Experimental ductus arteriosus: the relationships of atrial pressure, dilatation and flow with ANF secretion

The design of the study was to determine whether an increased blood flow as seen in shunt lesions could serve as a stimulus for the secretion of atrial natriuretic factor (ANF). Since atrial pressure, flow, and dilatation are closely related, an experimental ductus arteriosus model was utilized, in which acute changes of flow are assumed not to dilate the left atrium. In six dogs, a Dacron graft was constructed between the main pulmonary artery and the innominate artery. Constricting and releasing the tape around the graft adjusted the amount of "ductal" shunting. The total pulmonary flow and the shunt flow were measured by electromagnetic-flow transducers around the aortic root and around the graft. Plasma ANF concentration was measured from both cardiac atria. The size of the left atrium was determined from echocardiographic measurements made from a short-axis view. The total pulmonary flow varied between 1.2 and 5.8 1/min. The highest measured ANF was 396 pg/ml, and this was from the left atrium when the pressure was 18 mmHg, the highest left atrial pressure recorded. The highest right atrial pressure (5 mmHg) also correlated with the highest right-atrial level of ANF (366 pg/ml). The right atrial pressure had a significant correlation with plasma ANF concentration (R = 0.43, p less than 0.05). Pulmonary flow and plasma ANF concentration did not correlate; neither did left atrial size and ANF levels in 16 flow states where the size was measured. In the absence of atrial dilatation there was minimal stimulus for ANF secretion. A transient increase of left atrial pressure, without a concomitant significant atrial dilatation, did not serve as a significant stimulus for ANF secretion.     

Head-up suspension in humans: effects on sympathetic vasomotor activity and cardiovascular responses

Wehypothesized that muscle sympathetic nerve activity (MSNA) andcardiovascular responses to the conventional head-up tilt (HUT) aredifferent from those to head-up suspension (HUS) because of antigravitymuscle activity. The MSNA from the tibial nerve, heart rate, bloodpressure, stroke volume, cardiac output, and calf blood flow weremeasured in 13 healthy young subjects. Left atrial diameter wasmeasured by two-dimensional echocardiography in another nine subjects.The resting MSNA and cardiovascular responses at a low level (20°)of orthostasis were similar during both modes. At higher levels (40 and60°), the responses of MSNA, heart rate, stroke volume, and cardiacoutput were significantly stronger and there was a smaller reduction incalf blood flow during HUT than during HUS(P < 0.05). Left atrial diameter was decreased significantly from the resting values during HUT and HUSwithout any significant difference between the modes of orthostasis. The results provide evidence that the engagement of antigravity musclesduring HUT may have additive effects on sympathetic vasoconstrictor andcardiovascular responses to orthostatic stress.

     

Effect of continuous negative-pressure breathing on skin blood flow during exercise in a hot environment

To assessthe impact of continuous negative-pressure breathing (CNPB) on theregulation of skin blood flow, we measured forearm blood flow (FBF) byvenous-occlusion plethysmography and laser-Doppler flow (LDF) at theanterior chest during exercise in a hot environment (ambienttemperature = 30°C, relative humidity = ~30%). Seven malesubjects exercised in the upright position at an intensity of 60% peakoxygen consumption rate for 40 min with and without CNPB after 20 minof exercise. The esophageal temperature(T_es) in both conditionsincreased to 38.1°C by the end of exercise, without any significantdifferences between the two trials. Mean arterial pressure (MAP)increased by ~15 mmHg by 8 min of exercise, without any significantdifference between the two trials before CNPB. However, CNPB reducedMAP by ~10 mmHg after 24 min of exercise (P < 0.05). The increasein FBF and LDF in the control condition leveled off after 18 min ofexercise above a T_es of37.7°C, whereas in the CNPB trial the increase continued, with arise in T_es despite the decreasein MAP. These results suggest that CNPB enhances vasodilation of skinabove a T_es of ~38°C bystretching intrathoracic baroreceptors such as cardiopulmonarybaroreceptors.

