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.
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.
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).
These results suggest that LDL lipid peroxides play a role in modulating and attenuating platelet aggregation during strenuous 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: email@example.com.