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Lower body negative pressure (LBNP) is an established and important technique used to physiologically stress the human body, particularly the cardiovascular system. LBNP is most often used to simulate gravitational stress, but it has also been used to simulate hemorrhage, alter preload, and manipulate baroreceptors. During experimentation, the consequences of LBNP and the reflex increases in heart rate and blood pressure can be manipulated and observed in a well-controlled manner, thus making LBNP an important research tool. Numerous laboratories have developed LBNP devices for use in research settings, and a few devices are commercially available. However, it is often difficult for new users to find adequately described design plans. Furthermore, many available plans require sophisticated and expensive materials and/or technical support. Therefore, we have created an affordable design plan for a LBNP chamber. The purpose of this article was to share our design template with others. In particular, we hope that this information will be of use in academic and research settings. Our pressure chamber has been stress tested to 100 mmHg below atmospheric pressure and has been used successfully to test orthostatic tolerance and physiological responses to -50 mmHg.

Early diastolic left ventricular (LV) untwisting has been evaluated as a manifestation of LV recoil, reflecting the release of elastic energy stored during systole. The primary goal of this study was to characterize the relationship between systolic strain (e.g., circumferential strain and the shear strains that comprise twist) with the resulting early diastolic shear strain rates, including the rate of untwisting. A further goal was to characterize these relationships regionally from apical to basal locations. Cardiac magnetic resonance imaging tissue tagging was used to measure circumferential strain, global and regional (apex, mid, basal) twist ([theta]), and circumferential-longitudinal ([[member].sub.CL]) and circumferential-radial ([[member of].sub.CR]) shear strains along with the corresponding untwisting rates (d[theta]/dt and diastolic shear strain rates (d[member of]/dt in 32 healthy males (33 [+ or -] 7 yr). LV untwisting rates and shear strain rates measured during early diastole varied significantly with the measurement location from apex to base (P < 0.001) but demonstrated significant linear correlation with their corresponding preceding systolic strains (P < 0.001). Untwisting rates and diastolic shear strain rates were not significantly correlated with circumferential systolic strain or endsystolic volume (P > 0.05). Normalization of the untwisting rates to the peak twist (d[theta]/[dt.sub.Norm] = -13.6 [+ or -] 2.1 [s.sup.-1]) or shear strain rates to peak systolic shear strain (d[[member of].sub.CL]/[dt.sub.Norm] = -15.0 [+ or -] 5.4 [s.sup.-1], and d[[member of].sub.CR]/[dt.sub.Norm] = -14.2 [+ or -] 7.7 [s.sup.-1]) yielded a uniform measure of early diastolic function that was similar for all shear strain and twist components and for all locations from apex to base. These findings support a linear model of torsional recoil in the healthy heart, where diastolic shear strain rates (e.g., untwisting rates) are linearly related to the corresponding preceding systolic shear stain component. Furthermore, these findings suggest that torsional recoil is uncoupled from end-systolic volumes or the associated strains, such as circumferential strain. relaxation; torsion; untwisting doi: 10.1152/ajpheart.00353.2010.

Left ventricular (LV) active relaxation begins before aortic valve closure and is largely completed during isovolumic relaxation (IVR), before mitral valve opening. During IVR, despite closed mitral and aortic valves, indirect assessments of LV volume have suggested volume increases during this period. The aim of this study is to measure LV volume throughout IVR and to determine the sources of any volume changes. For 10 healthy individuals (26.0 [+ or -] 3.8 yr), magnetic resonance imaging was used to measure time courses of LV volume, principal myocardial strains (circumferential, longitudinal, radial), and LV twist. Mitral leaflet motion was observed using echocardiography. During IVR, LV volume measurements showed an apparent increase of 4.6 [+ or -] 1.5 ml (5.0 [+ or -] 2.0% of the early filling volume change), the LV untwisted by 4.5 [+ or -] 1.9[degrees] (36.6 [+ or -] 18.0% of peak systolic twist), and changes in circumferential, longitudinal, and radial strains were +0.87 [+ or -] 0.64%, +0.93 [+ or -] 0.57%, and - 1.46 [+ or -] 1.66% (4.2 [+ or -] 3.3%, 5.9 [+ or -] 3.3%, and 5.3 [+ or -] 7.5% of peak systolic strains), respectively. The apparent changes in volume correlated (P < 0.01) with changes in circumferential, longitudinal, and radial strains (r = 0.86, 0.69, and -0.37, respectively) and untwisting (r = 0.83). The closed mitral valve leaflets were observed to descend into the LV throughout IVR in all subjects in apical four- and three-chamber and parasternal long-axis views by 6.0 [+ or -] 3.3, 5.1 [+ or -] 2.4, and 2.1 [+ or -] 5.0 mm, respectively. In conclusion, LV relaxation during IVR is associated with changes in principal strains and untwisting, which are all correlated with an apparent increase in LV volume. Since closed mitral and aortic valves ensure true isovolumic conditions, the apparent volume change likely reflects expansion of the LV myocardium and the inward bowing of the closed mitral leaflets toward the LV interior. diastolic function; active relaxation; mitral valve leaflets doi: 10.1152/ajpheart.00131.2010.

