Short-term vascular responses to spring and fall daylight savings time shifts.

Daylight saving time (DST) is a Western biannual time transition, setting the clock back 1 h in the fall and forward 1 h in the spring. There is an epidemiological link between DST and acute myocardial infarction risk in the first week following the spring shift; however, the mechanisms underlying the effect of DST on cardiovascular function remain unclear. The purpose of this study was to explore the short-term cardiovascular changes induced by fall and spring shifts in DST in a convenience sample of healthy adults. We hypothesized that spring, but not fall, DST shifts would acutely increase central pulse wave velocity, the gold standard measurement of central arterial stiffness. Twenty-one individuals (fall: n = 10; spring: n = 11) participated in four visits, occurring 1 wk before and at +1, +3, and +5 days after spring and fall time transitions. Central, brachial, and radial pulse wave velocity as well as carotid augmentation index were assessed with applanation tonometry. Sleep quality and memory function were assessed via questionnaire and the Mnemonic Similarities Task, respectively. Neither fall or spring transition resulted in changes to cardiovascular variables (carotid-femoral pulse wave velocity, carotid-brachial pulse wave velocity, carotid-radial pulse wave velocity, heart rate, mean arterial pressure, or augmentation index), sleep quality, or cognitive function (all P > 0.05). Our findings do not provide evidence that DST shifts influence cardiovascular outcomes in healthy adults. This study emphasizes the need for further research to determine the mechanisms of increased cardiovascular disease risk with DST that help explain epidemiological trends.NEW & NOTEWORTHY The debate of whether to abolish daylight savings time (DST) is, in part, motivated by the population-level increase in all-cause mortality and incidence of cardiovascular events following DST; however, there is an absence of data to support a physiological basis for risk. We found no changes in pulse wave velocity or augmentation index during the subacute window of DST. Large multisite trials are necessary to address the small, but meaningful, effects brought on by a societal event.

Physiological basis for longitudinal motion of the arterial wall.

As opposed to arterial distension in the radial plane, longitudinal wall motion (LWM) is a multiphasic and bidirectional displacement of the arterial wall in the anterograde (i.e., in the direction of blood flow) and retrograde (i.e., opposing direction of blood flow) directions. Although initially disregarded as imaging artifact, LWM has been consistently reported in ultrasound investigations in the past decade and is reproducible beat-to-beat, albeit with large interindividual variability across healthy and diseased populations. Emerging literature has sought to examine the mechanistic control of LWM to explain the shape and variability of the motion pattern but lacks considerations for key foundational vascular principles at the level of the arterial wall ultrastructure. The purpose of this review is to summarize the potential factors that underpin the causes and control of arterial LWM, spanning considerations from the arterial extracellular matrix to systems-level integrative theories. First, an overview of LWM and relevant aspects wall composition will be discussed, including major features of the multiphasic pattern, arterial wall extracellular components, tunica fiber orientations, and arterial longitudinal prestretch. Second, current theories on the systems-level physiological mechanisms driving LWM will be discussed in the context of available evidence including experimental human research, porcine studies, and mathematical models. Throughout, we discuss implications of these observations with suggestions for future priority research areas.

Seated Elliptical Exercise, But Not Periodic Standing, Alleviates Sitting-Induced Changes to Arterial Wave Reflections.

PURPOSE: Sedentary behavior may contribute to increased central wave reflection due to associated peripheral vasoconstriction, yet its impact on central hemodynamics and the mitigating effects of interventional strategies have not been thoroughly investigated. We tested whether standing or seated elliptical breaks alleviate the deleterious effects of prolonged sitting on central wave reflections. METHODS: Eighteen healthy adults (9 9 females, 25 ± 3 yr) completed three 3-h protocols on separate days: uninterrupted sitting, sitting with periodic standing, and sitting with periodic seated elliptical activity. Central wave reflection, central pulse wave velocity, and lower-limb pulse wave velocity were measured before and after each intervention. RESULTS: Central relative wave reflection magnitude (RM) increased during sitting (0.31 ± 0.05 to 0.35 ± 0.05; P < 0.01) but did not change after standing (0.30 ± 0.05 to 0.32 ± 0.04; P = 0.19) or elliptical protocols (0.30 ± 0.05 to 0.30 ± 0.04; P > 0.99). The change in RM during prolonged sitting (ΔRM) was attenuated with elliptical activity (0.04 ± 0.05 vs 0.00 ± 0.03; P = 0.02) but not with periodic standing (0.04 ± 0.04 vs 0.02 ± 0.05; P = 0.54). In addition, augmentation index and central pulse wave velocity increased after sitting (both P < 0.01) and periodic standing (both P < 0.01) but were unchanged after elliptical activity. Lower limb pulse wave velocity did not change after sitting ( P = 0.73) or standing ( P = 0.21) but did decrease after elliptical activity ( P = 0.03). CONCLUSIONS: Prolonged sitting without interruptions increased central wave reflection, whereas elliptical but not standing interruptions were able to ameliorate multiple sitting-induced vascular consequences. More work is required to examine the long-term effectiveness of interruption strategies, as well as the optimal type, frequency, and duration for reducing vascular risk associated with sedentary behaviors.

The influence of physical activity and sex on carotid artery longitudinal wall motion in younger healthy adults.

