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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... Theoretically, impaired endothelial function may be associated with adverse cardiovascular events. However, previous studies have presented discrepant findings in healthy middle-aged men [8][9][10], hypertensive or healthy postmenopausal women [11][12][13], and healthy elderly subjects [14,15], suggesting that the association between endothelial function and cardiovascular risk is not yet well established in the asymptomatic population, especially from the standpoint of CVD risk profiles. In fact, it is ubiquitous that risk factors, such as serum uric acid and oxidized low-density lipoprotein (LDL) cholesterol, play a different role in CVD risk under different population profiles [16]. ...
... Similarly, cross-sectional studies revealed an inverse relationship between FMD and the 10-year Framingham risk in 5314 Japanese adults [18] and 200 subjects free of coronary heart disease [36]. Across different characteristics, there were inconsistent findings in the association of FMD with cardiovascular risk [8][9][10][11][12][13][14][15]. Notably, the association between FMD and cardiovascular risk was significant in older and postmenopausal women [13,14] but not in middle-aged men [8,9]. ...
... Across different characteristics, there were inconsistent findings in the association of FMD with cardiovascular risk [8][9][10][11][12][13][14][15]. Notably, the association between FMD and cardiovascular risk was significant in older and postmenopausal women [13,14] but not in middle-aged men [8,9]. In general, our study on the association between FMD and cardiovascular risk is in accordance with the previous studies. ...
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Impaired vascular endothelial function has attracted attention as a prognostic indicator of cardiovascular prevention. The association between impaired endothelial function and cardiovascular risk in the asymptomatic population, however, has been poorly explored. We evaluated the association of brachial artery flow-mediated dilation (FMD) with Framingham-estimated 10-year cardiovascular disease (CVD) risk in subjects free of CVD, especially by cardiovascular risk profiles. In total, 680 adults aged 30-74 years were enrolled from Rongan and Rongshui of Liuzhou, Guangxi, China, through a cross-sectional study in 2015. In the full-adjusted model, the odds ratio for the estimated 10-year CVD risk comparing the low FMD (<6%) with the high FMD (≥10%) was 2.81 (95% confidence interval [CI]: 1.21, 6.53; P for trend = 0.03). In subgroup analyses, inverse associations between FMD and the estimated 10-year CVD risk were found in participants with specific characteristics. The adjusted odds ratios, comparing the 25th and the 75th percentiles of FMD, were 2.77 (95% CI: 1.54, 5.00) for aged ≥60 years, 1.77 (95% CI: 1.16, 2.70) for female, 1.59 (95% CI: 1.08, 2.35) for nonsmokers, 1.74 (95% CI: 1.02, 2.97) for hypertension, 1.59 (95% CI: 1.04, 2.44) for normal glycaemia, 2.03 (95% CI: 1.19, 3.48) for C-reactive protein ≥10 mg/L, and 1.85 (95% CI: 1.12, 3.06) for eGFR <106 mL/minute per 1.73 m ² . Therefore, impaired endothelial function is associated with increased CVD risk in asymptomatic adults. This inverse association is more likely to exist in subjects with higher cardiovascular risk.
... The contribution of sport practice is often considered positive for the well-being and health of the human being [1,2]. Studies indicate that frequent practitioners of sports suffer from vascular remodeling over time [2][3][4]. Remodeling occurs differently between the central and peripheral arteries due to their different structural characteristics (i.e., peripheral arteries are more rigid and have less elastin than the central ones) [5,6]. The remodeling occurs more extensively on the different peripheral arteries, specifically in response to the blood flow and tension patterns to which each vessel is exposed during exercise [4][5][6]. ...
... Another study [3] reported that increased blood pressure and associated hemodynamic during exercise sessions can translate into vascular adaptation, even in distant vascular beds of the active muscle. The same author reported that the physiological adaptations to exercise may depend on the exercise intensity, as well as its modality, duration, and frequency. ...
