ArticleLiterature Review

Exercise Training as Vascular Medicine: Direct Impacts on the Vasculature in Humans

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Abstract

Exercise training decreases cardiovascular risk, but effects on traditional risk factors do not fully account for this benefit. Exercise directly impacts upon arterial shear stress, a stimulus to antiatherogenic adaptation in vascular function and remodeling. This review considers the impact of exercise training on vascular adaptation in large and small arteries in humans.

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... Approximately 40%-60% of the beneficial effects of exercise training in preventing/treating cardiovascular disease, including stroke, are unrelated to the reduction in traditional cardiovascular risk factors (Mora et al., 2007;Green, 2009). Several authors FIGURE 4 | Boxplot of Endothelial Shear Stress (ESS) by exercise modality and intensity with comparisons within modalities at each intensity. ...
... *, p < 0.05 low vs. moderate, low vs. high, and moderate vs. high; †, p < 0.05 low vs. moderate Bench press; ‡, p < 0.05 low vs. high and moderate vs. high; †, p < 0.05 low vs. moderate Biceps and Squat. (Laughlin, 1995;Hambrecht et al., 2000;Green et al., 2002;Green et al., 2008;Laughlin et al., 2008;Green, 2009) have established a close relationship between exercise training and improvements in endothelial function. In addition, previous studies have shown that the lack of or low ESS can result in vascular inflammation, upregulation of matrix-degrading proteases, and arterial wall remodeling, which promotes the transition of stable to unstable plaque in atherosclerotic lesions (Koskinas et al., 2009). ...
... Approximately 40%-60% of the beneficial effects of exercise training in preventing/treating cardiovascular disease, including stroke, are unrelated to the reduction in traditional cardiovascular risk factors (Mora et al., 2007;Green, 2009). Several authors FIGURE 4 | Boxplot of Endothelial Shear Stress (ESS) by exercise modality and intensity with comparisons within modalities at each intensity. ...
... *, p < 0.05 low vs. moderate, low vs. high, and moderate vs. high; †, p < 0.05 low vs. moderate Bench press; ‡, p < 0.05 low vs. high and moderate vs. high; †, p < 0.05 low vs. moderate Biceps and Squat. (Laughlin, 1995;Hambrecht et al., 2000;Green et al., 2002;Green et al., 2008;Laughlin et al., 2008;Green, 2009) have established a close relationship between exercise training and improvements in endothelial function. In addition, previous studies have shown that the lack of or low ESS can result in vascular inflammation, upregulation of matrix-degrading proteases, and arterial wall remodeling, which promotes the transition of stable to unstable plaque in atherosclerotic lesions (Koskinas et al., 2009). ...
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Endothelial dysfunction is the first pathophysiological step of atherosclerosis, which is responsible for 90% of strokes. Exercise programs aim to reduce the risk of developing stroke; however, the majority of the beneficial factors of exercise are still unknown. Endothelial shear stress (ESS) is associated with endothelial homeostasis. Unfortunately, ESS has not been characterized during different exercise modalities and intensities in the carotid artery. Therefore, the purpose of this study was to determine exercise-induced blood flow patterns in the carotid artery. Fourteen apparently healthy young adults (males = 7, females = 7) were recruited for this repeated measures study design. Participants completed maximal oxygen consumption (VO2max) tests on a Treadmill, Cycle-ergometer, and Arm-ergometer, and 1-repetition maximum (1RM) tests of the Squat, Bench Press (Bench), and Biceps Curl (Biceps) on separate days. Thereafter, participants performed each exercise at 3 different exercise intensities (low, moderate, high) while a real-time ultrasound image and blood flow of the carotid artery was obtained. Blood flow patterns were assessed by estimating ESS via Womersley’s estimation and turbulence via Reynold’s number (Re). Data were analyzed using a linear mixed-effects model. Pairwise comparisons with Holm-Bonferroni correction were conducted with Hedge’s g effect size to determine the magnitude of the difference. There was a main effect of intensity, exercise modality, and intensity * exercise modality interaction on both ESS (p < 0.001). Treadmill at a high intensity yielded the greatest ESS when compared to the other exercise modalities and intensities, while Bench Press and Biceps curls yielded the least ESS. All exercise intensities across all modalities resulted in turbulent blood flow. Clinicians must take into consideration how different exercise modalities and intensities affect ESS and Re of the carotid artery.
... In nonpregnant populations, exercise reduces cardiovascular risk through improvements in vascular structure and function (16,17). Specifically, in healthy trained populations, vascular conductance is increased (lower resistance) by vascular remodeling (increased diameter) to accommodate an increase in resting cardiac output and shear stress (16). ...
... In nonpregnant populations, exercise reduces cardiovascular risk through improvements in vascular structure and function (16,17). Specifically, in healthy trained populations, vascular conductance is increased (lower resistance) by vascular remodeling (increased diameter) to accommodate an increase in resting cardiac output and shear stress (16). Moreover, exercise training also increases carotid artery distensibility (decrease stiffness [18]), independent of a change in cardiorespiratory fitness (19). ...
Article
Purpose: Healthy pregnancy is typically associated with favorable vascular adaptations to both structure and function of the peripheral arteries. Exercise is independently associated with improvements in peripheral vascular health; however, the impact of exercise on prenatal adaptations is unclear. Therefore, we hypothesized that a structured aerobic exercise intervention between the second and third trimester (TM2 and TM3, respectively) of pregnancy would augment the already-positive changes in vascular outcomes. Methods: We recruited 59 inactive pregnant women (<20 weeks gestation) and randomized them into control (standard care; n = 28) or exercise (moderate intensity aerobic exercise, 3-4 days/week, 25-40 minutes, 14 ± 1 weeks; n = 31) conditions. Before and after the intervention all women completed comprehensive peripheral vascular assessment, which included blood markers of vascular health, carotid distensibility metrics, measures of arterial stiffness (pulse wave velocity; PWV), and [superficial] femoral artery reactivity during cold pressor test (CPT). Results: Carotid artery diameter increased from 6.5 mm to 6.9 mm (p < 0.001) strain (%)decreased from 9.9% to 8.4% (p < 0.001). Carotid artery blood flow, compliance and distensibility coefficients, stiffness (β), distensibility (1/β), and Elastic modulus were not different across gestation. PWV was not different across gestation. Superficial femoral artery diameter was increased from 5.4 mm to 5.6 mm (p = 0.004) while blood flow, conductance, and resistance at rest and during CPT were not different across gestation. None of our measures of vascular health were impacted by exercise. Conclusion: We did not observe an impact of aerobic exercise on altering the changes across pregnancy in blood vessel health. However, the present study was conducted in women who were overall at low risk for developing gestational hypertension and should be interpreted with caution. Future work in high-risk women is needed.
... Thus, it may be expected that patients who have a better capacity for exercise during hospitalization, may present with some benefits already accumulated in vascular health, causing this endothelium to be less affected in exacerbation of the disease, while patients who walk a minor distance may have a worse vascular prognosis. In general, physical exercise has been shown to improve exercise capacity and arterial function in particular endothelium-dependent vasodilation 44 , which seems to be an important key to upgrade vascular health and CV events prevention at AECOPD. www.nature.com/scientificreports/ ...
... In the study of Ozben et al. 46 , patients presented about 6% of FMD, though the exacerbation was not severe. The exercise is also responsible for decreasing levels of inflammatory markers such as cytokines and C-reactive protein 44 . A study described for the first time the association between airway inflammation and endothelial dysfunction related to NO activity in patients with COPD 47 . ...
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Severe acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are associated with significant poor outcomes including an increased risk of cardiovascular (CV) events and exercise intolerance. Endothelial dysfunction might contribute to an impaired vascular homeostasis and consequently to CV events and exercise capacity. This study aimed to evaluate the association between exercise capacity and endothelial function in patients with severe AECOPD. Forty-five COPD patients diagnosed with severe AECOPD and admitted to the University Hospital of São Carlos from 2017 to 2019 were enrolled in this observational clinical study. Endothelial Function was assessed by brachial artery ultrasonography (M-Turbo, Sonosite, Bottle, WA, USA) and Flow Mediated Dilatation (FMD) technique in absolute (mm) and percentage values (%). Walking distance (6MWD) obtained by six-minute walk test was considered to characterize the exercise capacity. Pearson’s correlation analysis and linear regression model were applied and a significance level of 5%. There was a significant positive correlation between exercise capacity and endothelial function. Pearson correlation coefficient were 0.36 (p = 0.02) and 0.40 (p = 0.01) between 6MWD and FMD in mm and %, respectively. Linear regression model revealed 6MWD (p = 0.007), accounting for 15% of FMD (%) variance (R ² adjusted). FMD (%) = 2.11 + (0.0081*6MWD). Exercise capacity is associated with endothelial function in patients with severe AECOPD. FMD was found to be increasing with increasing walked distance. Further research is needed to provide evidence of effectiveness of rehabilitation on exercise capacity and endothelial function in these patients and its prognostic value.
... Therefore, the effect of aquatic HIIT is better under the same conditions. Different types or intensities of exercise interventions are associated with different anterograde and retrograde shear stress patterns (Green, 2009). The intensity of HIIT during high-intensity exercise enhances the blood supply capacity of the heart, accelerates the blood flow speed, enhances the stimulation of the blood vessel wall, and the vascular smooth muscle passively contracts and diastole rapidly under mechanical stress to meet the needs of blood flow (Ramos et al., 2015). ...
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Objective: To investigate the effects of 8-week aquatic and land high intensity interval training (HIIT) on hemodynamics and vascular function in middle-aged men. Methods: Thirty middle-aged men with low physical activity were selected and divided into 15 men (52.43 ± 4.11) in aquatic group and 15 men (52.74 ± 5.62) in land group by random number table. They performed HIIT exercise in aquatic and land 3 times a week for 8 weeks. Pre-test, inter-test and post-test respectively measure hemodynamics and blood vessel function. Results: (1) Body composition: After 8 weeks of exercise, weight, body mass index (BMI) and body fat rate (BF) were lower than before exercise (aquatic group: p < 0.01, land group: p < 0.05). The improvement of BF in the aquatic group was better than that in the land group (p < 0.05); (2) Cardiac function: After 8 weeks of exercise, stroke volume (SV), left ventricular end-diastolic volume (EDV), cardiac output (CO), and left ventricular fractional shortening (FS), were higher than before exercise (aquatic group: p < 0.01, land group: p < 0.05), heart rate (HR) and left ventricular end-systolic volume (ESV) were lower than before exercise (aquatic group: p < 0.01, land group: p < 0.05). The improvement of SV, HR, EDV, ESV, CO and FS in the aquatic group was better than that in the land group (p < 0.05); (3) Hemodynamics: After 8 weeks of exercise, systolic blood pressure (SBP), diastolic blood pressure (DBP) were lower than before exercise (aquatic group: p < 0.01, land group: p < 0.05), wall shear stress (WSS) and peak systolic velocity (PSV) were higher than before exercise (aquatic group: p < 0.01, land group: p < 0.05). The improvement of SBP, WSS and PSV in the aquatic group was better than that in the land group (p < 0.05); (4) Vascular function: basal diameter and brachial artery flow-mediated dilatation (FMD) level in aquatic group and land group was higher than before exercise, pulse wave velocity (PWV) level was lower than before exercise (aquatic and land group: p < 0.05). The improvement of FMD in the aquatic group was better than that in the land group. Conclusion: The body composition, hemodynamics and vascular function of middle-aged men were improved by 8-week aquatic and land HIIT. Aquatic HIIT has better effect on body fat rate, hemodynamics and vascular endothelial function in middle-aged men due to the effect of aquatic pressure and temperature.
... Meta-analyses on FMD studies concluded that for every 1% increase in FMD, there is an 8 to 13% decreased risk of cardiovascular disease [3,4]. The beneficial effects of exercise training on FMD are well established [5,6]. A meta-analysis [7] and other studies [8,9] show that high-intensity interval training (HIIT) is more effective than moderate-intensity continuous training (MICT) in improving FMD, but some studies show similar effects between protocols [10][11][12][13]. ...
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Researchers have hypothesized that high-intensity interval exercise (HIIE) and moderate-intensity continuous exercise (MOD) lead to different patterns of shear stress in the brachial artery. These differing patterns of shear stress are thought to partially explain the differing chronic adaptations to these two types of exercise. No study has directly compared blood flow characteristics during HIIE and MOD. Sixteen healthy males (Age: 23 ± 3 years) completed two randomly assigned exercise visits: HIIE (10 × 1 min intervals at 90–95% of HRmax with 1 min of recovery between) or MOD (30 min at 70% of HRmax) on an electronically braked cycle ergometer. Brachial artery blood flow velocity and diameter were measured for a total of 12 min during each of the exercise sessions. Both anterograde blood flow (MOD: 191.3 ± 80.3 mL/min, HIIE: 153.9 ± 67.5 mL/min, p = 0.03) and shear rate (MOD: 203.5 ± 78.1 s−1, HIIE: 170.8 ± 55.5 s−1, p = 0.04) were higher during MOD compared to HIIE. Both retrograde blood flow (MOD: −48.7 ± 21.3 mL/min, HIIE: −63.9 ± 23.3 cm/s, p < 0.01) and shear rate (MOD: −51.5 ± 19.8 s−1, HIIE: −73.8 ± 28.4 s−1, p < 0.01) were of greater magnitude during HIIE compared to MOD. During exercise, brachial artery diameter (p = 0.34) did not differ between HIIE and MOD. Continuous moderate cycling exercise leads to higher brachial artery anterograde shear rate and blood flow, but lower retrograde shear rate and blood flow when compared to high-intensity interval exercise. These differences during exercise in blood flow characteristics could shed light on the differing chronic adaptations to these two types of exercise.
... The decrease in the risk score is due to the significant decrease in the risk factors of CVD due to yoga and diet intervention as it shifts the autonomic nervous system towards parasympathetic dominance, which lowers inflammatory cytokines, improves sensitivity of baroreflex, and decrease in heart rate and blood pressure. [31,[37][38][39][40][41] Table 4 depicts a correlation analysis of FRS score with cardiovascular risk variables; results show that there was a significant weak correlation with SBP, DBP, TG, VLDL, LDL, and a significant moderate correlation with TC/HDL and strong significant positive and negative correlations with TC and HDL, respectively, which was similar to the study conducted by Yadav R et al., [20] who reported a strong positive correlation between the FRS score and serum TC. There was a moderate positive correlation between FRS and LDL and a weak positive correlation between FRS and TG, VLDL, and SBP. ...
