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Objective: The aim of this study was to assess the effects of a single bout of maximal walking on blood and muscle nitric oxide (NO) bioavailability, oxidative stress, and inflammation in symptomatic peripheral artery disease (PAD) patients. Methods: A total of 35 men with symptomatic PAD performed a graded maximal exercise test on a treadmill (3.2 km/h, 2% increase in grade every 2 minutes). Plasma samples and gastrocnemius muscle biopsies were collected preexercise and postexercise for assessment of NO bioavailability (plasma NO and muscle, endothelial NO synthase), oxidative stress and antioxidant function (lipid peroxidation [LPO], catalase [CAT], and superoxide dismutase), and inflammation (interleukin-6, C-reactive protein, tumor necrosis factor-α, intercellular adhesion molecules, and vascular adhesion molecules). The effects of the walking exercise were assessed using paired t tests or Wilcoxon tests. Results: After maximal walking, plasma NO and LPO were unchanged (P > .05), plasma CAT decreased, and all blood inflammatory markers increased (all P ≤ .05). In the disease-affected skeletal muscle, endothelial NO synthase, CAT, LPO, and all inflammatory markers increased, whereas superoxide dismutase decreased (all P ≤ .05). Conclusion: In patients with symptomatic PAD, maximal exercise induces local and systemic impairments, which may play a key role in atherogenesis. Exercise strategies that avoid maximal effort may be important to reduce local and systemic damage and enhance clinical benefits. [ABSTRACT FROM AUTHOR]

This study examined the impact of submaximal walking training (WT) on local and systemic nitric oxide (NO) bioavailability, inflammation, and oxidative stress in patients with intermittent claudication (IC). The study employed a randomised, controlled, parallel group design and was performed in a single centre. Thirty-two men with IC were randomly allocated to two groups: WT (n = 16, two sessions/week, 15 cycles of two minutes walking at an intensity corresponding to the heart rate obtained at the pain threshold interspersed by two minutes of upright rest) and control (CO, n = 16, two sessions/week, 30 minutes of stretching). NO bioavailability (blood NO and muscle nitric oxide synthase [eNOS]), redox homeostasis (catalase [CAT], superoxide dismutase [SOD], lipid peroxidation [LPO] measured in blood and muscle), and inflammation (interleukin-6 [IL-6], C-reactive protein [CRP], tumour necrosis factor α [TNF-α], intercellular adhesion molecules [ICAM], vascular adhesion molecules [VCAM] measured in blood and muscle) were assessed at baseline and after 12 weeks. WT statistically significantly increased blood NO, muscle eNOS, blood SOD and CAT, and muscle SOD and abolished the increase in circulating and muscle LPO observed in the CO group. WT decreased blood CRP, ICAM, and VCAM and muscle IL-6 and CRP and eliminated the increase in blood TNF-α and muscle TNF-α, ICAM and VCAM observed in the CO group. WT at an intensity of pain threshold improved NO bioavailability and decreased systemic and local oxidative stress and inflammation in patients with IC. The proposed WT protocol provides physiological adaptations that may contribute to cardiovascular health in these patients. [ABSTRACT FROM AUTHOR]

Background and Aims: The purpose of this study was to investigate whether an intervention with physical activity (PA) would promote positive effects on the angiogenic factors, mobilization, and functionality of circulating endothelial progenitor cells (EPCs) in children with low birth weight (LBW).Methods and Results: Thirty-five children participated in a 10-week PA program (intensity: 75-85% of heart rate reserve, frequency: four times/week, and duration: 45 min). Before and after the PA program, we evaluated anthropometric parameters, blood pressure levels, biochemical profile, number of EPCs, number of EPC colony forming units, and plasma levels of vascular endothelial growth factor-A (VEGF-A), nitric oxide (NO), and matrix metalloproteinases (MMPs) 2 and 9. We found a significant main effect of the PA program on waist circumference (ηp2 = 0.489), cardiorespiratory fitness (ηp2 = 0.463), and MMP-9 (ηp2 = 0.582). Birth weight or the PA program produced significant independent effects on systolic blood pressure (birth weight: ηp2 = 0.431; PA program: ηp2 = 0.615) and EPC colony forming units (birth weight: ηp2 = 0.541; PA program: ηp2 = 0.698) with no significant interactions. The combination of birth weight and the PA program produced a significant interaction effect on the number of circulating EPCs (ηp2 = 0.123), NO (ηp2 = 0.258), and VEGF-A (ηp2 = 0.175). The variation in the number of EPCs from baseline to 10 weeks of the PA program correlated positively with the change in NO (P = 0.002) and VEGF-A (P = 0.004).Conclusions: A 10-week PA program attenuates the adverse effect of LBW on the number and functionality of EPCs; this effect occurs through an improvement in circulating levels of NO and VEGF-A. CLINICAL TRIALS: https://www.clinicaltrials.gov. Unique Identifier: NCT02982967. Date: December/2016. [ABSTRACT FROM AUTHOR]

The article presents a study on aerobic exercise training and its significance in the prevention and treatment of hypertension. The investigation proves the activity reduces blood pressure, improves vascularization and regulates microRNAs. An overview of the methodology and data analysis is also provided.

