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Effect of Air Travel on Exercise-Induced Coagulatory and Fibrinolytic Activation in Marathon Runners

Parker, Beth PhD*; Augeri, Amanda MS*; Capizzi, Jeffrey MS*; Troyanos, Christopher ATC; Kriz, Peter MD; D'Hemecourt, Pierre MD; Thompson, Paul MD*

Clinical Journal of Sport Medicine: March 2011 - Volume 21 - Issue 2 - p 126-130
doi: 10.1097/JSM.0b013e31820edfa6
Original Research

Objective: Air travel and exercise change hemostatic parameters. This study investigated the effect of air travel on exercise-induced coagulation and fibrinolysis in endurance athletes.

Design: A prospective longitudinal study.

Setting: The 114th Boston Marathon (April 19, 2010).

Participants: Forty-one adults were divided into travel (T: 23 participants, living >4-hour plane flight from Boston) and nontravel (C: 18 participants, living <2-hour car trip from Boston) groups.

Independent Variables: Age, anthropometrics, vital signs, training mileage, and finishing time were collected.

Main Outcome Measures: Subjects provided venous blood samples the day before (PRE), immediately after (FINISH), and the day following the marathon after returning home (POST). Blood was analyzed for thrombin–antithrombin complex (TAT), tissue plasminogen activator (t-PA), hematocrit (Hct), and the presence of Factor V Leiden R506Q mutation.

Results: Thrombin–antithrombin complex increased more in T subjects in PRE to FINISH samples (5.0 ± 4.0 to 12.9 ± 15.6 μg/L) than in C subjects (4.0 ± 1.2 to 6.1 ± 1.2 μg/L; P = 0.02 for comparison). The t-PA increased in both the T (5.4 ± 2.3 to 25.1 ± 12.2 ng/mL) and C (5.6 ± 2.0 to 27.7 ± 11.3 ng/mL) groups in PRE to FINISH samples, and this response did not differ between groups (P = 0.23 for comparison). Both groups exhibited similar t-PA and TAT values at POST that were not different than PRE (all P > 0.35). Age was related to the FINISH TAT values in T (r2 = 0.19; P = 0.04) but not in C (r2 = 0.03; P = 0.53) subjects.

Conclusions: Results suggest that the combination of air travel and marathon running induces an acute hypercoaguable state; this hemostatic imbalance is exaggerated with increasing age.

From the *Henry Low Heart Center, Department of Cardiology, Hartford Hospital, Hartford, Connecticut; and †Department of Sports Medicine, Children's Hospital, Boston, Massachusetts.

Submitted for publication July 29, 2010; accepted January 6, 2011.

Dr Paul Thompson is a consultant for AstraZeneca International, Merck & Co, Inc, Schering-Plough Corporation, Takeda Pharmaceutical Company Limited, Roche, and Genomas, Inc, and is a member of the speaker's bureau for Merck & Co, Inc, Pfizer Inc, Abbot Laboratories, AstraZeneca International, and Schering-Plough Corporation.

The authors report no conflicts of interest.

Corresponding Author: Beth Parker, PhD, Henry Low Heart Center, Hartford Hospital, Hartford, CT 06102 (e-mail:

© 2011 Lippincott Williams & Wilkins, Inc.