Ventilation and cardiac output during the onset of exercise, and during voluntary hyperventilation, in humans.

Damgaard

Journal of Applied Physiology

et al. 2011

PetersenLG, Damgaard M, Petersen JCG, Norsk P. Mechanisms of increase in cardiac output during acute weightlessness in humans. J Appl Physiol 111: 407-411, 2011. First published June 2, 2011 doi:10.1152/japplphysiol.01188.2010.-Based on previous water immersion results, we tested the hypothesis that the acute 0-Ginduced increase in cardiac output (CO) is primarily caused by redistribution of blood from the vasculature above the legs to the cardiopulmonary circulation. In seated subjects (n ϭ 8), 20 s of 0 G induced by parabolic flight increased CO by 1.7 Ϯ 0.4 l/min (P Ͻ 0.001). This increase was diminished to 0.8 Ϯ 0.4 l/min (P ϭ 0.028), when venous return from the legs was prevented by bilateral venous thigh-cuff inflation (CI) of 60 mmHg. Because the increase in stroke volume during 0 G was unaffected by CI, the lesser increase in CO during 0 G ϩ CI was entirely caused by a lower heart rate (HR). Thus blood from vascular beds above the legs in seated subjects can alone account for some 50% of the increase in CO during acute 0 G. The remaining increase in CO is caused by a higher HR, of which the origin of blood is unresolved. In supine subjects, CO increased from 7.1 Ϯ 0.7 to 7.9 Ϯ 0.8 l/min (P ϭ 0.037) when entering 0 G, which was solely caused by an increase in HR, because stroke volume was unaffected. In conclusion, blood originating from vascular beds above the legs can alone account for one-half of the increase in CO during acute 0 G in seated humans. A Bainbridge-like reflex could be the mechanism for the HR-induced increase in CO during 0 G in particular in supine subjects. regional blood flow; blood pressure; vascular resistance; gravity GRAVITY CONSTANTLY STRESSES the cardiovascular system in upright humans by diminishing venous return. It decreases stroke volume (SV) and thus cardiac output (CO) and, through the baroreflex system, induces arteriolar constriction and an increase in heart rate (HR) to counteract a fall in blood pressure (4,21,30). Compared with the upright 1-G position, sudden entry into weightlessness (0 G) causes a redistribution of blood from the lower vascular beds to the central circulation (4, 29), leading to an increase in venous return, and thus in SV and CO, and, through stimulation of the baroreflexes, to arteriolar vasodilatation and a decrease in HR (18,21,23,29).Our laboratory has previously observed that, in upright seated humans, short-term 0 G created by parabolic airplane flights increases CO by as much as 1.8 l/min, which corresponds to some 0.6 liters over the 20-s period of 0 G (21). Bailliart et al. (2) estimated that, in standing humans, some 165 ml of fluid disappeared from each leg during 20 s of 0 G. These and our observations collectively suggest that the contribution of blood from the legs to the acute 0-G-induced increase in CO amounts to some 50%. In another study from our laboratory, we have, however, observed that water immersion in humans, which is used to simulate the effects of 0 G, increases the diameter of the left atrium to the same degree, whethe...

Section: Discussionmentioning

confidence: 99%

Mechanisms of increase in cardiac output during acute weightlessness in humans

Damgaard

Journal of Applied Physiology

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

“…Some authors, however, soon identified two components of the V O 2 kinetics: 1) a rapid, almost immediate phase (phase I) (5,54,55), which they attributed to an immediate increase in cardiac output (Q ) at exercise start; and 2) a subsequent slower phase (phase II), to which they restricted the influence of muscle metabolic adjustments. The strongest support to this view came from the demonstration that the kinetics of Q (12,13,16,60) and arterial O 2 flow (Q a O 2 ) (27) are very rapid.…”

mentioning

confidence: 85%

Phase I dynamics of cardiac output, systemic O₂ delivery, and lung O₂ uptake at exercise onset in men in acute normobaric hypoxia

