Vascular Ageing and Aerobic Exercise

Impairment of vascular function, in particular endothelial dysfunction and large elastic artery stiffening, represents a major link between ageing and cardiovascular risk. Clinical and experimental studies identified numerous mechanisms responsible for age-related decline of endothelial function and arterial compliance. Since most of these mechanisms are related to oxidative stress or low-grade inflammation, strategies that suppress oxidative stress and inflammation could be effective for preventing age-related changes in arterial function. Indeed, aerobic physical activity, which has been shown to improve intracellular redox balance and mitochondrial health and reduce levels of systemic inflammatory markers, also improves endothelial function and arterial distensibility and reduces risk of cardiovascular diseases. The present paper provides a brief overview of processes underlying age-related changes in arterial function, as well as the mechanisms through which aerobic exercise might prevent or interrupt these processes, and thus attenuate vascular ageing.

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Edward F. Adolph Distinguished Lecture: The remarkable anti-aging effects of aerobic exercise on systemic arteries

Journal of Applied Physiology ◽

10.1152/japplphysiol.00362.2014 ◽

2014 ◽

Vol 117 (5) ◽

pp. 425-439 ◽

Cited By ~ 58

Author(s):

Douglas R. Seals

Keyword(s):

Oxidative Stress ◽

Endothelial Function ◽

Aerobic Exercise ◽

Arterial Compliance ◽

Vascular Inflammation ◽

Public Health Approach ◽

Low Grade ◽

Structural Protein ◽

Aging Effects ◽

Elastic Artery

Cardiovascular diseases (CVD) remain the leading cause of morbidity and mortality in modern societies, and advancing age is the major risk factor for CVD. Arterial dysfunction, characterized by large elastic artery stiffening and endothelial dysfunction, is the key event leading to age-associated CVD. Our work shows that regular aerobic exercise inhibits large elastic artery stiffening with aging (optimizes arterial compliance) and preserves endothelial function. Importantly, among previously sedentary late middle-aged and older adults, aerobic exercise improves arterial stiffness and enhances endothelial function in most groups and, therefore, also can be considered a treatment for age-associated arterial dysfunction. The mechanisms by which regular aerobic exercise destiffens large elastic arteries are incompletely understood, but existing evidence suggests that reductions in oxidative stress associated with decreases in both adventitial collagen (fibrosis) and advanced glycation end-products (structural protein cross-linking molecules), play a key role. Aerobic exercise preserves endothelial function with aging by maintaining nitric oxide bioavailability via suppression of excessive superoxide-associated oxidative stress, and by inhibiting the development of chronic low-grade vascular inflammation. Recent work from our laboratory supports the novel hypothesis that aerobic exercise may exert these beneficial effects by directly inducing protection to aging arteries against multiple adverse factors to which they are chronically exposed. Regular aerobic exercise should be viewed as a “first line” strategy for prevention and treatment of arterial aging and a vital component of a contemporary public health approach for reducing the projected increase in population CVD burden.

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Age-Related Changes in Activation of Mitogen-Activated Protein Kinase Cascades by Oxidative Stress

Journal of Investigative Dermatology ◽

10.1038/jidsp.1998.7 ◽

1998 ◽

Vol 3 (1) ◽

pp. 23-27 ◽

Cited By ~ 9

Author(s):

Kathryn Z Guyton ◽

Myriani Gorospe ◽

Xiantao Wang ◽

Yolanda D Mock ◽

Gertrude C Kokkonen ◽

...

Keyword(s):

Oxidative Stress ◽

Protein Kinase ◽

Mitogen Activated Protein Kinase ◽

Age Related ◽

Mitogen Activated Protein ◽

Age Related Changes

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Metaflammation: Tissue-Specific Alterations of the NLRP3 Inflammasome Platform in Metabolic Syndrome

Current Medicinal Chemistry ◽

10.2174/0929867324666170407123522 ◽

2018 ◽

Vol 25 (11) ◽

pp. 1294-1310 ◽

Cited By ~ 23

Author(s):

Raffaella Mastrocola ◽

Manuela Aragno ◽

Giuseppe Alloatti ◽

Massimo Collino ◽

Claudia Penna ◽

...

