Individuals with spinal cord injury (SCI) experience a markedly elevated risk of cardiometabolic disease, including obesity, dysglycaemia, insulin resistance, dyslipidaemia, and hypertension. These abnormalities emerge early following injury and contribute substantially to reduced life expectancy. The physiological drivers of cardiometabolic dysfunction in SCI are multifactorial, arising from paralysis-induced reductions in skeletal muscle mass, impaired autonomic regulation, altered body composition, and substantial barriers to engaging in sufficient physical activity.

The nutritional needs of individuals with SCI remain poorly characterised, and dietary recommendations developed for the general population are unlikely to be appropriate. Injury-related physiological changes mean that standard nutritional guidelines may systematically overestimate or underestimate true requirements, potentially exacerbating metabolic dysregulation. Such nutritional mismatches may contribute to the early development of obesity, dysglycaemia, and insulin resistance following SCI, highlighting the need for condition-specific dietary and metabolic strategies.

Although physical activity is commonly advocated as a cornerstone of cardiometabolic disease prevention, its effectiveness in SCI is inherently constrained. Current guidelines predominantly recommend upper-body exercise; however, absolute exercise capacity and energy expenditure are limited compared with lower-limb exercise, restricting the achievable cardiometabolic stimulus. While exercise interventions can improve certain aspects of cardiorespiratory fitness and metabolic health in chronic SCI, evidence for consistent improvements in glycaemic control remains equivocal. Acute studies demonstrate minimal effects of pre-meal exercise on postprandial glucose, and although high-intensity interval training can induce metabolic adaptations, responses are variable and feasibility remains challenging.

Neuromuscular electrical stimulation (NMES) represents a promising adjunct or alternative strategy by activating large lower-limb muscle groups independent of voluntary motor control, with evidence indicating improvements in postprandial glucose regulation. This talk will present preliminary findings from our ongoing work quantifying the acute effects of NMES on glucose control using dual stable isotope tracer methodology during an oral glucose tolerance test, alongside assessments of real-world feasibility and acceptability.

Ultimately, beyond its clinical relevance, SCI provides a unique human model of extreme deconditioning, muscle atrophy, and disrupted central and peripheral regulation, offering a powerful opportunity to interrogate the physiological mechanisms governing metabolic control in vivo and inform targeted nutritional and metabolic interventions.