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Exercise shifts the platelet aggregation modulatory role from native to mildly oxidized low-density lipoprotein


Medicine & Science in Sports & Exercise: May 2000 - Volume 32 - Issue 5 - pp 933-939
BASIC SCIENCES: Original Investigations

HSU, H-C., Y-T. LEE, and M-F. CHEN. Exercise shifts the platelet aggregation modulatory role from native to mildly oxidized low-density lipoprotein. Med. Sci. Sports Exerc., Vol. 32, No. 5, pp. 933–939, 2000.

Purpose: The role of low-density lipoprotein (LDL) lipid peroxides in strenuous exercise-induced changes in platelet function was studied in 30 patients (male/female = 22/8) aged 30–62 yr (mean ± SD = 508). Methods: All subjects were subjected to a treadmill exercise test, using the standard Bruce protocol. Blood samples were collected pre-, peak, and 10 min postexercise to assess hematological and biochemical parameters and platelet aggregation. Ex vivo whole blood platelet aggregation during treadmill exercise was assessed in 10 subjects by adding mildly oxidized LDL.

Results: Preexercise, a correlation existed between plasma thromboxane (TX) levels and plasma LDL cholesterol or β-thromboglobulin (β-TG) levels (r = 0.48, P < 0.05; r = 0.47, P < 0.05, respectively), whereas, at peak exercise, TX and β-TG levels increased, but no correlation was seen. At peak exercise, platelets showed hyperaggregability in terms of maximal amplitude and reaction slope (P < 0.001 and P < 0.01, respectively). In contrast to the increase in plasma lipid peroxide levels seen during peak exercise (P < 0.05), LDL lipid peroxides decreased during exercise, this decrease reaching a statistical significance at 10 min postexercise (P < 0.05). In addition, the ex vivo addition of mildly oxidized LDL (10 mg protein·L−1) to peak exercise blood resulted in a significant attenuation of platelet aggregation and a decrease in TX release. At 10 min postexercise, a correlation was seen between LDL lipid peroxides and TX levels (r = 0.78, P < 0.001) or β-TG levels (r = 0.68, P < 0.005).

Conclusion: These results suggest that LDL lipid peroxides play a role in modulating and attenuating platelet aggregation during strenuous exercise.

It has been suggested that regular physical activity prevents ischemic heart disease (21,28). However, exercise enhances oxygen consumption, resulting in oxygen-related free radical generation and oxidative stress, which are linked to membrane damage, lipid peroxidation, and platelet activation (9,22,32). Low-density lipoprotein (LDL) is reported to activate platelet functions, such as enhancement of thromboxane (TX) release and induction of platelet aggregation (41,45,48), and to be modified under oxidative stress such as exercise (19,20). Recently, it has been reported that the platelet-activating function of LDL resides more in the modified forms of LDL than in native LDL (23,46). Because both forms of LDL are major risk factors for cardiovascular disease, their interactions with platelets, therefore, may play an important role in the pathogenesis of atherosclerosis (25,39).

No reports have appeared on the combined effect of exercise and LDL (native or modified) on platelet-activating activities, such as TX release and platelet aggregation. Oldroyd et al. (31) reported that plasma lipid peroxide activity and TX production can be simultaneously increased under oxidative stress. In a previous study, we observed that the levels of LDL lipid peroxides seen during atrial pacing-induced ischemia correlated with myocardial ischemia and TX release (20). The purpose of this study was therefore to investigate the interaction between strenuous exercise and LDL, as well as their effects on platelet activity. We also attempted to determine whether lipid peroxides in plasma or LDL are a contributing factor for platelet activity during exercise.

Department of Internal Medicine (Cardiology), National Taiwan University Hospital, Chung-Shan South Road, Taipei, TAIWAN

Submitted for publication June 1998.

Accepted for publication June 1999.

Address for correspondence: Dr. Ming-Fong Chen, Department of Internal Medicine (Cardiology), National Taiwan University Hospital, No.7, Chung-Shan South Road, Taipei, 100, Taiwan. E-mail:

©2000The American College of Sports Medicine