scholarly journals Exercise heat acclimation has minimal effects on left ventricular volumes, function and systemic hemodynamics in euhydrated and dehydrated trained humans

2020 ◽  
Vol 319 (5) ◽  
pp. H965-H979
Author(s):  
Gavin Travers ◽  
José González-Alonso ◽  
Nathan Riding ◽  
David Nichols ◽  
Anthony Shaw ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Left Ventricle ◽  
Blood Volume ◽  
Heat Acclimation ◽  
Left Ventricular ◽  
Systemic Hemodynamics ◽  
Diastolic Filling ◽  
Left Ventricular Volumes ◽  
Ventricular Volumes

This study demonstrates that 10 days of exercise heat acclimation has minimal effects on left ventricular volumes, intrinsic cardiac function, and systemic hemodynamics during prolonged, repeated semirecumbent exercise in moderate heat, where heart rate and blood volume are similar to preacclimation levels. However, progressive dehydration is consistently associated with similar degrees of hyperthermia and tachycardia and reductions in blood volume, diastolic filling of the left ventricle, stroke volume, and cardiac output, regardless of acclimation state.

In the Loop—Left Ventricular Pressures

2011 ◽  
pp. 42-47
Author(s):  
James R. Munis
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Aortic Valve ◽  
Left Ventricle ◽  
Stroke Volume ◽  
Cardiovascular System ◽  
Aortic Root ◽  
Left Ventricular ◽  
Root Pressure ◽  
The Third

We've already looked at 2 types of pressure that affect physiology (atmospheric and hydrostatic pressure). Now let's consider the third: vascular pressures that result from mechanical events in the cardiovascular system. As you already know, cardiac output can be defined as the product of heart rate times stroke volume. Heart rate is self-explanatory. Stroke volume is determined by 3 factors—preload, afterload, and inotropy—and these determinants are in turn dependent on how the left ventricle handles pressure. In a pressure-volume loop, ‘afterload’ is represented by the pressure at the end of isovolumic contraction—just when the aortic valve opens (because the ventricular pressure is now higher than aortic root pressure). These loops not only are straightforward but are easier to construct just by thinking them through, rather than by memorization.

Atrial natriuretic peptide reverses angiotensin-induced venoconstriction in dogs

1989 ◽  
Vol 257 (4) ◽  
pp. H1062-H1067 ◽  
Author(s):  
R. W. Lee ◽  
R. G. Gay ◽  
S. Goldman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Left Ventricular ◽  
Ang Ii ◽  
Central Blood Volume ◽  
Venous Compliance ◽  
Induced Hypertension

To determine whether atrial natriuretic peptide (ANP) can reverse angiotensin (ANG II)-induced venoconstriction, ANP was infused (0.3 micrograms.kg-1.min-1) in the presence of ANG II-induced hypertension in six ganglion-blocked dogs. ANG II was initially administered to increase mean arterial blood pressure (MAP) 50% above control. ANG II did not change heart rate or left ventricular rate of pressure development (LV dP/dt) but increased total peripheral vascular resistance (TPVR) and left ventricular end-diastolic pressure (LVEDP). Mean circulatory filling pressure (MCFP) increased, whereas cardiac output and venous compliance decreased. Unstressed vascular volume did not change, but central blood volume increased. ANP infusion during ANG II-induced hypertension resulted in a decrease in MAP, but TPVR did not change. There were no changes in heart rate or LV dP/dt. ANP decreased cardiac output further. LVEDP returned to base line with ANP. ANP also decreased MCFP and normalized venous compliance. There was no significant change in total blood volume, but central blood volume decreased. In summary, ANP can reverse the venoconstriction but not the arterial vasoconstriction produced by ANG II. The decrease in MAP was due to a decrease in cardiac output that resulted from venodilatation and aggravation of the preload-afterload mismatch produced by ANG II alone. Because TPVR did not change when MAP fell, we conclude that the interaction between ANG II and ANP occurs primarily in the venous circulation.

Dimensional analysis of right and left ventricles during positive-pressure ventilation in dogs

1982 ◽  
Vol 242 (4) ◽  
pp. H549-H556 ◽  
Author(s):  
S. S. Cassidy ◽  
J. H. Mitchell ◽  
R. L. Johnson
Keyword(s):  
Left Ventricle ◽  
Stroke Volume ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Left Ventricular Volumes ◽  
Ventricular Volumes ◽  
End Diastolic Volume ◽  
Left And Right ◽  
The Right ◽  
Ventricular Dimensions