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A BSTRACT Introduction Cardiovascular diseases (CVDs) are a cluster of disorders of blood vessels and the heart. As a form of physical activity, yoga postures, and pranayama have been shown to be beneficial in various health conditions, i.e. hypertension, prediabetes, and diabetes among high-risk subjects. This study aimed to evaluate the impact of yoga and diet on the Framingham risk score (FRS) among high-risk cardiovascular subjects. Materials and Methods The experimental interventional study was conducted at “RUHS College of Medical Sciences” and Associated Group of Hospitals”, Jaipur among high-risk cardiovascular subjects. FRS was used as a measurement for the outcome of interest at baseline and six months of yoga diet intervention in the study and control groups. Results Mean age of participants was 48.43 ± 6.4 years. Baseline values (mean ± SD) of FRS 24.59 ± 10.15 after six months of yogic lifestyle 15.1 ± 7.05. After six months of yogic lifestyle FRS scores and estimated 10-year cardiovascular risk were statistically significantly ( P < 0.0001) decreased. Pearson correlation analysis results depict that FRS correlation. There was a strong positive correlation between the FRS score and total cholesterol ( r = 0.787; P < 0.001) and a negative strong correlation between the FRS score and high-density lipoprotein was observed ( r =−0.621; P < 0.002). Conclusion The findings of this study conclude that six months of yoga and diet lifestyle intervention significantly decreased FRS among high-risk CVD subjects compared to the control group.
... Furthermore, extensive research supports the notion that increased physical activity levels correlate with a reduced risk of CVD mortality [24]. The beneficial impact of physical exercise on cardiovascular health cannot be solely ascribed to enhancements in conventional risk factors (such as inflammatory/hemostatic biomarkers, blood pressure, lipids, and BMI [25]), but may also stem from improvements to vascular function, leading to augmented endothelium-dependent activity [26]. Given its significant benefits, moderate physical activity is vital for individuals with OSA. ...
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Background The relationship between the multivariable apnea prediction (MAP) index and lipid levels was examined using a cross-sectional and retrospective study of National Health and Nutrition Examination Surveys (2015–2018). A total of 3195 participants with MAP scores were included in the analysis. Methods The MAP index, an algorithm leveraging sleep apnea symptom frequency, body mass index (BMI), age, and sex, estimates the risk of obstructive sleep apnea (OSA). We investigated the associations between the MAP index and lipid profiles—specifically, high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) —using weighted linear regression and restricted cubic splines (RCS) analysis. Additionally, mediation analysis was conducted to explore the potential mediating role of physical activity on the link between OSA risk, hyperlipidemia, and cardiovascular mortality. Results A non-linear relationship was observed between OSA severity and lipid profiles, including elevated levels of TC, increased LDL-C, higher TG, and decreased HDL-C (All p for non-linearity <0.05). The findings remained consistent across the stratified sensitivity analyses. Furthermore, physical activity served as a mediator in the association between the MAP index and both hyperlipidemia and cardiovascular mortality, accounting for 16.6% and 16.7% of the indirect effects, respectively. Conclusions Participants at high risk for OSA demonstrated an increased prevalence of dyslipidemia. Additionally, engagement in physical activity was shown to have beneficial effects on lipid metabolism.
... every day; Cluster 2: peaks at around 8 a.m. and 6 p.m. daily; Cluster 3: a relatively uniform distribution of physical activity intensity throughout the day; Cluster 4: an even daily distribution of physical activity intensity The mechanisms whereby increase in physical activity exerts a beneficial effect on blood pressure are uncertain. These include alterations during exercise in the cardiac output, sympathetic nerve function, and the total peripheral vascular resistance with concomitant changes in circulating plasma norepinephrine and renin levels and favourable alterations in weight, insulin sensitivity, and vascular endothelial function [20,21]. The impact is affected by the exercise type, intensity, and duration where a metaanalysis by Cornelisson et al. showed that both dynamic aerobic and resistance exercise (but not combined training) could lower systolic and diastolic blood pressure in pre-hypertensive cases [7]. ...
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Purpose of Review It has recently been suggested that the timing of exercise is important in the subsequent development of hypertension. We used the UK Biobank database which prospectively collates data in over 500,000 people aged between 40 and 69 years to determine the relationship between the chronoactivity pattern of exercise and the risk of incident hypertension. Recent Findings We analyzed data from 70,617 participants with 7-day Axivity AX3 triaxial accelerometry information available. Comparisons were made by a K-means clustering analysis separating groups according to the daily timing of physical activity and intensity. Subgroup, sensitivity analyses, and Cox proportional hazard model were performed. The mean age of the cohort was 61.17 (± 7.89) years with 40.05% men, and there was a mean follow-up of 7.54 (± 1.65) years. Participants were separated into 4 clusters with 6341 developing hypertension. Cluster 1 (early morning physical activity) and Cluster 2 (early morning and later physical activity) had a significantly reduced risk of incident hypertension (adjusted HR 0.870 [95%CI 0.812–0.932) vs. 0.895 [95%CI 0.825–0.972], respectively) when compared with Cluster 3 (physical activity intensity spread evenly throughout the day). Cluster 1 and Cluster 2 cases with High Intensity physical activity had a lower risk of hypertension; however, Low Intensity physical activity in Cluster 1 still reduced the risk of incident hypertension. There was a lower risk of hypertension in Cluster 1 and Cluster 2 in both morning and evening sleep chronotypes. Summary The development of incident hypertension is significantly reduced in those who engage in some level of physical activity earlier in the day. Lay Summary Hypertension (high blood pressure) is a global problem with a high economic health burden that has been shown to be a major risk factor for diabetes, cardiovascular, and kidney disease. Our study has used a large maintained UK biological database to determine the impact of physical exercise on reducing the subsequent development of hypertension during follow-up from data provided by more than 70,000 participants. When we segregated patients into clusters of exercise timing, we found that the risk of developing hypertension over time was reduced for patients who performed exercise earlier in the morning than at other times of the day. This benefit was still evident even when the intensity of regular physical activity was low.
... Similar to a previous study, cuff inflation was used to modulate blood flow and WSS during handgrip exercise (Green, 2009). The results of our study showed that WSS in obese individuals was significantly higher after HIIE than that at baseline, and could effectively improve vascular endothelial function. ...
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Objective: To investigate the mechanisms of wall shear stress (WSS) responsible for the effects of high-intensity interval exercise (HIIE) on vascular endothelial function in young obese males. Methods: A within-subject study design was used. We examined the response of the reactive hyperemia index (RHI) to acute HIIE in young obese males (n = 20, age = 20.38 ± 1.40 years, body mass index [BMI] = 31.22 ± 3.57, body fat percentage [BF (%)] = 31.76 ± 3.57). WSS was manipulated using 100, 80, or 60 mmHg cuff inflation during the HIIE to determine the proper inflation capable of maintaining WSS near baseline levels. One-way repeated measures analysis of variance and LSD post hoc tests were performed to compare changes in WSS and vascular endothelial function at baseline HIIE and following HIIE using different cuff inflations. Results: There were no significant differences in RHI and WSS between the three cuff inflation values (p > 0.05). WSS was significantly higher in obese male individuals after HIIE and HIIE with 100 mmHg cuff inflation (p = 0.018, p = 0.005) than that at baseline, with no significant differences observed comparing HIIE and HIIE with 100 mmHg inflation (p = 0.23). The RHI after HIIE was significantly higher (p = 0.012) than that at baseline, while no significant differences were detected after HIIE at 100 mmHg (p = 0.91). The RHI was significantly lower after HIIE with 100 mmHg than that after HIIE (p = 0.007). WSS (p = 0.004) and RHI (p = 0.017) were significantly higher after HIIE than that at baseline, while no significant differences were observed after HIIE with either 80 or 60 mmHg cuff inflation (baseline vs. HIIE + 80 mmHg: WSS: p = 0.33, RHI: p = 0.38; baseline vs. HIIE + 60 mmHg: WSS: p = 0.58, RHI: p = 0.45). WSS was similar to HIIE, after HIIE with either 80 or 60 mmHg inflation (p = 0.36, p = 0.40). However, RHI was significantly higher for HIIE than for HIIE with both 80 and 60 mmHg inflation (p = 0.011, p = 0.006). Conclusion: HIIE could significantly improve WSS and vascular endothelial function. HIIE intervention with 60 or 80 mmHg inflation might enhance WSS near the baseline level. HIIE-induced acute changes in WSS may provide the primary physiological stimulus for vascular endothelial adaptation to HIIE in young obese males.
... For example, similar reasoning 369 on the need to limit motor preparedness would suggest that vascular dilation should also be 370 limited to the threat targeted limb, rather than across the entire body. While the neural 371 architecture for limb-specific vascular responding is well established -localized patterns of 372 dilation are well documented during motor activity and exercise (Wang, 2005;Green, 2009;373 Green et al., 2017) -it is unclear whether this localized vascular responding can be used by the 374 ANS preceding a threat-reduction response as well. It is also unclear whether limb-specific 375 cutaneous activity is observed in response limb-localized non-tactile threats, such the sight of a 376 spider approaching the hand. ...
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In times of stress or danger, the autonomic nervous system (ANS) signals the fight or flight response. A canonical function of ANS activity is to globally mobilize metabolic resources, preparing the organism to respond to threat. Yet a body of research has demonstrated that, rather than displaying a homogenous pattern across the body, autonomic responses to arousing events, as measured through changes in electrodermal activity (EDA), can differ between right and left body locations. Surprisingly, an attempt to identify a function of ANS asymmetry consistent with its metabolic role has not been investigated. In the current study, we investigated whether asymmetric autonomic responses could be induced through limb-specific aversive stimulation. Participants were given mild electric stimulation to either the left or right arm while EDA was monitored bilaterally. In a group-level analyses, an ipsilateral EDA response bias was observed, with increased EDA response in the hand adjacent to the stimulation. This effect was observable in ∼50% of individual participants. These results demonstrate that autonomic output is more complex than canonical interpretations suggest. We suggest that, in stressful situations, autonomic outputs can prepare either the whole-body fight or flight response, or a simply a limb-localized flick, which can effectively neutralize the threat while minimizing global resource consumption. These findings are consistent with recent theories proposing evolutionary leveraging of neural structures organized to mediate sensory responses for processing of cognitive emotional cues.
... 0.59 for MCAv) and little evidence of any familial correlation for response to exercise. There is evidence to suggest that exercise remodels peripheral blood vessels in humans (Green, 2009;Green et al., 2010;Green et al., 2017;Joyner & Green, 2009;Naylor et al., 2011;Tinken et al., 2010), although most studies utilise TCD to assess CBF in intracranial arteries, which assumes that the diameter of these vessels does not change. This assumption could result in overlooking potential changes in diameter during the cerebrovascular assessments (CR, autoregulation and acute exercise), or in response to the training interventions. ...
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We studied monozygotic (MZ) and dizygotic (DZ) twin pairs following resistance (RES) and endurance (END) training to assess genetic and environmental contributions to cerebrovascular function. Cerebrovascular function (rest, autoregulation, hypercapnia, exercise) was assessed in 86 healthy same‐sex MZ (30 pairs) and DZ (13 pairs) twins, who underwent 3 months of END and RES. Carbon dioxide (PETCO2${P_{{\rm{ETC}}{{\rm{O}}_{\rm{2}}}}}$), mean arterial pressure (MAP) and middle cerebral artery velocity (MCAv) were measured and MCAv resistance (MCACVRi) was calculated. Resting MCAv reduced by −2.8 cm/s following RES (P = 0.024), with no change following END (−0.3 cm/s, P = 0.758). Change in MCACVRi following RES was +0.11 mmHg/cm/s (P < 0.001), which was significantly greater than END (+0.02 mmHg/cm/s, P = 0.030). MAP also increased following RES (+4 mmHg, P = 0.010), but not END (+1 mmHg, P = 0.518). No changes were apparent in PETCO2${P_{{\rm{ETC}}{{\rm{O}}_{\rm{2}}}}}$. At rest, positive response rates following RES ranged from 27 to 71% and from 40 to 64% following END. Intraclass correlations between twins were moderate for most variables at baseline. In response to training, only MZ pairs were significantly correlated for a change in MCAv (P = 0.005) and low frequency phase (P = 0.047) following RES.This study is the first to compare cerebrovascular function following RES and END in MZ and DZ twins. Most individuals who did not respond to one modality were able to respond by switching modality, and baseline heritability estimates were higher than training response. Exercise professionals should therefore consider modality and environmental factors when optimising interventions. Key points Characterising individual responses to resistance and endurance exercise training can inform optimal strategies for exercise prescription. This study utilised monozygotic and dizygotic twins in a randomised cross‐over study to determine individual responsiveness to different modalities of exercise training. The influence of environment vs. genetics on cerebrovascular responses to training was determined. It is apparent that individuals respond differently to distinct exercise stimuli and that switching modality may be a beneficial way to obtain positive responses in cerebrovascular function. This study has implications for improving individualised exercise prescription to maintain or improve cerebrovascular structure and function.
... Reduced arterial stiffness as measured by PWV in response to aerobic-based exercise training has been demonstrated in the general population [47,48] and may precede clinically detectable changes in BP [49]. More pronounced improvements in PWV with exercise training have been reported in studies enrolling participants with higher baseline PWV values (>9.3 m/s) and those not receiving antihypertensive medication [47]. ...
