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

2008 ◽  
Vol 295 (2) ◽  
pp. R624-R632 ◽  
Author(s):  
Frédéric Lador ◽  
Enrico Tam ◽  
Marcel Azabji Kenfack ◽  
Michela Cautero ◽  
Christian Moia ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Phase I ◽  
Acute Hypoxia ◽  
Vagal Activity ◽  
Rapid Phase ◽  
Lower Phase ◽  
Model Flow ◽  
O2 Delivery ◽  
Dual Origin ◽  
Vagal Withdrawal

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 ± 3.4 yr, 82.1 ± 13.7 kg, maximal aerobic power 330 ± 67 W), we determined beat-by-beat cardiac output (Q̇), oxygen delivery (Q̇aO2), and breath-by-breath lung oxygen uptake (V̇o2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O2 = 0.11), because the latter reduces resting vagal activity. We computed Q̇ from stroke volume (Qst, by model flow) and heart rate ( fH, electrocardiography), and Q̇aO2 from Q̇ and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state fH and Q̇ were higher, and Qst and V̇o2 were unchanged. Q̇aO2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A1) for V̇o2 was unchanged. For fH, Q̇ and Q̇aO2, A1 was lower. Phase I time constant (τ1) for Q̇aO2 and V̇o2 was unchanged. The same was the case for Q̇ at 100 W and for fH at 50 W. Qst 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 A1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Qst. Thus the dual origin of the phase I of Q̇ and Q̇aO2, neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed.

scholarly journals Simultaneous determination of the kinetics of cardiac output, systemic O2 delivery, and lung O2 uptake at exercise onset in men

2006 ◽  
Vol 290 (4) ◽  
pp. R1071-R1079 ◽  
Author(s):  
Frédéric Lador ◽  
Marcel Azabji Kenfack ◽  
Christian Moia ◽  
Michela Cautero ◽  
Denis R. Morel ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Steady State ◽  
Phase I ◽  
Time Course ◽  
Hemoglobin Concentration ◽  
Two Phase ◽  
Rapid Phase ◽  
Steady State Method ◽  
Exercise Onset ◽  
Kinetics Of

We tested whether the kinetics of systemic O2 delivery (Q̇aO2) at exercise start was faster than that of lung O2 uptake (V̇o2), being dictated by that of cardiac output (Q̇), and whether changes in Q̇ would explain the postulated rapid phase of the V̇o2 increase. Simultaneous determinations of beat-by-beat (BBB) Q̇ and Q̇aO2, and breath-by-breath V̇o2 at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 ± 3.2 years, maximal aerobic power 333 ± 61 W). V̇o2 was determined using Grønlund's algorithm. Q̇ was computed from BBB stroke volume (Qst, from arterial pulse pressure profiles) and heart rate ( fh, electrocardiograpy) and calibrated against a steady-state method. This, along with the time course of hemoglobin concentration and arterial O2 saturation (infrared oximetry) allowed computation of BBB Q̇aO2. The Q̇, Q̇aO2 and V̇o2 kinetics were analyzed with single and double exponential models. fh, Qst, Q̇, and V̇o2 increased upon exercise onset to reach a new steady state. The kinetics of Q̇aO2 had the same time constants as that of Q̇. The latter was twofold faster than that of V̇o2. The V̇o2 kinetics were faster than previously reported for muscle phosphocreatine decrease. Within a two-phase model, because of the Fick equation, the amplitude of phase I Q̇ changes fully explained the phase I of V̇o2 increase. We suggest that in unsteady states, lung V̇o2 is dissociated from muscle O2 consumption. The two components of Q̇ and Q̇aO2 kinetics may reflect vagal withdrawal and sympathetic activation.

scholarly journals Acute Moderate Hypoxia Reduces One-Legged Cycling Performance Despite Compensatory Increase in Peak Cardiac Output: A Pilot Study

2021 ◽  
Vol 18 (7) ◽  
pp. 3732
Author(s):  
Hannes Gatterer ◽  
Verena Menz ◽  
Martin Burtscher
Keyword(s):  
Cardiac Output ◽  
Oxygen Uptake ◽  
Power Output ◽  
Acute Hypoxia ◽  
Peak Oxygen Uptake ◽  
Peak Power Output ◽  
Moderate Altitude ◽  
Moderate Hypoxia ◽  
Leg Cycling ◽  
O2 Delivery

