High-Intensity Exercise Training Improves Basal Platelet Prostacyclin Sensitivity and Potentiates the Response to Dual Anti-Platelet Therapy in Postmenopausal Women

Figures

• 

  Figure 1. Average time spent in each training zone (%) over the 8-week high-intensity exercise training period (n = 13). The training zones were pre-defined by POLAR TEAM Pro. Zone 1 was ≤60% HRmax, Zone 2 was 61 to 70% HRmax, Zone 3 was 71 to 80% HRmax, Zone 4 was 81 to 90% HRmax, and Zone 5 was ≥91% HRmax (Polar Electro Oy, Kempele, Finland).

• 

  Figure 2. Basal platelet reactivity (expressed as platelet aggregation (%)) to 6 concentrations of the platelet agonists before and after 8 weeks of exercise training with and without dual anti-platelet therapy (DAPT): (A) collagen, (B) thrombin receptor activator peptide 6 (TRAP6), (C) U46619 (U4), (D) U46619-induced aggregation at (1.98 µM), (E) adenosine 5′-diphosphate (ADP), and (F) epinephrine. *, indicates a statistically significant increase compared with pre-training (n = 13 for all agonists).

• 

  Figure 3. The half maximal effective concentration (EC50) for platelet aggregation with (B,D,F,H) or without (A,C,E,G,I) dual anti-platelet therapy (DAPT): (A) collagen, (B) collagen with DAPT, (C) thrombin receptor activator peptide 6 (TRAP6), (D) TRAP6 with DAPT, (E) U46619, (F) U46619 with DAPT, (G) ADP, (H) ADP with DAPT, and (I) epinephrine. *, indicates a statistically significant decrease with training (n = 13 for all agonists).

• 

  Figure 4. Platelet sensitivity to the anti-aggregatory effects of prostacyclin (1–300 nM), with and without dual anti-platelet therapy (DAPT). Agonist-induced platelet aggregation to (A) 10 µg∙mL−1 collagen (n = 12), (B) 10 µM thrombin receptor activator peptide 6 (TRAP6) (n = 13), (C) 20 µM adenosine 5′-diphosphate (ADP) (n = 12), and (D) 10 µM U46619 (n = 12). *, indicates a statistically significant decrease with training with the control treatment. #, indicates a statistically significant decrease with training with the DAPT treatment.

• 

  Figure 5. The half maximal inhibitory concentration (IC50) for inhibition of platelet aggregation by prostacyclin (1–300 nM) with (B,D,F,H) or without (A,C,E,G) dual anti-platelet therapy (DAPT). (A) collagen (n = 12), (B) collagen with DAPT (n = 12), (C) thrombin receptor activator peptide 6 (TRAP6; n = 13), (D) TRAP6 with DAPT (n = 13), (E) U46619 (n = 12), (F) U46619 with DAPT (n = 12), (G) adenosine 5′-diphosphate (ADP) (n = 12), and (H) ADP with DAPT (n = 12). *, indicates a statistically significant decrease with training. $, indicates a trend for a decrease with training.

• 

  Figure 6. Western blots on platelets isolated from whole blood (n = 10 for all proteins): (A) Thromboxane A2 Synthase (p = 0.829), (B) Thromboxane A2 Receptor (p = 0.686), (C) Cyclooxygenase-1 (p = 0.844), (D) Prostacyclin Receptor (p = 0.296), and (E) Representative Western blots and TGX Stain-Free image. Protein content is expressed in arbitrary units (AU).

• 

  Figure 7. Plasma levels of (A) 6-keto prostaglandin F1α (6-keto PGF1α) (p = 0.895) and (B) thromboxane B2 (p = 0.579) measured pre- and post-training (n = 13).