Exercise training elevates arterial compliance at rest, but the effects of acute exercise in this regard are unknown. This study investigated the effects of a single, 30-min bout of cycling exercise at 65% of maximal oxygen consumption on indexes of arterial compliance. Whole body arterial compliance determined noninvasively from simultaneous measurements of aortic flow and carotid pressure was elevated (66 ± 26%) at 0.5 h postexercise ( P = 0.04), followed by a decline to baseline 1 h after exercise. Aortic pulse-wave velocity, which is inversely related to compliance, was reduced (4 ± 2%; P = 0.04) at 0.5 h postexercise. Pulse-wave velocity in the leg decreased by 10 ± 4% at this time ( P = 0.01). Mean arterial pressure was unchanged; however, central systolic blood pressure was reduced postexercise ( P = 0.03). Cardiac output was elevated after exercise ( P = 0.007) via heart rate elevation ( P = 0.001), whereas stroke volume was unchanged. Total peripheral resistance was therefore reduced ( P = 0.01) and would be expected to contribute to an elevation in arterial compliance. In conclusion, a single bout of cycling exercise increased whole body arterial compliance by mechanisms that may relate to vasodilation.

Using a noninvasive technique we have investigated the effect of 4 wk of exercise training on total systemic arterial compliance (SAC) in 13 previously sedentary young males. SAC is assessed from simultaneous measurements of ascending aortic blood velocity using Doppler velocimetry and surrogate estimates of aortic root pressure obtained by applanation tonometry of the right carotid artery. Subsequent calibration of the pressure waveform is by linear interpolation against brachial arterial pressures measured sphygmomanometrically. Exercise training increased the overall mean maximum oxygen consumption (VO2 max) by 5.1 ml.min-1 x kg-1 (95% confidence limits 1.30-8.80, P < 0.01) and decreased mean systolic blood pressure by 8.4 mmHg [95% confidence interval (CI) 2.9-13.9, P < 0.01]. Mean SAC increased by 0.26 units (95% CI 0.10-0.43, P < 0.01) with the regional stiffness of the aortic arch (measured echocardiographically using the beta-index) showing a complementary decrease of 1.03 (95% CI -2.25-0.19, P < 0.05). Assuming a logarithmic arterial volume-pressure relationship, we were able to dissociate the change in SAC due to the exercise training-induced decrease in blood pressure from that due to change in the intrinsic compliance of the systemic arteries. Our results indicate that 1) exercise training increases SAC; 2) that the increase in SAC is greater than that due to changes in blood pressure and is likely to include a component due to change in intrinsic arterial compliance; and 3) that the induced change in SAC is linearly related to change in VO2 max.

The present study investigated arterial compliance as a possible influence on mean arterial pressure-heart rate (MAP-HR) reflex function in athletes and hypertensives. Aortic stiffness and systemic arterial compliance (SAC) were estimated in 25 elite male athletes and 25 age-matched sedentary controls. Blood pressure did not vary between groups, but SAC was higher in the athletic compared with the sedentary group (0.46 +/- 0.04 vs. 0.37 +/- 0.02 arbitrary compliance units; P = 0.03). In five hypertensives and six age-matched normals and in a subgroup of seven athletes and seven age-matched controls the sigmoidal MAP-HR reflex was assessed using phenylephrine and nitroprusside. In athletes compared with sedentary subjects MAP-HR reflex sensitivity was the same; however, the maximum tachycardia in response to blood pressure reduction was lower in the athletic group (87.1.1 +/- 3.7 vs. 97.1 +/- 2.9 beats/min; P = 0.05). Athletes had a higher blood pressure corresponding to 95% of the HR range (64.2 +/- 3.2 vs. 54.0 +/- 2.1 mmHg; P = 0.02), but there was no difference in the blood pressure corresponding to 5% of the HR range. The blood pressure excursion necessary to traverse the baroreceptor transducer range (MAPd) was therefore less in athletes compared with normals. The beta-index of aortic stiffness correlated closely with MAPd (R = 0.70; P < 0.01). In hypertensives reflex sensitivity was reduced, the minimum HR was elevated, and the MAPd was 56% greater compared with normals.(ABSTRACT TRUNCATED AT 250 WORDS)

Objective:To compare the efficacy of IV chlorpromazine with that of IV metoclopramide in the treatment for acute migraine headache in the ED. Methods:A prospective randomized double-blind trial was undertaken at two university-affiliated urban EDs with a combined annual census of more than 85,000 patients. Included in the study were patients presenting to the E D with a diagnosis of migraine headache. The subjects were randomized to receive 0.1 mg/kg/dose IV of either chlorpromazine (CPZ) or metoclopramide (MC), up to a total of three doses.Results: Ninety-one patients completed the protocol; 44 received MC and 47 received CPZ. The demographics of the two groups were similar. Both drugs provided, for the majority of patients, adequate pain relief as measured on a visual analog scale (VAS) completed every 15 minutes from T = 0 minutes t o T = 45 minutes. The average pain relief over 45 minutes (AVAS) for CPZ was 4.87 cm, vs 4.34 cm for MC (p = 0.35). There also was no statistically significant difference in blood pressure (BP) changes (ABP < 2 mm Hg for both systolic and diastolic BPs, p = 0.47 and 0.33) or numbers of patients reporting adverse effects (AEs) (CPZ: 16 of 35; MC: 13 of 29, p = 0.43). There was no severe A € with either study drug. Conclusions:Metoclopramide and chlorpromazine administered 1V are both effective in the management of acute migraine headache. They are associated with similar minor side-effect profiles.

