Mechanical ventilation in a conscious male during exercise: A case report.

We recently explored the cardiopulmonary interactions during partial unloading of the respiratory muscles during exercise. Expanding upon this work, we present a noteworthy case study whereby we eliminated the influence of respiration on cardiac function in a conscious but mechanically ventilated human during exercise. This human was a young healthy endurance-trained male who was mechanically ventilated during semi-recumbent cycle exercise at 75 Watts (W) (~30% Wmax). During mechanically ventilated exercise, esophageal pressure was reduced to levels indistinguishable from the cardiac artefact which led to a 94% reduction in the work of breathing. The reduction in respiratory pressures and respiratory muscle work led to a decrease in cardiac output (-6%), which was due to a reduction in stroke volume (-13%), left ventricular end-diastolic volume (-15%) and left-ventricular end-systolic volume (-17%) that was not compensated for by heart rate. Our case highlights the influence of extreme mechanical ventilation on cardiac function while noting the possible presence of a maximal physiological limit to which respiration (and its associated pressures) impacts cardiac function when the work of breathing is maximally reduced.

Are Wearable Photoplethysmogram-Based Heart Rate Variability Measures Equivalent to Electrocardiogram? A Simulation Study.

BACKGROUND: Traditional electrocardiography (ECG)-derived heart rate variability (HRV) and photoplethysmography (PPG)-derived "HRV" (termed PRV) have been reported interchangeably. Any potential dissociation between HRV and PRV could be due to the variability in pulse arrival time (PAT; time between heartbeat and peripheral pulse). OBJECTIVE: This study examined if PRV is equivalent to ECG-derived HRV and if PRV's innate error makes it a high-quality measurement separate from HRV. METHODS: ECG data from 1084 subjects were obtained from the PhysioNet Autonomic Aging dataset, and individual PAT dispersions for both the wrist (n = 42) and finger (n = 49) were derived from Mol et al. (Exp Gerontol. 2020; 135: 110938). A Bayesian simulation was constructed whereby the individual arrival times of the PPG wave were calculated by placing a Gaussian prior on the individual QRS-wave timings of each ECG series. The standard deviation (σ) of the prior corresponds to the PAT dispersion from Mol et al. This was simulated 10,000 times for each PAT σ. The root mean square of successive differences (RMSSD) and standard deviation of N-N intervals (SDNN) were calculated for both HRV and PRV. The Region of Practical Equivalence bounds (ROPE) were set a priori at ± 0.2% of true HRV. The highest density interval (HDI) width, encompassing 95% of the posterior distribution, was calculated for each PAT σ. RESULTS: The lowest PAT σ (2.0 SD) corresponded to 88.4% within ROPE for SDNN and 21.4% for RMSSD. As the σ of PAT increases, the equivalence of PRV and HRV decreases for both SDNN and RMSSD. The HDI interval width increases with increasing PAT σ, with the HDI width increasing at a higher rate for RMSSD than SDNN. CONCLUSIONS: For individuals with greater PAT variability, PRV is not a surrogate for HRV. When considering PRV as a unique biometric measure, SDNN may have more favorable measurement properties than RMSSD, though both exhibit a non-uniform measurement error.

Characterization of internal jugular vein region-specific distension and flow patterns during progressive volume shifting.

Blood volume shifts during postural adjustment leads to irregular distension of the internal jugular vein (IJV). In microgravity, distension may contribute to flow stasis and thromboembolism, though the regional implications and associated risk remain unexplored. We characterized regional differences in IJV volume distension and flow complexity during progressive head-down tilt (HDT) (0°, -6°, -15°, -30°) using conventional ultrasound and vector flow imaging. We also evaluated low-pressure thigh cuffs (40 mmHg) as a fluid shifting countermeasure during -6° HDT. Total IJV volume expanded 139±95% from supine (4.6±2.7 mL) to -30° HDT (10.3±5.0 mL). Blood flow profiles had greater vector uniformity at the cranial IJV region (P<0.01) and became more dispersed with increasing tilt (P<0.01). Qualitatively, flow was more uniform throughout the IJV during its early flow cycle phase, and more disorganized during late flow phase. This disorganized flow was accentuated closer to the vessel wall, near the caudal region, and during greater HDT. Low-pressure thigh cuffs during -6° HDT decreased IJV volume at the cranial region (-12±15%; P<0.01) but not the caudal region (P=0.20), although flow uniformity was unchanged (both regions,P>0.25). We describe a distensible IJV accommodating large volume shifts along its length. Prominent flow dispersion was primarily found at the caudal region, suggesting multi-directional blood flow. Thigh cuffs appear effective for decreasing IJV volume but effects on flow complexity are minor. Flow complexity along the vessel length is likely related to IJV distension during chronic volume shifting and may be a precipitating factor for flow stasis and future thromboembolism risk.

