| Summary: | 碩士 === 長庚大學 === 復健科學研究所 === 92 === Background: Platelet aggregation induced by pulsatile shear stress occurring in a stenosed artery is one of the mechanisms of thrombosis. It is also noticed that on one hand, regular exercise can reduce the risk of cardiovascular diseases, and on the other hand, vigorous exercise Provokes sudden cardiac death. This is the first study to demonstrate that effect of strenuous exercise on pulsatile shear-induced platelet aggregation (PSIPA) and how exercise training and detraining affects pulsatile PSIPA, and elucidates mechanisms that underlie PSIPA. Methods: Thirty sedentary healthy men engoaged in acute, strenuous exercise（VO2max）on a bicycle ergometer, then randomly divided into control and training groups. The trained men were trained on a bicycle ergometer at 60% maximal heart rate for 30 minutes per day, 5 day per week for 8 weeks, then detraining for 8 weeks, acute, strenuous re-operation at the after trained and detraining. The same acute, strenuous exercise was applied to the control group at the beginning of this study 8 weeks thereafter. At rest and immediately after acute exercise, platelets were exposed to a pulsatile shear stress, to closely approximate in vivo conditions such as those in stenotic arteries. Platelet aggregation and vWF binding, GPIIb/IIIa activation, and P-selectin expression on platelets induced by pulsatile shear stress were analyzed both before and immediately after acute exercise.
Results: Analytical results demonstrated that pulsatile shear stress was associated with a higher binding of vWF to platelets and expression of P-selectin and activation of GPIIb/IIIa on platelets than low-shear condition. Acute, strenuous exercise increased the extent of PSIPA and was accompanied by an increase in vWF binding and P-selectin expression on platelets, but not GPIIb/IIIa activation. Moreover, treating the platelet with P-selectin monoclone antibodies decreased pulsatile shear-induced platelet aggregation. Although the extent of PSIPA was increased by strenuous exercise; the enhancement of PSIPA disappeared after exercise training. However, this training effect seems reverse to pre-exercise training after detraining.
Conclusion: Exercise training suppresses the extent of PSIPA, probably by reducing vWF binding to platelets and P-selectin expression on platelets. However, detraining reverses the training effects. These findings provide new insight into possible protective effects of exercise training against the risk of thrombosis associated with stenotic arteries.
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