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Background: Sports athletes, namely high-intensity practitioners, suffer from vascular remodeling overtime. The purpose of this study was to analyze the systolic and diastolic velocities’ variation between non-athletes and futsal athletes by means of arterial lower limb doppler ultrasound. Additionally, we intended to verify if the velocity variations occur primarily at the systolic or the diastolic level and in which arteries. Methods: Seventy-six young males (mean ± SD: 24.9 ± 2.8 years old) volunteered to participate in this cross-sectional study and were divided into two groups: a futsal athletes group (n = 38; 24 ± 2.78 years) in the central region of Portugal playing on the 2nd national league with the same level of practice (16 ± 2.4 years of practice) and a non-athletes group (n = 38: 26 ± 1.8 years) who did not practice sports regularly and were not federated in any sport. All the subjects agreed to participate in the study with the aim of assessing the arterial lower limb through doppler ultrasound (Philips HD7 echograph with linear transducer 7–12 MHz). Results: Differences between groups (p ≤ 0.05) in the systolic velocity of the left deep femoral artery (p = 0.022; d = 0.546, small) and in the right superficial femoral artery (p = 0.028; d = −0.515, small) were found. We also found differences in the diastolic velocity: in the left common femoral artery (p = 0.002; d = −0.748, moderate), in the right deep femoral artery (p = 0.028; d = −0.521, small), in the right superficial femoral artery (p = 0.026; d = −0.522, small), in the right popliteal artery (p = 0.002; d = −0.763, moderate), and in the left popliteal artery (p = 0.007; d = −0.655, moderate). Moreover, the athletes’ group presented the highest mean values, with the exception of the systolic velocity of the left deep femoral artery. In intragroup analysis of variance referring to systolic and diastolic velocities in arterial levels in the right and left arteries, differences were found in all analyses (p ≤ 0.05). Conclusions: We conclude that futsal athletes of our sample go through a process of changes such as increased blood flow velocity in systolic and diastolic cardiac phase in all studied lower limb arteries, showing that the remodeling occurs regardless of vessel radius. Our results reinforce the existence of vascular remodeling that may vary with the sport and its intensity.
... 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.
... 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 . ...
... 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.
... e World Health Organization (WHO) estimates that over 75% of premature CVD is preventable, and protective factors can contribute to reduce the growing burden on both affected individuals and health care systems [2]. Carotid arterial stiffness is closely related to the occurrence and development of atherosclerosis and refers to as the surrogate markers for CVD [3]. Local hemodynamic parameters play a crucial role in regulating the carotid arterial elasticity (stiffness) [4]; therefore, illustrating the parameter alterations of carotid arterial function and hemodynamics may have an advantage in the prediction of CVD and provide valuable clinical guidance to prevent and treat CVD. ...
... Carotid artery is one of the main blood supply organs for cerebral circulation system, and its local hemodynamic changes may affect the health condition of intracerebral vascular system [16]. It is well acknowledged that physical exercise can give rise to whole-body or local hemodynamic changes by accelerating blood flow [3]. Endothelial cells covering arteries respond to hemodynamic changes via corresponding receptor sensations and induce the alteration of endothelial cell morphology, function, and gene expression [17]. ...
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Background: Cardiovascular disease (CVD) contributes to be one of the leading causes of death in the population worldwide. Carotid arterial stiffness and local hemodynamics are associated with the occurrence and development of CVD. Therefore, understanding the alterations of human carotid arterial stiffness and hemodynamics is of great clinical value in the prevention and treatment of CVD. Objective: In this study, we aimed to investigate the acute effect of high-intensity interval cycling (HIIC) on carotid arterial stiffness and hemodynamics in sedentary. Methods: Thirty volunteered healthy sedentary males were enrolled in this study. HIIC intervention (3 sets, 20 s per set) was performed individually. A color Doppler ultrasound was applied to detect the images of the arterial inner diameters and center-line velocity waveforms at the right common carotid artery at different time points (at rest, 3 min, 15 min, and 30 min) after HIIC. Synchronously, electronic manometer was used to measure the systolic and diastolic pressures at the left brachial artery. Results: Arterial stiffness increased and arterial diameter decreased significantly after acute HIIC. The variation in stiffness persisted for 30 min, at least 15 min longer than the change in diameter. At 3 min after exercise, maximum and mean wall shear stresses (WSS) increased and minimum WSS was also higher than the resting value. At 30 min after exercise, WSS returned to the baseline, but oscillating shear index was still higher than the resting value. Conclusions: In summary, arterial stiffness and hemodynamics changed significantly not only at 3 min but also at 30 min after acute HIIC.
... 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.
... 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. ...
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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. ...
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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.
