The effect of acute aerobic exercise on hemostasis in obstructive sleep apnea
Individuals with obstructive sleep apnea (OSA) have an altered hemostatic balance; however, the exercise response is less described. The purpose of this study is to determine the hemostatic response after acute aerobic exercise in obstructive sleep apnea.
Eighteen males (nine OSA vs. nine controls) were recruited from the university and local community. Individuals with evidence of cardiovascular, pulmonary, or metabolic disease were excluded. An apnea-hypopnea index (AHI) of >5 was a criterion for OSA. Subjects performed a treadmill exercise test at 35 and 70% predicted VO2 reserve during the morning hours. Pre-exercise blood samples were obtained after 15 min supine rest and within 2 min following exercise. Repeated measures ANOVA were performed for factor VIII antigen, tissue plasminogen activator (tPA) antigen, tPA activity, and PAI-1 activity. Correlational analysis compared resting and post-exercise hemostatic factors with age, BMI, and AHI.
Mean AHI was 13.00 ± 12.6. No exercise × condition interactions were observed for hemostatic markers. There was a main effect for exercise in factor VIII, tPA antigen, and tPA activity in both groups. PAI-1 activity tended to be elevated in OSA (145%) compared to controls which remained after exercise (205%) (P = 0.05). Post-exercise FVIII/Ag correlated with BMI (r = 0.52), while resting tPA/Ag correlated with AHI (r = 0.49) and age (r = 0.50).
The hemostatic response after acute aerobic exercise is unaffected in mild OSA, although PAI-1 activity seems to be elevated, reducing fibrinolytic potential. BMI seems to correlate with FVIII/Ag, while tPA/Ag is associated with AHI and age.
KeywordsCoagulation Fibrinolysis Sleep Obstructive sleep apnea Exercise
- 1.Somers VK, White DP, Amin R, Abraham WT, Costa F, Culebras A, Daniels S, Floras JS, Hunt CE, Olson LJ (2008) Sleep apnea and cardiovascular disease: an American heart association/American college of cardiology foundation scientific statement from the American heart association council for high blood pressure research professional education committee, council on clinical cardiology, stroke council, and council on cardiovascular nursing in collaboration with the national heart, lung, and blood institute national center on sleep disorders research (National Institutes of Health). J Am Coll Cardiol 52(8):686–717PubMedCrossRefGoogle Scholar
- 3.Pataka A, Riha RL (2009) The obstructive sleep apnoea/hypopnoea syndrome—an overview. Resp Med 2(3):111–117Google Scholar
- 9.Fox H, Purucker H-C, Holzhacker I, Tebtmann U, Bitter T, Horstkotte D, Graml A, Woehrle H, Oldenburg O (2016) Prevalence of sleep-disordered breathing and patient characteristics in a coronary artery disease cohort undergoing cardiovascular rehabilitation. J Cardpulm Rehabil 36(6):421–429CrossRefGoogle Scholar
- 14.Pinsky DJ, Liao H, Lawson CA, Yan S-F, Chen J, Carmeliet P, Loskutoff DJ, Stern DM (1998) Coordinated induction of plasminogen activator inhibitor-1 (PAI-1) and inhibition of plasminogen activator gene expression by hypoxia promotes pulmonary vascular fibrin deposition. J Clin Invest 102(5):919PubMedPubMedCentralCrossRefGoogle Scholar
- 16.Bärtsch P, Haeberli A, Hauser K, Gubser A, Straub P (1988) Fibrinogenolysis in the absence of fibrin formation in severe hypobaric hypoxia. Aviat Space Envir MD 59(5):428–432Google Scholar
- 22.Medicine ACoS (2013) ACSM’s guidelines for exercise testing and prescription. Lippincott Williams & Wilkins, USAGoogle Scholar
- 29.Thögersen AM, Jansson J-H, Boman K, Nilsson TK, Weinehall L, Huhtasaari F, Hallmans G (1998) High plasminogen activator inhibitor and tissue plasminogen activator levels in plasma precede a first acute myocardial infarction in both men and women evidence for the fibrinolytic system as an independent primary risk factor. Circulation 98(21):2241–2247PubMedCrossRefGoogle Scholar