pressure (termed “boosting”), as low blood pressure is a limiting factor for exercise performance in many people with SCI. Due to our understanding of the capacity of autonomic/cardiovascular disability to impact sport performance, classification of athletes with disability should consider autonomic injury to allow for equality between teams and help obviate the need to induce autonomic dysreflexia to improve performance.