Carotid artery longitudinal wall motion (CALM) is a novel preclinical marker for atherosclerosis that describes the axial anterograde and retrograde motion of the intima-media complex. While regular physical activity and sex are known to independently influence arterial stiffness, their roles on axial arterial wall behaviour are unknown. The purpose of this study is to examine whether physical activity and sex impact CALM. We hypothesized that CALM retrograde displacement and total amplitude would be greater in females and active individuals, as a function of arterial stiffness. Fifty-seven young healthy adults (30 females; aged 22 ± 3 years) were evaluated for CALM outcomes and arterial stiffness and grouped by physical activity based on active (V̇O2 = 44.2 ± 8.9 mL/kg/min) or sedentary (V̇O2 = 33.7 ± 6.7 mL/kg/min) lifestyles defined by the Canadian 24-Hour Movement Guidelines. Arterial stiffness and CALM were measured by carotid-femoral pulse wave velocity (cfPWV) and vascular ultrasound at the right common carotid artery with speckle tracking analysis, respectively. cfPWV was greater in males (p < 0.01) with no interaction between sex and physical activity (p = 0.90). CALM anterograde displacement was greater in males (p = 0.03) resulting in a forward shift in total CALM pattern, which became less prominent when controlling for mean arterial pressure (p = 0.06). All other CALM outcomes were not different between activity and sex. V̇O2max was not correlated to any CALM outcome (all p > 0.05). Apparent sex differences in vascular function extend to novel CALM outcomes but may be confounded by blood pressure. We recommend sex-balanced design and reporting in future studies due to possible anterograde-shifted CALM patterns in healthy males.

The influence of respiration, neck flexion, and arterial segment on carotid artery longitudinal wall motion.

Although carotid artery longitudinal wall motion (CALM) has been highly detailed in cross-sectional studies, there is little evidence to explain population interindividual variability. This study was conducted to investigate how common external factors impact CALM. Twenty-one young healthy adults (11 females, aged 22 ± 2 yr) underwent three within-subject protocols. To evaluate probe positioning, vascular ultrasound was performed at a proximal and distal location along the common carotid artery. To evaluate neck angle, scans were acquired with the neck positioned at 70°, 90°, maximum extension (112 ± 9°), and maximum flexion (51 ± 7°). For the respiratory cycle condition, scans were taken during 7 s of inhalation, 7 s of exhalation, and 7 s of breath hold. CALM was evaluated for anterograde, retrograde, and maximum displacements, as well as radial-axial displacement. CALM was greater at proximal versus distal locations (retrograde = 1.14 ± 0.62 vs. 0.63 ± 0.24 mm, maximal = 1.32 ± 0.59 vs. 0.73 ± 0.24 mm; all P < 0.05). Minimum neck angles had greater motion than maximum angles (maximum displacement = 1.03 ± 0.43 vs. 0.77 ± 0.23 mm, P < 0.05). Without correcting breathing bias, retrograde displacement was greater during inspiration versus expiration (1.06 ± 0.34 vs. 0.58 ± 0.24 mm) and breath hold (1.06 ± 0.34 vs. 0.58 ± 0.24 mm), diastolic CALM was greater during expiration versus breath hold (1.10 ± 0.44 vs. 0.76 ± 0.33 mm), and maximum CALM was smaller during breath hold versus expiration (0.89 ± 0.31 vs. 1.21 ± 0.39 mm) and inspiration (0.89 ± 0.31 vs. 1.41 ± 0.70 mm). We recommend scanning 1-2 cm proximal to the carotid bifurcation, maintaining a neutral neck angle (70°-90°) for optimal CALM data collection in humans.NEW & NOTEWORTHY Carotid artery longitudinal wall motion (CALM) provides unique cardiovascular health information, yet a standardized approach to measurement is nonexistent. We tested CALM during manipulation of common external factors including probe position, neck angle, and breathing. All three conditions were found to alter CALM with drift in the breathing condition correctable by use of a linear bias correction. Consistent techniques should be used in CALM acquisition to reduce variability between individuals and population groups.

Heating-induced peripheral limb microvascular vasodilation reduces arterial wave reflection.

Arterial wave reflection augments cardiac afterload increasing myocardial demands. Mathematical models and comparative physiology suggest that the lower limbs are the primary source of reflected waves; however, in vivo human evidence corroborating these observations is lacking. This study was designed to determine whether the vasculature of the lower or upper limbs contributes more to wave reflection. We hypothesized that lower limb heating will result in larger reductions in central wave reflection compared with upper limb heating due to local vasodilation of a larger microvascular bed. Fifteen healthy adults (8 females, 24 ± 3.6 yr) completed a within-subjects experimental crossover protocol with a washout period. The right upper and lower limbs were heated in a randomized order using 38°C water-perfused tubing with a 30-min break between protocols. Central wave reflection was calculated using pressure-flow relationships derived from aortic blood flow and carotid arterial pressure at baseline and after 30 min of heating. We observed a main effect of time for reflected wave amplitude (12.8 ± 2.7 to 12.2 ± 2.6 mmHg; P = 0.03) and augmentation index (-7.5 ± 8.9% to -4.5 ± 9.1%; P = 0.03). No significant main effects or interactions were noted for forward wave amplitude, reflected wave arrival time, or central relative wave reflection magnitude (all P values >0.23). Unilateral limb heating reduced reflected wave amplitude; however, the lack of a difference between conditions does not support the hypothesis that the lower limbs are the primary source of reflection. Future investigations should consider alternative vascular beds, such as splanchnic circulation.NEW & NOTEWORTHY Lower limb contributions to central wave reflections have been theorized without direct evidence in humans. In this study, mild passive heating was used to locally vasodilate either the right arm or leg to control local wave reflection sites. Heating in general reduced the reflected wave amplitude, but there were no differences between the arm or leg heating intervention, failing to provide support for the lower limbs as a primary contributor to wave reflection in humans.