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.

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.

Supramaximal Testing to Confirm the Achievement of V̇O 2max in Acute Hypoxia.

PURPOSE: We sought to determine if supramaximal exercise testing confirms the achievement of V̇O 2max in acute hypoxia. We hypothesized that the incremental and supramaximal V̇O 2 will be sufficiently similar in acute hypoxia. METHODS: Twenty-one healthy adults (males n = 13, females n = 8) completed incremental and supramaximal exercise tests in normoxia and acute hypoxia (fraction inspired oxygen = 0.14) separated by at least 48 h. Incremental exercise started at 80 and 60 W in normoxia and 40 and 20 W in hypoxia for males and females, respectively, with all increasing by 20 W each minute until volitional exhaustion. After a 20-min postexercise rest period, a supramaximal test at 110% peak power until volitional exhaustion was completed. RESULTS: Supramaximal exercise testing yielded a lower V̇O 2 than incremental testing in hypoxia (3.11 ± 0.78 vs 3.21 ± 0.83 L·min -1 , P = 0.001) and normoxia (3.71 ± 0.91 vs 3.80 ± 1.02 L·min -1 , P = 0.01). Incremental and supramaximal V̇O 2 were statistically similar, using investigator-determined equivalence bounds ±150 mL·min -1 , in hypoxia ( P = 0.02, 90% confidence interval [CI] = 0.05-0.14) and normoxia ( P = 0.03, 90% CI = 0.01-0.14). Likewise, using ±2.1 mL·kg -1 ·min -1 bounds, incremental and supramaximal V̇O 2 values were statistically similar in hypoxia ( P = 0.04, 90% CI = 0.70-2.0) and normoxia ( P = 0.04, 90% CI = 0.30-2.0). CONCLUSIONS: Despite differences in the oxygen cascade, incremental and supramaximal V̇O 2 values were statistically similar in both hypoxia and normoxia, demonstrating the utility of supramaximal verification of V̇O 2max in the setting of acute hypoxia.

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.

Supporting evidence for an "arterial pump" venous return mechanism in humans.

Blood flow in large veins is dependent on arterial-atrial pressure gradients and pumping mechanisms in concert with valve recruitment. Classic descriptions of muscle and respiratory pumps describe venous transmural pressure changes that cause flow. Not often considered is the transmission of pulsatile energy from arteries to veins directly adjacent to each other. Recently, an ex vivo study demonstrated a novel arterial pump effect in venoarterial bundles when valves were active in managing venous flow. We sought to show in vivo evidence of this arterial pump mechanism in 16 healthy young adults. Venous blood flow was measured in the venoarterial bundled deep femoral vein (DFV) and the greater saphenous vein (GSV), which is not bundled with an artery. Veins were studied through randomized body positions of -6° head-down tilt (HDT), supine, 20° head-up tilt (HUT), and 40° HUT, with the assumption that greater HUT postures increased valve dependence to observe the arterial pump effect. Between 20° and 40° HUT conditions, bundled DFV blood flow did not change (68 ± 36 vs. 71 ± 56 mL·min-1; Padj > 0.99), whereas nonbundled GSV blood flow decreased (6.1 ± 4.8 vs. 3.5 ± 3.9 mL·min-1; P = 0.01). Diameters between 20° and 40° HUT conditions increased in DFV (0.90 ± 0.16 vs. 1.04 ± 0.19 cm; P < 0.01), but not in GSV (0.33 ± 0.10 vs. 0.32 ± 0.08 cm; P = 0.60). These data support previous ex vivo observations that when venous pressure gradients rely on valve recruitment, presence of an adjacent artery may protect against further decreases in blood flow. The arterial pump mechanism is an underappreciated contributor to venous return and warrants further investigation.NEW & NOTEWORTHY Venous return mechanisms have classically considered muscle and respiratory pumps; however, recent ex vivo evidence suggests that pulsatile energy imparted from arteries to adjacent bundled veins can increase venous flow under certain driving pressures. We tested this concept in humans by manipulating hydrostatic pressures and measuring flow in bundled and nonbundled veins. The bundled vein exhibited flow preservation at the highest hydrostatic pressure. We suggest a novel conservation of energy mechanism within the circulatory system.

