Lower body negative pressure vs. lower body positive pressure to prevent cardiac atrophy after bed rest and spaceflight. What caused the controversy?

2006 ◽  
Vol 100 (3) ◽  
pp. 1090-1090 ◽  
Author(s):  
Marieta V. Pancheva ◽  
Vladimir S. Panchev ◽  
Adelina V. Suvandjieva

Cardiac muscle adapts well to changes in loading conditions. For example, left ventricular (LV) hypertrophy may be induced physiologically (via exercise training) or pathologically (via hypertension or valvular heart disease). If hypertension is treated, LV hypertrophy regresses, suggesting a sensitivity to LV work. However, whether physical inactivity in nonathletic populations causes adaptive changes in LV mass or even frank atrophy is not clear. We exposed previously sedentary men to 6 ( n = 5) and 12 ( n = 3) wk of horizontal bed rest. LV and right ventricular (RV) mass and end-diastolic volume were measured using cine magnetic resonance imaging (MRI) at 2, 6, and 12 wk of bed rest; five healthy men were also studied before and after at least 6 wk of routine daily activities as controls. In addition, four astronauts were exposed to the complete elimination of hydrostatic gradients during a spaceflight of 10 days. During bed rest, LV mass decreased by 8.0 ± 2.2% ( P = 0.005) after 6 wk with an additional atrophy of 7.6 ± 2.3% in the subjects who remained in bed for 12 wk; there was no change in LV mass for the control subjects (153.0 ± 12.2 vs. 153.4 ± 12.1 g, P = 0.81). Mean wall thickness decreased (4 ± 2.5%, P = 0.01) after 6 wk of bed rest associated with the decrease in LV mass, suggesting a physiological remodeling with respect to altered load. LV end-diastolic volume decreased by 14 ± 1.7% ( P = 0.002) after 2 wk of bed rest and changed minimally thereafter. After 6 wk of bed rest, RV free wall mass decreased by 10 ± 2.7% ( P = 0.06) and RV end-diastolic volume by 16 ± 7.9% ( P = 0.06). After spaceflight, LV mass decreased by 12 ± 6.9% ( P = 0.07). In conclusion, cardiac atrophy occurs during prolonged (6 wk) horizontal bed rest and may also occur after short-term spaceflight. We suggest that cardiac atrophy is due to a physiological adaptation to reduced myocardial load and work in real or simulated microgravity and demonstrates the plasticity of cardiac muscle under different loading conditions.

2001 ◽  
Vol 91 (2) ◽  
pp. 645-653 ◽  
Author(s):  
Merja A. Perhonen ◽  
Fatima Franco ◽  
Lynda D. Lane ◽  
Jay C. Buckey ◽  
C. Gunnar Blomqvist ◽  
...  

Cardiac muscle adapts well to changes in loading conditions. For example, left ventricular (LV) hypertrophy may be induced physiologically (via exercise training) or pathologically (via hypertension or valvular heart disease). If hypertension is treated, LV hypertrophy regresses, suggesting a sensitivity to LV work. However, whether physical inactivity in nonathletic populations causes adaptive changes in LV mass or even frank atrophy is not clear. We exposed previously sedentary men to 6 ( n = 5) and 12 ( n = 3) wk of horizontal bed rest. LV and right ventricular (RV) mass and end-diastolic volume were measured using cine magnetic resonance imaging (MRI) at 2, 6, and 12 wk of bed rest; five healthy men were also studied before and after at least 6 wk of routine daily activities as controls. In addition, four astronauts were exposed to the complete elimination of hydrostatic gradients during a spaceflight of 10 days. During bed rest, LV mass decreased by 8.0 ± 2.2% ( P = 0.005) after 6 wk with an additional atrophy of 7.6 ± 2.3% in the subjects who remained in bed for 12 wk; there was no change in LV mass for the control subjects (153.0 ± 12.2 vs. 153.4 ± 12.1 g, P = 0.81). Mean wall thickness decreased (4 ± 2.5%, P = 0.01) after 6 wk of bed rest associated with the decrease in LV mass, suggesting a physiological remodeling with respect to altered load. LV end-diastolic volume decreased by 14 ± 1.7% ( P = 0.002) after 2 wk of bed rest and changed minimally thereafter. After 6 wk of bed rest, RV free wall mass decreased by 10 ± 2.7% ( P = 0.06) and RV end-diastolic volume by 16 ± 7.9% ( P = 0.06). After spaceflight, LV mass decreased by 12 ± 6.9% ( P = 0.07). In conclusion, cardiac atrophy occurs during prolonged (6 wk) horizontal bed rest and may also occur after short-term spaceflight. We suggest that cardiac atrophy is due to a physiological adaptation to reduced myocardial load and work in real or simulated microgravity and demonstrates the plasticity of cardiac muscle under different loading conditions.