... Habitual exercise is a well-established intervention for reducing risk factors for cardiovascular disease (Mora et al., 2007) and improving arterial vascular function and structure (Green, 2009). Traditionally, moderate-intensity continuous training has been recommended (Pescatello et al., 2004;Haskell et al., 2007), and has increased endothelial function (Tinken et al., 2008;Birk et al., 2012), decreased arterial stiffness (Kakiyama et al., 2005), and improved arterial dilator capacity as surrogate measure for structural remodeling (Tinken et al., 2008). ...
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We examined whether the effect of short‐term endurance exercise training on venous compliance in the calf and forearm differed between continuous and interval workloads. Young healthy volunteers (10 women and 16 men) were randomly assigned to continuous (C‐TRA; n = 8) and interval (I‐TRA; n = 9) exercise training groups, and a control group (n = 9). Subjects in the C‐TRA group performed a continuous cycling exercise at 60% of heart rate reserve (HRR), and subjects in the I‐TRA group performed a cycling exercise consisting of alternating 2‐min intervals at 40% HRR and 80% HRR. Training programs were performed for 40 min/day, 3 days/week for 8 weeks. Before and after training, limb volume in the calf and forearm was measured with subjects in the supine position by venous occlusion plethysmography using a venous collecting cuff placed around the thigh and upper arm. Cuff pressure was held at 60 mmHg for 8 min and then decreased to 0 mmHg at a rate of 1 mmHg/s. Venous compliance was calculated as the numerical derivative of the cuff pressure–limb volume curve. Calf venous compliance was increased after I‐TRA, but not C‐TRA. Forearm venous compliance was unchanged after C‐TRA or I‐TRA. These results suggest that the adaptation of venous compliance in response to endurance training for 8 week may occur in interval but not continuous exercise bouts and may be specific to the exercising limb. This study demonstrated that 8 weeks of endurance interval exercise training, but not continuous exercise, increased calf venous compliance in young adults while forearm venous compliance remained unchanged. These findings suggest that the adaptation of venous compliance in response to short‐term endurance training could be induced by not moderate continuous exercise but interval exercise at low and high intensities, and might be specific to the exercising limb.
... 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). ...
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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.
... Thus our aerobic exercise intervention essentially restored brachial artery FMD in previously sedentary older adults to almost normal values. We hypothesis that this improvements were independent of changes among other factors, suggesting a direct physiological impact of the training program, as already reported (DeSouza et al., 2000;Green, 2009;Moreau, Donato, Seals, DeSouza, & Tanaka, 2003). Along with the impact of AT on increasing forearm blood flow responses to acetylcholine (DeSouza et al., 2000), the present results provide evidence that IATP-R improves endothelium-dependent dilation in both conduit arteries and resistance vessels of originally sedentary seniors. ...
... The cardiovascular benefits of exercise extend beyond the reduction of traditional cardiovascular risk factors and direct vascular effects, initiated by repeated episodes of exercise-induced shear stress, have been identified. [15] However, many of the mechanisms that mediate these favorable adaptations in vascular structure and function are disrupted in CKD. For instance, CKD is associated with endothelial dysfunction and markedly reduced NO bioavailability as well as increased activity of the sympathetic and renin-angiotensin systems. ...
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Background and objectives Management of hypertension in chronic kidney disease (CKD) remains a major challenge. We conducted a systematic review to assess whether exercise is an effective strategy for lowering blood pressure in this population. Design, setting, participants, and measurements We searched MEDLINE, EMBASE, the Cochrane Library, CINAHL and Web of Science for randomized controlled trials (RCTs) that examined the effect of exercise on blood pressure in adults with non-dialysis CKD, stages 3–5. Outcomes were non-ambulatory systolic blood pressure (primary), other blood pressure parameters, 24-hour ambulatory blood pressure, pulse-wave velocity, and flow-mediated dilatation. Results were summarized using random effects models. Results Twelve studies with 505 participants were included. Ten trials (335 participants) reporting non-ambulatory systolic blood pressure were meta-analysed. All included studies were a high risk of bias. Using the last available time point, exercise was not associated with an effect on systolic blood pressure (mean difference, MD -4.33 mmHg, 95% confidence interval, CI -9.04, 0.38). The MD after 12–16 and 24–26 weeks of exercise was significant (-4.93 mmHg, 95% CI -8.83, -1.03 and -10.94 mmHg, 95% CI -15.83, -6.05, respectively) but not at 48–52 weeks (1.07 mmHg, 95% CI -6.62, 8.77). Overall, exercise did not have an effect on 24-hour ambulatory blood pressure (-5.40 mmHg, 95% CI -12.67, 1.87) or after 48–52 weeks (-7.50 mmHg 95% CI -20.21, 5.21) while an effect was seen at 24 weeks (-18.00 mmHg, 95% CI -29.92, -6.08). Exercise did not have a significant effect on measures of arterial stiffness or endothelial function. Conclusion Limited evidence from shorter term studies suggests that exercise is a potential strategy to lower blood pressure in CKD. However, to recommend exercise for blood pressure control in this population, high quality, longer term studies specifically designed to evaluate hypertension are needed.