We investigated a change in vascular reactivity as a potential adaptive mechanism to chronic exercise. The study consisted of 2 separate protocols with 10 male athletes and 10 age-matched sedentary male control subjects participating in each. Protocol 1 investigated forearm blood flow responses to intra-arterial infusions of acetylcholine and sodium nitroprusside by use of venous occlusion plethysmography. Protocol 2 used identical techniques to study responses to norepinephrine, angiotensin II (ANG II), and NG-monomethyl-L-arginine (L-NMMA). The percent reduction in forearm vascular resistance to acetylcholine was significantly greater in the athletic compared with the sedentary group (multivariate analysis of variance for repeated measures, P = 0.03). Covariance analysis suggested that the lower total cholesterol level of the athletic group (P = 0.03) may contribute to their enhanced responsiveness to acetylcholine. There were no differences between athletic and sedentary groups in the forearm vascular resistance responses to norepinephrine, ANG II, sodium nitroprusside, or L-NMMA. These data support the hypothesis that long-term endurance training is associated with enhanced endothelium-dependent dilator reserve due to altered lipoprotein levels in athletes. This finding may have therapeutic application in conditions of elevated cholesterol and impaired vasodilator capacity including hypertension, hypercholesterolemia, atherosclerosis, and cardiac failure.

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Arterial elastic properties are altered with increasing age and in various disease states, including non-insulin-dependent diabetes mellitus (NIDDM). Whether young patients with insulin-dependent diabetes mellitus (IDDM) have reduced arterial compliance before developing endothelial dysfunction or overt micro- and macrovascular disease is unclear. Systemic arterial compliance and endothelium-dependent, flow-mediated vasodilation (FMD) was assessed in 25 individuals with uncomplicated IDDM (23 ± 4 yr, 14 females and 11 males) and compared with 30 age-matched controls (15 females and 15 males). Arterial compliance was determined via simultaneous measurements of aortic blood flow and carotid arterial pressure. The relationship between arterial compliance and endothelial function (assessed by brachial artery FMD) was also examined. Arterial compliance was 29% lower in IDDM subjects compared with control subjects (0.46 ± 0.05 vs. 0.65 ± 0.07 arbitrary compliance units, P < 0.05). Blood pressure, lipid levels, and daily energy expenditure (a measure of physical activity levels) were not different between groups. Compliance in the IDDM group was not related to the integrity of endothelial vasodilator function, disease duration, or degree of glycemic control. Arterial compliance is reduced in young patients with IDDM before the development of overt micro- or macrovascular disease. Early assessment of arterial compliance may be useful in predicting the development of diabetic vascular complications.

epicardial adipose tissue (eAt) is associated with cardiovascular risk. the longitudinal change in eAt volume (eAtv) and density (eAtd), and potential modulators of these parameters, has not been described. We prospectively recruited 90 patients with non-obstructive coronary atherosclerosis on baseline computed tomography coronary angiography (ctcA) performed for suspected coronary artery disease to undergo a repeat research CTCA. EATv in millilitres (mL) and EATd in Hounsfield units (HU) were analysed and multivariable regression analysis controlling for traditional cardiovascular risk factors (cVRf) performed to assess for any predictors of change. Secondary analysis was performed based on statin therapy. The median duration between CTCA was 4.3years. Mean EATv increased at follow-up (72 ± 33 mL to 89 ± 43 mL, p < 0.001) and mean EATd decreased (baseline −76 ± 6 HU vs. −86 ± 5 HU, p < 0.001). There were no associations between baseline variables of body mass index, age, sex, hypertension, hyperlipidaemia, diabetes or smoking on change in EATv or EATd. No difference in baseline, follow-up or delta EATv or EATd was seen in patients with (60%) or without baseline statin therapy. in this select group of patients, eAtv consistently increased and eAtd consistently decreased at long-term follow-up and these changes were independent of cVRf, age and statin use. together with the knowledge of strong associations between EAT and cardiac disease, these findings may suggest that eAt is an independent parameter rather than a surrogate for cardiovascular risk. open Scientific RepoRtS | (2020) 10:7109 | https://doi.org/10.1038/s41598-020-63135-z www.nature.com/scientificreports www.nature.com/scientificreports/ Scientific RepoRtS | (2020) 10:7109 | https://doi.org/10.1038/s41598-020-63135-zwww.nature.com/scientificreports www.nature.com/scientificreports/ however, this is reflective of the current literature in examining relevant associations of EAT. Finally, there is potential for error in using delta EAT values with potential overlap from test-retest variability. Our previous work has demonstrated limits of agreement up to 10 mL higher or lower between observers with a mean bias however of only 1 mL, however our inter-observer correlation was excellent at 0.98 with assessors blinded to scan timing and patient details. conclusion Epicardial adipose tissue volume and density demonstrate significant longitudinal changes in patients with non-obstructive coronary artery disease with a consistent increase in EAT volume and consistent decrease in EAT density. There are no clinical risk factors that appear to associate with the change in EAT parameters and this effect is also independent of statin therapy. This finding may suggest that EAT is an independent marker, rather than surrogate of cardiovascular risk.