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Introduction: Exercise is an effective strategy for blood pressure (BP) reduction in the general population, but efficacy for the management of hypertension in CKD is not known. We evaluated the difference in 24-hour ambulatory systolic BP with exercise training in people with moderate to severe chronic kidney disease (CKD). Methods: Participants with an estimated glomerular filtration rate (eGFR) of 15-44 mL/min per 1.73m2 and SBP >120 mmHg were randomized to receive thrice weekly, moderate intensity aerobic-based exercise over 24 weeks, or usual care. Phase 1 included supervised in-center and home-based sessions for eight weeks. Phase 2 was 16 weeks of home-based sessions. BP, arterial stiffness, cardiorespiratory fitness, and markers of CV risk were analyzed using mixed linear regression. Results: We randomized 44 people; 36% were female, median age was 69 years, 55% had diabetes and the median eGFR was 28 mL/min per 1.73m2. Compared with usual care, there was no significant change in 24-ambulatory SBP at eight weeks 2.96 mmHg (95% CI -2.56, 8.49) or 24 weeks. Peak oxygen uptake improved by 1.9 mL/kg/min in the exercise group (95% CI 0.03, 3.79) at eight weeks with a trend toward higher BMI 1.84 kg/m2 (95% CI -0.10, 3.78) and fat free mass, but this was not sustained at 24 weeks. Markers of CV risk were unchanged. Conclusions: Despite an improvement in VO2peak and body composition, we did not detect a change in 24-hour ambulatory systolic BP in people with moderate to severe chronic kidney disease.
... Furthermore, an increased release of vasodilators, such as histamine and creatine (Peake et al., 2005) could drive a decrease in SBP after eccentric exercise. Exercise-induced shear stress is intensity-dependent (Gurovich & Braith, 2012) and exercise training at higher intensities, like during HIIT, would enhance nitric oxide bioavailability improving endothelial function (Green, 2009;Ishibazawa et al., 2011;Jin & Loscalzo, 2010). Similarly, Bond et al. (2015) showed an increase in endothelial function after 2 weeks (6 sessions) of concentric HIIT training, which was in absence of other cardiovascular risk markers and aerobic capacity (Bond et al., 2015). ...
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Background: Steady-state eccentric exercise training improves cardiometabolic risk (CMR) despite lesser cardiovascular demands compared with load-matched concentric training. Whether a high-intensity interval eccentric training is also effective reducing CMR is unknown. Aim: To compare the effects of a short-term high-intensity interval eccentric training (ECC-HIIT) with high-intensity interval concentric training (CONC-HIIT) on CMR in sedentary overweight men. Methods: Twenty men (age: 27.9 ± 5.3y, body massindex: 29.1 ± 3.1 kg·m-2) were randomly assigned to ECC-HIIT (n = 10) or CONC-HIIT (n = 10) delivered as six sessions, including 4 x 5:2 min work-to-rest ratio, at 80% peak concentric power output. Heart rate (HR), rate of perceived exertion (RPE) and muscle soreness weremonitored during training sessions. Training effects on lipid profile, insulin sensitivity (HOMA-IR), body composition, thigh circumference, isometric knee extensors maximal strength, resting systolic and diastolic blood pressure (SBP and DBP) were determined. Results: Average training HR and RPE were -29%and -50%lower in ECC-HIIT in comparison with CONC-HIIT. Muscle soreness was initially greater after ECC-HIIT compared with CONC-HIIT. Significant changes in total and low-density lipoprotein cholesterol (-7.0 ± 8.7%; p = .02 and -6.3 ± 14.4%; p = .03), SBP (-9.8 ± 7.8%; p = .002), and maximal thigh circumference (+2.5 ± 3.1%; p = .02) were observed following ECC-HIIT. No changes in any CMR marker were observed after CONC-HIIT. Moderate-to-large training effect sizes were obtained in thigh circumference, SBP, total cholesterol and low-density lipoprotein cholesterol in response to ECC-HIIT. Conclusion: A two-week ECC-HIIT was well-tolerated and induced rapid onset improvements in cholesterol and blood pressure compared to conventional CONC-HIIT in sedentary overweight men.
... Exercise habits have been shown to improve vascular stiffness not only in the limbs but also many other regions of the body [7], whereas effects of exercise habits on the ocular circulation remain unknown Effects of exercise habits on improving vascular stiffness can vary between individuals and body [8]. Exercise habits are strongly recommended, but a large proportion of adults cannot meet these recommendations, including in Japan [9]. ...
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Purpose We examined the effects of aging and exercise habits on the ocular blood flow (OBF) and its profiles throughout the optic nerve head region and choroidal area. We hypothesized that exercise habits reduce the stiffness of vessels in the ocular circulation, which generally increases with aging. Methods Participants in a medical checkup program (698 males and 192 females aged 28 to 80 years) were categorized into 2 groups (with and without exercise habits) based on participant self-reporting and the definition of the Ministry of Health, Labor and Welfare of Japan (MHLW). OBF in the right eye was measured and analyzed using laser speckle flowgraphy. The blowout time (BOT), which is the time during which the blood flow is higher than half of the mean of the minimum and maximum signals during one heartbeat, was calculated as an index of the blood flow profile. BOT has been used as an indicator of the flexibility of blood vessels. Results BOT significantly decreased with aging. Neither the self-reported nor MHLW-based exercise habits significantly affected the ocular circulation. Conclusion These results indicate that the stiffness of the ocular vessels increases with aging, and this cannot be prevented by exercise habits.
... An impaired endothelial function may be associated with adverse CV events. However, previous studies have presented discrepant findings in healthy middle-aged men [89], hypertensive or healthy postmenopausal women, and healthy elderly subjects [90], suggesting that the association between endothelial function and CV risk is not yet well established in the asymptomatic population, especially concerning the CVD risk profiles. ...
Article
Atherosclerosis has a long preclinical phase, and the risk of cardiovascular (CV) events may be high in asymptomatic subjects. Conventional risk factors provide information for the statistical probability of developing CV events, but they lack precision in asymptomatic subjects. This review aims to summarize the role of some widely publicized indicators of early atherosclerosis in predicting CV events. The earliest measurable indicator of the atherosclerotic process is endothelial dysfunction, measured by flow-mediated dilation (FMD) of the brachial artery. However, reduced FMD is a stronger predictor of future CV events in patients with existing CV disease than in apparently healthy persons. Alternatively, measurement of carotid artery intima-media thickness does not improve the predictive value of risk factor scores, while detection of asymptomatic atherosclerotic plaques in carotid or common femoral arteries by ultrasound indicates high CV risk. Coronary calcium is a robust and validated help in the estimation of vascular changes and risk, which may improve risk stratification beyond traditional risk factors with relatively low radiation exposure. Arterial stiffness of the aorta, measured as the carotid-femoral pulse wave velocity is an independent marker of CV risk at the population level, but it is not recommended as a routine procedure because of measurement difficulties. Low ankle-brachial index (ABI) indicates flow-limiting atherosclerosis in the lower limbs and indicates high CV risk, while normal ABI does not rule out advanced asymptomatic atherosclerosis. Novel circulating biomarkers are associated with the atherosclerotic process. However, because of limited specificity, their ability to improve risk classification at present remains low.
... The powerful stimuli generated by aerobic exercise are associated with vascular remodeling (Green, 2009;Green et al., 2017). Small arteries are the main resistance vessels that regulate flow to different tissues of the body and control blood pressure. ...
Article
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The treatment and prevention of hypertension has been a worldwide medical challenge. The key pathological hallmark of hypertension is altered arterial vascular structure and function, i.e., increased peripheral vascular resistance due to vascular remodeling. The aim of this review is to elucidate the molecular mechanisms of vascular remodeling in hypertension and the protective mechanisms of aerobic exercise against vascular remodeling during the pathological process of hypertension. The main focus is on the mechanisms of oxidative stress and inflammation in the pathological condition of hypertension and vascular phenotypic transformation induced by the trilaminar structure of vascular endothelial cells, smooth muscle cells and extracellular matrix, and the peripheral adipose layer of the vasculature. To further explore the possible mechanisms by which aerobic exercise ameliorates vascular remodeling in the pathological process of hypertension through anti-proliferative, anti-inflammatory, antioxidant and thus inhibiting vascular phenotypic transformation. It provides a new perspective to reveal the intervention targets of vascular remodeling for the prevention and treatment of hypertension and its complications.
... However, the underlying mechanisms behind arterial remodeling are complex. Training induces a direct impact on the vasculature (43). The pattern of blood flow and the amount of shear stress that occur during exercise may be related to the specific training characteristics, including training intensities (44). ...
Article
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Background Endothelial function by flow-mediated dilatation assesses early markers of atherosclerotic progression. Greater amounts of physical activity and physical fitness in children are associated with cardiovascular health benefits. We aimed to explore factors, influencing endothelial function and arterial compliance in a cohort of healthy school children. Methods The 94 participants (41 girls, 53 boys) in the study were young, healthy children from a German school cohort. Anthropometric data, body composition and blood pressure were assessed. Blood was drawn (8 h overnight fast), assessing total cholesterol, high density lipoprotein and low density lipoprotein and triglycerides. Endothelial function was diagnosed by flow-mediated dilatation with ultrasonography (ALOKA/Hitachi, Prosound alpha 6). Tracking gates were set on the intima in B-mode. The waveform of diameter changes over the cardiac cycle was displayed in real time using the FMD-mode of the eTRACKING system. Changes in arterial diameter at baseline, ischaemia and vasodilatation were measured. A symptom limited pulmonary exercise test on a bicycle ergometer was performed to test cardiorespiratory fitness. Physical activity was assessed using GT3x accelerometers (Actigraph, USA), over 4 days (including 1 week-end day), with a minimum wear-time duration of 10 h. Results The median age was 12.2 years (11.8–12.8). Children were normal weight, blood lipid profiles (cholesterol, high-density lipoprotein, low-density lipoprotein, triglyceride) were in normal range. Baseline measurements during the diagnostics of endothelial function revealed higher arterial compliance of the brachial artery in boys. Boys' cardiorespiratory fitness was higher than compared to girls. Boys met the recommendations of 60 min moderate to vigorous activity, whereas girls were significantly less active and did not meet current recommendations. More time spent in sedentary activity was the main predictor for lower arterial compliance (adjusted for age and sex), accounting for 14% of the variance. No significant model revealed, analyzing the influencing factors such as anthropometric data, blood lipids, physical activity and fitness on endothelial function. Conclusion This is the first study on endothelial function in association to objectively measured physical activity and cardiorespiratory fitness in healthy school children in Germany. The study highlights the importance of reducing time spent being sedentary to maintain endothelial health.
... It is well established that aerobic exercise can improve endothelial function and flowmediated dilation (FMD) responses [153], particularly in those with cardiovascular disease and related risk factors [154]. Despite this link, the diurnal effects of exercise on FMD have received relatively little attention, even though FMD has been shown previously to vary with time of day [155]. ...
Article
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Compelling research has documented how the circadian system is essential for the maintenance of several key biological processes including homeostasis, cardiovascular control, and glucose metabolism. Circadian clock disruptions, or losses of rhythmicity, have been implicated in the development of several diseases, premature ageing, and are regarded as health risks. Redox reactions involving reactive oxygen and nitrogen species (RONS) regulate several physiological functions such as cell signalling and the immune response. However, oxidative stress is associated with the pathological effects of RONS, resulting in a loss of cell signalling and damaging modifications to important molecules such as DNA. Direct connections have been established between circadian rhythms and oxidative stress on the basis that disruptions to circadian rhythms can affect redox biology, and vice versa, in a bi-directional relationship. For instance, the expression and activity of several key antioxidant enzymes (SOD, GPx, and CAT) appear to follow circadian patterns. Consequently, the ability to unravel these interactions has opened an exciting area of redox biology. Exercise exerts numerous benefits to health and, as a potent environmental cue, has the capacity to adjust disrupted circadian systems. In fact, the response to a given exercise stimulus may also exhibit circadian variation. At the same time, the relationship between exercise, RONS, and oxidative stress has also been scrutinised, whereby it is clear that exercise-induced RONS can elicit both helpful and potentially harmful health effects that are dependent on the type, intensity, and duration of exercise. To date, it appears that the emerging interface between circadian rhythmicity and oxidative stress/redox metabolism has not been explored in relation to exercise. This review aims to summarise the evidence supporting the conceptual link between the circadian clock, oxidative stress/redox homeostasis, and exercise stimuli. We believe carefully designed investigations of this nexus are required, which could be harnessed to tackle theories concerned with, for example, the existence of an optimal time to exercise to accrue physiological benefits.
... For example, similar reasoning on the need to limit motor preparedness would suggest that vascular dilation should also be limited to threat targeted limb, rather than across the entire body. While the neural architecture for limb-specific vascular responding is well establishedlocalized patterns of dilation are well documented during motor activity and exercise (Green, 2009;Green et al., 2017;Wang, 2005) it is unclear whether this localized vascular responding can be used by the ANS for motor preparation as well. It is also unclear whether limb-specific cutaneous activity is observed in response to perception of threat through senses other than others, such the sight of a spider approaching the hand. ...
Preprint
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In times of stress or danger, the autonomic nervous system (ANS) signals the fight or flight response. A canonical function of ANS activity is to globally mobilize metabolic resources, preparing the organism to respond to threat. Yet a body of research has demonstrated that, rather than displaying a homogenous pattern across the body, autonomic responses to arousing events - as measured through changes in electrodermal activity (EDA) - can differ between right and left body locations. Surprisingly, the metabolic function of such ANS asymmetry has not been investigated. In the current study, we investigated whether asymmetric autonomic responses could be induced through limb-specific aversive stimulation. Participants were given mild electric stimulation to either the left or right arm while EDA was monitored bilaterally. Across participants, a strong ipsilateral EDA response bias was observed, with increased EDA response in the hand adjacent to the stimulation. This effect was observable in over 50% of individual subjects. These results demonstrate that autonomic output is more complex than canonical interpretations suggest. We suggest that, in stressful situations, autonomic outputs can prepare either the whole-body fight or flight response, or a simply a limb-localized flick, which can effectively neutralize the threat while minimizing global resource consumption. These findings provide insight into the evolutionary pathway of neural systems processing general arousal by linking observed asymmetry in the peripheral arousal response to a historical leveraging of neural structures organized to mediate responses to localized threat.
... Exercise is a front-line therapy that can reduce CVD by directly influencing vascular outcomes including endothelial-dependent dilation and arterial stiffness 5 . Specifically in pregnancy, exercise reduces the odds of developing gestational diabetes, gestational hypertension and pre-eclampsia by 40%, and therefore protects against future CVD 6 . ...
