Is exercise training an effective therapy targeting endothelial dysfunction and vascular wall inflammation?

Ribeiro, Fernando; Alves, Alberto Jorge; Duarte, José Alberto; Oliveira, José

doi:10.1016/j.ijcard.2009.09.548

Cited by 143 publications

(107 citation statements)

References 106 publications

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“…One explanation for these findings is thought to be because of beneficial effects of physical activity (PA) on endothelial function and the relatively less well‐studied biomarkers of atherosclerosis 5, 6, 7, 8, 9, 10, 11, 12. The anti‐inflammatory effects of PA have been well documented with consistent findings of decreases in pro‐inflammatory markers C‐reactive protein (CRP) and interleukin‐6 (IL‐6) following brief exercise interventions,8, 9 in addition to decreases in leptin and increases in adiponectin levels with exercise‐induced fat loss 5.…”

Section: Introductionmentioning

confidence: 99%

Physical Activity, Sedentary Time, and Cardiovascular Disease Biomarkers at Age 60 to 64 Years

Elhakeem

Cooper

Whincup

et al. 2018

JAHA

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BackgroundWe examined associations of objectively measured physical activity (PA) and sedentary time with cardiovascular disease biomarkers at age 60 to 64 years. This included investigation of sex differences and the extent to which associations may be mediated by adiposity.Methods and ResultsParticipants were 795 men and 827 women aged 60 to 64 years from the Medical Research Council National Survey of Health and Development. Combined heart rate and movement sensors worn for 5 consecutive days were used to derive overall PA energy expenditure, kJ/kg per day) and time spent sedentary (<1.5 metabolic equivalent of tasks), in light PA (1.5–3 metabolic equivalent of tasks) and moderate‐to‐vigorous intensity PA (>3 metabolic equivalent of tasks). Linear regression models were used to relate each PA parameter to inflammatory (C‐reactive protein, interleukin‐6), endothelial (tissue‐plasminogen activator, E‐selectin) and adipokine (leptin, adiponectin) markers extracted from fasting blood samples. Greater time in light PA and moderate‐to‐vigorous intensity PA and less sedentary time were associated with more favorable biomarker levels. For C‐reactive protein, interleukin‐6, and leptin, these differences were greater among women than men. For example, % differences (95% confidence intervals) in leptin for men and women per SD increases in sedentary time: 7.9 (2.7, 13.0) and 20.6 (15.3, 25.8); moderate‐to‐vigorous intensity PA: −3.8 (−8.9, 12.7) and −17.7 (−23.1, −12.4), moderate‐to‐vigorous intensity PA: −12.9 (−17.9, −8.0) and −18.3 (−23.4, −13.1). Fat mass mediated a greater proportion of these associations in women than men.ConclusionsGreater light PA and moderate‐to‐vigorous intensity PA and less sedentary time in early old age were associated with more favorable cardiovascular biomarker profiles. Fat mass partially mediated these associations but more strongly in women than men, which explained sex differences.

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Section: Introductionmentioning

confidence: 99%

Physical Activity, Sedentary Time, and Cardiovascular Disease Biomarkers at Age 60 to 64 Years

Elhakeem

Cooper

Whincup

et al. 2018

JAHA

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“…Previous studies have also demonstrated that exercise lowers blood pressure in L-NAME-treated rats by increasing NOS activity, improving NO bioavailability, and by inducing the NO-dependent relaxation pathway (2,32). NO bioavailability increased by exercise could be the result of increased activity/expression of eNOS and/or the diminished degradation of NO due to reduced interaction with ROS (33). This phenomenon could be attributed to an elevation of shear stress-induced vasodilation during exercise accompanied by increased blood fl ow (20,28,33).…”

Section: Discussionmentioning

confidence: 98%

“…NO bioavailability increased by exercise could be the result of increased activity/expression of eNOS and/or the diminished degradation of NO due to reduced interaction with ROS (33). This phenomenon could be attributed to an elevation of shear stress-induced vasodilation during exercise accompanied by increased blood fl ow (20,28,33).…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Aerobic Exercise Against L-Name-Induced Kidney Damage in Rats

Peeri

Habibian

Azarbayjani

et al. 2013

Archives of Industrial Hygiene and Toxicology

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Exercise, alone or combined with changes in lifestyle, can prevent or reduce the need for pharmacotherapy in patients with compromised endothelium-dependent function. The aim of this study was to examine the protective effect of aerobic exercise against (L-NAME)-kidney damage in male rats induced by Nω-nitro-L-arginine methyl ester (L-NAME). L-NAME was administered to rats intraperitoneally in doses of 10 mg kg -1 six days a week over eight weeks. Rats exercised by running on a treadmill at the speed of (15 to 22) m min -1 , 25 min to 64 min per day, fi ve days a week over eight weeks. The rats were killed 48 h after the last dose, and their kidneys removed and homogenised to measure the levels of heat shock protein70 (HSP70), superoxide dismutase activity (SOD), and thiobarbituric acid reactive substances (TBARS). We also measured serum nitrite/nitrate. Chronic administration of L-NAME signifi cantly increased renal HSP70 and TBARS levels and decreased renal SOD activity and serum nitrites/nitrates. Training modifi ed abnormal renal HSP70, lowered TBARS, and increased SOD and serum nitrite/nitrate. Our results have confi rmed that regular aerobic exercise protects against nitric oxide defi ciency-induced kidney damage by modifying HSP70, up-regulating SOD activity, and depleting TBARS. Arh Hig Rada Toksikol 2013;64:229-235 KEY WORDS: heat shock protein70, nitric oxide, renal injury, superoxide dismutase Peeri M, et al. EXERCISE EFFECTS ON L-NAME-INDUCED KIDNEY INJURIES