In severe hypoxia, single-leg peak oxygen uptake (VO2peak) is reduced mainly due to the inability to increase cardiac output (CO). Whether moderate altitude allows CO to increase during single-leg cycling, thereby restoring VO2peak, has not been extensively investigated. Five healthy subjects performed an incremental, maximal, two-legged cycle ergometer test, and on separate days a maximal incremental one-leg cycling test in normoxia and in moderate hypoxia (fraction of inspired oxygen (FiO2) = 15%). Oxygen uptake, heart rate, blood pressure responses, power output, and CO (PhysioFlow) were measured during all tests. Moderate hypoxia lowered single-leg peak power output (154 ± 31 vs. 128 ± 26 watts, p = 0.03) and oxygen uptake (VO2) (36.8 ± 6.6 vs. 33.9 ± 6.9 mL/min/kg, p = 0.04), despite higher peak CO (16.83 ± 3.10 vs. 18.96 ± 3.59 L/min, p = 0.04) and systemic oxygen (O2) delivery (3.37 ± 0.84 vs. 3.47 ± 0.89 L/min, p = 0.04) in hypoxia compared to normoxia. Arterial–venous O2 difference (a–vDO2) was lower in hypoxia (137 ± 21 vs. 112 ± 19 mL/l, p = 0.03). The increases in peak CO from normoxia to hypoxia were negatively correlated with changes in mean arterial pressure (MABP) (p < 0.05). These preliminary data indicate that the rise in CO was not sufficient to prevent single-leg performance loss at moderate altitude and that enhanced baroreceptor activity might limit CO increases in acute hypoxia, likely by reducing sympathetic activation. Since the systemic O2 delivery was enhanced and the calculated a–vDO2 reduced in moderate hypoxia, a potential diffusion limitation cannot be excluded.

Gastrointestinal blood flow and oxygen consumption in awake newborn piglets: effect of feeding

1983 ◽  
Vol 245 (5) ◽  
pp. G697-G702 ◽  
Author(s):  
P. T. Nowicki ◽  
B. S. Stonestreet ◽  
N. B. Hansen ◽  
A. C. Yao ◽  
W. Oh
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
O2 Consumption ◽  
Gi Tract ◽  
Local Blood Flow ◽  
O2 Uptake ◽  
O2 Extraction ◽  
Gastrointestinal Blood Flow ◽  
O2 Delivery ◽  
Effect Of Feeding

Regional and total gastrointestinal (GI) blood flow, O2 delivery, and whole-gut O2 extraction and O2 consumption were measured before and 30, 60, and 120 min after feeding in nonanesthetized, awake 2-day-old piglets. Cardiac output and blood flow to kidneys, heart, brain, and liver were also determined. Blood flow was measured using the radiolabeled microsphere technique. In the preprandial condition, total GI blood flow was 106 +/- 9 ml X min-1 X 100 g-1, while O2 extraction was 17.2 +/- 0.9% and O2 consumption was 1.99 +/- 0.19 ml O2 X min-1 X 100 g-1. Thirty minutes after slow gavage feeding with 30 ml/kg artificial pig milk, O2 delivery to the GI tract and O2 extraction rose significantly (P less than 0.05) by 35 +/- 2 and 33 +/- 2%, respectively. The increase in O2 delivery was effected by a significant increase in GI blood flow, which was localized to the mucosal-submucosal layer of the small intestine. O2 uptake by the GI tract increased 72 +/- 4% 30 min after feeding. Cardiac output and blood flow to non-GI organs did not change significantly with feeding, whereas arterial hepatic blood flow decreased significantly 60 and 120 min after feeding. The piglet GI tract thus meets the oxidative demands of digestion and absorption by increasing local blood flow and tissue O2 extraction.

The Role of the Aortic Body Chemoreceptors in the Cardiac and Respiratory Responses to Acute Hypoxia in the Anesthetized Dog

1973 ◽  
Vol 51 (4) ◽  
pp. 249-259 ◽  
Author(s):  
G. P. Biro ◽  
J. D. Hatcher ◽  
D. B. Jennings
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Acute Hypoxia ◽  
Control Period ◽  
Indirect Evidence ◽  
Minute Volume ◽  
Significant Rise ◽  
Cardiac Response ◽  
Cardiac Responses ◽  
Respiratory Parameters