Aerobic exercise training (ET) lowers hypertension and improves patient outcomes in cardiovascular disease. The mechanisms of these effects are largely unknown. We hypothesized that ET modulates microRNAs (miRNAs) involved in vascularization. miRNA-16 regulates the expression of vascular endothelial growth factor and antiapoptotic protein Bcl-2. miRNA-21 targets Bcl-2. miRNA-126 functions by repressing regulators of the vascular endothelial growth factor pathway. We investigated whether miRNA-16, -21 and -126 are modulated in hypertension and by ET. Twelve-week-old male spontaneously hypertensive rats (SHRs; n=14) and Wistar Kyoto (WKY; n=14) rats were assigned to 4 groups: SHRs, trained SHRs (SHR-T), Wistar Kyoto rats, and trained Wistar Kyoto rats. ET consisted of 10 weeks of swimming. ET reduced blood pressure and heart rate in SHR-Ts. ET repaired the slow-to-fast fiber type transition in soleus muscle and the capillary rarefaction in SHR-Ts. Soleus miRNA-16 and -21 levels increased in SHRs paralleled with a decrease of 48% and 25% in vascular endothelial growth factor and Bcl-2 protein levels, respectively. Hypertension increased Bad and decreased Bcl-x and endothelial NO synthase levels and lowered p-Bad(ser112):Bad ratio. ET in SHR-Ts reduced miRNA-16 and -21 levels and elevated vascular endothelial growth factor and Bcl-2 levels. ET restored soleus endothelial NO synthase levels plus proapoptotic and antiapoptotic mediators in SHR-Ts, indicating that the balance between angiogenic and apoptotic factors may prevent microvascular abnormalities in hypertension. miRNA-126 levels were reduced in SHRs with an increase of 51% in phosphoinositol-3 kinase regulatory subunit 2 expression but normalized in SHR-Ts. Our data show that ET promoted peripheral revascularization in hypertension, which could be associated with regulation of select miRNAs, suggesting a mechanism for its potential therapeutic application in vascular diseases. [ABSTRACT FROM AUTHOR]

Aerobic exercise training leads to a physiological, nonpathological left ventricular hypertrophy; however, the underlying biochemical and molecular mechanisms of physiological left ventricular hypertrophy are unknown. The role of microRNAs regulating the classic and the novel cardiac renin-angiotensin (Ang) system was studied in trained rats assigned to 3 groups: (1) sedentary; (2) swimming trained with protocol 1 (T1, moderate-volume training); and (3) protocol 2 (T2, high-volume training). Cardiac Ang I levels, Ang-converting enzyme (ACE) activity, and protein expression, as well as Ang II levels, were lower in T1 and T2; however, Ang II type 1 receptor mRNA levels (69% in T1 and 99% in T2) and protein expression (240% in T1 and 300% in T2) increased after training. Ang II type 2 receptor mRNA levels (220%) and protein expression (332%) were shown to be increased in T2. In addition, T1 and T2 were shown to increase ACE2 activity and protein expression and Ang (1-7) levels in the heart. Exercise increased microRNA-27a and 27b, targeting ACE and decreasing microRNA-143 targeting ACE2 in the heart. Left ventricular hypertrophy induced by aerobic training involves microRNA regulation and an increase in cardiac Ang II type 1 receptor without the participation of Ang II. Parallel to this, an increase in ACE2, Ang (1-7), and Ang II type 2 receptor in the heart by exercise suggests that this nonclassic cardiac renin-angiotensin system counteracts the classic cardiac renin-angiotensin system. These findings are consistent with a model in which exercise may induce left ventricular hypertrophy, at least in part, altering the expression of specific microRNAs targeting renin-angiotensin system genes. Together these effects might provide the additional aerobic capacity required by the exercised heart. [ABSTRACT FROM AUTHOR]

Cardiac hypertrophy is a major mechanism of adaptation of the heart by workload. We evaluate the effect of aerobic exercise training on the miRNAs expression profiling in the heart of spontaneously hypertensive rats (SHR), as well as we selected miRNAs with altered pattern in SHR and reversed by physical training. Also, we analyze their functional role through bioinformatics applications. Male rats were assigned into 3 groups: sedentary hypertensive rats (SHR-S), trained SHR (SHR-T) and sedentary Wistar Kyoto rats (WKY-S). The SHR-T group performed a swimming training protocol of 60 min/5x/week, 1x/day/10 weeks, with 4% caudal body weight workload. We analyzed hemodynamic (blood pressure, BP and resting heart rate, HR), functional (physical capacity, oxygen consumption and echocardiogram), biochemical (349 cardiac microRNAs by microarray and Real Time-PCR to miRNAs) and computational (prediction of targets and annotation cell signaling pathways) parameters. The main findings were: 1. The BP and HR decreased in SHR-T group compared to the SHR-S; 2. The exercise tolerance and VO2 peak increased in SHR-T group; 3.Echocardiographic analysis showed that the E wave, A wave and E/A ratio improved in SHR-T group; 4. Microarray analysis found six different miRNAs expression profile in the comparison groups WKY-S, SHR-S and SHR-T; 5. Six miRNAs were altered in SHR-S and were reversed in the SHR-T (miR-1,22, 27a, 27b, 29c and 451); 7. Bioinformatics analysis showed that this miRNA cluster has multiple predicted targets in signaling pathways related to cardiac remodeling as MAPK, Wnt and TGF-beta and others genes associate to cytoskeletal structure and energetic metabolism.These results suggest that miRNAs: 1, 22, 27a, 27b, 29c and 451 can be controlling cell signaling pathways involved in the process of reversing the disease. These results open new perspectives on the use of these molecules as a therapeutic treatment. [ABSTRACT FROM AUTHOR]