How do we teach simulation-based dental education? Time for an evidence-based, best-practice framework.

Historically, simulation-based dental education was taught using practical skills and the action of doing. An increased awareness of the importance of patient safety in healthcare education and delivery has seen considerable advances in the application of simulation-based education across several healthcare disciplines including medicine, nursing and anaesthetics. Dental simulation-based education requires improved standards of best-practice, and evidence-based, curriculum design that is based on theoretical frameworks, conceptual frameworks and educational theories. In this commentary, we explore the educational theory and the development of healthcare simulation, including internationally recognised standards of best practice and the simulation-based activity cycle. Given simulation-based education should be fit-for purpose, the components of these standards are examined within the specific context of dental education. We propose an evidence-based, best-practice framework that can be applied in the design and delivery of contemporary simulation-based dental curriculum.

Association between magnesium intake and risk of colorectal cancer among postmenopausal women.

PURPOSE: Data relating to magnesium intake and colorectal cancer (CRC) risk in postmenopausal women are incomplete. We investigated the association between total magnesium intake and the risk of CRC in an ethnically diverse cohort of postmenopausal women enrolled in the Women's Health Initiative. METHODS: Self-reported dietary and supplemental magnesium were combined to form total magnesium intake. Invasive incident CRC was the primary outcome. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CI). RESULTS: During an average follow-up of 13 years (1,832,319 person-years), of the 140,601 women included for analysis, 2,381 women were diagnosed with CRC (1,982 colon cancer and 438 rectal cancer). After adjustment for potential confounding variables, an inverse association was observed in the highest quintile of total magnesium intake compared to the lowest quintile for risk of CRC (HR 0.79, 95% CI 0.67, 0.94, p trend < 0.0001) and colon cancer (HR 0.80, 95% CI 0.66, 0.97, p trend < 0.0001). A borderline significant inverse association was detected in the highest versus the lowest quintile of total magnesium intake for rectal cancer (HR 0.76, 95% CI 0.51, 1.13, p trend < 0.001). CONCLUSIONS: Findings from this study support the hypothesis that magnesium intake around 400 mg/day from both dietary and supplemental sources is associated with a lower incidence of CRC in postmenopausal women.

Antioxidant vitamin C prevents decline in endothelial function during sitting.

BACKGROUND: This study was designed to test the hypothesis that antioxidant Vitamin C prevents the impairment of endothelial function during prolonged sitting. MATERIAL AND METHODS: Eleven men (24.2 ± 4.4 yrs) participated in 2 randomized 3-h sitting trials. In the sitting without vitamin C (SIT) and the sitting with vitamin C (VIT) trial, participants were seated for 3 h without moving their legs. Additionally, in the VIT trial, participants ingested 2 vitamin C tablets (1 g and 500 mg) at 30 min and 1 h 30 min, respectively. Superficial femoral artery (SFA) flow-mediated dilation (FMD) was measured hourly for 3 h. RESULTS: By a 1-way ANOVA, there was a significant decline in FMD during 3 h of SIT (p<0.001). Simultaneously, there was a significant decline in antegrade (p=0.04) and mean (0.037) shear rates. For the SIT and VIT trials by a 2-way (trial x time) repeated measures ANOVA, there was a significant interaction (p=0.001). Pairwise testing revealed significant between-SFA FMD in the SIT and VIT trial at each hour after baseline, showing that VIT prevented the decline in FMD 1 h (p=0.009), 2 h (p=0.016), and 3 h (p=0.004). There was no difference in the shear rates between SIT and VIT trials (p>0.05). CONCLUSIONS: Three hours of sitting resulted in impaired SFA FMD. Antioxidant Vitamin C prevented the decline in SFA FMD, suggesting that oxidative stress may contribute to the impairment in endothelial function during sitting.

Brachial artery endothelial function is stable across the morning in young men.