The article presents a study which investigates the consequences of a 169-km ultramarathon to the cardiac function with the use of traditional echocardiography, speckle tracking imaging, cardiac biomakers, and heart rate variability (HRV). In the course of the study, the cardiac function of the subjects were examined before and after the ultramarathon. Left ventricular systolic and diastolic measurements were assessed with the use of traditional echocardiography. Meanwhile, the myocardial peak strain and strain rate were analyzed using speckle tracking. Results suggest that reductions in left ventricular function are not significantly associated with changes in cardiac biomakers and HRV.

Background: It is well known that hypoxic exercise in healthy individuals increases limb blood flow, leg oxygen extraction and limb vascular conductance during knee extension exercise. However, the effect of hypoxia on cardiac output, and total vascular conductance is less clear. Furthermore, the oxygen delivery response to hypoxic exercise in well trained individuals is not well known. Therefore our aim was to determine the cardiac output (Doppler echocardiography), vascular conductance, limb blood flow (Doppler echocardiography) and muscle oxygenation response during hypoxic knee extension in normally active and endurance-trained males. Methods: Ten normally active and nine endurance-trained males (VO2max = 46.1 and 65.5 mL/kg/ min, respectively) performed 2 leg knee extension at 25, 50, 75 and 100% of their maximum intensity in both normoxic and hypoxic conditions (FIO2 = 15%; randomized order). Results were analyzed with a 2-way mixed model ANOVA (group x intensity). Results: The main finding was that in normally active individuals hypoxic sub-maximal exercise (25 - 75% of maximum intensity) brought about a 3 fold increase in limb blood flow but decreased stroke volume compared to normoxia. In the trained group there were no significant changes in stroke volume, cardiac output and limb blood flow at sub-maximal intensities (compared to normoxia). During maximal intensity hypoxic exercise limb blood flow increased approximately 300 mL/min compared to maximal intensity normoxic exercise. Conclusion: Cardiorespiratory fitness likely influences the oxygen delivery response to hypoxic exercise both at a systemic and limb level. The increase in limb blood flow during maximal exercise in hypoxia (both active and trained individuals) suggests a hypoxic stimulus that is not present in normoxic conditions. [ABSTRACT FROM AUTHOR]

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Background: Near infrared spectroscopy (NIRS) is used to assess muscle oxygenation (MO) within skeletal muscle at rest and during aerobic exercise. Previous investigations have used a single probe placement to measure MO during various forms of exercise. However, regional MO differences have been shown to exist within the same muscle which suggests that different areas of the same muscle may have divergent MO. Thus, the aim of this study was to examine whether regional differences in MO exist within the same muscle during different types of incremental (rest, 25, 50, 75, 100 % of maximum) exercise (1 leg knee extension (KE), 2 leg KE, or cycling). Methods: Nineteen healthy active males (Mean ± SD: Age 27 ± 4 yrs; VO2max: 55 ± 11 mL/kg/min) performed incremental exercise to fatigue using each mode of exercise. NIRS probes were placed on the distal and proximal portion of right leg vastus lateralis (VL). Results were analyzed with a 3- way mixed model ANOVA (probe x intensity x mode). Results: Differences in MO exist within the VL for each mode of exercise, however these differences were not consistent for each level of intensity. Comparison of MO revealed that the distal region of VL was significantly lower throughout KE exercise (1 leg KE proximal MO - distal MO = 9.9 %; 2 leg KE proximal MO - distal MO = 13 %). In contrast, the difference in MO between proximal and distal regions of VL was smaller in cycling and was not significantly different at heavy workloads (75 and 100 % of maximum). Conclusion: MO is different within the same muscle and the pattern of the difference will change depending on the mode and intensity of exercise. Future investigations should limit conclusions on MO to the area under assessment as well as the type and intensity of exercise employed. [ABSTRACT FROM AUTHOR]

