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Mental stress and physical exercise increase platelet-dependent thrombin generation
1Second Department of Internal Medicine, Kyorin University School of Medicine, Mitaka, Tokyo, Japan.
Insights
Physical exercise and mental stress both increase thrombin generation, a key factor in blood clots. Beta-blocker therapy, but not aspirin, effectively suppressed this increase, suggesting a potential therapeutic target.
Area of Science:
- Cardiovascular Physiology
- Hemostasis and Thrombosis
Background:
- Thrombin generation is implicated in thrombotic disorders and acute coronary syndromes.
- Mental stress is linked to acute coronary syndromes, but the mechanism remains unclear.
Purpose of the Study:
- To investigate the impact of physical exercise and mental stress on platelet-dependent thrombin generation.
- To explore the role of catecholamines and specific inhibitors in stress-induced thrombin generation.
Main Methods:
- Twelve healthy men underwent treadmill exercise and mental arithmetic stress tests.
- Measurements included platelet-dependent thrombin generation, catecholamines, thrombin-antithrombin III complex (TAT), plasmin-alpha2 plasmin inhibitor complex (PIC), and plasminogen activator inhibitor-1 (PAI-1).
- Interventions included aspirin and metoprolol to assess their effects on thrombin generation.
Main Results:
- Both exercise and mental stress significantly increased thrombin generation.
- Exercise led to transient elevations in catecholamines (epinephrine, norepinephrine, dopamine), while mental stress elevated norepinephrine.
- Metoprolol, a beta-blocker, inhibited the increase in thrombin generation, whereas aspirin did not.
Conclusions:
- Physical exercise and mental stress activate platelet-dependent thrombin generation.
- Beta-blocker therapy can suppress exercise and stress-induced thrombin generation.
- The findings suggest a role for beta-adrenergic pathways in mediating thrombin generation during stress.
Abstract:
Thrombin generation is an important factor in the pathogenesis of thrombogenic disorders and acute coronary syndromes. Increase in mental stress has been associated with the initiation of the acute coronary syndromes, but the exact mechanism is not known. The present study examined the effects of physical exercise and mental stress on platelet-dependent thrombin generation. Twelve healthy men (mean age 34.2 +/- 2.4 years) underwent a treadmill exercise test and a mental stress test by performing mental arithmetic. Platelet-dependent thrombin generation and plasma concentrations of catecholamines, thrombin-antithrombin III complex (TAT), plasmin-alpha2 plasmin inhibitor complex (PIC), and plasminogen activator inhibitor-1 (PAI-1) were measured before, immediately after, and at 10 and 30 min after stress. Thrombin generation increased significantly immediately after exercise, followed by rapid normalization. Mental stress caused a significant increase in thrombin generation 10 min after stress. While plasma concentrations of epinephrine, norepinephrine, and dopamine were elevated immediately after exercise, and rapidly returned to baseline, only plasma norepinephrine increased immediately after mental stress. TAT and PIC concentrations did increase immediately after exercise; however, PAI-1 remained unchanged. The increase in thrombin generation with exercise and mental stress was unaffected by treatment with 81 mg/day of aspirin of 7 days. However, it was inhibited by a single oral 40-mg dose of metoprolol. Both exercise and mental stress cause an increase in platelet-dependent thrombin generation, which was suppressed by beta-blocker therapy, but not by aspirin.