BACKGROUND: The morning hours are associated with increased cardiovascular (CV) risk, and vascular endothelial function (VEF) is a strong predictor of CV disease. A diurnal rhythm in VEF has been established but the morning variation in VEF is not well-documented. Thus, we tested if VEF is impaired across the vulnerable morning period. METHODS: After overnight fasts, eight healthy men (age 26.3 ± 3 yr) underwent assessments of VEF under standardized testing conditions every 2 h from 0700 to 1300 h on two separate days. VEF was estimated following 5 min brachial artery occlusions by hyperemic flow-mediated dilation (FMD). RESULTS: There was no significant change in FMD or hyperemic shear stimulus across the 6 h vulnerable period on either day, despite changes in physical activity and meals across these periods. CONCLUSION: In this healthy group of young men, VEF is stable across the vulnerable morning period when typical behaviors occurred (breakfast and physical activity). Future research should focus on the roles of sleep, physical inactivity during sleep and endogenous circadian rhythm in VEF.

Differences in brachial and femoral artery responses to prolonged sitting.

INTRODUCTION: It is unknown if there are limb differences in vascular function during prolonged sitting. PURPOSE: This study was designed to test whether the effects of prolonged sitting on brachial artery (BA) and the superficial femoral artery (SFA) are similar. METHODS: Twelve men (24.2 ± 4 yrs.) participated in a 3 hr prolonged sitting trial (SIT). SFA and BA flow mediated dilation (FMD) and respective flow patterns were measured at baseline, 1 hr, 2 hr and 3 hr. RESULTS: By a one-way ANOVA there was a significant decline in SFA FMD during 3 hrs of SIT (p < 0.001). Simultaneously, there was a significant decline in antegrade (p = 0.04) and mean (0.037) shear rates. By a one way ANOVA there were no significant differences in BA FMD during 3 hrs of sitting. There were no changes in the shear rates in the BA except for a significant decrease in antegrade shear rate (p = 0.029) and a significant increase in oscillatory shear index (p = 0.034) during 3 hrs of sitting. Furthermore, there was no correlation between BA and SFA FMD measurements. CONCLUSION: Three hours of sitting resulted in impaired SFA FMD but not BA FMD. Although 3 hours of sitting did not impair BA FMD, it impaired shear patterns in the BA.

Sitting and endothelial dysfunction: the role of shear stress.

Sedentary activity is a modifiable life-style behavior and a key component in the etiology of atherosclerotic cardiovascular disease (ACVD). US adults and children spend more than half their waking time in sedentary pursuits. Sedentary activity has been shown to result in impaired insulin sensitivity, impaired metabolic function and attenuated endothelial function, which are classic markers of ACVD. Sedentary activity is defined as 'sitting without otherwise being active.' This behavior promotes reduced muscular activity of the lower extremities which decreases leg blood flow, increases blood pooling in the calf, augments mean arterial pressure, and deforms arterial segments resulting in low mean shear stress (SS). SS activates distinct physiological mechanisms which have been proposed to be protective against ACVD; specifically through a SS-induced endothelium-derived nitric oxide mechanism. Reduced bioavailability of nitric oxide creates a pro-oxidant milieu resulting in increased oxidative stress. There is sufficient evidence which demonstrates that endothelial function is attenuated in the presence of oxidative stress. Sedentary activity results in low SS in the lower extremities which may result in increased oxidative stress and impaired endothelial function. This review furthers the use of sitting as model to study the effects of inactivity, discusses possible physiological mechanisms and suggests future directions.

Brachial artery flow-mediated dilation following exercise with augmented oscillatory and retrograde shear rate.