Article
Of all physiological systems, the cardiovascular system takes on the most profound adaptation in pregnancy to support fetal growth and development. The adaptations that arise are systemic and involve structural and functional changes that can be observed at the cerebral, central, peripheral, and microvascular beds. This includes, although is not limited to increased heart rate, stroke volume and cardiac output with negligible change to blood pressure, reductions in vascular resistance and cerebral blood flow velocity, systemic artery enlargement, enhanced endothelial function. All of this takes place to accommodate blood volume expansion and ensure adequate fetal and maternal oxygen delivery. In some instances, the demand placed on the vasculature can manifest as cardiovascular maladaptation and thus, cardiovascular complications can arise. Exercise is recommended in pregnancy because of its powerful ability to reduce the incidence and severity of cardiovascular complications in pregnancy. However, the mechanism by which it acts is poorly understood. The first aim of this review is to describe the systemic adaptations that take place in pregnancy. Secondly, this review aims to describe the influence of exercise on these systemic adaptations. It is anticipated that this review can comprehensively capture the extent of knowledge in this area while identifying areas that warrant further investigation.
... Reduced vagal tone also causes a reduction in heart rate as a result of change in the sympathetic stimulation and a change in the vascular system due to parasympathetic stimulation [19]. Another reason as mentioned by iyagarajan et al. could be the "vascular conditioning" effect due to exercises [20]. Exercises produce a shearing force on the internal vasculature and increase the levels and availability of endothelial nitric oxide synthase enzyme which causes vasodilation and reduction in BP [21]. ...
Article
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Introduction. Prehypertension is a precursor for developing hypertension and is a risk factor for cardiovascular diseases. Yoga therapy may have a role in lowering the blood pressures in prehypertension and hypertension. This systematic review aims to synthesize the available literature for the same. Methodology. Databases such as PubMed, Embase, Scopus, and Web of Science were searched for randomised control trials only in the time duration of 2010–2021. The main outcome of interest was systolic and diastolic blood pressures. Articles were screened based on the inclusion criteria, and 8 articles were recruited for the review. Meta-analysis was done for suitable articles. RevMan 5.4 by Cochrane was used for meta-analysis and forest plot construction. Risk of bias was determined using the Downs and Black checklist by three independent authors. Results. The meta-analysis of the articles favoured yoga intervention over the control intervention. Yoga therapy had significantly reduced the systolic pressure (−0.62 standard mean difference, at IV fixed 95% CI: −0.83, −0.41) and diastolic pressure (−0.81 standard mean difference, at IV random 95% CI: −1.39, −0.22). Secondary outcome measures studied were heart rate, weight, BMI, waist circumference, and lipid profile. The main protocol of yoga therapy included postures, breathing exercises, and different meditation techniques. A significant reduction in secondary outcomes was observed, except for HDL values in lipid profile which showed a gradual increase in yoga group in comparison with alternative therapy. Conclusion. Yoga therapy has shown to be significant in the reduction of systolic and diastolic pressure in prehypertensive population. Supporting evidence lacks in providing a proper structured dosage of yoga asanas and breathing techniques. Considering the existing literature and evidence, Yoga therapy can be used and recommended in prehypertensive population and can be beneficial in reducing the chances of developing hypertension or cardiovascular diseases. 1. Introduction Prehypertension and hypertension are one of the treatable diseases in the world. There has been strong evidence on the progression of prehypertension to hypertension, provided by the American Heart Association (AHA) in 2011. One of the studies also gives a probability of prehypertensive adults progressing to hypertension [1]. Prehypertension is defined as systolic blood pressure (SBP) 120–129 mmHg and diastolic blood pressure (DBP) 80–89 mmHg by the 2017 guidelines of AHA [2]. According to the update on the 8th guideline by Joint National Committee (JNC), it was SBP 120–139 mmHg and DBP 80–89 mmHg [1]. Prehypertension is a sign and can give the probability of developing cardiovascular diseases in the future. The Framingham heart study (FRS) has found the epidemiology for developing cardiovascular diseases and has identified elevated cholesterol levels and blood pressures as the important predisposing factors [3]. Elevated stress levels have also been correlated with a rise in blood pressure [4, 5]. Yoga improves flexibility, reduces stress levels, and causes strengthening of muscles. The neurobiological causes for increased stress levels were incorporated in a systematic review by Pascoe et al. in 2017 [6]. This systematic review and meta-analysis included the articles which used MBSR and yoga therapy in reducing stress levels and studied its physiological effects. This review did not solely concentrate on elevated blood pressures as a main outcome measure. Yoga therapy may prove to be beneficial in hypertensive and prehypertensive population. There was a significant effect of yoga on hypertensive population [7]. As per the review by Park and Hans, yoga therapy and meditation are successful in reducing the systolic and diastolic blood pressures [8]. Yoga therapy has been proven to be more effective in comparison to meditation. This review has focused on both hypertensive and prehypertensive population and has not isolated prehypertension as the primary health condition. Supporting literature also has been found on both hypertension and prehypertensive population [7, 8]. Yoga therapy is proven to be beneficial in reducing the cardiovascular risks as per the review by Chu et al. in 2016 [9]. This review has included all the predisposing comorbidities for developing cardiovascular disease and not solely elevated blood pressures. A review solely focusing on prehypertension was not found. Therefore, this review aims at providing evidence for stand-alone effect of yoga on prehypertensive population. To ensure high level evidence, this review will also aim to provide a meta-analysis for the blood pressure, systolic and diastolic. 2. Methodology 2.1. Literature Search The protocol of this systematic review was registered in Open Science Framework (OSF) with the registration DOI: 10.17605/OSF.IO/YH2FQ. MEDLINE, Scopus, EMBASE, and Web of Science were screened, and searches were run using various search strategies with a combination of Booleans, AND and OR, separately and later combined to get the desired articles as shown in Table 1 through the search engines of PubMed and Embase. The articles which were unsuitable according to inclusion criteria were excluded. Inclusion criteria and exclusion criteria are given in the following. A total of 126 articles were shortlisted based on the various filters of databases mentioned above and selected for title and abstract screening. 40 articles were identified from sources other than the databases referred to above. After title, abstract and full-text screening, eight appropriate articles were finalised and taken for the systematic review as shown in Figure 1, and then they were reviewed. Synonyms and MeSH terms were identified using Cochrane and PubMed MeSH finders and search strategy builders. The synonyms which were used are described in Table 2. Sr. no. Strategy 1. Basic keyword yoga with ‘OR’ 2. Basic keyword blood pressure with ‘OR’ 3. Basic keyword prehypertension with ‘OR’ 4. Combined searches with ‘AND’ 5. Time span filter (2010–2021) 6. Full-text filter 7. RCT filter RCT- Randomised control trial.
... While OSA poses a significant cardiovascular disease burden, cardiovascular disease risk is lower among adults who perform regular aerobic exercise (9). It has been proposed that this cardioprotection may be partly explained by the direct beneficial effect of exercise on the same vascular properties that are impaired in OSA (10). Indeed, favorable changes in endothelial function and arterial stiffness have been observed within weeks (11,12) of initiating exercise-training programs, and patient populations with less favorable endothelial function and arterial stiffness at baseline have enhanced improvement in these parameters following training (13,14). ...
Article
Obstructive sleep apnea (OSA) is associated with increased cardiovascular morbidity due, in part, to impaired vascular function. Exercise confers cardioprotection by improving vascular health. Yet, whether OSA severity affects the vascular improvements conferred with exercise training is not known. Overweight (body mass index (BMI) >27 kg/m²) adults were evaluated for OSA and enrolled in a six‐week exercise intervention. Baseline assessments of brachial artery flow‐mediated dilation (BAFMD), central augmentation index (AIx) and pulse wave velocity (PWV) were repeated post training. Fifty‐one participants (25 men; 26 women) completed the study. Despite improved aerobic capacity (p=0.0005) and total fat mass (p=0.0005), no change in vascular function was observed. Participants were divided into two severity groups according to their baseline total apnea‐hypopnea index (AHI) as either 5 to 14.9 events•hr‐1 (n= 21; Age=48 ± 7 yrs; BMI=33.7 ± 4.6kg•m‐2) or 15 ≥events•hr‐1 (n=30; Age=56 ± 13 yrs; BMI = 34.3 ± 4.2 kg•m‐2). No effect of OSA group was observed for BAFMD (p=0.82), AIx (p=0.37) or PWV (p=0.44), suggesting that OSA severity does not influence the effect of exercise on vascular function. The vascular effects of extended exercise programs of greater intensity in overweight OSA patients should be examined.
... 20,21 At the same time, there is abundant evidence that exercise training is associated with improvement in measures of endothelium-dependent, and NO-mediated, vasodilator function in humans. [27][28][29] The benefits of exercise are largely independent of impacts on traditional cardiovascular risk factors 30,31 and may relate to hemodynamic effects, as a result of repetitive endothelial shear stress associated with episodic exercise. 28 As exercise training primarily upregulates the endothelium, 28,29 and some evidence suggests testosterone treatment enhances vascular smooth muscle function in men with coronary artery disease, 26,32 the possibility of combining testosterone and exercise training for additive benefit, warrants investigation. ...
Article
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The endothelium is integral to the maintenance of vascular health in humans, and advancing age and low testosterone levels are associated with endothelial dysfunction in men. We compared the impacts of testosterone and exercise training, alone and in combination, on endothelium-dependent flow-mediated dilation % and endothelium-independent glyceryl trinitrate % responses. In this 2×2 factorial 12-week randomized controlled trial, 80 men aged 50 to 70 years with waist girth ≥95 cm and low-normal serum testosterone levels (6–14 nmol/L) were randomized to transdermal AndroForte5 (testosterone 5.0% w/v, 100 mg/2 mL; testosterone), or matching placebo; and to supervised centre-based exercise or no additional exercise. Testosterone increased serum testosterone levels (testosterone×time, P =0.003) to the extent that 62% of subjects in testosterone groups increased levels to >14 nmol/L, whereas placebo treatment had no impact on testosterone levels. Exercise training increased flow-mediated dilation % (exercise×time, P =0.033; testosterone+exercise: +0.5, placebo+exercise: +1.0 versus testosterone+no additional exercise: −0.7, placebo+no additional exercise: +0.2%), whereas testosterone did not impact flow-mediated dilation, nor was it additive to exercise (all P >0.05). There were no significant exercise or drug main effects on glyceryl trinitrate responses (all P >0.05). Exercise training improved endothelium-dependent vasodilator function, whereas administration of testosterone at therapeutic doses did not impact flow-mediated dilation % or add to the exercise benefit. Vascular smooth muscle sensitivity to nitric oxide was not modified by exercise, testosterone, or their combination. In middle-to-older-aged men with central adiposity and low/normal testosterone levels, we observed no evidence that testosterone added to the beneficial impact of exercise on vascular function and health. REGISTRATION URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=368611 ; Unique identifier: ACTRN12615000600549.
... Nevertheless, the number of EMPs showed different changes in both single and long-term exercise. It is widely believed that repeated episodes of high shear stress was the main physiological signal of endothelial cells adapting to exercise training [60,61]. The duration of exercise bouts is usually within 2 h. ...
Article
Full-text available
This study aimed to explore the relationship between exercise and circulating microparticles (CMPs). PubMed, Web of Science, Embase, and the Cochrane Library databases were searched until August 13, 2020, using the terms “exercise” and “cell-derived microparticles.” The Cochrane tool of risk of bias and the Methodological Index for Non-Randomized Studies were used to grade the studies. Twenty-six studies that met criteria were included in this review, including one before–after self-control study, 2 cohort studies, 4 randomized control trials, 5 case–control studies, and 14 descriptive studies. The studies were divided into a single bout and long-term exercise. The types of MPs contained endothelium-derived microparticles (EMPs), leukocyte-derived microparticles (LMPs), platelet-derived microparticles (PMPs), and erythrocyte-derived microparticles (ErMPs). This first systematic review found that the levels of CMPs continued to increase after a single bout of exercise in untrained subjects and were lower in trained subjects. PMPs expressed a transient increase after a single bout of exercise, and the proportion and duration of PMPs increment reduced in long-term exercise. Most studies showed a decline in LMPs in trained subjects after a single bout and long-term exercise, and variable changes were found in EMPs and ErMPs after exercise. A single bout of exercise drives the vessels exposed to high shear stress that promotes the formation of CMPs. However, the decline in CMPs in trained subjects may be attributed to the fact that they have a better ability to adapt to changes in hemodynamics and cellular function during exercise. Graphical abstract
... Whether the longitudinal changes across gestation result in differences in forearm or femoral blood flow, reactivity, or transduction is yet to be elucidated. Aerobic exercise may alter blood pressure regulation through improvements in vascular function (i.e., enhanced endothelial function) (56). Data from our nonburst sequences would suggest that basal vasodilatory status is not altered by prenatal physical activity; however, the ability to dilate in response to increases in shear stress may be enhanced with aerobic exercise (57). ...
Article
Purpose: Women who develop gestational hypertension have evidence of elevated muscle sympathetic nerve activity (MSNA) in early pregnancy which continues to rise following diagnosis. Exercise has been shown to play a preventative role in the development of gestational hypertension and has been shown to reduce resting and reflex MSNA in non-pregnant populations., We sought to investigate whether aerobic exercise impacted sympathetic regulation of blood pressure between the second and third trimester of pregnancy. Methods: We conducted a randomized controlled trial of structured aerobic exercise (n=31) compared to no intervention (control, n=28) beginning at 16-20 weeks and continuing until 34-36 weeks gestation (NCT02948439). Women in the exercise group were prescribed aerobic activity at 50-70% of their heart rate reserve, on 3-4 days per week for 25-40minutes with a 5-minute warm up and 5-minute cool down (i.e. up to 160 minutes total activity per week). At pre- and post-intervention assessments, data from ~10-minutes of quiet rest and a 3-minute cold pressor test (CPT) were analyzed to determine sympathetic nervous system activity and reactivity. Results: MSNA was obtained in 51% of assessments. Resting MSNA BF and BI increased across gestation (main effect of gestational age, p=0.002). Neurovascular transduction (NVT) was blunted in the control group (p=0.024) but not in exercisers (p=0.873) at the post-intervention time-point. Lastly, MSNA reactivity during CPT by was not impacted by gestational age or exercise (p=0.790, interaction). Conclusion: These data show that exercise attenuates both the rise in MSNA and the blunting of NVT. This may partially explain the lower risk of developing gestational hypertension in women who are active during their pregnancies.
