Emily V Nosova1, Priscilla Yen2, Karen C Chong1, Hugh F Alley1, Eveline O Stock3, Alex Quinn4, Jason Hellmann5, Michael S Conte6, Christopher D Owens7, Matthew Spite5, S Marlene Grenon8. 1. Department of Surgery, University of California, San Francisco, California; VIPERx Laboratory, San Francisco, California. 2. Department of Biostatistics, University of California, Los Angeles, California. 3. Cardiovascular Research Institute, University of California, San Francisco, California; Department of Medicine, University of California, San Francisco, California. 4. Cardiovascular Research Institute, University of California, San Francisco, California. 5. Division of Cardiovascular Medicine, University of Louisville, Kentucky. 6. Department of Surgery, University of California, San Francisco, California; Cardiovascular Research Institute, University of California, San Francisco, California. 7. Department of Surgery, University of California, San Francisco, California; VIPERx Laboratory, San Francisco, California; Department of Surgery, Veterans Affairs Medical Center, San Francisco, California. 8. Department of Surgery, University of California, San Francisco, California; VIPERx Laboratory, San Francisco, California; Department of Surgery, Veterans Affairs Medical Center, San Francisco, California. Electronic address: marlene.grenon@ucsfmedctr.org.
Abstract
BACKGROUND: Sedentarism, also termed physical inactivity, is an independent risk factor for cardiovascular diseases. Mechanisms thought to be involved include insulin resistance, dyslipidemia, hypertension, and increased inflammation. It is unknown whether changes in vascular and endothelial function also contribute to this excess risk. We hypothesized that short-term exposure to inactivity would lead to endothelial dysfunction, arterial stiffening, and increased vascular inflammation. METHODS: Five healthy subjects (four men and one woman) underwent 5 d of bed rest (BR) to simulate inactivity. Measurements of vascular function (flow-mediated vasodilation to evaluate endothelial function; applanation tonometry to assess arterial resistance), inflammation, and metabolism were made before BR, daily during BR, and 2 d after BR recovery period. Subjects maintained an isocaloric diet throughout. RESULTS: BR led to significant decreases in brachial artery and femoral artery flow-mediated vasodilation (brachial: 11 ± 3% pre-BR versus 9 ± 2% end-BR, P = 0.04; femoral: 4 ± 1% versus 2 ± 1%, P = 0.04). The central augmentation index increased with BR (-4 ± 9% versus 5 ± 11%, P = 0.03). Diastolic blood pressure increased (58 ± 7 mm Hg versus 62 ± 7 mm Hg, P = 0.02), whereas neither systolic blood pressure nor heart rate changed. 15-Hydroxyeicosatetraenoic acid, an arachidonic acid metabolite, increased but the other inflammatory and metabolic biomarkers were unchanged. CONCLUSIONS: Our findings show that acute exposure to sedentarism results in decreased endothelial function, arterial stiffening, increased diastolic blood pressure, and an increase in 15-hydroxyeicosatetraenoic acid. We speculate that inactivity promotes a vascular "deconditioning" state characterized by impaired endothelial function, leading to arterial stiffness and increased arterial tone. Although physiologically significant, the underlying mechanisms and clinical relevance of these findings need to be further explored. Published by Elsevier Inc.
BACKGROUND: Sedentarism, also termed physical inactivity, is an independent risk factor for cardiovascular diseases. Mechanisms thought to be involved include insulin resistance, dyslipidemia, hypertension, and increased inflammation. It is unknown whether changes in vascular and endothelial function also contribute to this excess risk. We hypothesized that short-term exposure to inactivity would lead to endothelial dysfunction, arterial stiffening, and increased vascular inflammation. METHODS: Five healthy subjects (four men and one woman) underwent 5 d of bed rest (BR) to simulate inactivity. Measurements of vascular function (flow-mediated vasodilation to evaluate endothelial function; applanation tonometry to assess arterial resistance), inflammation, and metabolism were made before BR, daily during BR, and 2 d after BR recovery period. Subjects maintained an isocaloric diet throughout. RESULTS: BR led to significant decreases in brachial artery and femoral artery flow-mediated vasodilation (brachial: 11 ± 3% pre-BR versus 9 ± 2% end-BR, P = 0.04; femoral: 4 ± 1% versus 2 ± 1%, P = 0.04). The central augmentation index increased with BR (-4 ± 9% versus 5 ± 11%, P = 0.03). Diastolic blood pressure increased (58 ± 7 mm Hg versus 62 ± 7 mm Hg, P = 0.02), whereas neither systolic blood pressure nor heart rate changed. 15-Hydroxyeicosatetraenoic acid, an arachidonic acid metabolite, increased but the other inflammatory and metabolic biomarkers were unchanged. CONCLUSIONS: Our findings show that acute exposure to sedentarism results in decreased endothelial function, arterial stiffening, increased diastolic blood pressure, and an increase in 15-hydroxyeicosatetraenoic acid. We speculate that inactivity promotes a vascular "deconditioning" state characterized by impaired endothelial function, leading to arterial stiffness and increased arterial tone. Although physiologically significant, the underlying mechanisms and clinical relevance of these findings need to be further explored. Published by Elsevier Inc.
