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J Surg Res. 2014 Aug;190(2):672-82. doi: 10.1016/j.jss.2014.02.001. Epub 2014 Feb 12.

Short-term physical inactivity impairs vascular function.

Author information

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.

KEYWORDS:

Arterial stiffness; Endothelial dysfunction; Inflammation; Physical inactivity

PMID:
24630521
PMCID:
PMC4096607
DOI:
10.1016/j.jss.2014.02.001
[Indexed for MEDLINE]
Free PMC Article

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