... Studies have shown that WSS plays an important role in the occurrence and development of atherosclerosis, which mainly occurs in areas of low [4]. After exercise training, obvious retrograde blood flow can be observed locally in some arteries, and the magnitude of the retrograde flow is affected by the exercise modes [33]. In this study, the minimum value of WSS (τ w min ) decreased and was negative, which means that there was retrograde WSS. ...
Article
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Background: Cardiovascular disease (CVD) is closely related to arterial elasticity and hemodynamics. Exercises have been reported to immediately decrease arterial apparent elasticity and regulate hemodynamic variables. However, the relationship between them and exercise intensity remains elusive. The purpose of this study was to determine the acute effects of different intensities of acute cycling exercise on carotid arterial apparent elasticity and hemodynamics. Methods: 32 healthy men (age: 19.4 ± 0.6 years) attended the laboratory on five occasions and completed cycling acute exercise for 20 minutes at five intensities (40%, 50%, 60%, 70%, and 80% heart rate reserve (HRR)). At the right carotid artery, center-line velocity and arterial inner diameter waveforms were examined before and immediately after exercise. Based upon the measured data, the classical hemodynamic theory was used to calculate the apparent elasticity and the local hemodynamic variables. Results: The arterial apparent stiffness and the apparent elastic modulus following acute cycling exercise at 60% to 80% HRR were significantly higher than baseline. The mean center-line velocity accelerated from 50% to 80% HRR, but no intensity of intervention altered mean blood flow. Immediately after intervention, the mean wall shear stress and oscillatory shear index increased. Conclusions: Aerobic cycling intervention, with intensity from 40% to 80% HRR, did not change the brain blood supply. A bout of cycling intervention decreased apparent elasticity, and there was an intensity-dependent effect on apparent elasticity and hemodynamic variables. This study would provide referable data for the further study on the effects of aerobic exercise on arterial hemodynamics and elasticity and underlying physiological mechanisms.
... Indeed, it is possible that the principle of specificity that is commonly used in the exercise physiology and human performance literature can be extended to exercise training-induced vascular adaptations. Stated differently, because during each bout of physical activity the vasculature perfusing the working limbs is naturally exposed to an episode of shear-induced dilation, it is credible that, over time, the vasculature adapts to be highly responsive to increased shear stress (i.e., hence the increase in FMD), a concept also referred as "vascular conditioning" (29,31,69). Finally, aortic stiffness, as assessed via cfPWV, was not reduced after the walking intervention; thus, systemic vascular dysfunction was not completely resolved. ...
Article
We aimed to examine if individuals with type 2 diabetes (T2D) exhibit suppressed leg vascular conductance and skeletal muscle capillary perfusion in response to a hyperinsulinemic-euglycemic clamp, and to test whether these two variables are positively correlated. Subsequently, we examined if T2D-associated skeletal muscle microvascular insulin resistance, as well as overall vascular dysfunction, would be ameliorated by an eight-week walking intervention (45 minutes at 60% of heart rate reserve, 5 sessions/week). We report that, relative to healthy subjects, overweight and obese individuals with T2D exhibit depressed insulin-stimulated increases in leg vascular conductance, skeletal muscle capillary perfusion, and Akt phosphorylation. Notably, we found that within individuals with T2D, those with lesser increases in leg vascular conductance in response to insulin exhibited the lowest increases in muscle capillary perfusion, suggesting that limited muscle capillary perfusion may be, in part, linked to the impaired ability of the upstream resistance vessels to dilate in response to insulin. Furthermore, we show that the eight-week walking intervention, which did not evoke weight loss, was insufficient to ameliorate skeletal muscle microvascular insulin resistance in previously sedentary, overweight/obese subjects with T2D, despite high adherence and tolerance. However, the walking intervention did improve (P<0.05) popliteal artery flow-mediated dilation (+4.52%) and reduced HbA1c (-0.75%). It is possible that physical activity interventions that are longer in duration, engage large muscle groups with recruitment of the maximum number of muscle fibers, and lead to a robust reduction in metabolic risk factors may be required to overhaul microvascular insulin resistance in T2D.
... In the resting pre exercise condition, a progressive increase in FMD was observed within Groups 1, 2, and 3, i.e., in healthy asymptomatic participants with a progressive increase in physical fitness due to their moderate training programs. This increase has been regularly reported and denotes an improvement of vascular endothelial function (Green et al., 2004;Green, 2009). The underlying mechanisms likely rely on the release of endothelial-derived factors such as nitric oxide (NO), which has antiproliferative, anti−inflammatory, and antithrombotic properties and causes vasodilation (Vanhoutte et al., 2017). ...
Article
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The effect of training status on post-exercise flow-mediated dilation (FMD) is not well characterized. We tested the hypothesis that the more trained the subjects, the lower the reduction in FMD after an acute bout of aerobic exercise. Forty-seven men (mean ± SD, age: 20.1 ± 1.2 years, body mass: 75.5 ± 5.1 kg, height 178.1 ± 5.4 cm) were divided into five groups with different training characteristics (sedentary, two different groups of active subjects, two different groups of well-trained subjects – runners and weightlifters). Brachial artery FMD (blood pressure cuff placed around the arm distal to the probe with the proximal border adjacent to the medial epicondyle; 5 min at a pressure of 220 mmHg) was assessed before and during 3 min immediately after a bout of cycling exercise at a relative intensity of 170 bpm [(physical work capacity (PWC170)]. At baseline, a progressive increase in FMD was observed in the participants with the higher training status, if the training remained moderate. Indeed, FMD was reduced in runners and weightlifters compared to those who were moderately trained. After PWC170, FMD did not significantly change in sedentary and highly trained runners, significantly increased in the two groups of active subjects but significantly decreased in highly trained weightlifters. These results showed that endothelium-dependent vasodilation evaluated using brachial FMD is maintained or improved following acute aerobic exercise in moderately trained participants, but not in well-trained participants, especially if they are engaged in resistance training.
Article
Objective Using a rat model, we investigated the effect of multidisciplinary rehabilitation, including aerobic training and ointment, on the ROM, vWF, VEGF content, and femoral artery hemodynamics in rats with joint contracture. Methods A total of 44 Wistar rats were divided into the normal control group (NC, eight rats) and the experimental group (EG). A joint contracture model was established for the rats in the EG group by an external fixator. After fixator removal, 32 rats are further divided into the MC, SC, RE, and SR groups ( n = 8). Before and after the 42 day intervention, the ROM, vWF, VEGF, PS, ED, and RI were measured using X-ray imaging, ELISA, and color Doppler ultrasound, respectively. Results After fixator removal, ROM for EG group was lower than that of the NC group ( p < .01). After the intervention, ROM for the SR, RE, and SC groups was improved. The ROM for the SR group reached a similar value for NC group. vWF and VEGF levels in SR group were lower than in the MC, SC, and RE groups ( p < .05), and had a similar value to the NC groups. PS value for SR and RE groups was higher than the MC and SC groups. The RI value for SR group was higher than that of NC and MC groups. Conclusion Multidisciplinary rehabilitation used in this study can treat joint contracture synergistically. It improves the ROM of the joint, reduces the content of vWF and VEGF, and improves the femoral artery hemodynamics.
Article
Background We aimed to evaluate whether the association between long-term temperature variability (TV) and CCVDs was affected by famine exposure in different age stages. Methods We used data from the fourth national Urban and Rural Elderly Population survey (2015). Participants were categorized into six groups based on their age at famine exposure (famine exposure under age 5, between ages 5 and 18, and during adulthood) and the severity (severely affected areas versus mildly affected areas) of the Great Chinese Famine (1959-1961) in their province of residence. Mixed-effects logistic regression model was used to quantify the association between long-term TV and the prevalence of CCVDs across six famine-exposed groups. Findings A total of 222,179 participants were included. In severely affected areas, the odds ratio (OR) of CCVDs associated with per 1°C increase in 5-year average TV were 1.07 (95% confidence interval [CI]: 1.02, 1.13) for those exposed to famine during adulthood, 1.28 (95% CI: 1.17, 1.40) under the age of 5 years. Urban residence, higher education, increased household income, and more frequent physical activity could mitigate the association between TV and CCVDs, particularly among those exposed to severe famine before the age of 5. Conclusion Individuals exposed to famine before the age of 5 are more susceptible to TV-related CCVDs compared to those exposed during adulthood. Our findings highlight the importance of early-life nutrition in lowering susceptibility to CCVDs later in life.
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BACKGROUND: Recent evidence highlights racquet sports as being associated with a substantially reduced risk of CVD mortality. The purpose of this investigation was to evaluate clustered cardiometabolic risk (CMR) and arterial stiffness in recreational adult tennis players. METHODS: Forty-three recreational tennis players (T) and a matched group of 45 healthy, active non-tennis (NT) players, mean age (± SEM) 41.6 ± 1.8 years participated in this cross-sectional comparative study. Measurements included emerging and traditional CMR factors with pulse wave analysis/velocity utilised to assess indexes of arterial stiffness. Clustered cardiometabolic risk was calculated using two composites: CMR1 (central aortic systolic blood pressure, carotid-femoral pulse wave velocity, percentage body fat, HDL-C and maximal oxygen uptake) and CMR2 (brachial systolic blood pressure, triglycerides, TC:HDL-C, percentage body fat, HbA1c and maximal oxygen uptake). RESULTS: Analysis of covariance, controlling for age, revealed T had significantly lower (healthier) CMR1 scores than NT (EMM ± SEM, T: -0.48 ± 0.3 vs NT: 0.50 ± 0.3, P = 0.03). Similarly, T also demonstrated lower clustered CMR2 scores (EMM, T: -0.66 ± 0.4 vs NT: 0.59 ± 0.4, P = 0.04). Augmentation index of the pulse pressure wave, normalised to heart rate 75 bpm (AIx75), was lower in T vs NT (EMM, T: 10.7 ± 1.7% vs NT: 12.7 ± 1.6%; P = 0.03), when controlling for age and gender. CONCLUSIONS: Tennis appears to be a suitable and effective physical activity modality for targeting cardiometabolic and vascular health and should be more frequently advocated in physical activity promotion strategies.
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In healthy and overweight/obese adults, interrupting prolonged sitting with activity bouts mitigates impairment in vascular function. However, it is unknown whether these benefits extend to those with type 2 diabetes (T2D); nor, whether an optimal frequency of activity interruptions exist. We examined the acute effects on vascular function in T2D of interrupting prolonged sitting with simple resistance activities (SRA) at different frequencies. In a randomized crossover trial, 24 adults with T2D (35-70 years) completed three 7-hour conditions: 1) uninterrupted sitting (SIT); 2) sitting with 3 minute bouts of SRA every 30 min (SRA3); and, 3) sitting with 6 minute bouts of SRA every 60 min (SRA6). Femoral artery flow-mediated dilation (FMD), resting shear rate, blood flow and endothelin-1 were measured at 0h, 1h, 3.5h, 4.5h, and 6.5-7h. Mean femoral artery FMD over 7 hours was significantly higher in SRA3 (4.1 ± 0.3%) compared to SIT (3.7 ± 0.3%, p = 0.04), but not in SRA6. Mean resting femoral shear rate over 7 hours was increased significantly for SRA3 (45.3±4.1/s, p<0.001) and SRA6 (46.2±4.1/s, p<0.001) relative to SIT (33.1±4.1/s). Endothelin-1 concentrations were not statistically different between conditions. Interrupting sitting with activity breaks every 30 minutes, but not 60 minutes, significantly increased mean femoral artery FMD over 7 hours, relative to SIT. Our findings suggest that more-frequent and shorter breaks may be more beneficial than longer, less-frequent breaks for vascular health in those with T2D.
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Hypertension (HTN) is among the leading global preventable risk factors for cardiovascular disease and premature mortality. Early detection and effective management of HTN has demonstrated significant reductions in mortality, morbidity rate, and healthcare costs. Furthermore, screening for HTN by non-physician healthcare providers improves detection rates and medical management. As physical therapy practice advances to a more independent care model, physical therapists may serve as the first point of contact into the healthcare system, thereby necessitating a need for routine blood pressure (BP) monitoring. This is especially relevant in the outpatient physical therapy practice setting, where there is evidence for elevated BP measures among patients, yet omission of routine screening in this setting is well documented. Leading physical therapy professional organizations include statements in their guidelines that suggest that physical therapists have a duty to provide a standard of care which protects the safety and optimizes the overall health of patients under their care. Therefore, it is imperative not only that physical therapists include BP examination into routine practice protocols, but that the knowledge and skills to accurately measure and interpret BP at rest and during exercise be integrated into the standard of care. The authors suggest that the profession of physical therapy proactively embrace their potential to address the national and worldwide HTN epidemic through routine assessment of BP, appropriate referral for elevated BP measures, and exploration of HTN management by physical therapists.
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The cross-sectional area (CSA) of large-conductance arteries increases in response to endurance training in humans. To determine whether training-induced changes in arterial structure are systemic in nature or, rather, are confined to the arteries supplying exercising muscles, we studied 10 young men who performed one-legged cycle training [80% of one-legged peak O2 uptake (VO2 peak)), 40 min/day, 4 days/wk] for 6 wk and detraining for another 6 wk. There were no significant differences in baseline one-legged VO2 peak) and CSA of the common femoral artery and vein (via B-mode ultrasound) between experimental and control legs. In the experimental leg, one-legged VO2 peak) increased 16% [from 3.0 +/- 0.1 to 3.4 +/- 0.1 (SE) l/min], arterial CSA increased 16% (from 84 +/- 3 to 97 +/- 5 mm2), and venous CSA increased 46% (from 56 +/- 5 to 82 +/- 5 mm2) after endurance training. These changes returned to baseline during detraining. There were no changes in one-legged VO2 peak) and arterial CSA in the control leg, whereas femoral venous CSA in the control leg significantly increased 24% (from 54 +/- 5 to 67 +/- 4 mm2) during training. Changes in femoral arterial and venous CSA in the experimental leg were positively and significantly related to corresponding changes in one-legged VO2 peak) (r = 0.86 and 0.76, respectively), whereas there were no such relations in the control leg (r = 0.10 and 0.17). When stepwise regression analysis was performed, a primary determinant of change in VO2 peak) was change in femoral arterial CSA, explaining approximately 70% of the variability. These results support the hypothesis that the regional increase in blood flow, rather than systemic factors, is associated with the training-induced arterial expansion. Femoral arterial expansion may contribute, at least in part, to improvement in efficiency of blood transport from the heart to exercising muscles and may facilitate achievement of aerobic work capacity.
