Effects of exercise training and detraining on oxidized low-density lipoprotein-potentiated platelet function in men

Objective: To investigate how exercise training and detraining affect oxidized low-density lipoprotein (Ox-LDL)-potentiated platelet function in men. Design: Cohort study. Setting: Department of physical medicine and rehabilitation. Participants: Ten sedentary men (mean age +/- standard error of the mean, 21.6 +/- 0.2y) who did not engage in any regular physical activity for at least 1 year before the study. Interventions: Subjects cycled on an ergometer at about 50% of maximal oxygen consumption for 30 minutes daily, 5 days a week, for 8 weeks, then detrained for 12 weeks. Main Outcome Measures: During the experimental period, blood samples from the subjects were collected before and immediately after a progressive exercise test (ie, strenuous, acute exercise) every 4 weeks. The following measurements were taken when the subjects were at rest and immediately after exercise: plasma lipid profile, plasma Ox-LDL level, and platelet aggregation and intracellular calcium concentration ([Ca2+](i)) elevation induced by adenosine disphosphate (ADP) alone or simultaneous ADP and Ox-LDL addition. Results: Analytical results indicated that: (1) plasma total cholesterol and LDL levels were reduced after exercise training from 151 +/- 7mg/dL and 58 +/- 2mg/dL to 133 +/- 6mg/dL and 46 +/- 2mg/dL (P < .05), respectively, whereas the plasma OxLDL level remained unchanged; (2) platelet aggregation and [Ca2+](i) elevation promoted by 100mug/mL of Ox-LDL were significantly increased from 70% +/- 5% and 91% +/- 7% of resting level to 108% +/- 4% and 125% +/- 3% after strenuous, acute exercise (P < .05); (3) exercise training decreased resting and postexercise 100mug/mL Ox-LDL-potentiated platelet aggregation (ie, 31% +/- 4% and 82% +/- 4%, respectively; P < .05) and [Ca2+](i) elevation (ie, 35% +/- 6% and 71% +/- 4%, respectively; P < .05); (4) detraining reversed the training effects on lipid profile and platelet function; and (5) treating the platelet with L-arginine-inhibited Ox-LDL-potentiated platelet activation during the experimental period. Conclusions: Our results suggest that 8 weeks of exercise training decreased the plasma LDL level, but failed to influence production of plasma Ox-LDL. Importantly, resting and exercise-induced Ox-LDL-potentiated platelet activation was decreased by exercise training. However, this was reversed by detraining to the pretraining level.