2007 ◽  
Vol 102 (3) ◽  
pp. 904-912 ◽  
Author(s):  
Jack M. Goodman ◽  
Michael R. Freeman ◽  
Leonard S. Goodman

The purpose of this study was to characterize left ventricular (LV) diastolic filling and systolic performance during graded arm exercise and to examine the effects of lower body positive pressure (LBPP) or concomitant leg exercise as means to enhance LV preload in aerobically trained individuals. Subjects were eight men with a mean age (±SE) of 26.8 ± 1.2 yr. Peak exercise testing was first performed for both legs [maximal oxygen uptake (V̇o2) = 4.21 ± 0.19 l/min] and arms (2.56 ± 0.16 l/min). On a separate occasion, LV filling and ejection parameters were acquired using non-imaging scintography using in vivo red blood cell labeling with technetium 99m first during leg exercise performed in succession for 2 min at increasing grades to peak effort. Graded arm exercise (at 30, 60, 80, and 100% peak V̇o2) was performed during three randomly assigned conditions: control (no intervention), with concurrent leg cycling (at a constant 15% leg maximal V̇o2) or with 60 mmHg of LBPP using an Anti G suit. Peak leg exercise LV ejection fraction was higher than arm exercise (60.9 ± 1.7% vs. 55.9 ± 2.7%; P < 0.05) as was peak LV end-diastolic volume was reported as % of resting value (110.3 ± 4.4% vs. 97 ± 3.7%; P < 0.05) and peak filling rate (end-diastolic volume/s; 6.4 ± 0.28% vs. 5.2 ± 0.25%). Concomitant use of either low-intensity leg exercise or LBPP during arm exercise failed to significantly increase LV filling or ejection parameters. These observations suggest that perturbations in preload fail to overcome the inherent hemodynamic conditions present during arm exercise that attenuate LV performance.


2008 ◽  
Vol 104 (4) ◽  
pp. 1037-1044 ◽  
Author(s):  
Todd A. Dorfman ◽  
Boaz D. Rosen ◽  
Merja A. Perhonen ◽  
Tommy Tillery ◽  
Roddy McColl ◽  
...  

Bed rest deconditioning leads to physiological cardiac atrophy, which may compromise left ventricular (LV) filling during orthostatic stress by reducing diastolic untwisting and suction. To test this hypothesis, myocardial-tagged magnetic resonance imaging (MRI) was performed, and maximal untwisting rates of the endocardium, midwall, and epicardium were calculated by Harmonic Phase Analysis (HARP) before and after −6° head-down tilt bed rest for 18 days with ( n = 14) and without exercise training ( n = 10). LV mass and LV end-diastolic volume were measured using cine MRI. Exercise subjects cycled on a supine ergometer for 30 min, three times per day at 75% maximal heart rate (HR). After sedentary bed rest, there was a significant reduction in maximal untwisting rates of the midwall (−46.8 ± 14.3 to −35.4 ± 12.4 °/s; P = 0.04) where untwisting is most reliably measured, and to a lesser degree of certainty in the endocardium (−50.3 ± 13.8 to −40.1 ± 18.5 °/s; P = 0.09); the epicardium was unchanged. In contrast, when exercise was performed in bed, untwisting rates were enhanced at the endocardium (−48.4 ± 20.8 to −72.3 ± 22.3 °/ms; P = 0.05) and midwall (−39.2 ± 12.2 to −59.0 ± 19.6 °/s; P = 0.03). The differential response was significant between groups at the endocardium (interaction P = 0.02) and the midwall (interaction P = 0.004). LV mass decreased in the sedentary group (156.4 ± 30.3 to 149.5 ± 27.9 g; P = 0.07), but it increased slightly in the exercise-trained subjects (156.4 ± 34.3 to 162.3 ± 40.5 g; P = 0.16); (interaction P = 0.03). We conclude that diastolic untwisting is impaired following sedentary bed rest. However, exercise training in bed can prevent the physiological cardiac remodeling associated with bed rest and preserve or even enhance diastolic suction.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
R Egoriti ◽  
F Landreani ◽  
L Costantini ◽  
E Mulder ◽  
D Gerlach ◽  
...  