     

Effects of systole-specific pericardial pressure increases on coronary flow

It has been postulated that intrathoracic pressure increases may impair cardiac function by decreasing coronary flow. To determine whether altered coronary flow causes or results from change in cardiac function, we used 14 anesthetized dogs in propranolol-induced heart failure following atrioventricular node ablation. After thoracoabdominal binding, the animals were paced and ventilated at the same frequency, and inspiration was synchronized with cardiac systole, resulting in systole-specific pericardial pressure increases (SSPPI). At SSPPI magnitudes of 15 and 30 mmHg, left atrial transmural pressure decreased and cardiac output increased, whereas decreases in left ventricular end-systolic transmural pressure and myocardial O2 consumption were directly related. Concurrent decreases in coronary sinus flow (CSF) and coronary arteriovenous O2 gradient with SSPPI 15 mmHg indicate autoregulation. However, the arteriovenous O2 gradient remained unaltered with SSPPI 30 mmHg, despite further decrease in CSF. Because the absolute diastolic aortic pressure decreased, a limit may exist for increasing SSPPI above which CSF may be directly affected.     

Early mitral deceleration and left atrial stiffness

Left ventricular (LV) filling deceleration time (DT) is determined by the sum of atrial and ventricular stiffnesses (KLA + KLV). If KLA, however, is close to zero, then DT would reflect KLV only. The purpose of this study was to quantify KLA during DT. In 15 patients, KLV was assessed, immediately after cardiopulmonary bypass, from E wave DT as derived from mitral tracings obtained by transesophageal echocardiography and computed according to a validated formula. In each patient, a left atrial (LA) volume curve was also obtained combining mitral and pulmonary vein (PV) cumulative flow plus LA volume measured at end diastole. Time-adjusted LA pressure was measured simultaneously with Doppler data in all patients. KLA was then calculated during the ascending limb of the V loop and during DT. LA volume decreased by 7.3 +/- 6.5 ml/m2 during the first of mitral DT, whereas LV volume increased 9.4 +/- 8.4 ml/m2 (both P < 0.001). There was a small amount of blood coming from the PV during the same time interval, with the cumulative flow averaging 3.2 +/- 2.4 ml/m(2) (P < 0.001). Mean LA pressure was 10.0 +/- 5.1 mmHg, and it did not change during DT [from 7.8 +/- 4.3 to 8.0 +/- 4.3 mmHg, not significant (NS)], making KLA, which averaged 0.46 +/- 0.39 mmHg/ml during the V loop, close to zero during DT [KLA(DT): from -0.002 +/- 0.08 to -0.001 +/- 0.031 mmHg/ml, NS]. KLV, as assessed noninvasively from DT, averaged 0.25 +/- 0.32 mmHg/ml. In conclusion, notwithstanding the significant decrement in LA volume, KLA does not change and can be considered not different from zero during DT. Thus KLA does not affect the estimation of KLV from Doppler parameters.     

Three-dimensional computational model of left heart diastolic function with fluid-structure interaction

Aided by advancements in computer speed and modeling techniques, computational modeling of cardiac function has continued to develop over the past twenty years. The goal of the current study was to develop a computational model that provides blood-tissue interaction under physiologic flow conditions, and apply it to a thin-walled model of the left heart. To accomplish this goal, the Immersed Boundary Method was used to study the interaction of the tissue and blood in response to fluid forces and changes in tissue pathophysiology. The fluid mass and momentum conservation equations were solved using Patankar's Semi-Implicit Method for Pressure Linked Equations (SIMPLE). A left heart model was developed to examine diastolic function, and consisted of the left ventricle, left atrium, and pulmonary flow. The input functions for the model included the pulmonary driving pressure and time-dependent relationship for changes in chamber tissue properties during the simulation. The results obtained from the left heart model were compared to clinically observed diastolic flow conditions for validation. The inflow velocities through the mitral valve corresponded with clinical values (E-wave = 74.4 cm/s, A-wave = 43 cm/s, and E/A = 1.73). The pressure traces for the atrium and ventricle, and the appearance of the ventricular flow fields throughout filling, agreed with those observed in the heart. In addition, the atrial flow fields could be observed in this model and showed the conduit and pump functions that current theory suggests. The ability to examine atrial function in the present model is something not described previously in computational simulations of cardiac function.     

