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Regular Resistance Training Enhances Fibrinolytic Potential but Does Not Affect Coagulation
Paul R Nagelkirk1, Kayla Soave1, Cody Altherr
1Integrative Exercise Physiology Laboratory, Ball State University, Muncie, IN.
Medicine and Science in Sports and Exercise
|June 11, 2021
Summary
This study found that an 8-week resistance training (RT) program reduced plasminogen activator inhibitor-1 (PAI-1), decreasing fibrinolysis inhibition. These findings suggest RT may lower thrombotic event risk.
Area of Science:
- Exercise Physiology
- Hemostasis Research
- Biochemistry
Background:
- Resistance training (RT) is known to improve body composition and strength.
- The effects of RT on hemostasis, particularly coagulation and fibrinolysis, require further investigation.
- Understanding these effects is crucial for assessing the overall health benefits of RT.
Purpose of the Study:
- To determine the impact of an 8-week whole-body RT program on markers of coagulation and fibrinolysis in healthy adults.
- To investigate changes in specific hemostatic factors following a structured RT intervention.
Main Methods:
- Sixteen healthy participants (23 ± 5 years) underwent an 8-week RT program (3x/week, 2-3 sets, 8-12 reps, 60-80% 1RM).
- Assessed strength, body composition, and circumferences pre- and post-training.
- Analyzed plasma for tissue plasminogen activator (tPA) activity and antigen, plasminogen activator inhibitor-1 (PAI-1) activity and antigen, fibrinogen, and coagulation factors VII (FVII) and VIII (FVIII).
Main Results:
- RT significantly increased lean mass and strength (chest press, leg press) (P < 0.05).
- A significant decrease in PAI-1 activity and antigen was observed post-RT (P < 0.05).
- No significant changes were found in tPA activity/antigen, fibrinogen, FVII, or FVIII.
Conclusions:
- The 8-week RT program effectively decreased PAI-1 levels, indicating reduced inhibition of fibrinolysis.
- Coagulation parameters remained unaffected by the RT intervention.
- These results suggest that regular RT may favorably modulate thrombotic risk by improving fibrinolytic capacity.
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