... With exercise training, peripheral arteries experience repeated increases in blood flow and shear stress; the dragging force of blood across the inner arterial wall. These stresses provide a stimulus to enhanced endothelial function (Black, Green, & Cable, 2008;Green, 2009;Green et al., 2010Green et al., , 2017Green, Spence, Halliwill, Cable, & Thijssen, 2011;Naylor et al., 2011;Thijssen et al., 2010;Tinken et al., 2010). If this is also true in the cerebral circulation, then repeated episodic increases in brain blood flow that accompany exercise should improve cerebrovascular function and promote healthy cognitive aging Maiorana et al., 2001;Maiorana et al., 2000;Maiorana et al., 2003;Walsh, Bilsborough, et al., 2003;Walsh, Yong, et al., 2003). ...
... The positive effects observed in the present study, in terms of %FMD/SR increase, may suggest that RMT is able to raise the peripheral blood flow, which, with chronic training, triggering a series of events, [57] that lead finally to an improvement in the vascular structure and function. [58] The implications of these findings effect of RMT may benefit the recovery of the endothelium after deconditioning, which can be useful in those populations characterized by low mobility, such as the elderly or in athletes recovering from an injury. ...
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Vasomotor response is related to the capacity of the vessel to maintain vascular tone within a narrow range. Two main control mechanisms are involved: the autonomic control of the sympathetic neural drive (global control) and the endothelial smooth cells capacity to respond to mechanical stress by releasing vasoactive factors (peripheral control). The aim of this study was to evaluate the effects of respiratory muscle training (RMT) on vasomotor response, assessed by flow-mediated dilation (FMD) and heart rate variability, in young healthy females. The hypothesis was that RMT could enhance the balance between sympathetic and parasympathetic neural drive and reduce vessel shear stress. Thus, twenty-four women were randomly assigned to either RMT or SHAM group. Maximal inspiratory mouth pressure and maximum voluntary ventilation were utilized to assess the effectiveness of the RMT program, which consisted of three sessions of isocapnic hyperventilation/ week for eight weeks, (twenty-four training sessions). Heart rate variability assessed autonomic balance, a global factor regulating the vasomotor response. Endothelial function was determined by measuring brachial artery vasodilation normalized by shear rate (%FMD/SR). After RMT, but not SHAM, maximal inspiratory mouth pressure and maximum voluntary ventilation increased significantly (+31% and +16%, respectively). Changes in heart rate variability were negligible in both groups. Only RMT exhibited a significant increase in %FMD/SR (+45%; p<0.05). These data suggest a positive effect of RMT on vasomotor response that may be due to a reduction in arterial shear stress, and not through modulation of sympatho-vagal balance.
... We read with interest the authors' opposing perspectives on the acute effects of exercise on healthy endothelium. As shear stress, and potentially endothelial damage, is considered a critical stimulus for vascular adaptation (Green 2009), we wish to highlight a caveat of research in this area: the disparity between in vitro and in vivo work that precludes the direct translation of findings between studies. Because of differences in milieu between isolated cells and the human body, shear patterns created in vitro (Uematsu et. ...
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Comment found in Supporting Information for Adams/Sapp CrossTalk: Acute exercise elicits damage to the endothelial layer of systemic blood vessels in health individuals
... 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. ...
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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.
... 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.
... 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.
... 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. ...
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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.
... 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. ...