Attenuating intrathoracic pressure swings decreases cardiac output at different intensities of exercise.

Intrathoracic pressure (ITP) swings that permit spontaneous ventilation have physiological implications for the heart. We sought to determine the effect of respiration on cardiac output ( Q ̇ $\dot Q$ ) during semi-supine cycle exercise using a proportional assist ventilator to minimize ITP changes and lower the work of breathing (Wb ). Twenty-four participants (12 females) completed three exercise trials at 30%, 60% and 80% peak power (Wmax ) with unloaded (using a proportional assist ventilator, PAV) and spontaneous breathing. Intrathoracic and intraabdominal pressures were measured with balloon catheters placed in the oesophagus and stomach. Left ventricular (LV) volumes and Q ̇ $\dot Q$ were determined via echocardiography. Heart rate (HR) was measured with electrocardiogram and a customized metabolic cart measured oxygen uptake ( V ̇ O 2 ${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}}}$ ). Oesophageal pressure swings decreased from spontaneous to PAV breathing by -2.8 ± 3.1, -4.9 ± 5.7 and -8.1 ± 7.7 cmH2 O at 30%, 60% and 80% Wmax , respectively (P = 0.01). However, the decreases in Wb were similar across exercise intensities (27 ± 42 vs. 35 ± 24 vs. 41 ± 22%, respectively, P = 0.156). During PAV breathing compared to spontaneous breathing, Q ̇ $\dot Q$ decreased by -1.0 ± 1.3 vs. -1.4 ± 1.4 vs. -1.5 ± 1.9 l min-1 (all P < 0.05) and stroke volume decreased during PAV breathing by -11 ± 12 vs. -9 ± 10 vs. -7 ± 11 ml from spontaneous breathing at 30%, 60% and 80% Wmax , respectively (all P < 0.05). HR was lower during PAV breathing by -5 ± 4 beats min-1 at 80% Wmax (P < 0.0001). Oxygen uptake decreased by 100 ml min-1 during PAV breathing compared to spontaneous breathing at 80% Wmax (P < 0.0001). Overall, attenuating ITPs mitigated LV preload and ejection, thereby suggesting that the ITPs associated with spontaneous respiration impact cardiac function during exercise. KEY POINTS: Pulmonary ventilation is accomplished by alterations in intrathoracic pressure (ITP), which have physiological implications on the heart and dynamically influence the loading parameters of the heart. Proportional assist ventilation was used to attenuate ITP changes and decrease the work of breathing during exercise to examine its effects on left ventricular (LV) function. Proportional assist ventilation with progressive exercise intensities (30%, 60% and 80% Wmax ) led to reductions in cardiac output at all intensities, primarily through reductions in stroke volume. Decreases in LV end-diastolic volume (30% and 60% Wmax ) and increases in LV end-systolic volume (80% Wmax ) were responsible for the reduction in stroke volume. The relationship between cardiac output and oxygen uptake is disrupted during respiratory muscle unloading.

Deep-learning-assisted and GPU-accelerated vector Doppler imaging with aliasing-resistant velocity estimation.

Vector flow imaging is a diagnostic ultrasound modality that is suited for the visualization of complex blood flow dynamics. One popular way of realizing vector flow imaging at high frame rates over 1000 fps is to apply multi-angle vector Doppler estimation principles in conjunction with plane wave pulse-echo sensing. However, this approach is susceptible to flow vector estimation errors attributed to Doppler aliasing, which is prone to arise when a low pulse repetition frequency (PRF) is inevitably used due to the need for finer velocity resolution or because of hardware constraints. Existing dealiasing solutions tailored for vector Doppler may have high computational demand that makes them unfeasible for practical applications. In this paper, we present the use of deep learning and graphical processing unit (GPU) computing principles to devise a fast vector Doppler estimation framework that is resilient against aliasing artifacts. Our new framework works by using a convolutional neural network (CNN) to detect aliased regions in vector Doppler images and subsequently applying an aliasing correction algorithm only at these affected regions. The framework's CNN was trained using 15,000 in vivo vector Doppler frames acquired from the femoral and carotid arteries, including healthy and diseased conditions. Results show that our framework can perform aliasing segmentation with an average precision of 90 % and can render aliasing-free vector flow maps with real-time processing throughputs (25-100 fps). Overall, our new framework can improve the visualization quality of vector Doppler imaging in real-time.