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1. In experimental animals chronic elevations in arterial blood flow increase the lumen diameter and reduce the intima-media thickness (IMT) of the arterial segment involved. We determined whether intermittent elevations in active muscle blood flow associated with regular aerobic leg exercise induced such expansive arterial remodelling in the common femoral artery of humans. 2. In the cross-sectional study 53 sedentary (47 +/- 2 years) and 55 endurance exercise-trained (47 +/- 2 years) men were studied. Common femoral artery lumen diameter (B-mode ultrasound) was 7 % greater (9.62 +/- 0.12 vs. 9.03 +/- 0.13 mm), and femoral IMT (0.46 +/- 0.02 vs. 0.55 +/- 0.02 mm) and IMT/lumen ratio were 16-21 % smaller in the endurance-trained men (all P < 0.001). Basal femoral artery blood flow (duplex ultrasound) was not different, shear stress tended to be lower (P = 0.08), and mean femoral tangential wall stress was 30 % higher in the endurance-trained men (P < 0.001). 3. In the intervention study 22 men (51 +/- 2 years) were studied before and after 3 months of regular aerobic leg exercise (primarily walking). After training, the femoral diameter increased by 9 % (8.82 +/- 0.18 vs. 9.60 +/- 0.20 mm), and IMT (0.65 +/- 0.05 vs. 0.56 +/- 0.05 mm) and the IMT/lumen ratio were approximately 15-20 % smaller (all P < 0.001). Basal femoral blood flow and shear stress were not different after training, whereas the mean femoral tangential wall stress increased by 31 %. The changes in arterial structure were not related to changes in risk factors for atherosclerosis. 4. Our results are consistent with the concept that regular aerobic leg exercise induces expansive arterial remodelling in the femoral artery of healthy men. This adaptive process is produced by even a moderate training stimulus, is not obviously dependent on corresponding improvements in risk factors for atherosclerosis, and is robust, occurring in healthy men of different ages.
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We have pooled data from a series of our exercise training studies undertaken in groups with a broad range of vascular (dys) function to the examine the hypothesis that exercise-induced improvements in the conduit and/or resistance vessel function are related to improvements in risk factors for cardiovascular (CV) disease. Endothelium-dependent and -independent conduit vessel function were assessed by using wall tracking of high-resolution ultrasound images of the brachial artery response to flow-mediated dilation (FMD) and glyceryl trinitrate. Resistance vessel function was assessed using intrabrachial administration of acetylcholine (ACh), sodium nitroprusside, and NG-monomethyl-l-arginine. Randomized cross-over studies of 8-wk exercise training were undertaken in untreated hypercholesterolemic (n = 11), treated hypercholesterolemic (n = 11), coronary artery disease (n = 10), chronic heart failure (n = 12), Type 2 diabetic (n = 15), and healthy control subjects (n = 16). Exercise training did not significantly alter plasma lipids, blood pressure, blood glucose, waist-to-hip ratio, or body mass index values, despite significant improvement in both FMD and ACh responses. There were no correlations between changes in any risk factor variables and indexes of either resistance or conduit vessel function. We conclude that, in these subjects with antecedent vascular dysfunction, the beneficial effects of relatively short-term exercise training on vascular function are not solely mediated by the effects of exercise on CV risk factors.
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Regular exercise in patients with stable coronary artery disease has been shown to improve myocardial perfusion and to retard disease progression. We therefore conducted a randomized study to compare the effects of exercise training versus standard percutaneous coronary intervention (PCI) with stenting on clinical symptoms, angina-free exercise capacity, myocardial perfusion, cost-effectiveness, and frequency of a combined clinical end point (death of cardiac cause, stroke, CABG, angioplasty, acute myocardial infarction, and worsening angina with objective evidence resulting in hospitalization). A total of 101 male patients aged < or =70 years were recruited after routine coronary angiography and randomized to 12 months of exercise training (20 minutes of bicycle ergometry per day) or to PCI. Cost efficiency was calculated as the average expense (in US dollars) needed to improve the Canadian Cardiovascular Society class by 1 class. Exercise training was associated with a higher event-free survival (88% versus 70% in the PCI group, P=0.023) and increased maximal oxygen uptake (+16%, from 22.7+/-0.7 to 26.2+/-0.8 mL O2/kg, P<0.001 versus baseline, P<0.001 versus PCI group after 12 months). To gain 1 Canadian Cardiovascular Society class, 6956 dollars was spent in the PCI group versus 3429 dollars in the training group (P<0.001). Compared with PCI, a 12-month program of regular physical exercise in selected patients with stable coronary artery disease resulted in superior event-free survival and exercise capacity at lower costs, notably owing to reduced rehospitalizations and repeat revascularizations.
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Assessment of flow-mediated dilation (FMD) after forearm ischemia is widely used as a noninvasive bioassay of stimulated nitric oxide (NO)-mediated conduit artery vasodilator function in vivo. Whether this stimulated endothelial NO function reflects basal endothelial NO function is unknown. To test this hypothesis, retrospective analysis of randomized crossover studies was undertaken in 17 subjects with Type 2 diabetes; 9 subjects undertook an exercise training or control period, whereas the remaining 8 subjects were administered an angiotensin II receptor blocker or placebo. FMD was assessed by using wall tracking of high-resolution brachial artery ultrasound images in response to reactive hyperemia. Resistance vessel basal endothelium-dependent NO function was assessed by using intrabrachial administration of NG-monomethyl-L-arginine (L-NMMA) and plethysmographic assessment of forearm blood flow (FBF). FMD was higher after intervention compared with control/placebo (6.15+/-0.53 vs. 3.81+/-0.72%, P<0.001). There were no significant changes in the FBF responses to L-NMMA. Regression analysis between FMD and L-NMMA responses at entry to the study revealed an insignificant correlation (r=-0.10, P=0.7), and improvements in FMD with the interventions were not associated with changes in the L-NMMA responses (r=-0.04, P=0.9). We conclude that conduit artery-stimulated endothelial NO function (FMD) does not reflect basal resistance vessel endothelial NO function in subjects with Type 2 diabetes.
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Current evidence indicates that the ability of physical activity to sustain a normal phenotype of arterial endothelial cells (ECs) plays a central role in the beneficial effects of exercise (Ex) on atherosclerotic disease. Here we evaluate the strength of evidence that shear stress (SS) and/or circumferential wall stress (stretch) are the primary signals, produced by bouts of Ex, that signal altered gene expression in arterial ECs, thereby resulting in a less atherogenic EC phenotype. Current literature indicates that SS is a signal for expression of antiatherogenic genes in cultured ECs, in ECs of isolated arteries, and in ECs of arteries in intact animals. Furthermore, SS levels in the arteries of humans during Ex are in the range that produces beneficial changes. In contrast, complex flow profiles within recirculation zones and/or oscillatory flow patterns can cause proatherogenic gene expression in ECs. In vivo evidence indicates that Ex decreases oscillatory flow/SS in some portions of the arterial tree but may increase oscillatory flow in other areas of the arterial tree. Circumferential wall stress can increase expression of some beneficial EC genes as well, but circumferential wall stress also increases production of reactive oxygen species and increases the expression of adhesion factors and other proatherogenic genes. Interactions of arterial pressure and fluid SS play an important role in arterial vascular health and likely contribute to how Ex bouts signal changes in EC gene expression. It is also clear that other local and circulating factors interact with these hemodynamic signals during Ex to produce the healthy arterial EC phenotype. We conclude that available evidence suggests that exercise signals formation of beneficial endothelial cell phenotype at least in part through changes in SS and wall stretch in the arteries.
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The contribution of endothelium-derived nitric oxide (NO) to exercise hyperaemia remains controversial. Disparate findings may, in part, be explained by different shear stress stimuli as a result of different types of exercise. We have directly compared forearm blood flow (FBF) responses to incremental handgrip and cycle ergometer exercise in 14 subjects (age +/-s.e.m.) using a novel software system which calculates conduit artery blood flow continuously across the cardiac cycle by synchronising automated edge-detection and wall tracking of high resolution B-mode arterial ultrasound images and Doppler waveform envelope analysis. Monomethyl arginine (L-NMMA) was infused during repeat bouts of each incremental exercise test to assess the contribution of NO to hyperaemic responses. During handgrip, mean FBF increased with workload (P < 0.01) whereas FBF decreased at lower cycle workloads (P < 0.05), before increasing at 120 W (P < 0.001). Differences in these patterns of mean FBF response to different exercise modalities were due to the influence of retrograde diastolic flow during cycling, which had a relatively larger impact on mean flows at lower workloads. Retrograde diastolic flow was negligible during handgrip. Although mean FBF was lower in response to cycling than handgrip exercise, the impact of L-NMMA was significant during the cycle modality only (P < 0.05), possibly reflecting the importance of an oscillatory antegrade/retrograde flow pattern on shear stress-mediated release of NO from the endothelium. In conclusion, different types of exercise present different haemodynamic stimuli to the endothelium, which may result in differential effects of shear stress on the vasculature.
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Shear stress is an important stimulus to arterial adaptation in response to exercise and training in humans. We recently observed significant reverse arterial flow and shear during exercise and different antegrade/retrograde patterns of shear and flow in response to different types of exercise. The purpose of this study was to simultaneously examine flow-mediated dilation, a largely NO-mediated vasodilator response, in both brachial arteries of healthy young men before and after 30-minute interventions consisting of bilateral forearm heating, recumbent leg cycling, and bilateral handgrip exercise. During each intervention, a cuff inflated to 60 mm Hg was placed on 1 arm to unilaterally manipulate the shear rate stimulus. In the noncuffed arm, antegrade flow and shear increased similarly in response to each intervention (ANOVA; P<0.001, no interaction between interventions; P=0.71). Baseline flow-mediated dilation (4.6%, 6.9%, and 6.7%) increased similarly in response to heating, handgrip, and cycling (8.1%, 10.4%, and 8.9%, ANOVA; P<0.001, no interaction; P=0.89). In contrast, cuffed arm antegrade shear rate was lower than in the noncuffed arm for all of the conditions (P<0.05), and the increase in flow-mediated dilation was abolished in this arm (4.7%, 6.7%, and 6.1%; 2-way ANOVA: all conditions interacted P<0.05). These results suggest that differences in the magnitude of antegrade shear rate transduce differences in endothelial vasodilator function in humans, a finding that may have relevance for the impact of different exercise interventions on vascular adaptation in humans.
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Changes in arterial shear stress induce functional and structural vasculature adaptations. Recent studies indicate that substantial retrograde flow and shear can occur through human conduit arteries. In animals, retrograde shear is associated with atherogenic effects. The aim of this study was to examine the impact of incremental levels of retrograde shear on endothelial function in vivo. On 3 separate days, we examined bilateral brachial artery flow-mediated dilation, an index of NO-mediated endothelial function, in healthy men (24+/-3 years) before and after a 30-minute intervention consisting of cuff inflation to 25, 50, or 75 mm Hg. Cuff inflations resulted in "dose"-dependent increases in retrograde shear rate, compared with the noncuffed arm, within subjects (P<0.001). Flow-mediated dilation in the cuffed arm did not change in response to the 25-mm Hg stimulus but decreased significantly after both the 50- and 75-mm Hg interventions (P<0.05). The decrease in flow-mediated dilation after the 75-mm Hg intervention was significantly larger than that observed after a 50-mm Hg intervention (P=0.03). In the noncuffed arm, no changes in shear rate or flow-mediated dilation were observed. These results demonstrate that an increase in retrograde shear rate induces a dose-dependent attenuation of endothelial function in humans. This finding contributes to our understanding regarding the possible detrimental effects of retrograde shear rate in vivo.
Article
Cycling is associated with a reproducible systolic anterograde and diastolic retrograde flow pattern in the brachial artery (BA) of the inactive upper limb, which results in endothelial nitric oxide (NO) release. The purpose of this study was to examine the impact of different types and intensities of lower limb exercise on the BA flow pattern. We examined BA blood flow and shear rate patterns during cycling, leg kicking, and walking exercise in 12 young subjects (24 +/- 3 yr). BA diameter, blood flow, and shear rate were assessed at baseline (1 min) and at three incremental intensity levels of cycling (60, 80, and 120 W), bilateral leg kicking (5, 7.5, and 10 kg), and walking (3, 4, and 5 km x h(-1)), performed for 3 min each. Edge detection and wall tracking of high-resolution B-mode arterial ultrasound images, combined with synchronized Doppler waveform envelope analysis, were used to calculate conduit artery diameter and anterograde/retrograde blood flow and shear rate continuously across the cardiac cycle. BA mean blood flow and shear rate increased significantly throughout each exercise protocol (P < 0.001), and BA anterograde blood flow and shear rate showed comparable increases throughout each protocol (P < 0.001). Retrograde blood flow and shear rate, however, demonstrated a significant increase during cycling and walking (P < 0.001) but not during leg kicking. Rhythmic lower limb exercise (cycling and walking) results in an increase in BA systolic anterograde blood flow and shear rate, directly followed by a large retrograde flow and shear rate. This typical pattern, previously linked with endothelial NO release, is not present during a different type of exercise such as leg kicking.
Article
To examine whether forearm vascular adaptations could occur after upright-leg exercise training, the reactive hyperemic blood flow after 10 min of forearm circulatory arrest (RHBF10) was studied. RHBF10 was examined in seven subjects before, at 2 wk, and after the completion of 4 wk of bicycle ergometer training. Maximal O2 consumption (VO2max) for leg ergometer work increased 13% (P less than 0.05) over 4 wk. Over that period of time RHBF10 in the forearm increased 50% (P less than 0.05), with a reciprocal drop in minimum vascular resistance. Resting heart rate decreased 15% (P less than 0.05) during the same period. Changes in RHBF10 and VO2max were noted after 2 wk of training. Mean arterial pressure did not change. We conclude that vascular adaptations can occur in the forearm muscle beds, even though the training regimen is designed to condition the lower extremities.
