The present study demonstrates that treadmill exercise induced platelet aggregation and increased TX levels and β-TG release and plasma lipid peroxide levels, whereas LDL lipid peroxides decreased during exercise, the decrease reaching a statistical significance at 10 min postexercise. The addition of mildly ox-LDL to peak exercise blood resulted in decreased platelet aggregation, suggesting that LDL lipid peroxides attenuate exercise-induced platelet aggregation.
The generally accepted concept that LDL possess platelet-activating properties was confirmed in the present study. At preexercise, plasma LDL cholesterol levels correlated with plasma TX levels; however, this correlation disappeared during strenuous exercise. It has been reported that plasma lipid peroxides might contribute to strenuous exercise-induced platelet activation (17), but no correlation between plasma lipid peroxides and TX levels was seen in this study. The most striking finding was the correlation at 10 min postexercise between LDL lipid peroxides and either plasma TX levels or β-TG levels. We speculate that LDL lipid peroxides play an important role in replacing plasma LDL cholesterol on platelet activation during strenuous exercise. To study what factors might contribute to this paradoxical result, we prepared mildly ox-LDL and observed that it inhibited ex vivo platelet aggregation and the amount of TX release when added to blood drawn during exercise.
Under physiological conditions, LDL is mildly oxidized by activated endothelial cells and monocytes and the mildly ox-LDL is retained in the circulation, because the minimally modified Apo B is not recognized by cellular scavenger receptors (13). In this study, mildly ox-LDL did not significantly affect collagen-induced platelet aggregation and TX release pre- or post-exercise. However, at peak exercise, platelet aggregation was significantly inhibited and TX release reduced, implying that mildly ox-LDL has an attenuating role on platelet activation that is only apparent during strenuous exercise. A possible explanation is that, under preexercise condition, native LDL exists a predominant role on platelet activity and that strenuous exercise shifts this modulatory role from native LDL to mildly ox-LDL, which affects platelet activation; however, other factors such as catecholamine release and neutrophile activation during exercise mask the role of mildly ox-LDL on platelet activation. At 10 min postexercise, these additional factors disappear and the effect of the mildly ox-LDL is seen.
The results of this study indicate that strenuous exercise changes the modulating roles of native and ox-LDL on platelet function. Mildly ox-LDL is formed under physiological conditions, but its role on platelet function is masked by the predominant activity of native LDL and is not seen until under exercise conditions. Further studies are required to clarify the precise mechanisms involved in the effects of strenuous exercise in modifying the effects of native and mildly ox-LDL on platelet function.
The authors are grateful to Hsiu-Tsu Yeh and Zu-Or Hsiao for technical assistance.
This study was supported in part by grants DOH86-TD-025 from the Department of Healthy, Executive Yuan and NSC 88–2314-B002–325 from the National Science Council, Republic of China.
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