BACKGROUND: Acute doses of elevated retrograde shear rate (SR) appear to be detrimental to endothelial function in resting humans. However, retrograde shear increases during moderate intensity exercise which also enhances post-exercise endothelial function. Since SR patterns differ with the modality of exercise, it is important to determine if augmented retrograde SR during exercise influences post-exercise endothelial function. This study tested the hypothesis that (1) increased doses of retrograde SR in the brachial artery during lower body supine cycle ergometer exercise would attenuate post-exercise flow-mediated dilation (FMD) in a dose-dependent manner, and (2) antioxidant vitamin C supplementation would prevent the attenuated post-exercise FMD response. METHODS: Twelve men participated in four randomized exercise sessions (90 W for 20 minutes) on separate days. During three of the sessions, one arm was subjected to increased oscillatory and retrograde SR using three different forearm cuff pressures (20, 40, 60 mmHg) (contralateral arm served as the control) and subjects ingested placebo capsules prior to exercise. A fourth session with 60 mmHg cuff pressure was performed with 1 g of vitamin C ingested prior to the session. RESULTS: Post-exercise FMD following the placebo conditions were lower in the cuffed arm versus the control arm (arm main effect: P < 0.05) and without differences between cuff pressures (20 mmHg: 5.7 ± 2.2%; 40 mmHg: 4.7 ± 1.3%; 60 mmHg: 5.4 ± 2.4%) (P > 0.05). Following vitamin C treatment, post-exercise FMD in the cuffed and control arm increased from baseline (P < 0.05) but were not different (control: 7.1 ± 3.5% vs. cuffed: 6.6 ± 3.3%) (P > 0.05). CONCLUSIONS: These results indicate that augmented oscillatory and retrograde SR in non-working limbs during lower body exercise attenuates post-exercise FMD without an evident dose-response in the range of cuff pressures evaluated. Vitamin C supplementation prevented the attenuation of FMD following exercise with augmented oscillatory and retrograde SR suggesting that oxidative stress contributes to the adverse effects of oscillatory and retrograde shear during exercise on FMD.

The exercise dose affects oxidative stress and brachial artery flow-mediated dilation in trained men.

The aim of this investigation was to establish whether changes in oxidative stress and endothelial function following acute aerobic exercise are dose-dependent. Ten healthy trained men completed four exercise sessions: 50% VO(2peak) for 30 min (moderate intensity moderate duration, MIMD), 50% VO(2peak) for 60 min (moderate intensity long duration, MILD), 80% VO(2peak) for 30 min (high intensity moderate duration, HIMD), and 80% VO(2peak) for the time to reach the caloric equivalent of MIMD (high intensity short duration, HISD). Thiobarbituric acid reactive substances (TBARS) were measured as an index of oxidative stress and brachial artery flow-mediated dilation (FMD) was assessed as an index of endothelial function. Variables were measured at baseline, immediately post-exercise, 1 and 2 h post-exercise. Both HIMD (14.2 ± 2.5 µmol/L) and HISD (14.7 ± 1.9 µmol/L) TBARS differed from MIMD (11.8 ± 1.5 µmol/L) immediately post-exercise. TBARS increased from pre to immediately post-exercise for HIMD (12.6 ± 2.1 vs.14.2 ± 2.5 µmol/L) and HISD (12.3 ± 2.8 vs. 14.7 ± 1.9 µmol/L). Both MIMD (7.2 ± 2.2%) and HISD (7.6 ± 2.7%) FMD immediately post-exercise were greater than HIMD (4.7 ± 2.2%). An increase of FMD from pre to immediately post-exercise was found for MIMD (5.0 ± 2.5 vs. 7.2 ± 2.2%) and HISD (5.9 ± 2.4 vs. 7.6 ± 2.7%). These data suggest that acute exercise-induced TBARS are exercise intensity-dependent whereas FMD appears to improve following energy expenditure equivalent to 30 min 50% VO(2peak), regardless of intensity or duration.

Mechanotransduction of shear in the endothelium: basic studies and clinical implications.

