Combined Aerobic and Resistance Exercise Training Reduces Acute Exercise‐Induced Platelet‐Monocyte Complex Formation in Overweight, Postmenopausal Women
Authors: Levitt Michael M , Cardenas Maria A , Cook Carmen A , O'Connor Jacob B , Orr Kaci L , Richie Bryan , Kreutzer Andreas , Haynes Jay , Cheek Dennis J , Phillips Melody D 
Published: June 2021

Inactivity‐related diseases such as cardiovascular disease (CVD) involve a complex interplay among endothelial cells, leukocytes and activated platelets in response to vascular injury. Activated platelets are involved in atherogenesis and can promote an inflammatory phenotype of both the vasculature and leukocytes, particularly monocytes. Platelet‐monocyte complexes (PMCs) are markers of in vivo platelet activation and may be early indicators of subclinical inflammation.

PURPOSE

To examine the influence of combined aerobic and resistance exercise training on platelet activation, as measured by PMCs, and to characterize the acute exercise‐induced response of PMCs in a population at risk for CVD.

METHODS

Thirty‐eight overweight‐obese (BMI: 32.8 ± 4.6 kg×m−2, age: 64 ± 5.1 years) post‐menopausal women were randomly assigned to either an exercise (EX, n=20) or education control (ED, n=18) group. EX performed 2 sets of 8 resistance exercises and 25 minutes of treadmill walking three times a week for 12 weeks while ED attended education classes (CPR certification, invited authors, health‐related talks) twice weekly for the same duration. Before (BT) and after (AT) the intervention, EX performed a single exercise bout during which blood was obtained pre‐exercise, immediately post‐exercise, 1‐hour and 2 hours post‐exercise. Blood was obtained at the same time points in resting ED. PMCs were identified via flow cytometry and analyzed in each monocyte phenotype. Monocyte phenotypes were defined as: Mon1 (CD14++CD16−), Mon2 (CD14++CD16+), and Mon3 (CD14loCD16++). All events positive for both CD14 and CD42a (marker for platelets) were considered PMCs.

RESULTS

Exercise training resulted in a significant increase in VO2max (BT: 21.1 ± 0.85, AT: 23.7 ± 0.90 ml×kg−1×min−1, p < 0.001) and leg press strength (BT: 70 ± 4.1, AT: 99 ± 5.9 kg, p < 0.001), while no changes in fitness were observed in ED. Exercise training (EX: BT = 27.6 ± 2.7, AT = 23.7 ± 2.9 %) prevented the observed increase in percent PMC in ED (ED: BT = 20.9 ± 2.9, AT = 26.4 ± 3.2 %, p = 0.029). We observed a group x training interaction where exercise training reduced mean PMC percentage across all time points (EX: BT = 27.6 ± 2.4, AT = 22.1 ± 2.8 %, p = 0.034) while ED did not change (ED: BT = 20.2 ± 2.5, AT = 23.6 ± 2.9 %). PMCs formed with Mon1 monocytes followed a similar response (p = 0.031), but no significant changes were observed with PMCs formed in Mon2 or Mon3. A single exercise bout did not influence PMCs in any phenotype.

CONCLUSION

Our results indicate that 12 weeks of combined exercise training reduces PMC formation in obese, postmenopausal women; however, a single bout of exercise did not significantly change percent PMC. The increase in PMCs in ED after the intervention is difficult to explain, but may be related to the time of year of the BT and AT experimental trials. These data may provide evidence that exercise training reduces CVD risk via reductions in platelet activation.

Support or Funding Information

TCU Invests in Scholarship Grant; TCU Research and Creative Activities Fund

This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.