Abstract Aims Prolonged immobilization generates cardiac deconditioning, a risk factor for cardiovascular disease, and efficient countermeasures (CM) are needed to prevent it. Our aim was to assess by Cine-MRI the effects of long-term strict head-down (−6 degrees) bed-rest (BR) deconditioning, and the effectiveness of high-intensity jump training CM, on left ventricular (LV) function and mass. Methods 23 male participants (29±6 years, 181±6 cm, 77±7 kg) were enrolled. The experiment was conducted at: envihab (Koln, DLR, Germany) as part of the European Space Agency BR studies. Volunteers were randomly allocated to the jump training group (JUMP, n=12) or the control group (CTRL, n=11). A typical training session consisted of 4x10 countermovement jumps and 2x10 hops in a sledge jump system, with 5–6 sessions per week. Steady-state free precession cine-MRI images were obtained (25 frames/cardiac cycle, 8mm thickness, no gap, no overlap) as stack of short-axis images covering the whole LV from base to apex, before (PRE) and after 58-days (HDT58) of BR. Endocardial and epicardial semi-automated contouring was performed using custom software. Results In CTRL group, at HDT58 a reduction in LV mass (9%), end-diastolic (21%), end-systolic (8%) and stroke volume (23%) were observed, while ejection fraction did not change. In JUMP group, the reduction in LV end-diastolic volume was only by 9%, followed by a decrease in end-systolic (10%) and stroke volume (10%), with a preservation of LV mass. In both groups, ejection fraction did not change. Left ventricular changes after 58d BR EDV (ml) ESV (ml) SV (ml) EF (%) Mass (g) CTRL PRE 171 (163; 191) 60 (58; 65) 113 (102; 124) 64 (63; 67) 133 (121; 160) HDT58 143 (131; 149)* 56 (50; 58)* 86 (83; 92)* 62 (60; 63)* 127 (106; 138)* JUMP PRE 156 (140; 204) 70 (61; 84) 91 (78; 117) 58 (56; 60) 118 (104; 134) HDT58 141 (135; 175)* 63 (54; 69)* 90 (78; 92)* 58 (55; 60) 113 (105; 128) Results expressed as median (25th; 75th percentiles). *p<0.05 Wilcoxon non parametric paired test (PRE vs HDT58). CTRL: control group; JUMP: countermeasure group. Conclusions Cardiac adaptation to deconditioning due to immobilization induced by BR resulted in a reduction of cardiac volumes and function, together with a decrease in LV mass. Interestingly, the applied JUMP countermeasure appeared able to partially reverse these effects, in particular by reducing the decrease in end-diastolic volume and preserving LV mass. This information could be useful for better understanding physiologic changes in patients undergoing long periods of immobilization, as well as to apply the studied countermeasure during space flight to reduce cardiac deconditioning. Acknowledgement/Funding Italian Space Agency (contract 2018-7-U.0),CNES/DAR 48ehz747.01950965,BELSPO, via the European Space Agency PRODEX program (PEA 4000110826)


Diagnostics ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1403
Author(s):  
Akira Yairo ◽  
Ahmed S. Mandour ◽  
Katsuhiro Matsuura ◽  
Tomohiko Yoshida ◽  
Danfu Ma ◽  
...  

Evaluation of diastolic function is a pivotal challenge due to limitations of the conventional echocardiography, especially when the heart rate is rapid as in rats. Currently, by using color M-mode echocardiography (CMME), intraventricular pressure difference (IVPD) and intraventricular pressure gradient (IVPG) in early diastole can be generated and are available as echocardiographic indices. These indices are expected to be useful for the early diagnosis of heart failure (HF), especially diastolic dysfunction. There have not been any studies demonstrating changes in IVPD and IVPG in response to changes in loading conditions in rats. Therefore, the present study aims to evaluate CMME-derived IVPD and IVPG changes in rats under various loading conditions. Twenty rats were included, divided into two groups for two different experiments, and underwent jugular vein catheterization under inhalational anesthetics. Conventional echocardiography, CMME, and 2D speckle tracking echocardiography were measured at the baseline (BL), after intravenous infusion of milrinone (MIL, n = 10), and after the infusion of hydroxyethyl starch (HES, n = 10). Left ventricular IVPD and IVPG were calculated from color M-mode images and categorized into total, basal, mid-to-apical, mid, and apical parts, and the percentage of the corresponding part was calculated. In comparison to the BL, the ejection fraction, mid-to-apical IVPG, mid IVPG, and apical IVPD were significantly increased after MIL administration (p < 0.05); meanwhile, the end-diastolic volume, E-wave velocity, total IVPD, and basal IVPD were significantly increased with the administration of HES (p < 0.05). The increase in mid-to-apical IVPD, mid IVPD, and apical IVPD indicated increased relaxation. A significant increase in basal IVPD reflected volume overloading by HES. CMME-derived IVPD and IVPG are useful tools for the evaluation of various loading conditions in rats. The approach used in this study provides a model for continuous data acquisition in chronic cardiac disease models without drug testing.


