A Prior High-Intensity Exercise Bout Attenuates the Vascular Dysfunction Resulting From a Prolonged Sedentary Bout

2019 ◽  
Vol 16 (10) ◽  
pp. 916-924
Author(s):  
Ryan S. Garten ◽  
Matthew C. Scott ◽  
Tiffany M. Zúñiga ◽  
Austin C. Hogwood ◽  
R. Carson Fralin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aerobic Exercise ◽  
Lower Limb ◽  
High Intensity ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Blood Samples ◽  
Prolonged Sitting ◽  
Leg Movement ◽  
High Intensity Interval

Background: This study sought to determine the impact of an acute prior bout of high-intensity interval aerobic exercise on attenuating the vascular dysfunction associated with a prolonged sedentary bout. Methods: Ten young (24 ± 1 y) healthy males completed two 3-hour sessions of prolonged sitting with (SIT-EX) and without (SIT) a high-intensity interval aerobic exercise session performed immediately prior. Prior to and 3 hours into the sitting bout, leg vascular function was assessed with the passive leg movement technique, and blood samples were obtained from the lower limb to evaluate changes in oxidative stress (malondialdehyde and superoxide dismutase) and inflammation (interleukin-6). Results: No presitting differences in leg vascular function (assessed via passive leg movement technique-induced hyperemia) were revealed between conditions. After 3 hours of prolonged sitting, leg vascular function was significantly reduced in the SIT condition, but unchanged in the SIT-EX. Lower limb blood samples revealed no alterations in oxidative stress, antioxidant capacity, or inflammation in either condition. Conclusions: This study revealed that lower limb vascular dysfunction was significantly attenuated by an acute presitting bout of high-intensity interval aerobic exercise. Further analysis of lower limb blood samples revealed no changes in circulating oxidative stress or inflammation in either condition.

Aerobic training status does not attenuate prolonged sitting-induced lower limb vascular dysfunction

2019 ◽  
Vol 44 (4) ◽  
pp. 425-433 ◽  
Author(s):  
Ryan S. Garten ◽  
Austin C. Hogwood ◽  
Jennifer B. Weggen ◽  
R. Carson Fralin ◽  
Kathryn LaRosa ◽  
...  
Keyword(s):  
Blood Flow ◽  
Lower Limb ◽  
Vascular Function ◽  
Aerobic Training ◽  
Vascular Dysfunction ◽  
Area Under The Curve ◽  
Training Status ◽  
Prolonged Sitting ◽  
Leg Movement ◽  
The Relationship

This study examined if the degree of aerobic training protects against the lower limb vascular dysfunction associated with a prolonged sitting bout. Ten young, aerobically trained (AT) and 10 young, untrained (UT) individuals completed a prolonged (3 h) sitting bout. Leg vascular function was measured prior to and at 1.5 and 3 h into the prolonged sitting bout using the passive leg movement (PLM) technique. PLM-induced hyperemia was significantly reduced from baseline at 1.5 and 3 h into the prolonged sitting bout in both groups when evaluated as peak change in leg blood flow from baseline (Δ LBF) (UT: 956 ± 140, 586 ± 80, and 599 ± 96 mL·min−1 at baseline, 1.5 h, and 3 h, respectively; AT: 955 ± 183, 789 ± 193, and 712 ± 131 mL·min−1 at baseline, 1.5 h, and 3 h, respectively) and LBF area under the curve (UT: 283 ± 73, 134 ± 31, and 164 ± 42 mL·min−1 at baseline, 1.5 h, and 3 h, respectively; AT: 336 ± 86, 242 ± 86, and 245 ± 73 mL·min−1 at baseline, 1.5 h, and 3 h, respectively), but no significant differences between groups were revealed. No significant correlations were observed when examining the relationship between maximal oxygen uptake (relative and absolute) and reductions in leg vascular function at 1.5 and 3 h into the prolonged sitting bout. This study revealed that aerobic training did not provide a protective effect against prolonged sitting-induced lower limb vascular dysfunction and further highlights the importance of reducing excessive sitting in all populations.

scholarly journals Age-Related Macular Degeneration: Role of Oxidative Stress and Blood Vessels

2021 ◽  
Vol 22 (3) ◽  
pp. 1296
Author(s):  
Yue Ruan ◽  
Subao Jiang ◽  
Adrian Gericke
Keyword(s):  
Oxidative Stress ◽  
Macular Degeneration ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Therapeutic Strategies ◽  
Vision Impairment ◽  
Age Related Macular Degeneration ◽  
Oxygen Species ◽  
Age Related

Age-related macular degeneration (AMD) is a common irreversible ocular disease characterized by vision impairment among older people. Many risk factors are related to AMD and interact with each other in its pathogenesis. Notably, oxidative stress and choroidal vascular dysfunction were suggested to be critically involved in AMD pathogenesis. In this review, we give an overview on the factors contributing to the pathophysiology of this multifactorial disease and discuss the role of reactive oxygen species and vascular function in more detail. Moreover, we give an overview on therapeutic strategies for patients suffering from AMD.