In vivo porcine left atrial wall stress: Computational model

Most computational models of the heart have so far concentrated on the study of the left ventricle, mainly using simplified geometries. The same approach cannot be adopted to model the left atrium, whose irregular shape does not allow morphological simplifications. In addition, the deformation of the left atrium during the cardiac cycle strongly depends on the interaction with its surrounding structures. We present a procedure to generate a comprehensive computational model of the left atrium, including physiological loads (blood pressure), boundary conditions (pericardium, pulmonary veins and mitral valve annulus movement) and mechanical properties based on planar biaxial experiments. The model was able to accurately reproduce the in vivo dynamics of the left atrium during the passive portion of the cardiac cycle. A shift in time between the peak pressure and the maximum displacement of the mitral valve annulus allows the appendage to inflate and bend towards the ventricle before the pulling effect associated with the ventricle contraction takes place. The ventricular systole creates room for further expansion of the appendage, which gets in close contact with the pericardium. The temporal evolution of the volume in the atrial cavity as predicted by the finite element simulation matches the volume changes obtained from CT scans. The stress field computed at each time point shows remarkable spatial heterogeneity. In particular, high stress concentration occurs along the appendage rim and in the region surrounding the pulmonary veins.     

Cardiac function adaptations in hibernating grizzly bears (Ursus arctos horribilis)

Research on the cardiovascular physiology of hibernating mammals may provide insight into evolutionary adaptations; however, anesthesia used to handle wild animals may affect the cardiovascular parameters of interest. To overcome these potential biases, we investigated the functional cardiac phenotype of the hibernating grizzly bear (Ursus arctos horribilis) during the active, transitional and hibernating phases over a 4 year period in conscious rather than anesthetized bears. The bears were captive born and serially studied from the age of 5 months to 4 years. Heart rate was significantly different from active (82.6 ± 7.7 beats/min) to hibernating states (17.8 ± 2.8 beats/min). There was no difference from the active to the hibernating state in diastolic and stroke volume parameters or in left atrial area. Left ventricular volume:mass was significantly increased during hibernation indicating decreased ventricular mass. Ejection fraction of the left ventricle was not different between active and hibernating states. In contrast, total left atrial emptying fraction was significantly reduced during hibernation (17.8 ± 2.8%) as compared to the active state (40.8 ± 1.9%). Reduced atrial chamber function was also supported by reduced atrial contraction blood flow velocities and atrial contraction ejection fraction during hibernation; 7.1 ± 2.8% as compared to 20.7 ± 3% during the active state. Changes in the diastolic cardiac filling cycle, especially atrial chamber contribution to ventricular filling, appear to be the most prominent macroscopic functional change during hibernation. Thus, we propose that these changes in atrial chamber function constitute a major adaptation during hibernation which allows the myocardium to conserve energy, avoid chamber dilation and remain healthy during a period of extremely low heart rates. These findings will aid in rational approaches to identifying underlying molecular mechanisms.     

Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans

Nóbrega, Antonio C. L., Jon W. Williamson, Jorge A. Garcia, and Jere H. Mitchell. Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans. J. Appl. Physiol. 83(3): 712-717, 1997.Ten patients with preserved inotropic function having adual-chamber (right atrium and right ventricle) pacemaker placed forcomplete heart block were studied. They performed static one-leggedknee extension at 20% of their maximal voluntary contraction for 5 minduring three conditions: 1)atrioventricular sensing and pacing mode [normal increase in heart rate (HR; DDD)], 2) HRfixed at the resting value (DOO-Rest; 73 ± 3 beats/min), and3) HR fixed at peak exercise rate(DOO-Ex; 107 ± 4 beats/min). During control exercise (DDD mode),mean arterial pressure (MAP) increased by 25 mmHg with no change instroke volume (SV) or systemic vascular resistance. During DOO-Rest andDOO-Ex, MAP increased (+25 and +29 mmHg, respectively) because of aSV-dependent increase in cardiac output (+1.3 and +1.8 l/min,respectively). The increase in SV during DOO-Rest utilized acombination of increased contractility and the Frank-Starling mechanism(end-diastolic volume 118-136 ml). However, during DOO-Ex, agreater left ventricular contractility (end-systolic volume 55-38ml) mediated the increase in SV.