Lador¹,

Tam²,

Kenfack³

et al. 2008

We tested the hypothesis that vagal withdrawal plays a role in the rapid (phase I) cardiopulmonary response to exercise. To this aim, in five men (24.6 Ϯ 3.4 yr, 82.1 Ϯ 13.7 kg, maximal aerobic power 330 Ϯ 67 W), we determined beat-by-beat cardiac output (Q ), oxygen delivery (Q a O 2 ), and breathby-breath lung oxygen uptake (V O2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O 2 ϭ 0.11), because the latter reduces resting vagal activity. We computed Q from stroke volume (Q st, by model flow) and heart rate (fH, electrocardiography), and Q a O 2 from Q and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state f H and Q were higher, and Qst and V O2 were unchanged. Q a O 2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A 1) for V O2 was unchanged. For fH, Q and Q a O 2 , A1 was lower. Phase I time constant (1) for Q a O 2 and V O2 was unchanged. The same was the case for Q at 100 W and for fH at 50 W. Q st kinetics were unaffected. In conclusion, the results do not fully support the hypothesis that vagal withdrawal determines phase I, because it was not completely suppressed. Although we can attribute the decrease in A 1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Q st. Thus the dual origin of the phase I of Q and Q a O 2 , neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed. cardiovascular response ALTHOUGH OUR KNOWLEDGE of the central (neural) control of the cardiovascular system at the exercise steady state is quite well established (19,42,57), how the circulatory readjustments upon exercise onset occur and match the increase in pulmonary oxygen uptake (V O 2 ) is less understood, as are the mechanisms underlying this matching. The kinetics of V O 2 at exercise onset were seen for a long time as reflecting essentially the metabolic adaptations in the working muscles (15,31,33). Some authors, however, soon identified two components of the V O 2 kinetics: 1) a rapid, almost immediate phase (phase I) (5, 54, 55), which they attributed to an immediate increase in cardiac output (Q ) at exercise start; and 2) a subsequent slower phase (phase II), to which they restricted the influence of muscle metabolic adjustments. The strongest support to this view came from the demonstration that the kinetics of Q (12, 13, 16, 60) and arterial O 2 flow (Q a O 2 ) (27) are very rapid.The concept of a close correspondence between V O 2 and muscle O 2 consumption was further undermined by the recent demonstration that, upon the onset of light exercise, the V O 2 kinetics are faster than the kinetics of muscle O 2 consumption estimated from the monoexponential decrease in phosphocreatine concentration (7,14,43). This would imply dissociation of the kinetics of V O 2 and muscle O 2 consumption, which should respond to different control mechanisms.Our postulate is that the V O 2 kinetics are dictated by ...

American Journal of Physiology-Regulatory, Integrative and Comp

“…It has been shown that short-term hyperventilation has no effect on MAP (14) and HR (6,19,28). The breathing rate and rebreathing volume also have no influence on CO (5,12,14,19).…”

Section: Cardiac Outputmentioning

confidence: 99%

Body height and blood pressure regulation in humans during anti-orthostatic tilting

Arvedsen

Damgaard

Norsk

2012

Arvedsen SK, Damgaard M, Norsk P. Body height and blood pressure regulation in humans during anti-orthostatic tilting. Am J Physiol Regul Integr Comp Physiol 302: R984 -R989, 2012. First published February 15, 2012 doi:10.1152/ajpregu.00036.2011.-The hypothesis was tested that the cardiovascular changes during an upper body anti-orthostatic maneuver in humans are more pronounced in tall than in short individuals, because of the larger intravascular hydrostatic pressure gradients. In 34 males and 41 females [20 -30 yr, body height (BH) ϭ 147-206 cm], inter-individual multiple linear regression analyses adjusted for gender and body weight were conducted between changes in cardiovascular variables versus BH during tilting of the upper body from vertical to horizontal while keeping the legs horizontal. In all the subjects, tilting induced increases in stroke volume and arterial pulse pressure and a decrease in heart rate, which each correlated significantly with BH. In males (n ϭ 51, BH ϭ 163-206 cm), 24-h ambulatory mean arterial pressure increased significantly with BH (P ϭ 0.004, r ϭ 0.40, ␣ ϭ 0.15 mmHg/cm) so that systolic/diastolic blood pressure increased by 2/2 mmHg per 15 cm increase in BH. There was no significant correlation between mean arterial pressure and BH in females (n ϭ 53, BH ϭ 147-193 cm). In conclusion, a larger BH induces larger cardiovascular changes during anti-orthostatic tilting, and in males 24-h ambulatory mean arterial pressure increases with BH. The lack of a mean arterial pressure to BH correlation in females is probably because of their lower BH and greater variability in blood pressure. cardiovascular system; hydrostatic pressure; gravity; orthostasis WHEN HUMANS CHANGE POSITION from supine to upright, blood is redistributed from the upper to the lower body. This results in a reduction in blood pressure (BP) in the upper body and an increase in the lower body. To ensure an adequate venous return and appropriate blood flow to the brain, baroreflexes originating from the carotid sinus, aorta, and atria of the heart induce contraction of the arterial resistance vessels and an increase in heart rate (HR) and cardiac contractility (1, 27). During anti-orthostatic maneuvers from upright to supine, the opposite changes occur.Because hydrostatic pressure gradients in upright individuals impede venous return to the heart and inhibit the carotid baroreceptors, it is possible that body height (BH) is a determinant of BP at heart level. That this might be the case is indicated by the giraffe, which exhibits the highest BP than any other creature (2, 10, 11). It is possible that to ensure an adequate perfusion of the brain in the giraffe, the high BP at heart level of more than 200 mmHg is required to overcome the high hydrostatic pressure gradient from head to heart. Therefore, it is possible that also in humans, however, much weaker BH and thereby the distance from the heart to the brain is one of the determinants of BP at heart level.It is known that BP during childhood is correlated to BH a...