Article
Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.
Article
In an effort to evaluate potential peripheral adaptations to training, maximal metabolic vasodilation was studied in the dominant and nondominant forearms of six tennis players and six control subjects. Maximal metabolic vasodilation was defined as the peak forearm blood flow measured after release of arterial occlusion, the reactive hyperemic blood flow (RHBF). Two ischemic stimuli were employed in each subject: 5 min of arterial occlusion (RHBF5) and 5 min of arterial occlusion coupled with 1 min of ischemic exercise (RHBF5ex). RHBF and resting forearm blood flows were measured using venous occlusion strain-gauge plethysmography (ml X min-1 X 100 ml-1). Resting forearm blood flows were similar in both arms of both groups. RHBF5ex was similar in both arms of our control group (dominant, 40.8 +/- 1.2 vs. nondominant, 40.9 +/- 2.1). However, RHBF5ex was 42% higher in the dominant than in the nondominant forearms of our tennis player population (dominant, 48.7 +/- 4.0 vs. nondominant, 34.4 +/- 3.4; P less than 0.05). This intraindividual difference in peak forearm blood flows was not secondary to improved systemic conditioning since the maximal O2 consumptions in the two study groups were similar (controls, 45.4 +/- 3.9 vs. tennis players, 46.1 +/- 1.7). These findings suggest a primary peripheral cardiovascular adaptation to exercise training in the dominant forearms of the tennis players resulting in a greater maximal vasodilatation.
Article
The purpose of this paper is to examine the role of endothelium-derived relaxing factors in the control of coronary vascular resistance in conditioned subjects (i.e., after exercise training for a period of time sufficient to complete adaptation processes). Results from studies with exercise trained (EX) dogs, miniature swine, and rats are summarized. Since the relative importance of vascular control mechanisms differ in various segments of the coronary arterial tree, the effects of EX on conduit arteries and the coronary arterial microcirculation are discussed separately. Results indicate that endothelium-mediated vasodilator responses are normal in conduit coronary arteries of EX dogs, miniature swine, and rats. It is proposed that endothelium-mediated vasodilation of conduit coronary arteries is enhanced early in the exercise-adaptive process but returns to normal as adaptation to EX is complete, when structural adaptations produce a relative decrease in coronary shear during exercise. EX miniature swine manifest enhanced endothelium-mediated vasodilation stimulated by bradykinin and flow in isolated coronary resistance arteries and appear to have increased expression of NO synthase (ecNOS). Brief training also appears to increase the expression of ecNOS. The role of endothelium-mediated vasodilation in regulation of coronary blood flow in EX animals remains uncertain.
Article
The purpose of the present study was to assess the size of great and medium caliber arterial and venous vessels (conductance vessels) in athletes of different sports and sedentary people. Vessel size was measured by two-dimensional echocardiography in 15 professional cyclists, 15 highly-trained long-distance runners, 15 professional volley-ball players, 10 wheelchair basketball players, 11 wheelchair distance runners and 20 sedentary controls. The following vessels were imaged and measured: aortic arch, left carotid and left subclavian artery, right pulmonary artery, abdominal aorta and mesenteric artery, superior and inferior vena cava. Vessel size was considered in absolute value and normalized for body surface area (BSA). Among the able-bodied athletes, both cyclists and long-distance runners showed a generalized increase in vessels size in respect to controls, either absolute or normalized for BSA. The increase was highly significant for normalized inferior vena cava: cyclists, mean 15.1 mm, 95% confidence intervals 14.2 to 15.8 mm; long-distance runners, 15.8 mm, 15.3 to 16.4; controls, 10.5 mm, 9.8 to 11.3. Volleyball players also showed larger vessels than controls, but this feature was clearly related to their greater body size because statistical differences were attenuated or abolished by normalization for BSA. Wheelchair athletes exhibited significantly larger upper-body vessels but significantly smaller lower-body vessels than controls when normalized for BSA. In addition, wheelchair distance runners, who trained more intensively, had larger abdominal aorta and inferior vena cava than wheelchair basket players. Long-term endurance training leads to a generalized increase in arterial and venous conductance vessels size.(ABSTRACT TRUNCATED AT 250 WORDS)
Article
The aim of this study was to determine whether a 4-wk handgrip training program would elicit changes in endothelium-dependent and endothelium-independent vasodilatation in resistance vessels of the human forearm. Minimum vascular resistance after a 10-min ischemic stimulus, an index of peak vasodilator capacity, was also determined. Forearm blood flow response to the endothelium-dependent vasodilator methacholine chloride did not change over the 4-wk-intervention period either in the group undertaking training (n = 11) or in control subjects (n = 6). Similarly, the response to sodium nitroprusside was not influenced by the handgrip training program. Peak vasodilator capacity of the trained forearms significantly increased, whereas no change was evident in the untrained limbs. These results suggest that 4 wk of forearm exercise training enhances peak vasodilator capacity of the vasculature without influencing stimulated activity of the nitric oxide dilator system.
Article
Increases in coronary artery size and dilating capacity have been observed in some animals after endurance training, and at autopsy, active men appear to have enlarged epicardial coronary arteries. This cross-sectional study was designed to test the hypothesis that highly trained endurance runners have larger epicardial coronary arteries and greater dilating capacity than inactive men. The subjects, ages 39-66 years, included 11 male volunteers who had participated in ultradistance running during the past 2 years and 11 physically inactive men who had been referred for arteriography but had no visible coronary artery disease. The internal diameter of the proximal segments of each major epicardial coronary artery was measured before and after nitroglycerin administration using a computer-based quantitative arteriographic analysis system. Measurements also included maximal oxygen uptake, plasma lipoprotein concentrations, body composition, and cardiac mass by echocardiography. Before nitroglycerin, the sum of the cross-sectional areas for the proximal right, left anterior descending, and circumflex arteries was not different for the runners and the inactive men: 22.7 +/- 4.79 versus 21.0 +/- 7.97 mm2 (p = 0.57), respectively. However, the increase in the sum of the cross-sectional area for the proximal right, left anterior descending, and circumflex arteries in response to nitroglycerin was greater for the runners (13.20 +/- 4.76 versus 6.00 +/- 3.02 mm2; p = 0.002). Left ventricular mass index (152 +/- 21 versus 116 +/- 41 g/m2; p < 0.05) but not left ventricular mass (284 +/- 40 versus 246 +/- 91 g; p = 0.22) was significantly greater for the runners. Among the runners, dilating capacity was positively correlated with aerobic capacity and negatively related to adiposity, resting heart rate, and plasma lipoprotein concentrations. Highly trained, middle-aged endurance runners demonstrated a significantly greater dilating capacity of their epicardial coronary arteries in response to nitroglycerin compared with inactive men. The causes of this greater dilating capacity and its clinical significance need to be determined.
Article
Flow-induced changes in vessel caliber tend to restore baseline wall shear stress (WSS) and have been reported to be endothelium-dependent. To investigate the role of endothelium-derived nitric oxide (NO) in the adaptive increase in artery diameter in response to a chronic increase in blood flow, an arteriovenous fistula was constructed between the left common carotid artery (CCA) and the external jugular vein in 22 New Zealand White rabbits, and NO synthesis was inhibited in 14 animals by long-term administration of NG-nitro-L-arginine-methyl ester (L-NAME) in drinking water given for 4 weeks. The remaining 8 animals served as controls. Mean arterial blood pressure was not significantly altered by L-NAME treatment (91 +/- 2 in control versus 98 +/- 3 mm Hg in L-NAME-treated rabbits). Blood flow significantly increased in the left CCA in both groups but was lower in L-NAME-treated than control animals (106.1 +/- 10.7 versus 196.2 +/- 32.3 mL/min, P < .003). The diameter of the flow-loaded left CCA also increased significantly in both groups compared with the right CCA (2.15 +/- 0.12 and 2.54 +/- 0.1 mm, respectively, P < .02), but the increase was less in the L-NAME-treated than the control group (3.24 +/- 0.09 and 4.64 +/- 0.17 mm, respectively, P < .0001). The diameter of the anastomosed veins was also increased but to a much lesser degree in L-NAME-treated animals than in controls (4.14 +/- 0.29 versus 7.94 +/- 0.51 mm, P < .0001). As a result of artery enlargement, WSS was normalized in the flow-loaded left CCA of the control group (8.87 +/- 0.77 dynes/cm2) regardless of blood flow values. In L-NAME-treated animals, however, WSS was only partially regulated, the mean value being significantly increased (18.7 +/- 2.2 dynes/cm2, P < .006). Moreover, a highly significant positive correlation between WSS and blood flow was obtained in L-NAME-treated animals (r = .84, P < .0001). We also found remodeling of the artery wall, with a larger increase in the medial cross-sectional area associated with an increased number of smooth muscle cells, in the control group compared with the L-NAME-treated group (0.75 +/- 0.09 versus 0.49 +/- 0.04 mm2 and 4504 +/- 722 versus 2717 +/- 282 cells/mm2, P < .03). We conclude that NO plays a role in the increase of vessel caliber in response to chronic increase in blood flow. As yet unidentified additional metabolic processes appear to be necessary for a complete regulatory response.
Article
The aim of this study was to determine whether physical conditioning induced by a repetitive exercise stimulus would elicit changes in the response of forearm resistance vessels to an infusion of substances that modulate nitric oxide synthesis. Forearm blood flow responses to a 5-min ischemic stimulus and intrabrachial infusion of acetylcholine, sodium nitroprusside, and NG-monomethyl-L-arginine were examined in the preferred and nonpreferred limbs of eight habitual tennis players. Forearm volume, girth, and grip strength were significantly greater in the preferred limb, indicating a bilateral difference in physical condition. This was associated with an enhanced reactive hyperemic response in the preferred limb (53.5 +/- 9.4 vs. 38.8 +/- 4.7 ml.100 ml-1.min-1; P < 0.05). No differences between the limbs were evident in response to acetylcholine, sodium nitroprusside, or NG-monomethyl-L-arginine. These results suggest that exercise training enhances the peak vasodilator capacity of the vasculature without influencing basal or stimulated activity of the nitric oxide dilator system in vivo.
Article
We sought to analyze the systemic effects of lower-limb exercise training (ET) on radial artery endothelial function in patients with chronic heart failure (CHF). Local ET has the potential to improve local endothelial dysfunction in patients with CHF. However, it remains unclear whether the systemic effects can be achieved by local ET. Twenty-two male patients with CHF were prospectively randomized to either ET on a bicycle ergometer (ET group, n = 11; left ventricular ejection fraction [LVEF] 26 +/- 3%) or an inactive control group (group C, n = 11; LVEF 24 +/- 2%). At the beginning of the study and after four weeks, endothelium-dependent and -independent vasodilation of the radial artery was determined by intra-arterial infusion of acetylcholine (ACh-7.5, 15 and 30 microg/min) and nitroglycerin (0.2 mg/min). The mean internal diameter (ID) of the radial artery was assessed using a high resolution ultrasound system (NIUS-02, Asulab Research Laboratories, Neuchâtel, Switzerland) with a 10-MHz probe. After four weeks of ET, patients showed a significant increase in the baseline-corrected mean ID in response to ACh (30 microg/min), from 33 +/- 10 to 127 +/- 25 microm (p < 0.001 vs. control group at four weeks). In the control group, the response to ACh (30 microg/min) remained unchanged. Endothelium-independent vasodilation was similar in both groups at the beginning of the study and at four weeks. In the training group, increases in agonist-mediated, endothelium-dependent vasodilation correlated to changes in functional work capacity (r = 0.63, p < 0.05). In patients with stable CHF, bicycle ergometer ET leads to a correction of endothelial dysfunction of the upper extremity, indicating a systemic effect of local ET on endothelial function.
Article
We describe a novel software system that utilizes automated algorithms to perform edge detection and wall tracking of high-resolution B-mode arterial ultrasound images, combined with synchronized Doppler waveform envelope analysis, to calculate conduit arterial blood flow (BF) across the cardiac cycle. Furthermore, we describe changes in brachial arterial BF to the resting forearm during incremental cycle ergometry in eight subjects. During exercise, peak BF during the cardiac cycle increased at each workload (P < 0.001), because of increased velocity in the presence of unaltered cross-sectional area. In contrast, mean BF calculated across each cardiac cycle decreased at lower workloads before increasing at 100 and 160 W (P < 0.001). Differences in the pattern of peak and mean cardiac cycle flows were due to the influence of retrograde diastolic flow, which had a larger impact on mean flows at lower workloads. In conclusion, BF can be measured with high temporal resolution across the cardiac cycle in humans. Resting brachial arterial flow, including retrograde flow, increases during lower limb exercise.
Article
Our objective was to test the hypothesis that short-term exercise training (STR) of pigs increases endothelium-dependent dilation (EDD) of coronary arteries but not coronary arterioles. Female Yucatan miniature swine ran on a treadmill for 1 h, at 3.5 mph, twice daily for 7 days (STR; n = 28). Skeletal muscle citrate synthase activity was increased in STR compared with sedentary controls (Sed; n = 26). Vasoreactivity was evaluated in isolated segments of conduit arteries (1-2 mm ID, 3-4 mm length) mounted on myographs and in arterioles (50-100 microm ID) isolated and cannulated with micropipettes with intraluminal pressure set at 60 cmH(2)O. EDD was assessed by examining responses to increasing concentrations of bradykinin (BK) (conduit arteries 10(-12)-10(-6) M and arterioles 10(-13)-10(-6) M). There were no differences in maximal EDD or BK sensitivity of coronary arterioles from Sed and STR hearts. In contrast, sensitivity of conduit arteries (precontracted with PGF(2alpha)) to BK was increased significantly (P < 0.05) in STR (EC(50), 2.33 +/- 0.62 nM, n = 12) compared with Sed animals (EC(50), 3.88 +/- 0.62 nM, n = 13). Immunoblot analysis revealed that coronary arteries from STR and Sed animals had similar levels of endothelial nitric oxide synthase (eNOS). In contrast, eNOS protein was increased in STR aortic endothelial cells. Neither protein nor mRNA levels of eNOS were different in coronary arterioles from STR compared with Sed animals. STR did not alter expression of superoxide dismutase (SOD-1) protein in any artery examined. We conclude that pigs exhibit increases in EDD of conduit arteries, but not in coronary arterioles, at the onset of exercise training. These adaptations in pigs do not appear to be mediated by alterations in eNOS or SOD-1 expression.