     

The heart-forming fields: one or multiple?

The recent identification of a second mesodermal region as a source of cardiomyocytes has challenged the views on the formation of the heart. This second source of cardiomyocytes is localized centrally on the embryonic disc relative to the remainder of the classic cardiac crescent, a region also called the pharyngeal mesoderm. In this review, we discuss the concept of the primary and secondary cardiogenic fields in the context of folding of the embryo, and the subsequent temporal events involved in formation of the heart. We suggest that, during evolution, the heart developed initially only with the components required for a systemic circulation, namely a sinus venosus, a common atrium, a 'left' ventricle and an arterial cone, the latter being the myocardial outflow tract as seen in the heart of primitive fishes. These components developed in their entirety from the classic cardiac crescent. Only later in the course of evolution did the appearance of novel signalling pathways permit the central part of the cardiac crescent, and possibly the contiguous pharyngeal mesoderm, to develop into the cardiac components required for the pulmonary circulation. These latter components comprise the right ventricle, and that part of the left atrium that derives from the mediastinal myocardium, namely the dorsal atrial wall and the atrial septum. It is these elements which are now recognized as developing from the second field of pharyngeal mesoderm. We suggest that, rather than representing development from separate fields, the cardiac components required for both the systemic and pulmonary circulations are derived by patterning from a single cardiac field, albeit with temporal delay in the process of formation.     

Right atrial dimension-pressure relation during volume expansion is unaltered by pregnancy in the rat

Blood volume expands significantly during pregnancy, but afferent signals from cardiac receptors are reduced. In addition, during exogenous volume expansion, right atrial pressure (RAP) increases more for equivalent volumes in pregnant animals, implying reduced atrial compliance. To examine possible gestational alterations in atrial dimension during volume expansion, we compared the effects of volume expansion on RAP and right atrial dimension (RAD) in pregnant vs. virgin rats. Anesthetized animals were ventilated and catheterized for measurement of arterial pressure and RAP and for drug infusion. Through a parasternal incision, ultrasonic crystals were glued to the medial and lateral surfaces of the right atrium for measurement of RAD. Plasma volume and hematocrit were determined before experimentation. RAP, RAD, and arterial pressure were recorded at baseline and during progressive volume expansion (6% dextran, 60% of initial blood volume). Baseline RAP was similar in the two groups: 2.82 +/- 0.40 and 2.72 +/- 0.47 mmHg in pregnant and virgin rats, respectively. Basal RAD was significantly larger in pregnant than in virgin rats: 4.36 +/- 0.66 vs. 3.36 +/- 0.48 mm. Despite increased basal RAD in pregnant rats, the slope of the RAD-RAP relation during volume expansion was similar in the two groups. Results indicate that resting RAD is increased in pregnant rats and that the change in dimension during volume loads is similar to that in virgin rats. Thus, during pregnancy, the right atrium appears to accommodate the increased blood volume, and reduced afferent signaling most likely is due to mechanisms other than mechanical alterations of the atrium by expanded volume.     

Noninvasive measurement of time-varying three-dimensional relative pressure fields within the human heart

Understanding cardiac blood flow patterns is important in the assessment of cardiovascular function. Three-dimensional flow and relative pressure fields within the human left ventricle are demonstrated by combining velocity measurements with computational fluid mechanics methods. The velocity field throughout the left atrium and ventricle of a normal human heart is measured using time-resolved three-dimensional phase-contrast MRI. Subsequently, the time-resolved three-dimensional relative pressure is calculated from this velocity field using the pressure Poisson equation. Noninvasive simultaneous assessment of cardiac pressure and flow phenomena is an important new tool for studying cardiac fluid dynamics.     

