Contributors to Metabolic Disease Risk Following Spinal Cord Injury

Abstract

Spinal cord injury (SCI) induced changes in neurological function have significant impact on the metabolism and subsequent metabolic-related disease risk in injured individuals. This metabolic-related disease risk relationship is differential depending on the anatomic level and severity of the injury, with high level anatomic injuries contributing a greater risk of glucose and lipid dysregulation resulting in type 2 diabetes and cardiovascular disease risk elevation. Although alterations in body composition, particularly excess adiposity and its anatomical distribution in the visceral depot or ectopic location in non-adipose organs, is known to significantly contribute to metabolic disease risk, changes in fat mass and fat-free mass do not fully account for this elevated disease risk in subjects with SCI. There are other negative adaptations in body composition including reductions in skeletal muscle mass and alterations in muscle fiber type, in addition to significant reduction in physical activity, that contribute to a decline in metabolic rate and increased metabolic disease risk following SCI. Recent studies in adult humans suggest cold- and diet-induced thermogenesis through brown adipose tissue metabolism may be important for energy balance and substrate metabolism, and particularly sensitive to sympathetic nervous signaling. Considering the alterations that occur in the autonomic nervous system (SNS) (sympathetic and parasympathetic) following a SCI, significant dysfunction of brown adipose function is expected. This review will highlight metabolic alterations following SCI and integrate findings from brown adipose tissue studies as potential new areas of research to pursue.

Energy balance following diets of varying fat content: metabolic dysregulation in a rodent model of spinal cord contusion

“…Spinal cord injury results in debilitating impact on motor and sensory control of the limbs. The long‐term reductions in mobility and locomotor activity result in negative impact on the metabolic health of injured persons (Smith and Yarar‐Fisher ). Even beyond the altered energy expenditure complexities following SCI, changes in energy intake and utilization may contribute to the increased MetS rates in this population (Smith and Yarar‐Fisher ).…”

“…The long‐term reductions in mobility and locomotor activity result in negative impact on the metabolic health of injured persons (Smith and Yarar‐Fisher ). Even beyond the altered energy expenditure complexities following SCI, changes in energy intake and utilization may contribute to the increased MetS rates in this population (Smith and Yarar‐Fisher ). Chronic injury to the cord can also alter the functioning of the central nervous system as whole, changing the neural connectivity within and between higher‐order brain centers and germane to the current work, body‐weight regulation (Smith and Yarar‐Fisher ).…”

“…Even beyond the altered energy expenditure complexities following SCI, changes in energy intake and utilization may contribute to the increased MetS rates in this population (Smith and Yarar‐Fisher ). Chronic injury to the cord can also alter the functioning of the central nervous system as whole, changing the neural connectivity within and between higher‐order brain centers and germane to the current work, body‐weight regulation (Smith and Yarar‐Fisher ). Finally, in the context of nutrient rich, palatable Western diets that are both high in saturated fats and carbohydrates, persons with SCI may fare worse than noninjured individuals because of the various neural and hormonal impairments associated with their injury (Smith and Yarar‐Fisher ).…”

Locomotor training with adjuvant testosterone preserves cancellous bone and promotes muscle plasticity in male rats after severe spinal cord injury

“…Skeletal muscle atrophy and impaired muscle function are hallmarks of spinal cord injury (SCI) that are negatively associated with walking function (DiPiro et al, 2015) and that worsen risk for several metabolic comorbidities (Smith & Yarar-Fisher, 2016). SCI also produces severe bone mineral density (BMD) deficits and deleterious alterations to skeletal microarchitecture in the unloaded limbs, which contribute to increased fracture risk (McCarthy, Bloomer, Gall, Keen, & Ferguson-Pell, 2012).…”

Effects of Arm-Crank Exercise on Fitness and Health in Adults With Chronic Spinal Cord Injury: A Systematic Review

“…Indeed, following an autonomic and motor-sensory complete, cervical SCI (i.e., greatest disruption to brainstem-spinal sympathetic pathways), peak heart rate, circulating catecholamines and venous return are reduced, brachial blood pressure is low and stroke volume is restricted ( Krassioukov and West, 2014 ; Cruz and Blauwet, 2018 ). Furthermore, the dimished descending sympathetic drive following high level SCI may impact substrate mobilization (lipolysis) during exercise and adipose tissue metabolism ( Smith and Yarar-Fisher, 2016 ; Cowley, 2018 ). The aformentioned exercise-related physiological dysfunctions caused by high-level SCI can impact exercise capacity and may influence the magnitude of a training effect with aerobic exercise interventions in this population.…”