Six months of aerobic exercise training does not prevent a worsening of glucose tolerance in individuals with acute spinal cord injury
Authors: Ely Matthew , Burns Kathryn , Middelbeek Roeland , Goodyear Laurie , Taylor J. Andrew 
Published: May 2023

Individuals with spinal cord injuries (SCI) have a greater incidence of Type 2 Diabetes (T2D) than their non-injured peers. The increased incidence of T2D has been noted in individuals within the first few years after injury, and incidence increases with time since injury. Aerobic exercise training improves long-term glycemic control in non-injured individuals and results in improved glycemic control in individuals with chronic SCI (>10 years). However, it is unknown whether individuals with acute injuries (<3 years) display altered glucose control, and if aerobic training may prevent worsening of glucose control and T2D. Therefore, we assessed blood glucose regulation in individuals <3 years post SCI injury. Glucose regulation was assessed through fasting blood glucose, insulin, hemoglobin A1C (HbA1C), homeostatic model assessment for insulin resistance (HOMA-IR), and an oral glucose tolerance test (OGTT). In addition, body composition was estimated via dual energy x-ray absorptiometry. These assessments were made prior to, and following 3- and 6-months (mo) of aerobic exercise training consisting of hybrid functional electrical stimulation rowing. Data were analyzed with 1-way RMANOVA. Eight individuals (1F, 7M, age 20-45 years) with SCI 9-27 mo post-injury and a neurological level of injury from spinal cord segments C3 to T3 were enrolled. Individuals exercised for 30min per session, at ~60% VO2peak, 2-3 times per week. Fasting glucose (Pre:85±9, 3m:88±8, 6m:86±2 mg/dL, p=0.55), insulin (Pre:6.0±3.8, 3m:5.7±2.5, 6m:3.9±2.5 uIU/mL, p=0.25), HbA1C (Pre:4.9±0.3, 3m:5.0±0.3, 6m:4.8±0.1%, p=0.73) and HOMA-IR (Pre:1.4±1.0, 3m:1.2±0.7, 6m:0.7±0.4, p=0.26) did not change after 6-mo of training. In contrast, the dynamic assessment of glucose tolerance (OGTT) showed dramatic worsening (AUC Pre:15.7±3.8, 3m:17.8±5.9, 6m:17.6±5.8 units, p=0.04) from pre-exercise to 3-mo. Moreover, following 6-mo of exercise training, 1 individual met the diagnostic criteria for impaired glucose tolerance and another 2 for diabetes. Exercise training did not change visceral adipose mass (Pre:1.4±0.9, 3m:1.4±1.2, 6m:1.3±1.2 kg, p=0.96) or total body lean mass (Pre:50.4±9.5, 3m:49.6±9.6, 6m:49.5±9.5kg, p=0.98). These results suggest that fasting measures alone are not sensitive enough in detecting impairments in glucose metabolism in the acute period following a SCI. Interestingly, in people with SCI, whole-body aerobic exercise does not prevent the occurrence of impaired glucose metabolism. The worsening of glucose tolerance occurs despite a conservation of lean mass and no increase in visceral adiposity. It will be of importance to determine the mechanisms underlying the worsening of glycemic control and develop therapies to prevent metabolic disease in SCI. R01 HL117037, F32 HL156675 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.