Article
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 particpants. 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.Significance statementThe present study constitutes novel evidence for an autonomic nervous response specific to the side of the body exposed to direct threat. We identify a robust pattern of electrodermal response at the body location that directly receives aversive tactile stimulation. Thus, we demonstrate for the first time in contemporary research that the ANS is capable of location-specific outputs within single effector organs in response to small scale threat. This extends the canonical view of the role of ANS responses in stressful or dangerous stresses - that of provoking a 'fight or flight' response - suggesting a further role of this system: preparation of targeted limb-specific action, i.e., a flick.
... 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]. ...
Article
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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). ...
Article
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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]. ...
Article
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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.
... 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.
... 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.
... Exercise training can modulate arterial stiffness and directly induce systemic and local arterial hemodynamic responses [5]. Cross-sectional comparisons between sedentary individuals and athletes, including runners, cyclists, and basketball players [6][7][8], have demonstrated that arterial stiffness and hemodynamic parameters, such as arterial diameter, blood supply to the brain, and blood pressure have been improved. ...
Article
Full-text available
This paper studied the alterations in arterial stiffness and hemodynamic responses during resting state and immediately following acute cycling intervention at different times across 12-week supervised exercise training. Twenty-six sedentary young males participated in the exercise training program at moderate intensity. Arterial stiffness and hemodynamic variables of the right common carotid artery were measured and computed during resting state and immediately following acute cycling intervention at weeks 0, 4, 8, and 12. Across the 12-week exercise training, carotid arterial stiffness was decreased at weeks 8 and 12 and hemodynamic variables were improved at week 12 during resting state. In response to acute cycling intervention, carotid arterial stiffness exhibited an acute increase foremost at 8 weeks, and arterial maximal and mean diameters showed acute decreases at weeks 0 and 4. Despite significant differences in arterial stiffness and hemodynamic variables between resting state and immediately after acute intervention for each time period, these differences presented a progressive decrease across the 12-week exercise training. In conclusion, long-term exercise training not only improved carotid arterial stiffness and hemodynamic alterations when at rest but also negated the acute responses of carotid arterial stiffness and hemodynamic variables to acute cycling intervention.
... 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.
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Generating precise in vivo arterial endothelial hemodynamic microenvironments using microfluidics is essential for exploring endothelial mechanobiology. However, a hemodynamic principle guiding the fabrication of microfluidic systems is still lacking. We propose a hemodynamic similarity principle for quickly obtaining the input impedance of the microfluidic system in vitro derived from that of the arterial system in vivo to precisely generate the desired endothelial hemodynamic microenvironments. First, based on the equivalent of blood pressure (BP) and wall shear stress (WSS) waveforms, we establish a hemodynamic similarity principle to efficiently map the input impedance in vivo to that in vitro, after which the multi-component microfluidic system is designed and fabricated using a lumped parameter hemodynamic model. Second, numerical simulation and experimental studies are carried out to validate the performance of the designed microfluidic system. Finally, the intracellular Ca²⁺ responses after exposure to different intensities of exercise-induced BP and WSS waveforms are measured to improve the reliability of EC mechanobiological studies using the designed microfluidic system. Overall, the proposed hemodynamic similarity principle can guide the fabrication of a multi-component microfluidic system for endothelial cell mechanobiology.
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Metabolic syndrome is a pathologic condition that has increasing prevalence in modern world and is a significant precursor of cardiovascular disease. One of the main mechanisms underlying metabolic syndrome and each of its components is the inflammatory state that favors the development of the atherosclerotic process leading to increased arterial stiffness. Indeed, a body of evidence has demonstrated a strict link between metabolic syndrome and its components with arterial stiffness. Regular physical activity represents a key strategy for antagonizing the adverse effects of metabolic syndrome including the impairment of arterial elasticity, thereby reducing the burden of cardiovascular disease. Thus, special attention should be paid by clinicians to people with metabolic syndrome in whom the untoward effects of metabolic disturbances on the arteries can be offset by a program of physical activity.KeywordsMetabolic syndromeArterial stiffnessPhysical activityExercise
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Physical activity remains a milestone of non-pharmacological treatment of hypertension and cardiovascular disease by means of its positive effect on vascular function. Regular aerobic exercise exerts its favourable action by reducing heart rate and blood pressure level, decreasing sympathetic activity and inflammation process. This leads to an improvement of arterial distensibility, reduction of arterial stiffness and through this to a reduction of cardiovascular disease. On the opposite side contrasting results exist on the effect of resistance training or combined training exercise.KeywordsExerciseAerobic physical activityArterial stiffnessArterial distensibility
Article
Prolonged sitting has been shown to affect endothelial function. Strategies that promote interruption of sitting have shown varying results on the shear rate (SR), flow-mediated dilation (FMD) and blood flow (BF). Thus, we conducted a systematic review and meta-analysis to 1) increase the existing knowledge of the impact of sitting interruption in the prevention of endothelial dysfunction in adults and 2) determine the effect of the sitting interruption strategies on SR, FMD, BF. Literature search was carried out through 7 databases. A random effects model was used to provide the overall mean difference with a 95%CI, and forest plots were generated for pooled estimates of each study outcome. Assessment of biases was performed using ROB2 and considerations for crossover trials. Prolonged sitting interruption strategies showed a significant effect in increasing SR (MD: 7.58 s-1; 95% CI: 3.00 to 12.17), FMD (MD: 1.74%; 95% CI: 0.55 to 2.93) and BF (MD: 12.08 ml/min; 95% CI: 7.61 to 16.55) when compared with the uninterrupted prolonged sitting condition. Prolonged sitting interruption strategies significantly increase SR, FMD and BF, therefore, they represent a considerable effective preventive method on endothelial dysfunction caused by acute exposure to uninterrupted prolonged sitting.