Mutation of weak atrium/atrial myosin heavy chain disrupts atrial function and influences ventricular morphogenesis in zebrafish

The embryonic vertebrate heart is composed of two major chambers, a ventricle and an atrium, each of which has a characteristic size, shape and functional capacity that contributes to efficient circulation. Chamber-specific gene expression programs are likely to regulate key aspects of chamber formation. Here, we demonstrate that epigenetic factors also have a significant influence on chamber morphogenesis. Specifically, we show that an atrium-specific contractility defect has a profound impact on ventricular development. We find that the zebrafish locus weak atrium encodes an atrium-specific myosin heavy chain that is required for atrial myofibrillar organization and contraction. Despite their atrial defects, weak atrium mutants can maintain circulation through ventricular contraction. However, the weak atrium mutant ventricle becomes unusually compact, exhibiting a thickened myocardial wall, a narrow lumen and changes in myocardial gene expression. As weak atrium/atrial myosin heavy chain is expressed only in the atrium, the ventricular phenotypes in weak atrium mutants represent a secondary response to atrial dysfunction. Thus, not only is cardiac form essential for cardiac function, but there also exists a reciprocal relationship in which function can influence form. These findings are relevant to our understanding of congenital defects in cardiac chamber morphogenesis.     

Fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model

This paper aims to investigate detailed mechanical interactions between the pulmonary haemodynamics and left heart function in pathophysiological situations (e.g. atrial fibrillation and acute mitral regurgitation). This is achieved by developing a complex computational framework for a coupled pulmonary circulation, left atrium and mitral valve model. The left atrium and mitral valve are modelled with physiologically realistic three-dimensional geometries, fibre-reinforced hyperelastic materials and fluid–structure interaction, and the pulmonary vessels are modelled as one-dimensional network ended with structured trees, with specified vessel geometries and wall material properties. This new coupled model reveals some interesting results which could be of diagnostic values. For example, the wave propagation through the pulmonary vasculature can lead to different arrival times for the second systolic flow wave (S2 wave) among the pulmonary veins, forming vortex rings inside the left atrium. In the case of acute mitral regurgitation, the left atrium experiences an increased energy dissipation and pressure elevation. The pulmonary veins can experience increased wave intensities, reversal flow during systole and increased early-diastolic flow wave (D wave), which in turn causes an additional flow wave across the mitral valve (L wave), as well as a reversal flow at the left atrial appendage orifice. In the case of atrial fibrillation, we show that the loss of active contraction is associated with a slower flow inside the left atrial appendage and disappearances of the late-diastole atrial reversal wave (AR wave) and the first systolic wave (S1 wave) in pulmonary veins. The haemodynamic changes along the pulmonary vessel trees on different scales from microscopic vessels to the main pulmonary artery can all be captured in this model. The work promises a potential in quantifying disease progression and medical treatments of various pulmonary diseases such as the pulmonary hypertension due to a left heart dysfunction.

     

Quantifying whole bladder biomechanics using the novel pentaplanar reflected image macroscopy system

Optimal bladder compliance is essential to urinary bladder storage and voiding functions. Calculated as the change in filling volume per change in pressure, bladder compliance is used clinically to characterize changes in bladder wall biomechanical properties that associate with lower urinary tract dysfunction. But because this method calculates compliance without regard to wall structure or wall volume, it gives little insight into the mechanical properties of the bladder wall during filling. Thus, we developed Pentaplanar Reflected Image Macroscopy (PRIM): a novel ex vivo imaging method to accurately calculate bladder wall stress and stretch in real time during bladder filling. The PRIM system simultaneously records intravesical pressure, infused volume, and an image of the bladder in five distinct visual planes. Wall thickness and volume were then measured and used to calculate stress and stretch during filling. As predicted, wall stress was nonlinear; only when intravesical pressure exceeded ~ 15 mmHg did bladder wall stress rapidly increase with respect to stretch. This method of calculating compliance as stress vs stretch also showed that the mechanical properties of the bladder wall remain similar in bladders of varying capacity. This study demonstrates how wall tension, stress and stretch can be measured, quantified, and used to accurately define bladder wall biomechanics in terms of actual material properties and not pressure/volume changes. This method is especially useful for determining how changes in bladder biomechanics are altered in pathologies where profound bladder wall remodeling occurs, such as diabetes and spinal cord injury.

