After spinal cord injury, the decrease in lean muscle mass, autonomic dysfunction, and relative physical inactivity (compared to the able-bodied population) contribute to the development of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM) to be leading causes of morbidity and mortality.1-3 There is increasing evidence that chronic low-grade inflammation, characterised by elevated resting concentrations of pro-inflammatory cytokines, mediate this relationship.4 Persons with SCI have elevated concentrations of pro-inflammatory markers compared with able-bodied (AB) individuals,3,5 impaired glucose utilization and vascular remodelling that occurs as soon as 3-6 weeks post injury.6,7 In the able-bodied (AB) population, exercise training increases lean body mass, improves glucose utilization, and importantly, also reduces chronic low-grade inflammation, potentially via the acute increase in plasma concentrations of interleukin (IL)-6 and anti-inflammatory cytokines following each session.10 While exercise is a cost-effective intervention to lower the risk for chronic disease, the reduced physical capacity of people with SCI often precludes participation in exercise and anti-inflammatory benefits of exercise are not seen in SCI compared to AB persons. There is growing and emerging evidence that acute (1 session only) and chronic (repeated sessions over 4-8 weeks) passive heating can decrease inflammation in AB persons. In persons with SCI, acute (one ~60min session) passive heat therapy decreases inflammation, but for a short time only. To impact morbidity and mortality, long-term attenuation of inflammation will be required and thus, the impact of chronic (i.e.; repeated sessions) passive heat therapy over a longer time period needs to be studied. This is the first study to investigate the impact of chronic passive heat therapy in persons with SCI and its impact on inflammation, glucose utilization, and endothelial function. We hypothesize that six weeks of passive heat therapy will decrease inflammatory mediators, glucose utilization and endothelial function. Methods: Ten persons with sensorimotor complete (AIS A) SCI (levels C2-T6) will participate in 8 weeks without passive heating (control = CON) followed by 8 weeks of passive heat stress (intervention = INT) using electrical heating blankets for 60min 2-3x/week. Inflammatory markers (TLR4, Hsp70, CRP, IL-6, TNF-α,IL-1β, IL-10), oral glucose tolerance and skin blood flow changes with local thermal hypermia (nitric oxide dependent) will be measured at baseline, after CON, then after INT. Anticipated outcomes: Chronic passive heat stress will decrease chronic inflammation, improve glucose utilization and improve endothelial function. Preliminary studies and future directions: This work utilizes a feasible and practical method of passive heating using electrical heating blankets and water perfused suits that has been well-developed in Dr. Trbovich’s lab.11 This proposal takes next ste...