The participation of the aortic chemoreceptors in the reflex cardiac responses to acute hypoxia is suggested only by the indirect evidence of pharmacological stimulation of these receptors. In order to assess their role more directly, the response to a 15 min period of hypoxia was determined after surgical denervation of the aortic chemoreceptors (A.D.), and compared with the response of sham-operated (S.O.) dogs, anesthetized with morphine–pentobarbital. In the control period, while breathing room air, the cardiovascular and respiratory parameters measured in the A.D. animals were not different from those of the S.O. dogs. Hypoxia (partial pressure of oxygen approximately 30 mm Hg) in the S.O. dogs was associated with a statistically significant rise in the heart rate (+71 ± 7 min−1, mean ± S.E.M.) and of the cardiac output (+25 ± 10 ml kg−1 min−1). In the A.D. animals, the significantly smaller increment in heart rate (+29 ± 6 min−1) was associated with a fall of the cardiac output (−16 ± 12 ml kg−1 min−1). The hypoxia-induced changes in heart rate and cardiac output in the S.O. animals were different (p < 0.05) from those in the A.D. group. The minute volume of ventilation was significantly augmented in both groups, and to a comparable extent. These findings indicate that the aortic chemoreceptors play a significant role in the cardiac response to hypoxia, but they do not affect, to a significant extent, the respiratory response.

Oxygen transport during exercise in large mammals. I. Adaptive variation in oxygen demand

1989 ◽  
Vol 67 (2) ◽  
pp. 862-870 ◽  
Author(s):  
J. H. Jones ◽  
K. E. Longworth ◽  
A. Lindholm ◽  
K. E. Conley ◽  
R. H. Karas ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Mammalian Species ◽  
Oxygen Demand ◽  
Tissue Resistance ◽  
Capillary Bed ◽  
The Difference ◽  
Hb Concentration ◽  
O2 Delivery ◽  
Arterial Po2

This study investigated mechanisms used by horses and steers to increase O2 uptake and delivery (VO2) from resting to maximal rates and identified the mechanisms that enable horses to achieve higher maximal rates of O2 consumption (VO2max) than steers. VO2 and circulatory variables were measured while Standardbred trotting horses and steers (450-kg body mass) stood quietly and ran on a treadmill at speeds up to those eliciting VO2max. As VO2 increased in both species, heart rate and circulating hemoglobin (Hb) concentration increased, thereby increasing O2 delivery by the circulation, while cardiac stroke volume remained unchanged. At VO2max arterial PCO2 increased from its resting value in horses but was unchanged in steers, and arterial PO2 decreased in both species. Although the horses hypoventilated and were hypoxemic at VO2max, no significant decrease in arterial Hb saturation occurred. VO2max of the horses was 2.6 times higher than that of the steers and was associated with a 100% larger cardiac output, 100% larger stroke volume, and 40% higher Hb concentration, whereas heart rates at VO2max were identical in the two species. The higher cardiac output of the horses at VO2max resulted from a 1.2-fold higher mean arterial pressure and 1.6-fold lower peripheral tissue resistance (associated with a larger skeletal muscle capillary bed). Both the magnitude of the difference in VO2max between horses and steers and the mechanisms used to achieve it are the same as observed in smaller pairs of mammalian species with large variation in aerobic capacity.

Higher Cardiac Vagal Activity Predicts Lower Peripheral Resistance Six Years Later in European but not African Americans

2021 ◽  
Author(s):  
DeWayne P. Williams ◽  
Julian F. Thayer ◽  
James D. Halbert ◽  
Xiaoling Wang ◽  
Gaston Kapuku
Keyword(s):  
Cardiac Output ◽  
Peripheral Resistance ◽  
Cardiovascular Complications ◽  
Vagal Activity ◽  
Differential Impact ◽  
Full Sample ◽  
Mortality And Morbidity ◽  
European Americans ◽  
Lower Blood

African American (AA) individuals are at a greater risk for the development of cardiovascular complications, such as hypertension, compared to European Americans (EAs). Higher vagally mediated heart rate variability (HRV) is typically associated with lower blood pressure (BP) and total peripheral resistance (TPR). However, research has yet to examine the differential impact of HRV on longitudinal hemodynamic activity between AAs and EAs. We sought to rectify this in a sample of 385 normotensive youths (207 AAs, 178 EAs; mean age 23.16 ± 2.9 years). Individuals participated in two laboratory evaluations spanning approximately six years. Bio-impedance was used to assess HRV at time 1 and cardiac output at both time 1 and time 2. Mean arterial pressure (i.e., BP) was measured at both timepoints via an automated BP machine. TPR was calculated as MAP divided by cardiac output. Results showed AAs to have higher BP and higher TPR at time 2 compared to EAs, independent of several important covariates. Also, higher HRV at time 1 significantly predicted both lower TPR and BP at time 2 among EAs only; these associations were attenuated and not significant in AAs. HRV did not significantly predict cardiac output at time 2 in the full sample or split by ethnicity. Our findings highlight that AAs show TPR mediated long-term increases in BP irrespective of resting HRV, providing a physiological pathway linking AAs with a greater risk for mortality and morbidity from hypertension and potentially other cardiovascular disease.