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Advanced Glycation Endproducts ◽

Low Grade ◽

Advanced Glycation ◽

Added Sugars ◽

Physiological Ageing ◽

Glycation Endproducts ◽

Inflammatory Status ◽

Age Related

In the last decades, the extension of life expectancy and the increased consumption of foods rich in saturated fats and added sugars have exposed the general population to emerging health problems. The prevalence of metabolic syndrome (MS), composed of a cluster of factors as obesity, dyslipidemia, hyperglycemia, and hypertension, is rapidly increasing in industrialized and developing countries leading to precocious onset of age-related diseases. Indeed, oxidative stress, accumulation of advanced glycation endproducts, and a chronic low-grade inflammation are common features of MS and physiological ageing. In particular, the entire set of MS factors contributes to the development of an inflammatory status named metaflammation, which has been associated with activation of early innate immune response through the assembling of the multiprotein complex inflammasome. The most investigated family of inflammasome platforms is the NOD-like receptor pyridine containing (NLRP) 3, which is activated by several exogenous and endogenous stimuli, leading to the sequential cleavage of caspase-1 and IL-1β, followed by secretion of active IL-1β. We here collect the most recent findings on NLRP3 activation in MS providing evidence of its central role in disease progression and organ dysfunction in target tissues of metaflammation, in particular in cardiovascular, hepatic and renal complications, with a focus on oxidative stress and advanced glycation endproducts. A wide overview of the most promising strategies for the modulation of NLRP3 activation and related metabolic repercussions is also provided, since the finding of specific pharmacological tools is an urgent requirement to reduce the social and economic burden of MS- and elderly-associated diseases.

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Response of endothelial function and oxidative stress after supervised aerobic exercise training in formerly preeclamptic women

Health Care For Women International ◽

10.1080/07399332.2021.2002331 ◽

2021 ◽

pp. 1-15

Author(s):

Wenjiang Sun ◽

Bin Liu ◽

Huan Zheng

Keyword(s):

Oxidative Stress ◽

Exercise Training ◽

Endothelial Function ◽

Aerobic Exercise ◽

Aerobic Exercise Training ◽

And Oxidative Stress

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Endothelial Function in Patients with Severe and Moderate Haemophilia A and B

Hämostaseologie ◽

10.1055/s-0038-1673415 ◽

2018 ◽

Vol 39 (02) ◽

pp. 195-202

Author(s):

Stephanie Böhmert ◽

Ralf Schubert ◽

Stephan Fichtlscherer ◽

Sonja Alesci ◽

Wolfgang Miesbach

Keyword(s):

Endothelial Function ◽

Adhesion Molecule ◽

Reactive Hyperemia ◽

Intercellular Adhesion Molecule ◽

Control Group ◽

Low Grade ◽

Haemophilia A ◽

Intercellular Adhesion Molecule 1 ◽

Age Related ◽

Artery Disease

AbstractThe life expectancy of patients with haemophilia has increased and therefore the interest in age-related comorbidities has grown. The aim of this study was to determine whether haemophilia patients have a different endothelial function compared with the general population. A total of 26 patients with severe or moderate haemophilia A or B, 14 controls and 36 patients with coronary artery disease (CAD) were included in this study. Five markers of endothelial dysfunction (MOEDs) were determined. Moreover, the endothelial function was examined using the Itamar Endo-PAT, and the reactive hyperemia index (RHI) was calculated from the results. The MOEDs soluble intercellular adhesion molecule-1 (p = 0.0095) and interleukin-6 (p = 0.010) were significantly higher for patients with haemophilia compared with the control group. The presence of increased adhesion molecule levels and low-grade inflammation is suggestive of a decreased endothelial function. RHI is impaired in CAD patients (1.862), whereas haemophilia patients have an RHI of 1.958 in comparison with 2.112 in controls (p = 0.127). Therefore, laboratory and functional measurements imply a possible higher risk for CAD in haemophilia patients.

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