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.

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.

Serum concentrations of ketones increase after hand-ergometer exercise in persons with cervical spinal cord injuries: a preliminary prospective study.

STUDY DESIGN: Experimental study. OBJECTIVES: To compare lipid profiles during moderate-intensity exercise between persons with cervical spinal cord injuries (SCIC) and able-bodied controls (AB). SETTING: Wakayama Medical University, Japan. METHODS: Six participants with SCIC and six AB performed 30-min arm-crank exercise at 50% VO2peak. Blood samples were collected before (PRE), immediately (POST), and 60 min after exercise (REC). Concentrations of serum free fatty acids ([FFA]s), total ketone bodies ([tKB]s), acetoacetic acid ([AcAc]s), insulin ([Ins]s), and plasma catecholamines and glucose ([Glc]p) were assessed. RESULTS: Catecholamine concentrations in SCIC were lower than AB throughout the experiment (P < 0.001) and remained unchanged, while increased at POST in AB (P < 0.01). [FFA]s remained unchanged in both groups with no differences between groups. [tKB]s in SCIC tended to increase at REC from PRE (P = 0.043), while remaining unchanged in AB (P > 0.42). [AcAc]s in SCIC increased at REC from PRE and POST (P < 0.01) while remaining unchanged in AB (interactions of Group × Time P = 0.014). [Glc]p and [Ins]s were comparable between the groups throughout the study. CONCLUSION: Serum ketone bodies in SCIC increased after exercise while remaining unchanged in AB, suggesting that suppressed uptakes of serum ketone bodies from blood to the muscles in SCIC would partially contribute the increased serum ketones.

Ambulatory Monitoring of Cerebrovascular Responses to Upright Posture and Walking in Older Adults With Heart Failure.

Background: Insufficient cardiac output in individuals with heart failure (HF) limits daily functioning and reduces quality of life. Although lower cerebral perfusion, secondary to limitations in cardiac output, has been observed during moderate-intensity efforts, individuals with HF also may be at risk for lower perfusion during even low-intensity ambulatory activities. Methods: We determined whether HF is associated with an altered cerebrovascular response to low-intensity activities representative of typical challenges of daily living. In this study, we monitored central hemodynamics and middle cerebral artery blood velocity (MCAv) and cerebral tissue oxygenation (near-infrared spectroscopy) in 10 individuals with HF (aged 78 ± 4 years; left ventricular ejection fraction 20%-61%) and 13 similar-aged controls (79 ± 8 years; 52%-73%) during 3 randomized transitions, as follows: (i) supine-to-standing; (ii) sitting-to-slow-paced over-ground walking; and (iii) sitting-to-normal-paced over-ground walking. Results: Throughout supine, sitting, standing, and both walking conditions, individuals with HF had lower cardiac index and cerebral tissue oxygenation than controls (P < 0.05), and MCAv was lower across the range of blood pressure in HF patients (P = 0.051) and during walking only (P = 0.011). Individuals with HF had an attenuated increase in stroke volume index and cardiac index during normal-paced walking, compared to controls (P < 0.01). Conclusions: The indices of cerebral perfusion from MCAv and cerebral oxygenation were lower during ambulatory activities in individuals with HF; however, relationships between MCAv and blood pressure were not different between those with HF and controls, indicating no difference in static cerebral autoregulation.