The endothelium plays an integral role in the development and progression of atherosclerosis. Hemodynamic forces, particularly shear stress, have a powerful influence on endothelial phenotype and function; however, there is no clear consensus on how endothelial cells sense shear. Nevertheless, multiple endothelial cell signal transduction pathways are activated when exposed to shear stress in vitro. The type of shear, laminar or oscillatory, impacts which signal transduction pathways are initiated as well as which subsequent genes are up- or down-regulated, thereby influencing endothelial phenotype and function. Recently, human studies have examined the impact of shear stress and different shear patterns at rest and during exercise on endothelial function. Current evidence supports the theory that augmented exercise-induced shear stress contributes to improved endothelial function following acute exercise and exercise training, whereas retrograde shear initiates vascular dysfunction. The purpose of this review is to examine the current theories on how endothelial cells sense shear stress, to provide an overview on shear stress-induced signal transduction pathways and subsequent gene expression, and to review the current literature pertaining to shear stress and shear patterns at rest as well as during exercise in humans and the related effects on endothelial function.

Health-related fitness and physical activity in patients with nonalcoholic fatty liver disease.

UNLABELLED: Nonalcoholic fatty liver disease (NAFLD) has been referred to as the hepatic manifestation of the metabolic syndrome. There is a lower prevalence of metabolic syndrome in individuals with higher health-related fitness (HRF) and physical activity (PA) participation. The relationship between NAFLD severity and HRF or PA is unknown. Our aim was to compare measures of HRF and PA in patients with a histological spectrum of NAFLD severity. Thirty-seven patients with liver biopsy-confirmed NAFLD (18 women/19 men; age = 45.9 +/- 12.7 years) completed assessment of cardiorespiratory fitness (CRF, VO(2peak)), muscle strength (quadriceps peak torque), body composition (%fat), and PA (current and historical questionnaire). Liver histology was used to classify severity by steatosis (mild, moderate, severe), fibrosis stage (stage 1 versus stage 2/3), necroinflammatory activity (NAFLD Activity Score; or=5 NAS2) and diagnosis of NASH by Brunt criteria (NASH versus NotNASH). Analysis of variance and independent t tests were used to determine the differences among groups. Fewer than 20% of patients met recommended guidelines for PA, and 97.3% were classified at increased risk of morbidity and mortality by %fat. No differences were detected in VO(2peak) (x = 26.8 +/- 7.4 mL/g/min) or %fat (x = 38.6 +/- 8.2%) among the steatosis or fibrosis groups. Peak VO(2) was significantly higher in NAS1 versus NAS2 (30.4 +/- 8.2 versus 24.4 +/- 5.7 mL/kg/min, P = 0.013) and NotNASH versus NASH (34.0 +/- 9.5 versus 25.1 +/- 5.7 mL/kg/min, P = 0.048). CONCLUSION: Patients with NAFLD of differing histological severity have suboptimal HRF. Lifestyle interventions to improve HRF and PA may be beneficial in reducing the associated risk factors and preventing progression of NAFLD.

Adjusting flow-mediated dilation for shear stress stimulus allows demonstration of endothelial dysfunction in a population with moderate cardiovascular risk.

BACKGROUND/AIMS: Although normalization of brachial artery flow-mediated dilation (FMD) to individual shear stress (FMD:shear stress ratio) has been proposed to improve this measure of endothelial function, the clinical utility of FMD normalization has not yet been demonstrated. We tested (1) whether following conventional 5-min forearm occlusion, the FMD:shear stress ratio would discriminate a population with moderate cardiovascular risk (MR) from a low-risk (LR) population, and (2) whether the dose-response profile relating shear stress to FMD would be different between the 2 populations. METHODS: Five different magnitudes of reactive hyperemia-induced shear stress were applied to 20 MR and 20 LR subjects by manipulating forearm cuff occlusion duration. Brachial artery diameters and velocities were measured via high-resolution ultrasound. To quantify the hyperemic stimulus, shear stress area under the curve was individually calculated for the duration of time-to-peak dilation. RESULTS: Following 5-min of forearm occlusion, FMD:shear stress ratio (p = 0.041), but not FMD (p = 0.286), discriminated MR from LR. The slope of the shear stress-FMD regression line was lower in MR compared to the LR (p < 0.001). CONCLUSION: The FMD:shear stress ratio distinguished reduced endothelial function in a population with MR. The dose-response profile of the shear stress-FMD relationship appears to differ between populations of distinct cardiovascular risk.