     

Fluid Dynamics of Ventricular Filling in the Embryonic Heart

The vertebrate embryonic heart first forms as a valveless tube that pumps blood using waves of contraction. As the heart develops, the atrium and ventricle bulge out from the heart tube, and valves begin to form through the expansion of the endocardial cushions. As a result of changes in geometry, conduction velocities, and material properties of the heart wall, the fluid dynamics and resulting spatial patterns of shear stress and transmural pressure change dramatically. Recent work suggests that these transitions are significant because fluid forces acting on the cardiac walls, as well as the activity of myocardial cells that drive the flow, are necessary for correct chamber and valve morphogenesis. In this article, computational fluid dynamics was used to explore how spatial distributions of the normal forces acting on the heart wall change as the endocardial cushions grow and as the cardiac wall increases in stiffness. The immersed boundary method was used to simulate the fluid-moving boundary problem of the cardiac wall driving the motion of the blood in a simplified model of a two-dimensional heart. The normal forces acting on the heart walls increased during the period of one atrial contraction because inertial forces are negligible and the ventricular walls must be stretched during filling. Furthermore, the force required to fill the ventricle increased as the stiffness of the ventricular wall was increased. Increased endocardial cushion height also drastically increased the force necessary to contract the ventricle. Finally, flow in the moving boundary model was compared to flow through immobile rigid chambers, and the forces acting normal to the walls were substantially different.     

4D subject-specific inverse modeling of the chick embryonic heart outflow tract hemodynamics

Blood flow plays a critical role in regulating embryonic cardiac growth and development, with altered flow leading to congenital heart disease. Progress in the field, however, is hindered by a lack of quantification of hemodynamic conditions in the developing heart. In this study, we present a methodology to quantify blood flow dynamics in the embryonic heart using subject-specific computational fluid dynamics (CFD) models. While the methodology is general, we focused on a model of the chick embryonic heart outflow tract (OFT), which distally connects the heart to the arterial system, and is the region of origin of many congenital cardiac defects. Using structural and Doppler velocity data collected from optical coherence tomography, we generated 4D (\(\hbox {3D}\,+\,\hbox {time}\)) embryo-specific CFD models of the heart OFT. To replicate the blood flow dynamics over time during the cardiac cycle, we developed an iterative inverse-method optimization algorithm, which determines the CFD model boundary conditions such that differences between computed velocities and measured velocities at one point within the OFT lumen are minimized. Results from our developed CFD model agree with previously measured hemodynamics in the OFT. Further, computed velocities and measured velocities differ by \(<\)15 % at locations that were not used in the optimization, validating the model. The presented methodology can be used in quantifications of embryonic cardiac hemodynamics under normal and altered blood flow conditions, enabling an in-depth quantitative study of how blood flow influences cardiac development.     

Moving Domain Computational Fluid Dynamics to Interface with an Embryonic Model of Cardiac Morphogenesis