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“…Vascular inflammation can be the first step to an endothelial dysfunction and an impaired blood flow that will originate the enhancement of the endothelial layer permeability, in turn facilitating the diffusion of low-density lipoproteins to the intima, which causes a decrease in the vasodilation endothelium dependently (37). Some recent studies have shown that the increases in BDNF levels resulting from exercise are accompanied by reductions in basal serum vascular cell adhesion molecule-1 and serum tumor necrosis factor-␣, which produces attenuation of inflammation and prevents atherosclerosis (52).…”

Section: Discussionmentioning

confidence: 99%

Peripheral vascular reactivity and serum BDNF responses to aerobic training are impaired by the BDNF Val66Met polymorphism

Lemos

Alves

Souza

et al. 2016

Physiological Genomics

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-Besides neuronal plasticity, the neurotrophin brain-derived neurotrophic factor (BDNF) is also important in vascular function. The BDNF has been associated with angiogenesis through its specific receptor tropomyosin-related kinase B (TrkB). Additionally, Val66Met polymorphism decreases activity-induced BDNF. Since BDNF and TrkB are expressed in vascular endothelial cells and aerobic exercise training can increase serum BDNF, this study aimed to test the hypotheses: 1) Serum BDNF levels modulate peripheral blood flow; 2) The Val66Met BDNF polymorphism impairs exercise training-induced vasodilation. We genotyped 304 healthy male volunteers (Val66Val, n ϭ 221; Val66Met, n ϭ 83) who underwent intense aerobic exercise training on a running track three times/wk for 4 mo. We evaluated pre-and post-exercise training serum BDNF and proBDNF concentration, heart rate (HR), mean blood pressure (MBP), forearm blood flow (FBF), and forearm vascular resistance (FVR). In the pre-exercise training, BDNF, proBDNF, BDNF/proBDNF ratio, FBF, and FVR were similar between genotypes. After exercise training, functional capacity (V O2 peak) increased and HR decreased similarly in both groups. Val66Val, but not Val66Met, increased BDNF (interaction, P ϭ 0.04) and BDNF/proBDNF ratio (interaction, P Ͻ 0.001). Interestingly, FBF (interaction, P ϭ 0.04) and the FVR (interaction, P ϭ 0.01) responses during handgrip exercise (HG) improved in Val66Val compared with Val66Met, even with similar responses of HR and MBP. There were association between BDNF/proBDNF ratio and FBF (r ϭ 0.64, P Ͻ 0.001) and FVR (r ϭ Ϫ0.58, P Ͻ 0.001) during HG exercise. These results show that peripheral vascular reactivity and serum BDNF responses to exercise training are impaired by the BDNF Val66Met polymorphism and such responsiveness is associated with serum BDNF concentrations in healthy subjects.BDNF Val66Met polymorphism; exercise training; vascular reactivity EXERCISE TRAINING HAS BEEN considered a key element in the improvement in brain-derived neurotrophic factor (BDNF) levels (39), which is the strongest factor linking exercise with cognitive benefits. However, the variability of individual responses may be linked to genetic differences.While BDNF promotes neuronal survival and enhanced synaptic plasticity by activating the tropomyosin kinase B (TrkB) receptor, the action of its precursor proBDNF results in apoptosis by interacting with the p75 neurotrophin receptor (p75NTR), and both are significantly involved in different physiological functions (15,53).Considering the fact that the BDNF gene and its TrkB receptor are expressed in several tissues, such as brain, heart, lungs, and endothelial cells (12, 28), besides neuronal plasticity, it is possible that the neurotrophin BDNF also is involved in the health of other tissues. Indeed, besides the hippocampus, the circulating BDNF is produced by a number of peripheral nonneuronal tissues, including vascular endothelial cells (28,53). Moreover, the neurotrophin BDNF has been associated with angiogenesis thro...

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Is exercise training an effective therapy targeting endothelial dysfunction and vascular wall inflammation?

Cited by 143 publications

References 106 publications

Physical Activity, Sedentary Time, and Cardiovascular Disease Biomarkers at Age 60 to 64 Years

Physical Activity, Sedentary Time, and Cardiovascular Disease Biomarkers at Age 60 to 64 Years

Protective Effect of Aerobic Exercise Against L-Name-Induced Kidney Damage in Rats

Peripheral vascular reactivity and serum BDNF responses to aerobic training are impaired by the BDNF Val66Met polymorphism

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