Normalization of flow-mediated dilation to shear stress area under the curve eliminates the impact of variable hyperemic stimulus.

BACKGROUND: Normalization of brachial artery flow-mediated dilation (FMD) to individual shear stress area under the curve (peak FMD:SSAUC ratio) has recently been proposed as an approach to control for the large inter-subject variability in reactive hyperemia-induced shear stress; however, the adoption of this approach among researchers has been slow. The present study was designed to further examine the efficacy of FMD normalization to shear stress in reducing measurement variability. METHODS: Five different magnitudes of reactive hyperemia-induced shear stress were applied to 20 healthy, physically active young adults (25.3 +/- 0. 6 yrs; 10 men, 10 women) by manipulating forearm cuff occlusion duration: 1, 2, 3, 4, and 5 min, in a randomized order. A venous blood draw was performed for determination of baseline whole blood viscosity and hematocrit. The magnitude of occlusion-induced forearm ischemia was quantified by dual-wavelength near-infrared spectrometry (NIRS). Brachial artery diameters and velocities were obtained via high-resolution ultrasound. The SSAUC was individually calculated for the duration of time-to-peak dilation. RESULTS: One-way repeated measures ANOVA demonstrated distinct magnitudes of occlusion-induced ischemia (volume and peak), hyperemic shear stress, and peak FMD responses (all p < 0.0001) across forearm occlusion durations. Differences in peak FMD were abolished when normalizing FMD to SSAUC (p = 0.785). CONCLUSION: Our data confirm that normalization of FMD to SSAUC eliminates the influences of variable shear stress and solidifies the utility of FMD:SSAUC ratio as an index of endothelial function.

Reproducibility of the flow-mediated dilation response to acute exercise in overweight men.

Flow-mediated dilation (FMD) has been established as a reliable noninvasive measurement of endothelial function. The reproducibility of FMD under resting conditions has previously been reported; however, the reproducibility of FMD in response to exercise remains to be investigated. On two separate days, we determined if flow-mediated dilation is reproducible in response to acute exercise in nine overweight men. Following pre-exercise FMD measurements, subjects were asked to walk on a treadmill for 45 min at 50% of their VO(2)peak. Subsequently, FMD was measured immediately, and every hour for 3 h thereafter. Reproducibility of FMD following exercise was assessed utilizing: (1) a two-way analysis of variance (ANOVA), (2) Intraclass correlation coefficients (ICC), (3) Pearson correlations (r), and (4) coefficient of variation (CV %) and coefficient of variation prime (CV') for FMD at each time-period. Four acceptable reproducibility assessments were required to confirm FMD reproducibility in response to acute exercise. No differences (F(1,8) = .01; p = 0.942) in FMD were observed between trials collapsing for time. All the ICC(FMD) fell within the reproducible criterion set and are as follows: pre-exercise 0.602, immediately post 0.840, 1 h post 0.632, 2 h post 0.724 and 3 h post 0.631. The correlation and the average CV% for FMD between trials was 0.579% and 25.2%, respectively. The FMD response to an acute bout of moderate treadmill exercise appears to be as reproducible as FMD measured during resting conditions. The findings of the present study support the use of FMD as an outcome variable in response to acute exercise.

Can the measurement of brachial artery flow-mediated dilation be applied to the acute exercise model?

