Passive hind-limb cycling improves cardiac function and reduces cardiovascular disease risk in experimental spinal cord injury : Cardio-metabolic effects of passive hind-limb cycling in SCI

Little is known about the structure of athletes' hearts of anatomic variations associated with training. Echocardiograms of 56 active athletes were obtained. Mean left ventricular end-diastolic volume and mass were increased in athletes involved in isotonic exercise, such as swimming (181 ml, 308 g) and running (160 ml, 302 g), compared with controls (101 ml, 211 g); wall thickness was normal (less than or equal to 12 mm). Athletes involved in isometric exercise, such as werstling and shot putting, had normal mean left ventricular end-diastolic volumes (110 ml, 122 ml), but increased wall thickness (13 to 14 mm) and mass (330 g, 348 g). Thus, athletes participating in isotonic exercise had increased left ventricular mass with cardiac changes similar to those in chronic volume overloads. Athletes participating in isometric exercise had increased left ventricular mass with cardiac changes similar to those in chronic pressure loads, recognizing greater left ventricular mass and volume in well-trained athletes aids in interpreting values deviating from "normal" limits.

Spinal cord injury (SCI) with resultant quadriplegia or high paraplegia is associated with significant dysfunction of the sympathetic nervous system. This alteration of sympathetic nervous system activity occurs as a consequence of loss of supraspinal control of the sympathetic nervous system and is further complicated by at least three subsequent phenomena that occur below the level of SCI: reduced overall sympathetic activity, morphologic changes in sympathetic preganglionic neurons, and peripheral alpha-adrenoceptor hyperresponsiveness. Reduced sympathetic activity below the level of SCI appears to result in orthostatic hypotension, low resting blood pressure, loss of diurnal fluctuation of blood pressure, reflex bradycardia, and, rarely, cardiac arrest. Peripheral alpha-adrenoceptor hyperresponsiveness likely accounts for some, if not the majority, of the excessive pressor response in autonomic dysreflexia and may also contribute to decreased blood flow in the peripheral microcirculation, potentially increasing susceptibility to pressure sores. What has yet to be established is whether this alpha-adrenoceptor hyperresponsiveness is a consequence of receptor hypersensitivity or a failure of presynaptic reuptake of noradrenaline at the receptor level. Better understanding of the pathophysiology of sympathetic nervous system dysfunction after high-level SCI should allow development of more effective measures to manage clinical complications.