scholarly journals Vascular function and arginine and dimethylarginines in gentamicin-induced renal failure: a possible effect of heme oxygenase 1 inducer hemin

2017 ◽  
Vol 95 (12) ◽  
pp. 1406-1413 ◽  
Author(s):  
Esra Aycan-Ustyol ◽  
Merve Kabasakal ◽  
Seldag Bekpinar ◽  
F. Ilkay Alp-Yıldırım ◽  
Ozge Tepe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Vascular Function ◽  
Asymmetric Dimethylarginine ◽  
Vascular Dysfunction ◽  
Cardiovascular Complication ◽  
Heme Oxygenase 1 ◽  
Antioxidant Enzyme Activities ◽  
Symmetric Dimethylarginine ◽  
Inflammatory Changes

Increased oxidative stress and disturbance in nitric oxide bioavailability lead to endothelial dysfunction and cardiovascular complication in renal disease. Gentamicin (GM), a commonly used antibiotic, exhibits a toxic effect on renal proximal tubules. Prevention of its nephrotoxicity is important. Therefore, we investigated whether heme oxygenase 1 HO-1) induction influenced kidney and vascular function in GM-administered rats. GM (100 mg·kg–1·day–1; i.p.) was given to rats alone or together with hemin (20 mg·kg–1 on alternate days; i.p.) for 14 days. Plasma and kidney l-arginine, asymmetric dimethylarginine (ADMA), and symmetric dimethylarginine (SDMA) as well as kidney 4-hydroxynonenal (HNE) levels and myeloperoxidase (MPO) activity were measured. Histopathological examinations of kidney and relaxation and contraction responses of aorta were also examined. GM increased serum SDMA, urea nitrogen (BUN), and creatinine levels and caused histopathological alterations in the kidney. GM elevated HO-1 protein and mRNA expressions, 4-HNE level, and MPO activity and decreased antioxidant enzyme activities and l-arginine levels in the kidney. Decreased relaxation and contraction were detected in the aorta. Hemin restored renal oxidative stress and inflammatory changes together with vascular dysfunction, but did not affect SDMA, BUN, or creatinine levels. We conclude that HO-1 induction may be effective in improving renal oxidative stress, inflammation, and vascular dysfunction mediated by GM.

scholarly journals High-intensity interval training modulates retinal microvascular phenotype and DNA methylation of p66Shc gene: a randomized controlled trial (EXAMIN AGE)

2019 ◽  
Vol 41 (15) ◽  
pp. 1514-1519 ◽  
Author(s):  
Lukas Streese ◽  
Abdul Waheed Khan ◽  
Arne Deiseroth ◽  
Shafaat Hussain ◽  
Rosa Suades ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Dna Methylation ◽  
High Intensity ◽  
Interval Training ◽  
Retinal Vessel ◽  
High Intensity Interval Training ◽  
Age Related ◽  
High Intensity Interval ◽  
Retinal Arteriolar

Abstract Aims Impairments of retinal vessel diameter are associated with major adverse cardiovascular (CV) events. Promoter DNA methylation is a repressor of the mitochondrial adaptor p66Shc gene transcription, a key driver of ageing-induced reactive oxygen species. The study aimed to investigate whether high-intensity interval training (HIIT) affects retinal microvascular phenotype as well as p66Shc expression and oxidative stress in ageing subjects with increased CV risk from the EXAMIN AGE cohort. Methods and results Eighty-four sedentary subjects (mean age 59.4 ± 7.0 years) with ≥2 CV risk factors were randomized into either a 12-week HIIT or standard physical activity recommendations. Retinal arteriolar and venular diameters were measured by use of a retinal vessel analyser. As a marker of oxidative stress plasma 3-nitrotyrosine (3-NT) level was determined by ELISA. Gene expression of p66Shc and DNA methylation were assessed in mononuclear cells by RT-qPCR and methylated-DNA capture (MethylMiner Enrichment Kit) coupled with qPCR, respectively. High-intensity interval training reduced body mass index, fat mass, low-density lipoprotein and increased muscle mass, as well as maximal oxygen uptake (VO2max). Moreover, HIIT restored microvascular phenotype by inducing retinal arteriolar widening (pre: 175 ± 14 µm vs. post: 181 ± 13 µm, P = 0.001) and venular narrowing (pre: 222 ± 14 µm vs. post: 220 ± 14 µm, P = 0.007). After HIIT, restoration of p66Shc promoter methylation (P = 0.034) reduced p66Shc gene expression (P = 0.037) and, in turn, blunted 3-NT plasma levels (P = 0.002). Conclusion High-intensity interval training rescues microvascular dysfunction in ageing subjects at increased CV risk. Exercise-induced reprogramming of DNA methylation of p66Shc gene may represent a putative mechanistic link whereby exercise protects against age-related oxidative stress. Clinical trial registration  ClinicalTrials.gov: NCT02796976 (https://clinicaltrials.gov/ct2/show/NCT02796976).

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