The measurement of flow-mediated dilation using high-resolution ultrasound has been utilized extensively in interventional trials evaluating the salutary effect of drugs and lifestyle modifications (i.e. diet or exercise training) on endothelial function; however, until recently researchers have not used flow-mediated dilation to examine the role of a single bout of exercise on vascular function. Utilizing the acute exercise model can be advantageous as it allows for an efficient manipulation of exercise variables (i.e. mode, intensity, duration, etc.) and permits greater experimental control of confounding variables. Given that the application of flow-mediated dilation in the acute exercise paradigm is expanding, the purpose of this review is to discuss methodological and physiological factors pertinent to flow-mediated dilation in the context of acute exercise. Although the scientific rationale for evaluating endothelial function in response to acute exercise is sound, few concerns warrant attention when interpreting flow-mediated dilation data following acute exercise. The following questions will be addressed in the present review: Does the measurement of flow-mediated dilation influence subsequent serial measures of flow-mediated dilation? Do we need to account for diurnal variation? Is there an optimal time to measure post-exercise flow-mediated dilation? Is the post-exercise flow-mediated dilation reproducible? How is flow-mediated dilation interpreted considering the hemodynamic and sympathetic changes associated with acute exercise? Can the measurement of endothelial-independent dilation affect the exercise? Evidence exists to support the methodological appropriateness for employing flow-mediated dilation in the acute exercise model; however, further research is warranted to clarify its interpretation following acute exercise.

Accumulation of physical activity leads to a greater blood pressure reduction than a single continuous session, in prehypertension.

BACKGROUND: Despite limited research, the accumulation of physical activity has been recommended for the treatment of prehypertension. OBJECTIVES: To compare the duration and magnitude of blood pressure reduction after accumulated physical activity with that after a single session of continuous physical activity, and to investigate sympathetic modulation as a possible mechanism for the reduction in blood pressure after each acute session. METHODS: Prehypertensive adults (n = 21) participated in a randomized crossover design. Ambulatory blood pressure and heart rate variability (Holter monitoring) were measured for 12 h after accumulated physical activity (4 x 10-min walks (1/h for 4 h) at 50% of VO2peak), continuous physical activity (40-min walk at 50% of VO2peak) and control treatments. Blood pressure and heart rate variability after each activity treatment were compared with the respective periods from the control treatment. Heart rate variability was correlated with reduction in blood pressure. RESULTS: Systolic blood pressure (SBP) was reduced for 11 h after accumulated physical activity (P < 0.01), and for 7 h after continuous physical activity (P < 0.05). Diastolic blood pressure (DBP) was reduced for 10 h after accumulated physical activity (P < 0.05) and for 7 h after continuous physical activity (P < 0.05). With accumulated physical activity, the differences in normalized low-frequency (r = 0.517, P < 0.01) and high-frequency (r = -0.503, P < 0.05) power were correlated with reduction in SBP and the differences in normalized low-frequency (r = 0.745, P < 0.001), high-frequency (r = -0.738, P < 0.001) powers, and low frequency: high frequency ratio (r = 0.756, P < 0.001) were correlated with reduction in DBP. With continuous physical activity, the difference in low frequency: high frequency ratio (r = 0.543, P < 0.05) was correlated with reduction in DBP. CONCLUSION: The accumulation of physical activity appears to be more effective than a single continuous session in the management of prehypertension. Sympathetic modulation was associated with reduced blood pressure after each session.

H-reflex and motor responses to acute ischemia in apparently healthy individuals.

