ORIGINAL CONTRIBUTION Lower-Extremity Functional Electrical Stimulation Decreases Platelet Aggregation and Blood Coagulation in Persons With Chronic Spinal Cord Injury: A Pilot Study

Background: Individuals with spinal cord injury (SCI) develop premature cardiovascular disease. Regular exercise reduces the incidence and symptoms of cardiovascular disease in able-bodied individuals; these salutary effects of exercise have not been documented in persons with SCI. Objective: To evaluate the effects of functional electrical stimulation leg cycle ergometry (FES-LCE) exercise training on platelet aggregation and blood coagulation in persons with SCI. Participants: Subjects (n 5 14) with stable chronic (.1 year) paraplegia (T1–T10) or tetraplegia (C4–C8). Methods: Blood samples were collected before and after the first and eighth sessions (2 sessions per week for 4 weeks) of FES exercise. Results: Platelet aggregation was inhibited by 20% after the first session and by 40% (P , 0.001) after the eighth session. Thrombin activity was unchanged after the first session (10.7 ± 0.85 s to 10.43 ± 0.56 s) and decreased after the eighth session (12.5 ± 1.98 s to 11.1 ± 1.7 s; P , 0.0003). Antithrombin III activity increased after the first (103.8% ± 8.9% to 110% ± 6.9%; P , 0.0008) and eighth sessions (107.8% ± 12.1% to 120.4% ± 13.1%; P , 0.0001). Cyclic adenosine monophosphate increased after the first (9.9% ± 2.5% to 15.8% ± 3%; P , 0.001) and eighth sessions (17.8% ± 4.2% to 36.5% ± 7.6%; P , 0.0001). After the eighth session, factors V and X increased significantly (88% ± 27% to 103% ± 23%, P , 0.0001; 100% ± 40% to 105% ± 7%, P , 0.01, respectively); factors VII and VIII and fibrinogen did not change significantly. A significant reduction in platelet activation/aggregation was demonstrated in response to FESLCE. The decrease in thrombin level was caused by the simultaneous increase in antithrombin activity. Conclusion: These findings provide new insight into the potential protective effects of FES-LCE against the risk of cardiovascular disease. J Spinal Cord Med. Apr 2010;33(2):150–158