Our purpose was to determine the effects of controlled ventilation with positive end-expired pressure (PEEP) on ventricular dimensions and to relate changes in shape to changes in stroke volume and left ventricular volumes. Left and right ventricular dimensions were measured using biplane cinefluorography of dogs with radiopaque markers implanted in their hearts, and left ventricular volumes were derived from left ventricular dimensions by assuming that the left ventricle conformed to the shape of a nonprolate ellipsoid. As PEEP increased from 0 to 5, 10, and 15 cmH2O, stroke volume fell 36%, and all three left ventricular end-diastolic dimensions fell, with apex-base falling 5%, anterior-posterior falling 7%, and septal-lateral falling nearly twice as much, 12%. This resulted in a 11.3 cm3 fall in left ventricular end-diastolic volume. The right ventricular end-diastolic dimensions changed in opposite directions with respect to each other as the level and PEEP was raised to 15 cmH2O; one axis fell 3.2 mm, and the midpoint of the right ventricular free wall moved outward by 1.7 mm. Thus the fall in cardiac output (and stroke volume) during PEEP was associated with a fall in left ventricular end-diastolic volume and a change both left and right ventricular configurations. It is not known whether the left ventricular septal-lateral narrowing is the consequence of lateral wall compression by the lungs or encroachment on the left ventricle by the septum.

scholarly journals Cardiac changes induced by immersion and breath-hold diving in humans

2009 ◽  
Vol 106 (1) ◽  
pp. 293-297 ◽  
Author(s):  
Claudio Marabotti ◽  
Alessandro Scalzini ◽  
Danilo Cialoni ◽  
Mirko Passera ◽  
Antonio L'Abbate ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Diastolic Function ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Breath Hold ◽  
Left Ventricular Volumes ◽  
Ventricular Diastolic Function ◽  
Condition C

To evaluate the separate cardiovascular response to body immersion and increased environmental pressure during diving, 12 healthy male subjects (mean age 35.2 ± 6.5 yr) underwent two-dimensional Doppler echocardiography in five different conditions: out of water (basal); head-out immersion while breathing ( condition A); fully immersed at the surface while breathing ( condition B) and breath holding ( condition C); and breath-hold diving at 5-m depth ( condition D). Heart rate, left ventricular volumes, stroke volume, and cardiac output were obtained by underwater echocardiography. Early (E) and late (A) transmitral flow velocities, their ratio (E/A), and deceleration time of E (DTE) were also obtained from pulsed-wave Doppler, as left ventricular diastolic function indexes. The experimental protocol induced significant reductions in left ventricular volumes, left ventricular stroke volume ( P < 0.05), cardiac output ( P < 0.001), and heart rate ( P < 0.05). A significant increase in E peak ( P < 0.01) and E/A ( P < 0.01) and a significant reduction of DTE ( P < 0.01) were also observed. Changes occurring during diving ( condition D) accounted for most of the changes observed in the experimental series. In particular, cardiac output at condition D was significantly lower compared with each of the other experimental conditions, E/A was significantly higher during condition D than in conditions A and C. Finally, DTE was significantly shorter at condition D than in basal and condition C. This study confirms a reduction of cardiac output in diving humans. Since most of the changes were observed during diving, the increased environmental pressure seems responsible for this hemodynamic rearrangement. Left ventricular diastolic function changes suggest a constrictive effect on the heart, possibly accounting for cardiac output reduction.

Left ventricular mechanical limitations to stroke volume in healthy humans during incremental exercise

2011 ◽  
Vol 301 (2) ◽  
pp. H478-H487 ◽  
Author(s):  
Eric J. Stöhr ◽  
José González-Alonso ◽  
Rob Shave
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Left Ventricular ◽  
Incremental Exercise ◽  
Diastolic Filling ◽  
Systolic Volume ◽  
Young Males ◽  
Healthy Humans ◽  
End Diastolic Volume

During incremental exercise, stroke volume (SV) plateaus at 40–50% of maximal exercise capacity. In healthy individuals, left ventricular (LV) twist and untwisting (“LV twist mechanics”) contribute to the generation of SV at rest, but whether the plateau in SV during incremental exercise is related to a blunting in LV twist mechanics remains unknown. To test this hypothesis, nine healthy young males performed continuous and discontinuous incremental supine cycling exercise up to 90% peak power in a randomized order. During both exercise protocols, end-diastolic volume (EDV), end-systolic volume (ESV), and SV reached a plateau at submaximal exercise intensities while heart rate increased continuously. Similar to LV volumes, two-dimensional speckle tracking-derived LV twist and untwisting velocity increased gradually from rest (all P < 0.001) and then leveled off at submaximal intensities. During continuous exercise, LV twist mechanics were linearly related to ESV, SV, heart rate, and cardiac output (all P < 0.01) while the relationship with EDV was exponential. In diastole, the increase in apical untwisting was significantly larger than that of basal untwisting ( P < 0.01), emphasizing the importance of dynamic apical function. In conclusion, during incremental exercise, the plateau in LV twist mechanics and their close relationship with SV and cardiac output indicate a mechanical limitation in maximizing LV output during high exercise intensities. However, LV twist mechanics do not appear to be the sole factor limiting LV output, since EDV reaches its maximum before the plateau in LV twist mechanics, suggesting additional limitations in diastolic filling to the heart.

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