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Physical deconditioning commonly occurs following spinal cord injury (SCI) due to loss of voluntary functional movement and resultant increased sedentary behavior. This lesser energy expenditure leads to increased fat mass, decreased lean tissue mass, increased body mass index, declines in cardiac structure and function, reduced insulin sensitivity, and lower cardiorespiratory fitness. Collectively these physiological changes increase the risk of morbidity and mortality from cardiovascular diseases. Exercise as a therapy after an SCI may mitigate these negative health effects and improve quality and longevity of life. However, current exercise interventions for individuals with SCI may not be sufficient to prevent the elevations in risk factors for cardiovascular disease. Therefore, interventions to enhance the effectiveness of exercise therapy may be needed in this population in order to experience the same benefits seen by the uninjured population. Further, adjunctive therapies that mimic exercise may induce health benefits to combat cardiovascular disease. This chapter highlights novel interventions that may enhance function, increase exercise capacity, and decrease disease risk in individuals following an SCI. An effort was made to concentrate this chapter on human investigations of SCI but, where appropriate, investigations using animal models of SCI are referenced and specifically stated. Although this chapter highlights novel interventions to enhance the positive health benefits of exercise, combinations of these interventions may be necessary to improve the health of these individuals and warrants future investigation.KeywordsSpinal cord injuryRehabilitationAerobic exerciseCardiovascular diseaseRegenerative medicine
Article
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 versus genetics in 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 cerebral structure and function. Abstract: Introduction 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. Methods Cerebrovascular function (rest, autoregulation, hypercapnia, exercise) was assessed in 86 healthy same-sex MZ (30 pairs) and DZ (13 pairs) twins, who underwent three-months of END and RES. Carbon dioxide (PET CO2 ), mean arterial pressure (MAP) and middle cerebral artery velocity (MCAv) were measured and MCAv resistance (MCACVRi ) was calculated. Results 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 PET CO2 . At rest, positive response rates following RES ranged from 27-71% and 40-64% following END. Intraclass correlations between twins were moderate for most variables at baseline. In response to training, only MZ pairs were significantly correlated for change in MCAv (P = 0.005) and low frequency phase (P = 0.047) following RES. Conclusion 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. Abstract figure legend Schematic summary of the assessment battery of cerebrovascular measures of function and health developed by Ainslie and Green. Transcranial Doppler (TCD) measures are complemented by contemporaneous assessment of whole brain blood flow, derived from simultaneous high-resolution ultrasound via insonation of the internal carotid and vertebral arteries. Results show that group response does not always reflect individual responses, and that switching exercise modality can increase individual responsiveness to exercise training. Low twin correlations in response to exercise training indicate nurture has a larger contribution to training response than nature. This article is protected by copyright. All rights reserved.