Contexte: Un débit cardiaque insuffisant chez les personnes atteintes d'insuffisance cardiaque limite les activités quotidiennes et affecte la qualité de vie. Par exemple, des efforts d'intensité modérée ont été associés à une perfusion cérébrale affaiblie chez ces personnes. Or, il semble que même des activités ambulatoires de faible intensité soient susceptibles d'avoir les mêmes conséquences. Méthodologie: Nous voulions déterminer si l'insuffisance cardiaque est associée à une altération de la réponse cérébrovasculaire à des activités de faible intensité qui sont typiques de la vie quotidienne. Dans le cadre de cette étude, nous avons surveillé l'hémodynamique centrale et la vitesse du sang dans l'artère cérébrale moyenne (VACM), ainsi que l'oxygénation tissulaire cérébrale (par spectroscopie dans le proche infrarouge) chez 10 personnes atteintes d'insuffisance cardiaque (âge : 78 ± 4 ans; fraction d'éjection du ventricule gauche de 20 à 61 %) et 13 témoins d'âge similaire (79 ± 8 ans; de 52 à 73 %) lors de 3 transitions réparties de façon aléatoire, soit : i) de la position couchée à debout; ii) de la position assise à une marche lente et iii) de la position assise à une marche à vitesse normale. Résultats: En position couchée, assise ou debout et avec les deux vitesses de marche, l'index cardiaque et l'oxygénation tissulaire cérébrale étaient plus faibles chez les personnes atteintes d'insuffisance cardiaque que chez les témoins (p < 0,05); la VACM était plus faible dans toutes les plages de pression artérielle chez les personnes atteintes d'insuffisance cardiaque (p = 0,051) et durant la marche seulement (p = 0,011). Les personnes atteintes d'insuffisance cardiaque présentaient une plus faible augmentation du volume d'éjection systolique et de l'index cardiaque durant la marche à vitesse normale, comparativement aux témoins (p < 0,01). Conclusions: Les indices de la perfusion cérébrale selon la VACM et l'oxygénation cérébrale étaient réduits durant les activités ambulatoires chez les personnes atteintes d'insuffisance cardiaque; cependant, les relations entre la VACM et la pression artérielle n'étaient pas différentes entre les personnes atteintes d'insuffisance cardiaque et les témoins, ce qui indique que l'autorégulation cérébrale statique n'est pas un facteur de différenciation.

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.

Case Studies in Physiology: Using premature ventricular contractions to understand the regulation of carotid artery longitudinal wall motion.

Recent observations have identified a distinct longitudinal motion pattern of the common carotid artery, where the wall oscillates along its length both with (anterograde) and against (retrograde) the direction of blood flow. The regulation of the longitudinal pattern remains largely undetermined, in part due to difficulty uncoupling local pressure and flow stimuli from upstream energy sources. In this case study of a 29-yr-old male, we examine the regulation of longitudinal wall motion from the perspective of spontaneous premature ventricular contractions (PVCs). With respect to the pre-PVC beat, during the PVC, there was an 81% reduction in carotid blood velocity (96.8 to 18.4 cm/s), a 69% reduction in pulse pressure (58 to 18 mmHg), and a 59% reduction in apical left ventricular (LV) rotation (6.9 to 2.8°) as a result of reduced LV filling time. During this time, anterograde longitudinal wall motion was unchanged (0.06 mm), whereas retrograde motion was reduced by 91% (0.75 to 0.07 mm). During the compensated post-PVC beat, there were large increases in all outcomes, except for anterograde wall motion. Taken together, there appears to be little influence of either local or upstream factors on anterograde wall motion. Although retrograde wall motion generally mirrored blood pressure, blood velocity, and upstream cardiac movement, the primary motion regulator remains unclear. In this Case Study, we provide evidence against the role of blood velocity in regulating local wall motion and reinforce the potential importance of cardiac mechanics dictating the unique longitudinal motion pattern at the common carotid artery.NEW & NOTEWORTHY Benign arrhythmias can be a useful tool to probe new hypotheses in physiology. We tested the control of longitudinal motion of the common carotid artery wall using observations from spontaneous premature ventricular contractions in a healthy male. Forwards wall motion remained unchanged despite large deviations in local blood velocity and backwards wall motion mirrored changes in pulse pressure, blood velocity, and cardiac motion, thereby revising our original hypothesis of the control of longitudinal wall motion.

Construct validation of the leisure time physical activity questionnaire for people with SCI (LTPAQ-SCI).