1992 ◽  
Vol 72 (3) ◽  
pp. 977-984 ◽  
Author(s):  
G. Geelen ◽  
P. Arbeille ◽  
J. L. Saumet ◽  
J. M. Cottet-Emard ◽  
F. Patat ◽  
...  

This study examined the hemodynamic consequences of prolonged lower body positive-pressure application and their relationship to changes in the plasma concentration of the major vasoactive hormones. Six men [36 +/- 2 (SE) yr] underwent 30 min of sitting and then 3 h of 70 degrees head-up tilt. An antigravity suit was applied (60 Torr legs, 30 Torr abdomen) during the last 2 h of tilt. In a similar noninflation experiment, the endocrine responses were measured in the suited subjects tilted for 3 h. Two-dimensional echocardiography was used to calculate ventricular volume and cardiac output. Measurements were made 30 min before and 30 and 90 min after inflation. Immediately after inflation, mean arterial pressure increased by 7 +/- 2 Torr and heart rate decreased by 16 +/- 4 beats/min. Left ventricular end-diastolic volume and systolic volume increased significantly (P less than 0.05) at 30 and 90 min of inflation. Cardiac output increased after 30 min of inflation and returned to the preinflation level at 90 min. Plasma norepinephrine and plasma renin activity were maximally suppressed after 15 and 90 min of inflation, respectively (P less than 0.05). No such hormonal changes occurred during control. Plasma sodium, potassium, and osmolality remained unchanged during both experiments. Thus, prolonged application of lower body positive pressure induces 1) a transient increase in cardiac output and 2) a marked and sustained decrease in plasma norepinephrine and plasma renin activity, which reflect an inflation-induced decrease in sympathetic activity.


1998 ◽  
Vol 85 (4) ◽  
pp. 1368-1375 ◽  
Author(s):  
R. L. Stepien ◽  
K. W. Hinchcliff ◽  
P. D. Constable ◽  
J. Olson

The cardiac morphology of 77 conscious Alaskan sled dogs before and after 5 mo of endurance training (20 km/day team pulling a sled and musher) was studied using two-dimensional and M-mode echocardiography. Subgroups included dogs with at least one season of previous training (“veterans”) and dogs undergoing their first season of training (“rookies”). Training resulted in a significant ( P< 0.05) decrease in resting heart rate (−15%) and significant increases in interventricular septal thickness (systole, 15%; diastole, 13%), left ventricular (LV) internal dimension in diastole (LVIDd, 4%), LV free wall thickness in systole (9%) and diastole (LVWd, 9%), and left atrial diameter (5%) in all dogs, but the increase in LVWd was greater in rookies (16%) than in veterans (7%). Training increased end-diastolic volume index (8%), LV mass index (24%), and heart weight index (24%) and decreased the LVIDd-to-LVWd ratio (−6%) but did not alter cardiac index. We conclude that increased LV mass attributable to LV dilation and hypertrophy is associated with endurance training in Alaskan sled dogs. Disproportionate LV wall thickening accompanying LV dilation suggests that cardiac morphological changes are due to volume and pressure loading. These training-induced changes are similar to those documented in human athletes undergoing combined isometric and isotonic training and differ from studies of dogs trained on treadmills.


Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Michael P Bancks ◽  
Mercedes Carnethon ◽  
Lisa S Chow ◽  
David R Jacobs ◽  
Satoru Kishi ◽  
...  

