Hemostatic and Inflammatory Responses to Exercise Induced Heat Stress in Highly Trained Males
Melanie A. Cyr, Alexandra G. Harding, Anne Ledyard, Mikayla R. Nemes
Dr. Denise L. Smith
The purpose of this study is to to examine the hemostatic and inflammatory responses to an acute bout of exercise in the heat as compared to in thermoneutral conditions in highly trained males.
Nine healthy highly trained men reported between 6:30 and 9:30am and cycled at 60%VO2max for 30 min on two occasions; one exercise bout was in a thermoneutral (TN) condition and the other was in heat stressed (HS) condition, with the order randomly assigned. Blood was drawn from the antecubital vein before exercise following five minutes rest on the cycle ergometer, and also immediately post-exercise.
ADP induced time to occlusion showed no effects of exercise over time or between conditions. There was a significant decrease over time for EPI-induced time to occlusion with no differences between HS and TN. There was increase in fibrinogen in both HS and TN conditions. Activated partial thromboplastin time (aPTT) decreased in both conditions. Prothrombin time (PT) remained unchanged in both HS and TN. These findings indicate increased coagulation with exercise, although there was no significant main effect for condition. Cell adhesion molecule concentration increased only in the TN environment. Plasminogen activator inhibitor (PAI-1) concentration increased significantly in both environments, which suggests a hypofibrinolytic state with exercise. There was no change in interleukin-10 (IL-10) or tumor necrosis factor-a (TNF-a) concentration with exercise in either condition.
The activation or depression of coagulation, fibrinolysis, and inflammation varies between a thermoneutral and heat stress exercise condition, and over time. During exercise induced heat stress, coagulation activity increased, fibrinolysis decreased, and inflammation was unaffected. This suggests enhanced clotting activity during exercise in the heat, and this imbalance between clotting and fibrinolysis is the pathogenesis for cardiovascular events, and requires further investigation.