Regular physical exercise is associated with overall reduced risk of primary cardiac arrest.[4] D Wosornu et al. showed that a three-month aerobic training program (3 sessions per week) decreased resting fibrinogen concentration.[9] A meta-analysis showed that an exercise intervention over 2 weeks is associated with reduced inflammatory activity in patients with coronary artery disease (CAD). C-reactive protein and fibrinogen have provided the strongest evidence.[10] Platelet activation by strenuous exercise has been studied in 12 physically active and 12 sedentary individuals before and after a standardized treadmill exercise test. Among sedentary subjects, exercise caused an augmentation of the platelet activation and reactivity. In contrast, in physically active subjects exercise failed to induce alteration in platelet activation state.[11] Our previous study identified that moderate-intensity exercise training (60% maximal oxygen consumption for 30 min per day, 5 days/week for 8 weeks) reduced resting and strenuous exercise-induced platelet aggregation and platelet adhesion under shear flow in healthy men,[12] which were accompanied by decreased vWF binding to platelets and expression of P-selectin on platelets.[13] Accordingly, our main research question is that whether the short-term CR program in the current investigation ameliorates hemostatic imbalance at rest and platelet and coagulation activation at maximal stress exercise.