Acute Low Force Electrically Induced Exercise Modulates Post Prandial Glycemic Markers in People with Spinal Cord Injury

Regular exercise involves daily muscle contractions helping metabolize up to 70% of daily ingested glucose. Skeletal muscle increases glucose uptake through two distinct pathways: insulin signaling pathway and muscle contraction mediated AMPK pathway. People with paralysis are unable to contract their muscles which atrophy, transform into insulin resistant glycolytic muscle, and develop osteoporosis. Our goal is to determine if low force electrically induced exercise (LFE) will modulate the post prandial insulin and glucose response in people with and without spinal cord injury (SCI). 18 people with SCI and 23 without SCI (Non-SCI) participated in an assessment of metabolic biomarkers during passive sitting (CTL) and a bout of LFE delivered to the quadriceps/hamstring muscle groups after a glucose challenge. Baseline fasting insulin (p = 0.003) and lactate (p = 0.033) levels were higher in people with SCI, but glucose levels (p = 0.888) were similar compared to the non-SCI population. After 1-h of muscle contractions using LFE, heart rate increased (p < 0.001), capillary glucose decreased (p = 0.004), insulin decreased (p < 0.001), and lactate increased (p = 0.001) in the SCI population. These findings support that LFE attenuates certain metabolic blood biomarkers during a glucose challenge and may offer a lifestyle strategy to regulate metabolic responses after eating among people with SCI.