Introduction: Whether trajectories in fasting glucose (FG) and insulin resistance (HOMA-IR) during young adulthood, before the onset of diabetes, are associated with cardiac function and structure in middle adulthood is unclear. Hypothesis: We tested the hypothesis that as compared to low-stable trajectory of FG and HOMA-IR, an increasing trajectory for each would be associated with worse cardiac structure and function in middle adulthood. Methods: We determined FG and HOMA-IR for 2,198 CARDIA participants, age 18-30 years, at baseline (1985-1986) and 7, 10, 15, 20, and 25 year follow-up exams who fasted for >8 hours and were not pregnant and were free from diabetes at all exams. At year 30 (2016), Doppler echocardiography and 2D-guided M-mode echocardiography was performed, measuring left atrial dimension, relative wall thickness, left ventricular (LV) mass, LV mass indexed to height, LV ejection fraction percentage, LV end-diastolic and systolic volume, and LV mass to volume ratio. Trajectories were determined using latent class analysis (SAS Proc Traj). We used multivariable linear regression to estimate adjusted means for echo measures according to FG and HOMA-IR trajectory group after adjustment for potential confounding factors. Results: For individuals free from diabetes in midlife, we identified three trajectory groups for both FG and HOMA-IR, low-stable to increasing, moderate-increasing, and high-increasing. Compared to low-stable trajectory for FG, increasing trajectory was associated with greater LV end-diastolic volume, whereas for HOMA-IR increasing trajectory was associated with lower LV end-diastolic volume ( Table ). Increasing FG trajectory was also associated with greater left atrial dimension, while HOMA-IR was not. Conclusion: Trajectory of both FG and HOMA-IR during young adulthood, in the absence of diabetes, was most prominently and differentially associated with LV end-diastolic volume. Future research should elaborate on differential associations of FG and HOMA-IR trajectory.


1978 ◽  
Vol 235 (6) ◽  
pp. H767-H775 ◽  
Author(s):  
G. A. Geffin ◽  
M. A. Vasu ◽  
D. D. O'Keefe ◽  
D. G. Pennington ◽  
A. J. Erdmann ◽  
...  

In dogs anesthetized with chloralose-urethan on right heart bypass, left ventricular (LV) performance was assessed at constant LV stroke work before and for up to 2.5 h after crystalloid hemodilution was established. Lowering the hematocrit from 43.3 +/- 1.3% to 13.6 +/- 1.7% (SE) did not significantly change LV end-diastolic pressure (LVEDP) initially. After 80 min LVEDP increased slightly by 1.7 +/- 0.6 cmH2O (P less than 0.05) at a stroke work of 17.3 +/- 2.3 g.m. The value of dP/dt did not change significantly throughout. When LV function curves were generated by increasing cardiac output, the stroke work attained at an LVEDP of 10 cmH2O decreased with hemodilution from 23.9 +/- 3.5 to 20.8 +/- 3.9 g.m (NS). LV wall water content increased with hemodilution, from which it could be calculated that there was an 18.6% increase in LV mass. Thus, despite an increase in LV external girth demonstrated by LV circumferential gauges, it is possible that increased wall thickness due to the water gain resulted in little change or an actual decrease in LV end-diastolic volume. Thus, profound hemodilution can be attained with only slight depression of LV performance.


Author(s):  
Laura Banks ◽  
Saif Al-Mousawy ◽  
Mustafa A Altaha ◽  
Kaja Koneiczny ◽  
Wesseem Osman ◽  
...  

Background: The relationship between structural and electrical remodeling in the heart, particularly after long-standing endurance training, remains unclear. Signal-averaged electrocardiogram (SAECG) may provide a more sensitive method to evaluate cardiac remodeling than a 12-lead electrocardiogram (ECG). Accurate measures of electrical function (SAECG filtered QRS duration (fQRSd) and late potentials (LP) and left-ventricular mass (cardiac magnetic resonance, CMR) can allow an assessment of structural and electrical remodeling. Methods: Endurance athletes (45-65 years old, >10 years of endurance sport), screened to exclude cardiac disease, had standardized 12-lead ECG, SAECG, resting echocardiogram (ECHO), and CMR performed. SAECG fQRSd was correlated with QRS duration on the 12-lead ECG, and ECHO and CMR-derived left ventricular (LV) mass. Results: Participants (n=82, 67% male, mean age: 54±6 years, mean VO2max: 50±7 ml/kg/min) had a CMR-derived LV mass of 118±28 g/m2 and a fQRSd of 112±8 ms (46% had abnormal fQRSd (>114 msec), and 51% met clinical threshold for abnormal SAECG). fQRSd was positively correlated with the 12-lead ECG QRS duration (r=0.83), ECHO-derived LV mass (r=0.60), CMR-derived LV mass (r=0.58) and LV end-diastolic volume (r=0.63, p<0.001 for all). fQRSd had higher correlations with ECHO and CMR-derived LV mass than 12-lead ECG (p<0.0008 and p<0.0005, respectively). Conclusion: In a healthy cohort of middle-aged endurance athletes, the SAECG is often abnormal by conventional criteria, and is correlated with structural remodeling, but CMR evaluation does not indicate pathologic structural remodeling. SAECG fQRSd is superior to the 12-lead ECG for the electrocardiographic evaluation of LV mass.


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