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We assessed the impact of a structured lower-limb aerobic exercise training intervention during pregnancy on brachial artery endothelial function, shear rate and patterns, and forearm blood flow and reactive hyperemia. Twenty-seven pregnant women were recruited and randomized into either a control group (n = 11; 31.0 ± 0.7 years), or an exercise intervention group (n = 16; 32.6 ± 0.9 years). The exercise group completed 40 minutes of aerobic exercise (50–70% heart rate reserve) 3–4 times per week, between the second and third trimester of pregnancy. Endothelial function was assessed using flow-mediated dilation (FMD, normalized for shear stress) at pre- (16–20 weeks) and post-intervention (34–36 weeks). The exercise training group experienced an attenuated increase in mean arterial pressure (MAP) relative to the control group (ΔMAP exercise: +2 ± 2 mm Hg vs. control: +7 ± 3 mm Hg; p = 0.044) from pre- to post-intervention. % FMD change corrected for shear stress was not different between groups (p = 0.460); however, the post-occlusion mean flow rate (exercise: 437 ± 32 mL/min vs. control: 364 ± 35 mL/min; p = 0.001) and post-occlusion anterograde flow rate (exercise: 438 ± 32 mL/min vs. control: 364 ± 46 mL/min; p = 0.001) were larger for the exercise training group compared with controls, post-intervention. Although endothelial function was not different between groups, we observed an increase in microcirculatory dilatory capacity, as suggested by the augmented reactive hyperemia in the exercise training group. Registered at ClinicalTrials.gov: NCT02948439. Novelty: Endothelial function was not altered with exercise training during pregnancy. Exercise training did contribute to improved cardiovascular outcomes, which may have been associated with augmented reactive hyperemia, indicative of increased microcirculatory dilatory capacity.
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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.
Article
Aim: It is generally considered that regular exercise maintains brain health and reduces the risk of cerebrovascular diseases such as stroke and dementia. Since the benefits of different 'types' of exercise are unclear, we sought to compare the impacts of endurance and resistance training on cerebrovascular function. Methods: In a randomized and cross-over design, 68 young healthy adults were recruited to participate in 3-months of resistance and endurance training. Cerebral hemodynamics through the internal carotid, vertebral, middle and posterior cerebral arteries were measured using Duplex ultrasound and transcranial Doppler at rest and during acute exercise, dynamic autoregulation and cerebrovascular reactivity (to hypercapnia). Results: Following resistance, but not endurance training, middle cerebral artery velocity and pulsatility index significantly decreased (P<0.01 and P=0.02, respectively), while mean arterial pressure and cerebrovascular resistance in the middle, posterior and internal carotid arteries all increased (P<0.05). Cerebrovascular resistance in response to acute exercise and hypercapnia also significantly increased following resistance (P=0.02), but not endurance training. Conclusions: Our findings, which were consistent across multiple domains of cerebrovascular function, suggest that episodic increases in arterial pressure associated with resistance training may increase cerebrovascular resistance. The implications of long-term resistance training on brain health require future study, especially in populations with pre-existing cerebral hypoperfusion and/or hypotension.
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Exercise exerts direct effects on the vasculature via the impact of hemodynamic forces on the endothelium, thereby leading to functional and structural adaptations that lower cardiovascular risk. The patterns of blood flow and endothelial shear stress during exercise lead to atheroprotective hemodynamic stimuli on the endothelium and contribute to adaptations in vascular function and structure. The structural adaptations observed in arterial lumen dimensions after prolonged exercise supplant the need for acute functional vasodilatation in case of an increase in endothelial shear stress due to repeated exercise bouts. In contrast, wall thickness is affected by rather systemic factors, such as transmural pressure modulated during exercise by generalized changes in blood pressure. Several mechanisms have been proposed to explain the exercise-induced benefits in patients with coronary artery disease (CAD). They include decreased progression of coronary plaques in CAD, recruitment of collaterals, enhanced blood rheological properties, improvement of vascular smooth muscle cell and endothelial function, and coronary blood flow. This review describes how exercise via alterations in hemodynamic factors influences vascular function and structure which contributes to cardiovascular risk reduction, and highlights which mechanisms are involved in the positive effects of exercise on CAD.