Authors: Dick H J Thijssen; Mark A Black; Kyra E Pyke; Jaume Padilla; Greg Atkinson; Ryan A Harris; Beth Parker; Michael E Widlansky; Michael E Tschakovsky; Daniel J Green Journal: Am J Physiol Heart Circ Physiol Date: 2010-10-15 Impact factor: 4.733
Authors: Lin T Guey; Clive R Pullinger; Brian Y Ishida; Patricia M O'Connor; Christian Zellner; Omar L Francone; Jason M Laramie; Josefina M Naya-Vigne; Ketevan A Siradze; Prakash Deedwania; Rita F Redberg; Philip H Frost; Albert B Seymour; John P Kane; Mary J Malloy Journal: Am J Cardiol Date: 2011-08-01 Impact factor: 2.778
Authors: S Marlene Grenon; Xinshu Xiao; Shelley Hurwitz; Craig D Ramsdell; Natalie Sheynberg; Christine Kim; Gordon H Williams; Richard J Cohen Journal: Ann Noninvasive Electrocardiol Date: 2005-07 Impact factor: 1.468
Authors: Melinda S Schaller; Greg J Zahner; Warren J Gasper; William S Harris; Michael S Conte; Nancy K Hills; S Marlene Grenon Journal: J Clin Lipidol Date: 2017-06-24 Impact factor: 4.766
Authors: Robert M Restaino; Lauren K Walsh; Takuma Morishima; Jennifer R Vranish; Luis A Martinez-Lemus; Paul J Fadel; Jaume Padilla Journal: Am J Physiol Heart Circ Physiol Date: 2016-01-08 Impact factor: 4.733
Authors: Ronald J Headid; Elizabeth J Pekas; TeSean K Wooden; Won-Mok Son; Gwenael Layec; John Shin; Song-Young Park Journal: Am J Physiol Heart Circ Physiol Date: 2020-07-10 Impact factor: 4.733
Authors: Breno Q Farah; Raphael M Ritti-Dias; Polly S Montgomery; Ana I Casanegra; Federico Silva-Palacios; Andrew W Gardner Journal: J Vasc Surg Date: 2015-10-27 Impact factor: 4.268
Authors: Nathan C Winn; Ryan Pettit-Mee; Lauren K Walsh; Robert M Restaino; Sean T Ready; Jaume Padilla; Jill A Kanaley Journal: Med Sci Sports Exerc Date: 2019-05 Impact factor: 5.411
Authors: Saurabh S Thosar; Alec M Berman; Maya X Herzig; Andrew W McHill; Nicole P Bowles; Christine M Swanson; Noal A Clemons; Matthew P Butler; Aaron A Clemons; Jonathan S Emens; Steven A Shea Journal: Arterioscler Thromb Vasc Biol Date: 2019-06 Impact factor: 8.311
Authors: Karen C Chong; Christopher D Owens; Meyeon Park; Hugh F Alley; W John Boscardin; Michael S Conte; Warren J Gasper; S Marlene Grenon Journal: J Vasc Surg Date: 2014-10-16 Impact factor: 4.268
Authors: Saurabh S Thosar; Alec M Berman; Maya X Herzig; Sally A Roberts; Michael R Lasarev; Steven A Shea Journal: Am J Physiol Regul Integr Comp Physiol Date: 2018-08-08 Impact factor: 3.619
Authors: Mihaela Jurdana; Zala Jenko-Pražnikar; Nina Mohorko; Ana Petelin; Tadeja Jakus; Boštjan Šimunič; Rado Pišot Journal: Age (Dordr) Date: 2015-11-13