STUDY DESIGN: Cross-sectional construct validation study. OBJECTIVES: To test the construct validity of the Leisure Time Physical Activity Questionnaire for People with Spinal Cord Injury (LTPAQ-SCI) by examining associations between the scale responses and cardiorespiratory fitness (CRF) in a sample of adults living with spinal cord injury (SCI). SETTING: Three university-based laboratories in Canada. METHODS: Participants were 39 adults (74% male; M age: 42 ± 11 years) with SCI who completed the LTPAQ-SCI and a graded exercise test to volitional exhaustion using an arm-crank ergometer. One-tailed Pearson's correlation coefficients were computed to examine the association between the LTPAQ-SCI measures of mild-, moderate-, heavy-intensity and total minutes per week of LTPA and CRF (peak volume of oxygen consumption [V̇O2peak] and peak power output [POpeak]). RESULTS: Minutes per week of mild-, moderate- and heavy-intensity LTPA and total LTPA were all positively correlated with V̇O2peak. The correlation between minutes per week of mild intensity LTPA and V̇O2peak was small-medium (r = 0.231, p = 0.079) while all other correlations were medium-large (rs ranged from 0.276 to 0.443, ps < 0.05). Correlations between the LTPAQ-SCI variables and POpeak were also positive but small (rs ranged from 0.087 to 0.193, ps > 0.05), except for a medium-sized correlation between heavy-intensity LTPA and POpeak (r = 0.294, p = 0.035). CONCLUSIONS: People with SCI who report higher levels of LTPA on the LTPAQ-SCI also demonstrate greater levels of CRF, with stronger associations between moderate- and heavy-intensity LTPA and CRF than between mild-intensity LTPA and CRF. These results provide further support for the construct validity of the LTPAQ-SCI as a measure of LTPA among people with SCI.

The impact of preconditioning exercise on the vascular response to an oral glucose challenge.

Exercise elicits direct benefits to insulin sensitivity but may also indirectly improve glucose uptake by hemodynamic conditioning of the vasculature. The purpose of this study was to examine the modifying effect of 3 different types of exercise on the vascular response to an oral glucose challenge. Twenty healthy adults (9 women, 11 men; aged 23 ± 3 years) completed a standard oral glucose tolerance test (OGTT) at rest, as well as 1.5 hours after moderate continuous cycling exercise (30 min; 65% peak oxygen consumption), high-intensity interval cycling exercise (10 × 1 min at 90% peak heart rate), and lower-load higher-repetition resistance exercise (25-35 repetitions/set, 3 sets). Brachial and superficial femoral artery blood flow, conductance, and oscillatory shear index were measured throughout the OGTT. Regardless of rested state or exercise preconditioning, the OGTT induced reductions in brachial artery blood flow and conductance (p < 0.001), and transient increases in brachial and superficial femoral artery oscillatory shear index and retrograde blood flow (p < 0.01). Continuous cycling and resistance exercise were followed with a small degree of protection against prolonged periods of oscillatory flow. Our findings imply transient peripheral vasoconstriction and decreased limb blood flow during a standard OGTT, for which prior exercise was unable to prevent in healthy adults. Novelty: We investigated the impact of continuous, interval, and resistance exercise on the hemodynamic response to an OGTT. Our findings suggest decreased upper-limb blood flow during an OGTT is not prevented by prior exercise in healthy adults.

A Deep Learning Approach to Resolve Aliasing Artifacts in Ultrasound Color Flow Imaging.

Despite being used clinically as a noninvasive flow visualization tool, color flow imaging (CFI) is known to be prone to aliasing artifacts that arise due to fast blood flow beyond the detectable limit. From a visualization standpoint, these aliasing artifacts obscure proper interpretation of flow patterns in the image view. Current solutions for resolving aliasing artifacts are typically not robust against issues such as double aliasing. In this article, we present a new dealiasing technique based on deep learning principles to resolve CFI aliasing artifacts that arise from single- and double-aliasing scenarios. It works by first using two convolutional neural networks (CNNs) to identify and segment CFI pixel positions with aliasing artifacts, and then it performs phase unwrapping at these aliased pixel positions. The CNN for aliasing identification was devised as a U-net architecture, and it was trained with in vivo CFI frames acquired from the femoral bifurcation that had known presence of single- and double-aliasing artifacts. Results show that the segmentation of aliased CFI pixels was achieved successfully with intersection over union approaching 90%. After resolving these artifacts, the dealiased CFI frames consistently rendered the femoral bifurcation's triphasic flow dynamics over a cardiac cycle. For dealiased CFI pixels, their root-mean-squared difference was 2.51% or less compared with manual dealiasing. Overall, the proposed dealiasing framework can extend the maximum flow detection limit by fivefold, thereby improving CFI's flow visualization performance.