Peristaltic contraction of the embryonic heart tube produces time- and spatial-varying wall shear stress (WSS) and pressure gradients (∇P) across the atrioventricular (AV) canal. Zebrafish (Danio rerio) are a genetically tractable system to investigate cardiac morphogenesis. The use of Tg(fli1a:EGFP)^y1 transgenic embryos allowed for delineation and two-dimensional reconstruction of the endocardium. This time-varying wall motion was then prescribed in a two-dimensional moving domain computational fluid dynamics (CFD) model, providing new insights into spatial and temporal variations in WSS and ∇P during cardiac development. The CFD simulations were validated with particle image velocimetry (PIV) across the atrioventricular (AV) canal, revealing an increase in both velocities and heart rates, but a decrease in the duration of atrial systole from early to later stages. At 20-30 hours post fertilization (hpf), simulation results revealed bidirectional WSS across the AV canal in the heart tube in response to peristaltic motion of the wall. At 40-50 hpf, the tube structure undergoes cardiac looping, accompanied by a nearly 3-fold increase in WSS magnitude. At 110-120 hpf, distinct AV valve, atrium, ventricle, and bulbus arteriosus form, accompanied by incremental increases in both WSS magnitude and ∇P, but a decrease in bi-directional flow. Laminar flow develops across the AV canal at 20-30 hpf, and persists at 110-120 hpf. Reynolds numbers at the AV canal increase from 0.07±0.03 at 20-30 hpf to 0.23±0.07 at 110-120 hpf (p< 0.05, n=6), whereas Womersley numbers remain relatively unchanged from 0.11 to 0.13. Our moving domain simulations highlights hemodynamic changes in relation to cardiac morphogenesis; thereby, providing a 2-D quantitative approach to complement imaging analysis.     

Phenylephrine-induced elevations in arterial blood pressure are attenuated in heat-stressed humans

To test the hypothesis that phenylephrine-induced elevations in blood pressure are attenuated in heat-stressed humans, blood pressure was elevated via steady-state infusion of three doses of phenylephrine HCl in 10 healthy subjects in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature by ~0.5 degrees C, muscle sympathetic nerve activity (MSNA), heart rate, and cardiac output and decreased total peripheral vascular resistance (TPR; all P < 0.005) but did not change mean arterial blood pressure (MAP; P > 0.05). At the highest dose of phenylephrine, the increase in MAP and TPR from predrug baselines was significantly attenuated during the heat stress [DeltaMAP 8.4 +/- 1.2 mmHg; DeltaTPR 0.96 +/- 0.85 peripheral resistance units (PRU)] compared with normothermia (DeltaMAP 15.4 +/- 1.4 mmHg, DeltaTPR 7.13 +/- 1.18 PRU; all P < 0.001). The sensitivity of baroreflex control of MSNA and heart rate, expressed as the slope of the relationship between MSNA and diastolic blood pressure, as well as the slope of the relationship between heart rate and systolic blood pressure, respectively, was similar between thermal conditions (each P > 0.05). These data suggest that phenylephrine-induced elevations in MAP are attenuated in heat-stressed humans without affecting baroreflex control of MSNA or heart rate.     

A Cycling Movement Based System for Real-Time Muscle Fatigue and Cardiac Stress Monitoring and Analysis

In this study, we defined a new parameter, referred to as the cardiac stress index (CSI), using a nonlinear detrended fluctuation analysis (DFA) of heart rate (HR). Our study aimed to incorporate the CSI into a cycling based fatigue monitoring system developed in our previous work so the muscle fatigue and cardiac stress can be both continuously and quantitatively assessed for subjects undergoing the cycling exercise. By collecting electrocardiogram (ECG) signals, the DFA scaling exponent α was evaluated on the RR time series extracted from a windowed ECG segment. We then obtained the running estimate of α by shifting a one-minute window by a step of 20 seconds so the CSI, defined as the percentage of all the less-than-one α values, can be synchronously updated every 20 seconds. Since the rating of perceived exertion (RPE) scale is considered as a convenient index which is commonly used to monitor subjective perceived exercise intensity, we then related the Borg RPE scale value to the CSI in order to investigate and quantitatively characterize the relationship between exercise-induced fatigue and cardiac stress. Twenty-two young healthy participants were recruited in our study. Each participant was asked to maintain a fixed pedaling speed at a constant load during the cycling exercise. Experimental results showed that a decrease in DFA scaling exponent α or an increase in CSI was observed during the exercise. In addition, the Borg RPE scale and CSI were positively correlated, suggesting that the factors due to cardiac stress might also contribute to fatigue state during physical exercise. Since the CSI can effectively quantify the cardiac stress status during physical exercise, our system may be used in sports medicine, or used by cardiologists who carried out stress tests for monitoring heart condition in patients with heart diseases.