Systemic and regional O2 delivery and uptake in bled dogs given hypertonic saline, whole blood, or dextran

1992 ◽  
Vol 262 (3) ◽  
pp. H778-H786 ◽  
Author(s):  
S. E. Curtis ◽  
S. M. Cain
Keyword(s):  
Cardiac Output ◽  
Hypertonic Saline ◽  
Special Effect ◽  
Shed Blood ◽  
Hindlimb Muscle ◽  
Dextran 70 ◽  
O2 Extraction ◽  
Negative Effect ◽  
Anesthetized Dogs ◽  
O2 Delivery

The mechanisms by which small volumes of hypertonic saline in dextran (HSD) resuscitate bled dogs are incompletely understood but may include a pulmonary osmolar reflex. A known negative effect of HSD is hemodilution that reduces O2-carrying capacity. Our goals in this study were to ascertain whether the putative osmotic reflex redistributed blood flow between muscle and gut and whether O2 delivery (DO2) was adequate at systemic and regional levels. Left hindlimb muscle and a segment of ileum were vascularly isolated in three groups (n = 8) of anesthetized dogs that were then bled to mean arterial pressure (MAP) of 40 mmHg for 30 min. At that point, all shed blood (approximately 40 ml/kg) was returned in the blood group (BLD); 20 ml/kg of Dextran 70 was given to the dextran group (DEX); and 5 ml/kg of 7.5% NaCl in dextran was given to the HSD group. MAP and cardiac output were restored to acceptable levels in all but was poorly maintained in HSD. The fall in hematocrit (41 to 25%) in HSD was matched by that in DEX (42 to 22%), so that DO2 only reached approximately 55% of that in BLD. Nevertheless, systemic and regional O2 uptakes were similar; O2 debt and repayment did not differ; and lactate metabolism was alike in all groups. O2 extraction did have to increase to near maximum in HSD, however. Other than a transient increase to muscle, HSD had no special effect on distribution of cardiac output. HSD was efficacious as a short-term resuscitative measure but did encroach markedly on O2 transport reserves.

scholarly journals Cardiac responses to hypoxia and reoxygenation in Drosophila

2015 ◽  
Vol 309 (11) ◽  
pp. R1347-R1357 ◽  
Author(s):  
Rachel Zarndt ◽  
Sarah Piloto ◽  
Frank L. Powell ◽  
Gabriel G. Haddad ◽  
Rolf Bodmer ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Genetic Model ◽  
Heart Function ◽  
Acute Hypoxia ◽  
Hypoxia Inducible Factor ◽  
High Energy ◽  
Hypoxic Exposure ◽  
Low Oxygen ◽  
Cardiac Responses ◽  
Organ Systems

An adequate supply of oxygen is important for the survival of all tissues, but it is especially critical for tissues with high-energy demands, such as the heart. Insufficient tissue oxygenation occurs under a variety of conditions, including high altitude, embryonic and fetal development, inflammation, and thrombotic diseases, often affecting multiple organ systems. Responses and adaptations of the heart to hypoxia are of particular relevance in human cardiovascular and pulmonary diseases, in which the effects of hypoxic exposure can range in severity from transient to long-lasting. This study uses the genetic model system Drosophila to investigate cardiac responses to acute (30 min), sustained (18 h), and chronic (3 wk) hypoxia with reoxygenation. Whereas hearts from wild-type flies recovered quickly after acute hypoxia, exposure to sustained or chronic hypoxia significantly compromised heart function upon reoxygenation. Hearts from flies with mutations in sima, the Drosophila homolog of the hypoxia-inducible factor alpha subunit (HIF-α), exhibited exaggerated reductions in cardiac output in response to hypoxia. Heart function in hypoxia-selected flies, selected over many generations for survival in a low-oxygen environment, revealed reduced cardiac output in terms of decreased heart rate and fractional shortening compared with their normoxia controls. Hypoxia-selected flies also had smaller hearts, myofibrillar disorganization, and increased extracellular collagen deposition, consistent with the observed reductions in contractility. This study indicates that longer-duration hypoxic insults exert deleterious effects on heart function that are mediated, in part, by sima and advances Drosophila models for the genetic analysis of cardiac-specific responses to hypoxia and reoxygenation.