The cardiovascular response to exercise in heart transplant recipients (HTR) has been compared with that of healthy individuals matched to the recipient age (RM controls). However, no study has compared HTR with donor age-matched (DM) controls. Moreover, the cardiovascular response to sustained submaximal exercise in HTR requires further evaluation. We therefore examined cardiovascular responses during incremental exercise and sustained (1 h) submaximal aerobic exercise in 9 clinically stable HTR [63 +/- 10 yr of age, 24.2 +/- 10.9 ml x kg(-1) x min(-1) peak O(2) uptake (Vo(2peak))] and 11 healthy age-matched controls (60 +/- 11 yr of age and 36.3 +/- 10.7 ml.kg(-1) x min(-1) Vo(2peak) for 6 RM controls and 35 +/- 8 yr of age and 51.1 +/- 10.4 ml x kg(-1) x min(-1) Vo(2peak) for 5 DM controls). Heart rate (HR) and left ventricular systolic and diastolic volumes (2-dimensional echocardiography) indexed to body surface area [end-systolic and end-diastolic volume indexes (EDVI and ESVI)], cardiac output (CI), ejection fraction (EF), systemic vascular resistance (SVRI), end-systolic elastance index, and arterial elastance index were determined. Although systolic function was maintained during incremental exercise, peak CI was significantly reduced (6.7 +/- 2.4 vs. 11.6 +/- 1.4 l x min(-1) x m(-2)), secondary to blunted HR, EDVI, and increased peak SVRI, in HTR compared with DM controls. The lower peak CI in HTR than in RM controls was due to blunted peak EDVI (54.1 +/- 13.2 vs. 68.6 +/- 5.7 ml/m(2)). During sustained submaximal exercise, HTR exhausted their preload reserve, a response for which changes in ESVI, HR, or EF did not fully compensate. Thus it appears that HTR are limited by impaired preload reserve, HR reserve, and vascular reserve during exercise conditions.

We tested the hypothesis that following an acute bout of exercise cardiovascular and cerebrovascular responses to lower-body negative pressure (LBNP) would be altered due to post-exercise hypotension (PEH). Ten healthy, male, endurance-trained athletes (mean age +/- SD = 29.6 +/- 5) were assessed for cardiovascular and cerebrovascular responses to LBNP following acute bouts of interval and continuous exercise. Mean arterial pressure (MAP), cardiac output, total peripheral resistance, heart rate variability, and total cerebral oxygen index were determined during a baseline LBNP session. These indices were also determined during two other LBNP sessions: following an acute bout of interval exercise, and following an acute bout of continuous exercise. Compared with baseline, MAP was reduced after both exercise conditions, similar to values previously reported (10 mmHg; p < 0.05 vs. pre-exercise). Total peripheral resistance was significantly reduced following both exercise bouts, and heart rate was significantly increased post-exercise (rest: 59.6 +/- 11.2; interval: 77.8 +/- 12.8; continuous: 80.3 +/- 15.2 beats.min(-1)). Both cardiac output and stroke volume responses to LBNP following exercise were not altered when compared with baseline measurements. Tissue oxygenation during -40 mmHg (interval: 74.31% +/- 7.82% vs. continuous: 69.13% +/- 5.23%) was significantly lower than during normobaric pressure (interval: 77.14% +/- 1.30% vs. continuous: 74.41% +/- 0.94%). It appears from these observations that although young, endurance-trained males experience PEH following acute bouts of interval or continuous exercise, this hypotension does not alter the cardiovascular and cerebrovascular responses to a moderate orthostatic stress.

Enhanced left-ventricular (LV) compliance is a common adaptation to endurance training. This adaptation may have differential effects under conditions of altered venous return. The purpose of this investigation was to assess the effect of cardiac (un)loading on right ventricular (RV) cavity dimensions and LV volumes in endurance-trained athletes and normally active males. Eight endurance-trained (Vo(2max), 65.4 +/- 5.7 ml.kg(-1).min(-1)) and eight normally active (Vo(2max), 45.1 +/- 6.0 ml.kg(-1).min(-1)) males underwent assessments of the following: 1) Vo(2max), 2) orthostatic tolerance, and 3) cardiac responses to lower-body positive (0-60 mmHg) and negative (0 to -80 mmHg) pressures with echocardiography. In response to negative pressures, echocardiographic analysis revealed a similar decrease in RV end-diastolic cavity area in both groups (e.g., at -80 mmHg: normals, 21.4%; athletes, 20.8%) but a greater decrease in LV end-diastolic volume in endurance-trained athletes (e.g., at -80 mmHg: normals, 32.3%; athletes, 44.4%; P < 0.05). Endurance-trained athletes also had significantly greater decreases in LV stroke volume during lower-body negative pressure. During positive pressures, endurance-trained athletes showed larger increases in LV end-diastolic volume (e.g., at +60 mmHg; normals, 14.1%; athletes, 26.8%) and LV stroke volume, despite similar responses in RV end-diastolic cavity area (e.g., at +60 mmHg: normals, 18.2%; athletes, 24.2%; P < 0.05). This investigation revealed that in response to cardiac (un)loading similar changes in RV cavity area occur in endurance-trained and normally active individuals despite a differential response in the left ventricle. These differences may be the result of alterations in RV influence on the left ventricle and/or intrinsic ventricular compliance.