Article
In a cross-sectional study, central and peripheral arteries were investigated noninvasively in high-performance athletes and in untrained subjects. The diastolic inner vessel diameter (D) of the thoracic and abdominal aorta, the subclavian artery (Sub), and common femoral artery (Fem) were determined by duplex sonography in 18 able-bodied professional tennis players, 34 able-bodied elite road cyclist athletes, 26 athletes with paraplegia, 17 below-knee amputated athletes, and 30 able-bodied, untrained subjects. The vessel cross-sectional areas (CSA) were set in relation to body surface area (BSA), and the cross-section index (CS-index = CSA/BSA) was calculated. Volumetric blood flow was determined in Sub and Fem via a pulsed-wave Doppler system and was set in relation to heart rate to calculate the stroke flow. A significantly increased D of Sub was found in the racket arm of able-bodied tennis players compared with the opposite arm (19%). Fem of able-bodied road cyclist athletes and of the intact limb in below-knee amputated athletes showed similar increases. D of Fem was lower in athletes with paraplegia (37%) and in below-knee amputated athletes proximal to the lesion (21%) compared with able-bodied, untrained subjects; CS-indexes were reduced 57 and 31%, respectively. Athletes with paraplegia demonstrated a larger D (19%) and a larger CS-index in Sub (54%) than able-bodied, untrained subjects. No significant differences in D and CS-indexes of the thoracic and abdominal aorta were found between any of the groups. The changes measured in Sub and Fem were associated with corresponding alterations in blood flow and stroke flow in all groups. The study suggests that the size and blood flow volume of the proximal limb arteries are adjusted to the metabolic needs of the corresponding extremity musculature and underscore the impact of exercise training or disuse on the structure and the function of the arterial system.
Article
In stable coronary artery disease (CAD), exercise training has well-documented positive effects on arterial endothelial function. NO derived from endothelial NO synthase (eNOS) is regarded as a protective factor against atherosclerosis. The aim of the present study was to investigate the effects of exercise training on the endothelial function in relation to the expression of eNOS and Akt-dependent eNOS phosphorylation in the left internal mammary artery (LIMA) of patients with stable CAD. In 17 training patients (T) and 18 control patients (C), endothelium-dependent vasodilation and average peak flow velocity (APV) in response to acetylcholine were measured invasively at study beginning and after 4 weeks in the LIMA. In LIMA tissue sampled during bypass surgery, eNOS expression and content of pospho-eNOS-Ser1177, Akt, and phospho-Akt were determined by Western blot and quantitative reverse transcriptase-polymerase chain reaction. After exercise training, LIMA APV in response to acetylcholine was increased by 56+/-8% (from +48+/-8% at beginning to +104+/-11% after 4 weeks, P<0.001). Patients in T had a 2-fold higher eNOS protein expression (T 1.0+/-0.7 versus C 0.5+/-0.3 arbitrary units, P<0.05) and 4-fold higher eNOS Ser1177-phosphorylation levels in LIMA-endothelium (1.2+/-0.9 versus 0.3+/-0.2 arbitrary units, P<0.01). A linear correlation was confirmed between Akt phosphorylation and phospho-eNOS levels (R=0.80, P<0.05) and between phospho-eNOS and Delta APV (R=0.59, P<0.05). Exercise training in stable CAD leads to an improved agonist-mediated endothelium-dependent vasodilatory capacity. The change in acetylcholine-induced vasodilatation was closely related to a shear stress-induced/Akt-dependent phosphorylation of eNOS on Ser1177.
Article
In this review the evidence for structural adaptations of the coronary circulation in the healthy adult heart in response to exercise and training is examined. Previously, it was thought that expansion of the coronary arteries and resistance vasculature occurred without angiogenesis. Detailed studies of the time course of coronary vascular remodelling now reveal that capillary proliferation is an integral response to exercise training, but is disguised by concurrent transformation of capillaries into arterioles by 'arteriolarization'. Increases in numbers of small arterioles < 30 micro m in diameter are accompanied by expansion in calibre of resistance and large coronary arteries. Stimuli related to increases in blood flow--shear stress and wall tension--and to mechanical deformation of the myocardium--stretch and compression--provide the main impetus for coronary vascular remodelling. Despite the technical difficulties of measuring such parameters in the heart in vivo, intervention studies using specific exercise components such as vasodilator, inotropic and chronotropic manipulations have allowed some insight into the differential regional effects of haemodynamic factors throughout the vascular tree. It remains to establish more clearly the involvement of mediators such as nitric oxide and growth factors in the temporal relationship to endothelial and smooth muscle growth and proliferation so that the endogenous attributes of exercise can be exploited for therapeutic purposes.
Article
In the past two decades, normal endothelial function has been identified as integral to vascular health. The endothelium produces numerous vasodilator and vasoconstrictor compounds that regulate vascular tone; the vasodilator, nitric oxide (NO), has additional antiatherogenic properties, is probably the most important and best characterised mediator, and its intrinsic vasodilator function is commonly used as a surrogate index of endothelial function. Many conditions, including atherosclerosis, diabetes mellitus and even vascular risk factors, are associated with endothelial dysfunction, which, in turn, correlates with cardiovascular mortality. Furthermore, clinical benefit and improved endothelial function tend to be associated in response to interventions. Shear stress on endothelial cells is a potent stimulus for NO production. Although the role of endothelium-derived NO in acute exercise has not been fully resolved, exercise training involving repetitive bouts of exercise over weeks or months up-regulates endothelial NO bioactivity. Animal studies have found improved endothelium-dependent vasodilation after as few as 7 days of exercise. Consequent changes in vasodilator function appear to persist for several weeks but may regress with long-term training, perhaps reflecting progression to structural adaptation which may, however, have been partly endothelium-dependent. The increase in blood flow, and change in haemodynamics that occur during acute exercise may, therefore, provide a stimulus for both acute and chronic changes in vascular function. Substantial differences within species and within the vasculature appear to exist. In humans, exercise training improves endothelium-dependent vasodilator function, not only as a localised phenomenon in the active muscle group, but also as a systemic response when a relatively large mass of muscle is activated regularly during an exercise training programme. Individuals with initially impaired endothelial function at baseline appear to be more responsive to exercise training than healthy individuals; that is, it is more difficult to improve already normal vascular function. While improvement is reflected in increased NO bioactivity, the detail of mechanisms, for example the relative importance of up-regulation of mediators and antioxidant effects, is unclear. Optimum training schedules, possible sequential changes and the duration of benefit under various conditions also remain largely unresolved. In summary, epidemiological evidence strongly suggests that regular exercise confers beneficial effects on cardiovascular health. Shear stress-mediated improvement in endothelial function provides one plausible explanation for the cardioprotective benefits of exercise training.
Article
The purpose of this study was to test the hypothesis that the content of endothelial nitric oxide synthase (eNOS) protein (eNOS protein/g total artery protein) increases with decreasing artery diameter in the coronary arterial tree. Content of eNOS protein was determined in porcine coronary arteries with immunoblot analysis. Arteries were isolated in six size categories from each heart: large arteries [301- to 2,500-microm internal diameter (ID)], small arteries (201- to 300-microm ID), resistance arteries (151- to 200-microm ID), large arterioles (101- to 150-microm ID), intermediate arterioles (51- to 100-microm ID), and small arterioles(<50-microm ID). To obtain sufficient protein for analysis from small- and intermediate-sized arterioles, five to seven arterioles 1-2 mm in length were pooled into one sample for each animal. Results establish that the number of smooth muscle cells per endothelial cell decreases from a number of 10 to 15 in large coronary arteries to 1 in the smallest arterioles. Immunohistochemistry revealed that eNOS is located only in endothelial cells in all sizes of coronary artery and in coronary capillaries. Contrary to our hypothesis, eNOS protein content did not increase with decreasing size of coronary artery. Indeed, the smallest coronary arterioles had less eNOS protein per gram of total protein than the large coronary arteries. These results indicate that eNOS protein content is greater in the endothelial cells of conduit arteries, resistance arteries, and large arterioles than in small coronary arterioles.
Article
Exercise training is a known stimulus for arteriogenesis, but it is unclear whether elite athletes, who exhibit increased conduit vessel diameter at rest, experience further structural vascular adaptations as a result of intense exercise training. Cross-sectional comparisons were performed between elite rowers (N = 17), following a respite from training, and eight untrained age- and gender-matched controls to assess the effects of long-term exercise on vessel structure. To determine the impact of the resumption of intensive exercise training on conduit artery structure, measures were repeated following 3 and 6 months of training in the athletes; the controls remained inactive. Conduit vessel structure was assessed, using high-resolution B-mode ultrasound, as brachial artery diameter at rest (BADr) and in response to 5-min (BAD5) and 10-min (BAD10) periods of forearm cuff ischemia. Shear rate profiles were also analyzed following cuff deflation at all time points. At entry, all measures of BAD were greater (all P < 0.05) in the athletes relative to controls (athletes vs controls; BADr 4.47 +/- 0.10 vs 3.84 +/- 0.22 mm; BAD5 4.70 +/- 0.10 vs 4.05 +/- 0.36 mm, and BAD10 4.93 +/- 0.10 vs 4.07 +/- 0.25 mm). Resumption of exercise training caused a further increase in brachial artery diameters in the athletes at 3 months (BADr, 4.71 +/- 0.10 mm, P < 0.01; BAD5 4.94 +/- 0.10 mm, P < 0.05; BAD10 5.12 +/- 0.10 mm, P < 0.001), which were maintained, but not further increased, after 6 months of training. Athletes exhibit enhanced conduit artery diameters at rest and in response to vasodilator stimuli. Despite this long-term training effect on arterial structure, resumption of training further enhances diameter, an effect that occurs within 3 months.
Article
Higher levels of physical activity are associated with fewer cardiovascular disease (CVD) events. Although the precise mechanisms underlying this inverse association are unclear, differences in several cardiovascular risk factors may mediate this effect. In a prospective study of 27,055 apparently healthy women, we measured baseline levels of hemoglobin A1c, traditional lipids (total, low-density lipoprotein, and high-density lipoprotein cholesterol), novel lipids [lipoprotein(a) and apolipoprotein A1 and B-100], creatinine, homocysteine, and inflammatory/hemostatic biomarkers (high-sensitivity C-reactive protein, fibrinogen, soluble intracellular adhesion molecule-1) and used women's self-reported physical activity, weight, height, hypertension, and diabetes. Mean follow-up was 10.9+/-1.6 years, and 979 incident CVD events occurred. The risk of CVD decreased linearly with higher levels of activity (P for linear trend < 0.001). Using the reference group of < 200 kcal/wk of activity yielded age- and treatment-adjusted relative risk reductions associated with 200 to 599, 600 to 1499, and > or = 1500 kcal/wk of 27%, 32%, and 41%, respectively. Differences in known risk factors explained a large proportion (59.0%) of the observed inverse association. When sets of risk factors were examined, inflammatory/hemostatic biomarkers made the largest contribution to lower risk (32.6%), followed by blood pressure (27.1%). Novel lipids contributed less to CVD risk reduction compared with traditional lipids (15.5% and 19.1%, respectively). Smaller contributions were attributed to body mass index (10.1%) and hemoglobin A1c/diabetes (8.9%), whereas homocysteine and creatinine had negligible effects (< 1%). The inverse association between physical activity and CVD risk is mediated in substantial part by known risk factors, particularly inflammatory/hemostatic factors and blood pressure.
Article
Ageing is associated with impaired endothelium-derived nitric oxide (NO) function in human microvessels. We investigated the impact of cardiorespiratory fitness and exercise training on physiological and pharmacological NO-mediated microvascular responses in older subjects. NO-mediated vasodilatation was examined in young, older sedentary and older fit subjects who had two microdialysis fibres embedded into the skin on the ventral aspect of the forearm and laser Doppler probes placed over these sites. Both sites were then heated to 42 degrees C, with Ringer solution infused in one probe and N-nitro-L-arginine methyl ester (L-NAME) through the second. In another study, three doses of ACh were infused in the presence or absence of L-NAME in similar subjects. The older sedentary subjects then undertook exercise training, with repeat studies at 12 and 24 weeks. The NO component of the heat-induced rise in cutaneous vascular conductance (CVC) was diminished in the older sedentary subjects after 30 min of prolonged heating at 42 degrees C (26.9 +/- 3.9%CVC(max)), compared to older fit (46.2 +/- 7.0%CVC(max), P < 0.05) and young subjects (41.2 +/- 5.2%CVC(max), P < 0.05), whereas exercise training in the older sedentary group enhanced NO-vasodilator function in response to incremental heating (P < 0.05). Similarly, the NO contribution to ACh responses was impaired in the older sedentary versus older fit subjects (low dose 3.2 +/- 1.3 versus 6.6 +/- 1.3%CVC(max); mid dose 11.4 +/- 2.4 versus 21.6 +/- 4.5%CVC(max); high dose 35.2 +/- 6.0 versus 52.6 +/- 7.9%CVC(max), P < 0.05) and training reversed this (12 weeks: 13.7 +/- 3.6, 28.9 +/- 5.3, 56.1 +/- 3.9%CVC(max), P < 0.05). These findings indicate that maintaining a high level of fitness, or undertaking exercise training, prevents age-related decline in indices of physiological and pharmacological microvascular NO-mediated vasodilator function. Since higher levels of NO confer anti-atherogenic benefit, this study has potential implications for the prevention of microvascular dysfunction in humans.
Regular aerobic exercise prevents and restores the age-related decline in endothelium-dependent vasodilation.
  • DeSouza
Topical review: Effects of exercise training on vascular endothelial nitric oxide function in humans.
  • Green
Exercise and cardiovascular risk reduction: Updating the rationale for exercise.
  • Green
Conduit artery functional adaptation is reversible and precedes structural changes to exercise training in humans.
  • Tinken