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Abstract The aim of the present study was to compare the sympathetic neural and endothelial responses of brachial artery to vasodilatory and constrictor stimuli in elite weightlifters and a sedentary age-matched control group. 7 elite weightlifters (age 23.5±2.2 yrs) and 8 sedentary healthy subjects (age 24.3±2.12 yrs) voluntarily participated in this study. High-resolution Doppler ultrasound was used to determine brachial artery diameters at rest, following 5 minutes of forearm occlusion [Flow Mediated Dilation (FMD)] and during acute sympathetic stimulation [cold pressure test (CPT)]. Vasoreactivity responses were calculated from the vasodilatory and constrictor peak changes in artery diameter. The acquired data were analyzed using independent t test and repeated measures method at P≤0.05. Brachial artery diameters in baseline [mean differences, 0.5 mm (P=0.001)], peak vasodilation [mean differences, 0.57 mm (P=0.002)] and peak constriction [mean differences, 0.498 mm (P=0.003)] were significantly greater in weightlifters than control group. However, no significant difference was observed in %FMD, %CPT and vascular operating range (VOR) between weightlifters and age-matched control group (P≤0.05). The present study indicated that the function of brachial artery is not necessarily enhanced in elite weightlifters. However, elite weightlifters had larger brachial artery diameter than age-matched healthy control subjects. Keywords brachial artery, elite weightlifters, endothelial function, vasoreactivity.
Article
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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IntroductionThe present study is an attempt to compare the effects of letrozole therapy plus monitored exercise and letrozole therapy alone on pregnancy outcomes in infertile patients with polycystic ovary syndrome (PCOS).MethodA total of 120 infertile women aged between 18 and 40 years with PCOS participated in this study. The patients were divided to two groups: treatment with letrozole and exercise workouts (Group 1) and treatment with letrozole only (Group 2). All data were analyzed using SPSS 22 software.ResultsThe group of women that received exercise had more live births than the group of women that received only letrozole, but this difference was not significant. Biochemical pregnancy rates in Group 1 were significantly lower than Group 2 (p-value < 0.001). The number of follicles and clinical pregnancies was significantly higher in Group 1.Conclusion Despite the well-proven benefits of exercise for the general population and the fact that it is recommended as a basis for PCOS management, few completely controlled studies have evaluated the impact of exercise on PCOS. The present study results revealed that regular exercise combined with letrozole therapy would lead to better pregnancy outcomes in women with PCOS compared to letrozole alone.
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Exercise promotes general metabolic wellness not only by preserving musculoskeletal function, increasing muscle flexibility, increasing cardiopulmonary fitness, decreasing inflammation, increasing blood flow, and improving mental health, but also by promoting bone health, decreasing the risk of osteoporosis, improving postural stability, reducing risk of falling and fractures, and range of motion, increasing lifespan, and improving quality of life. At the molecular level, beneficial effects of exercise are related, in part, to increase in insulin sensitivity, decrease in CRP and IL-6 levels, enhancement in heart function, increase in growth factors such as BDNF, IGF, and VEGF, and decrease inflammation in brain and peripheral tissues. These parameters contribute to maintenance of cognitive function.
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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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Objective To comprehensively examine the potential impacts of prenatal experience of the Chinese Great Famine on chronic disease risks in the middle age. Methods This study included 92 284 participants aged 39–51 years from China Kadoorie Biobank born around the famine period and without major chronic diseases at baseline. We categorised participants into non-famine births (born between 1 October 1956 and 30 September 1958, and 1 October 1962 and 30 September 1964) and famine births (born between 1 October 1959 and 30 September 1961). The outcomes were incident cardiovascular disease, cancer and respiratory system disease. Cox regression was used to estimate adjusted HR and 95% CI for famine exposure. Subgroup analyses were performed according to baseline characteristics. Results During a median 10.1 years of follow-up, we identified 4626 incident ischaemic heart disease (IHD) cases, 7332 cerebrovascular disease cases, 3111 cancer cases and 16 081 respiratory system disease cases. In the whole population, prenatal famine exposure was not statistically associated with the risks of developing any chronic diseases in adulthood. However, for urban participants, compared with non-famine births, famine births had a higher risk of cerebrovascular disease (HR 1.18; 95% CI 1.09 to 1.28); such association was not shown for rural participants (p for interaction <0.001). Also, we observed the associations of prenatal famine exposure with IHD (HR 1.15; 95% CI 1.05 to 1.26) and cerebrovascular disease (HR 1.13; 95% CI 1.05 to 1.21) in participants with lower physical activity level, but not in those with higher ones (all p for interaction=0.003). Conclusion Our findings indicate that prenatal exposure to the Chinese famine might be associated with an increased cardiovascular risk and such risk may be modified by adult lifestyle.
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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.
Article
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.
Article
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.