scholarly journals Hypoxia-induced vagal withdrawal is independent of the hypoxic ventilatory response in men

2019 ◽  
Vol 126 (1) ◽  
pp. 124-131 ◽  
Author(s):  
Christoph Siebenmann ◽  
Camilla K. Ryrsø ◽  
Laura Oberholzer ◽  
James P. Fisher ◽  
Linda M. Hilsted ◽  
...  
Keyword(s):  
Heart Rate ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Spontaneous Breathing ◽  
Animal Studies ◽  
Pulmonary Ventilation ◽  
Vagal Activity ◽  
Adrenergic Blockade ◽  
Controlled Breathing ◽  
Vagal Withdrawal

Hypoxia increases heart rate (HR) in humans by sympathetic activation and vagal withdrawal. However, in anaesthetized dogs hypoxia increases vagal activity and reduces HR if pulmonary ventilation does not increase and we evaluated whether that observation applies to awake humans. Ten healthy males were exposed to 15 min of normoxia and hypoxia (10.5% O2), while respiratory rate and tidal volume were volitionally controlled at values identified during spontaneous breathing in hypoxia. End-tidal CO2 tension was clamped at 40 mmHg by CO2 supplementation. β-Adrenergic blockade by intravenous propranolol isolated vagal regulation of HR. During spontaneous breathing, hypoxia increased ventilation by 3.2 ± 2.1 l/min ( P = 0.0033) and HR by 8.9 ± 5.5 beats/min ( P < 0.001). During controlled breathing, respiratory rate (16.3 ± 3.2 vs. 16.4 ± 3.3 breaths/min) and tidal volume (1.05 ± 0.27 vs. 1.06 ± 0.24 l) were similar for normoxia and hypoxia, whereas the HR increase in hypoxia persisted without (8.6 ± 10.2 beats/min) and with (6.6 ± 5.6 beats/min) propranolol. Neither controlled breathing ( P = 0.80), propranolol ( P = 0.64), nor their combination ( P = 0.89) affected the HR increase in hypoxia. Arterial pressure was unaffected ( P = 0.48) by hypoxia across conditions. The hypoxia-induced increase in HR during controlled breathing and β-adrenergic blockade indicates that hypoxia reduces vagal activity in humans even when ventilation does not increase. Vagal withdrawal in hypoxia seems to be governed by the arterial chemoreflex rather than a pulmonary inflation reflex in humans. NEW & NOTEWORTHY Hypoxia accelerates the heart rate of humans by increasing sympathetic activity and reducing vagal activity. Animal studies have indicated that hypoxia-induced vagal withdrawal is governed by a pulmonary inflation reflex that is activated by the increased pulmonary ventilation in hypoxia. The present findings, however, indicate that humans experience vagal withdrawal in hypoxia even if ventilation does not increase, indicating that vagal withdrawal is governed by the arterial chemoreflex rather than a pulmonary inflation reflex.

Regional blood flow and cardiac output during acute hypoxia in the anesthetized dog

1963 ◽  
Vol 204 (6) ◽  
pp. 963-968 ◽  
Author(s):  
John F. Murray ◽  
I. Maureen Young
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Acute Hypoxia ◽  
Arterial Oxygen Saturation ◽  
Head Kidney ◽  
Arterial Oxygen ◽  
Circulatory Effects ◽  
Low Concentrations ◽  
Anesthetized Dogs

The circulatory effects of breathing low concentrations of oxygen were studied in ten anesthetized dogs. Simultaneous measurements were made of cardiac output (indicator dilution technique) and blood flow to the head, kidney, and hind limb (electromagnetic flowmeters). Four experiments were performed with the addition of succinylcholine to inhibit the ventilatory response to hypoxia and maintain pCO2 constant. A rise in cardiac output and mean arterial pressure occurred which was significantly correlated to the decrease in arterial oxygen saturation. No threshold for these responses was found. Blood flow tended to increase during hypoxia in the regions studied but the responses were variable and only the change in renal blood flow had a significant correlation to arterial oxygen unsaturation. Systemic and regional vascular resistances during hypoxia varied both in direction and magnitude of change. The preponderant effects of hypoxia influence cardiac output more than peripheral vascular resistance.

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