The authors examined the effect of acute ischemia on peripheral nerve function in healthy subjects. It was hypothesized that acute ischemia would interfere with the ability of sensory and motor nerves to propagate an impulse. Twelve young, apparently healthy adults participated in the study. Soleus H-reflex and motor recruitment curves were determined for subjects during a control condition, after 5 minutes of ischemia by femoral artery occlusion, and after a 5-minute recovery. During ischemia, the stimulus intensity required to evoke an H-reflex or M-wave was reduced by 18.3% and 18.4%, respectively. Hmax/Mmax ratios were significantly reduced with acute ischemia (mean +/- standard error) 66.29% +/- 5.4% and 58.81% +/- 6.7% for control and ischemia, respectively, owing to a decrease in Hmax during acute ischemia with no change in Mmax. After ischemia, the Hmax/Mmax returned to control values, as did the M-threshold. However, although the H-threshold slightly recovered, it failed to return to control threshold after 5 minutes of recovery. The results suggest that acute ischemia decreases motor and H-reflex thresholds in healthy individuals with a longer lasting effect for the H-reflex. In addition, a decrease in Hmax/Mmax ratio was observed, suggesting that acute ischemia has differential effects on sensory nerve propagation and synapse transmission.

Accumulation of physical activity reduces blood pressure in pre- and hypertension.

PURPOSE: The effectiveness of lifestyle physical activity to reduce BP in prehypertension/hypertension is unclear. The purpose of this study was: 1) to investigate the magnitude and duration of ambulatory BP (AmBP) reduction after the accumulation of one day of lifestyle physical activity (PAaccum) in normotension, prehypertension, and hypertension; and 2) to determine the relationship between energy expenditure (EE) and BP reduction. METHODS: Subjects were eight normotensive (112.3/73.1 +/- 1.6/1.9 mm Hg), 10 prehypertensive (124.3/79.3 +/- 1.2/1.6 mm Hg), and 10 hypertensive (139.7/83.3 +/- 3.7/3.7 mm Hg) adults. EE was analyzed during the PA and corresponding control (C) treatment; AmBP was analyzed for 12 h after the PAaccum and corresponding C. EE of the PA (EEPA) was calculated as the total EE for the duration of the PA. Steps to analyze and compare the BP reduction after PAaccum were: 1) determination of the duration of the BP reduction (95% CI), 2) determination of the magnitude of the BP reduction (paired t-tests of C vs PA), 3) determination of the area of the BP reduction, and 4) comparison of the areas (independent t-test) between prehypertension and hypertension. Correlation between EE(PA-C) and BP reduction was examined RESULTS: No BP differences were found for normotension or for DBP in any group. Significant difference in SBP after the PAaccum were found for prehypertensives (magnitude; area = 6.6 +/- 2.3 mm Hg; 21.7 +/- 15.2 mm Hg x h(-1)) for 6 h and for hypertensives (12.9 +/- 4.3 mm Hg; 123.4 + 42.8 mm Hg x h(-1)) for 8 h; area was significantly different between groups. No correlation was found between EE(PA-C) and BP reduction. CONCLUSION: The PAaccum reduces SBP in hypertension and prehypertension but does not appear to be related to the EE(PA-C). PAaccum can be utilized as an approach to treat prehypertension and hypertension.

Time of day to monitor ambulatory blood pressure affects the outcome.

OBJECTIVES: The reproducibility of blood pressure variables from ambulatory blood pressure monitoring (AMBP) initiated at the same time of day (SAME: 1700-1900 h) was compared with the reproducibility of blood pressure variables when monitoring was initiated at opposite times of day (OPP: randomized, morning=0700-0900 h and evening=1700-1900 h). It was hypothesized that the reproducibility for SAME (n=18) would be no different than the reproducibility for OPP (n=13). METHODS: The order of AMBP sessions was randomized. The Accutracker II was used to determine average blood pressures, Crest (CrBP), Trough (TrBP), and TrBP : CrBP ratio; Averages were divided into 24-h, daytime (0600-2200 h), and night-time (2200-0600 h) for both systolic and diastolic blood pressures. A paired t-test with an intraclass correlation was used to determine the reproducibility of AMBP for both SAME and OPP. A chi-square was used to compare the distribution of reproducible AMBP variables between SAME and OPP. Significance was at P<0.05. RESULTS: The reproducibility of AMBP variables for SAME and OPP was a significantly different for systolic blood pressure. All of the ambulatory systolic variables measured in the SAME group were reproducible except for the TrBP : CrBP, whereas only the systolic night-time averages of the OPP group were reproducible. Similarly all of the ambulatory diastolic variables measured in the SAME group were reproducible except for TrBP : CrBP, whereas 24-h, night-time averages, and TrBP were reproducible in the OPP group. CONCLUSIONS: Ambulatory blood pressure variables were consistently higher when the monitoring session began in the morning hours.