In this review, we examine the growing body of evidence suggesting that the pericardium plays an important role in modulating cardiac function during conditions of physiological stress. Specifically, we discuss the effects of the pericardium on left ventricular filling and compliance. Furthermore, we reveal that there is increasing evidence to support the contention that the pericardium is capable of adaptation in response to volume loading. We also provide data that suggests endurance-training is a good example of a physiological stressor capable of causing pericardial remodelling. These adaptations appear particularly beneficial during exercise and may explain (in part) the common finding of stroke volume increasing during exercise to a greater extent in endurance-trained athletes. However, this adaptation may also partially explain the increased susceptibility to orthostatic intolerance in endurance athletes.

In this narrative review of the current literature, we examine the central and peripheral mechanisms responsible for the exercise intolerance of chronic heart failure and highlight briefly the benefits of exercise training in the treatment of this debilitating disorder. Specifically, we identify the common finding of reduced cardiac output reserve during exercise conditions leading to decreased exercise tolerance. We also reveal that the stroke volume response to exercise varies depending on the individual patient, the presence of mitral regurgitation, and the aetiology of heart failure. Chronic heart failure patients with left ventricular systolic dysfunction appear able to use the Frank-Starling mechanism to compensate (in part) for their decreased contractile reserve. Patients with left ventricular diastolic dysfunction have normal contractile function; however, they are unable to make use of the Frank-Starling mechanism during exercise conditions. We also reveal that pericardial constraint may limit diastolic filling and exercise capacity in patients with chronic heart failure. It appears that interventions that reduce pericardial constraint and mitral regurgitation enhance diastolic filling and increase exercise tolerance. A series of peripheral muscle changes also occur, including changes in muscle mass, cellular structure, energy metabolism, and blood flow. Each of these factors is associated with decreased exercise capacity and the symptoms of chronic heart failure. Exercise training has been shown to improve both central haemodynamics and peripheral muscle function leading to improvements in exercise capacity, functional status, and overall quality of life in patients with chronic heart failure.

The gravitational stress encountered by pilots of high-performance aircraft can cause dramatic shifts in blood volume and circulatory pressure, thus placing the cardiovascular system under significant stress, sometimes resulting in loss of consciousness due to cerebral under-perfusion. Since pilots experience both increased and decreased gravitational stress in high-risk environments, it is important not only to examine the cardiovascular effects of altered gravitational exposure, but also to create effective countermeasures that will increase pilot safety. In this review, we discuss the cardiovascular consequences of rapid changes in gravitational forces. We also examine the effectiveness of the countermeasures that have been developed to combat gravity-induced loss of consciousness. Finally, we examine those current laboratory-based techniques that simulate hyper-gravity and the "push-pull effect"; making it possible to investigate the cardiovascular mechanisms responsible for maintaining cerebral perfusion and consciousness.

Sex differences in neuroendocrine and metabolic responses to prolonged strenuous exercise (PSE) have been well documented. The aim of this investigation was to examine sex differences in left ventricular function and cardiac beta-receptor responsiveness following a single bout of PSE. Nine male and eight female triathletes were examined during three separate sessions: before, immediately after, and 24 h following a half-ironman triathlon using dobutamine stress echocardiography. Steady-state graded infusions of dobutamine were used to assess beta-receptor responsiveness. Slopes calculated from linear regressions between dobutamine doses and changes in heart rate and contractility for each participant were used as an index of beta-receptor responsiveness. Despite no change in preload, fractional area change decreased from baseline after the race in both men and women, with a greater decrease in men [men: 54.1% (SD 2.1) to 50.7% (SD 3.4) vs. women: 55.4% (SD 2.7) to 53.3% (SD 2.5); P < 0.05]. The amount of dobutamine necessary to increase heart rate by 25 beats/min [men: 29.6 microg x kg(-1) x min(-1) (SD 6.6) to 42.7 microg x kg(-1) x min(-1) (SD 12.9) vs. women: 23.5 microg x kg(-1) x min(-1) (SD 4.0) to 30.0 microg x kg(-1) x min(-1) (SD 7.8); P < 0.05] and contractility by 10 mmHg/cm2 [men: 20.9 microg x kg(-1) x min(-1) (SD 5.1) to 37.0 microg x kg(-1) x min(-1) (SD 11.5) vs. women: 22.6 microg x kg(-1) x min(-1) (SD 6.4) to 30.7 microg x kg(-1) x min(-1) (SD 7.2); P < 0.05] was greater in both men and women postrace. However, the amount of dobutamine required to induce these changes was greater in men, reflecting larger beta-receptor alterations in male triathletes following PSE relative to women. These data suggest that following an acute bout of PSE, male triathletes demonstrate an attenuated chronotropic and inotropic response to beta-adrenergic stimulation compared with female triathletes.