Effect of prolonged sitting and breaks in sitting time on endothelial function.

UNLABELLED: Sitting time (ST) is associated with cardiovascular disease risk factors, whereas breaking ST has been reported to be beneficial for reducing cardiovascular risk. PURPOSE: The objective of this study is to examine the effects of breaking ST on superficial femoral artery (SFA) endothelial function. HYPOTHESES: 1) Prolonged sitting would induce endothelial dysfunction and changes in shear forces, and 2) breaking ST with brief periods of activity would prevent attenuation in endothelial function. METHODS: Twelve nonobese men (24.2 ± 4.2 yr) participated in two randomized 3-h sitting trials. In the sitting (SIT) trial, subjects were seated on a firmly cushioned chair for 3 h without moving their lower extremities. In the breaking ST trial (ACT), subjects sat similar to the SIT trial but walked on a treadmill for 5 min at 2 mph at 30 min, 1 h 30 min, and 2 h 30 min during the sitting interval. SFA flow-mediated dilation (FMD) was assessed at baseline, 1 h, 2 h, and 3 h in each trial. Statistical analyses were performed using dependent variables SFA FMD and shear rates. Significance was set at P ≤ 0.05. RESULTS: In the SIT trial, there was a significant decline in SFA FMD from baseline to 3 h (baseline, 4.72% ± 3.78%; 1 h, 0.52% ± 0.85%; 2 h, 1.66% ± 1.11%; 3 h, 2.2% ± 2.15; P < 0.05 by ANOVA) accompanied by a decline in mean shear rate and antegrade shear rate but no difference in shear rate (area under the curve). By two-way repeated-measures ANOVA, ACT prevented the sitting-induced decline in FMD (baseline, 4.5% ± 2.3%; 1 h, 5.04% ± 2.85%; 2 h, 5.28% ± 5.05%; 3 h, 6.9% ± 4.5%) along with no decline in shear rates. CONCLUSION: Three hours of sitting resulted in a significant impairment in shear rate and SFA FMD. When light activity breaks were introduced hourly during sitting, the decline in FMD was prevented.

Exercise in hypertension. A clinical review.

The current exercise prescription for the treatment of hypertension is: cardiovascular mode, for 20-60 minutes, 3-5 days per week, at 40-70% of maximum oxygen uptake (VO2(max)). Cardiovascular exercise training is the most effective mode of exercise in the prevention and treatment of hypertension. Resistance exercise is not the preferred mode of exercise treatment, but can be incorporated into an exercise regime provided the diastolic blood pressure response is within safe limits. It is inconclusive whether durations longer than 30 minutes produce significantly greater reductions in blood pressure. A frequency of three exercise sessions per week has been considered to be the minimal frequency for blood pressure reduction. Higher frequencies tended to produce greater reductions, although not significantly different. Evidence still exists that high intensity exercise (>75% VO2(max)) may not be as effective as low intensity exercise (<70% VO2(max)) in reducing elevated blood pressures. Exercise can be effective without a change in bodyweight or body fat. Bodyweight or body fat loss and anti-hypertensive medications do not have an added effect on blood pressure reduction associated with exercise. beta-blockade is not the recommended anti-hypertensive medication for effective exercise performance in non-cardiac patients. Not all hypertensive patients respond to exercise treatment. Differences in genetics and pathophysiology may be responsible for the inability of some hypertensive patients to respond to exercise. Ambulatory technology may allow advances in individualising a more effective exercise prescription for low-responders and non-responders.