Haemoglobin, Blood Volume, Cardiac Function, and Aerobic Power

1999 ◽  
Vol 24 (1) ◽  
pp. 54-65 ◽  
Author(s):  
Norman Gledhill ◽  
Darren Warburton ◽  
Veronica Jamnik
Keyword(s):  
Cardiac Output ◽  
Aerobic Power ◽  
Endurance Performance ◽  
Endurance Athletes ◽  
Aerobic Performance ◽  
Arterial Oxygen ◽  
Blood Doping ◽  
Arterial Oxygen Content ◽  
The Difference ◽  
Key Words Blood

Alterations in [Hb], which are mediated through changes in arterial oxygen content, and alterations in BV, which are mediated through changes in cardiac output [Formula: see text] have a significant effect on both [Formula: see text] and aerobic performance. If BV is held constant, a decrease in [Hb] (anaemia) causes a decrease in [Formula: see text] and aerobic performance, while an increase in [Hb] (blood doping) causes an increase in [Formula: see text] and aerobic performance. If [Hb] is held constant, an increase in BV can cause an increase in both [Formula: see text] and aerobic performance, while a decrease in BV can cause a decrease in both [Formula: see text] and aerobic performance. In addition, an increase in BV can compensate for moderate reductions in [Hb] through increases in [Formula: see text], allowing [Formula: see text] to remain unchanged or even increase. Also, a large portion of the difference in the enhanced cardiovascular function of endurance athletes is due to their high BV and the resultant enhancement of diastolic function. Hence, optimizing both [Hb] and BV is a very important consideration for endurance performance. Key words: blood doping, sport anemia, stroke volume

scholarly journals Novel serum biomarkers for erythropoietin use in humans: a proteomic approach

2011 ◽  
Vol 110 (1) ◽  
pp. 149-156 ◽  
Author(s):  
Britt Christensen ◽  
Lucila Sackmann-Sala ◽  
Diana Cruz-Topete ◽  
Jens Otto L. Jørgensen ◽  
Niels Jessen ◽  
...  
Keyword(s):  
Serum Proteins ◽  
Endurance Performance ◽  
Serum Biomarkers ◽  
Arterial Oxygen ◽  
Total Serum ◽  
Two Dimensional Gel Electrophoresis ◽  
Arterial Oxygen Content ◽  
Serum Haptoglobin ◽  
Proteomic Approach ◽  
Male Subjects

Erythropoietin (Epo) is produced primarily in the kidneys upon low blood oxygen availability and stimulates erythropoiesis in the bone marrow. Recombinant human Epo (rHuEpo), a drug developed to increase arterial oxygen content in patients, is also illicitly used by athletes to improve their endurance performance. Therefore, a robust and sensitive test to detect its abuse is needed. The aim of the present study was to investigate potential human serum biomarkers of Epo abuse employing a proteomic approach. Eight healthy male subjects were injected subcutaneously with rHuEpo (5,000 IU) every second day for a 16-day period. Serum was collected before starting the treatment regime and again at days 8 and 16 during the treatment period. Samples were homogenized and proteins separated by two-dimensional gel electrophoresis (2DE). Spots that changed significantly in response to rHuEpo treatment were identified by mass spectrometry. Both the number of reticulocytes and erythrocytes increased throughout the study, leading to a significant increase in hematocrit and hemoglobin content. In addition, transferrin levels increased but the percentage of iron bound to transferrin and ferritin levels decreased. Out of 97 serum proteins, seven were found to decrease significantly at day 16 compared with pre-Epo administration, and were identified as four isoforms of haptoglobin, two isoforms of transferrin, and a mixture of hemopexin and albumin. In support, total serum haptoglobin levels were found to be significantly decreased at both days 8 and 16. Thus a 2DE proteomic approach for discovery of novel markers of Epo action appears feasible.

Systemic oxygen transport in induced normovolemic anemia and polycythemia

1962 ◽  
Vol 203 (4) ◽  
pp. 720-724 ◽  
Author(s):  
John F. Murray ◽  
Philip Gold ◽  
B. Lamar Johnson
Keyword(s):  
Cardiac Output ◽  
Oxygen Transport ◽  
Arterial Oxygen Saturation ◽  
Peripheral Resistance ◽  
Arterial Oxygen ◽  
Peripheral Vascular ◽  
Arterial Oxygen Content ◽  
Normovolemic Anemia ◽  
Systemic Oxygen ◽  
Negative Linear Relationship

The hemodynamic effects of normovolemic anemia and polycythemia were studied in 14 dogs. Anemia (5 dogs) and polycythemia (5 dogs) were induced by bleeding and simultaneously infusing dextran or packed erythrocytes. Measurements included cardiac output, arterial oxygen saturation, peripheral vascular resistance, and systemic oxygen transport (cardiac output X arterial oxygen content). Cardiac output had a significant negative linear relationship to hematocrit ( r = –0.74, P < 0.01) over the range studied (13–74%). Peripheral resistance fell 46% in anemic animals and increased 152% in four of five polycythemic animals. Arterial saturation was significantly correlated to changes in hematocrit ( r = 0.62, P < 0.01) and cardiac output ( r = –0.55, P < 0.01); these values were due primarily to the linearity encountered in the anemia experiments and a reversal in these relationships tended to occur at high hematocrits. Systemic oxygen transport was maximum at normal hematocrits and decreased in anemia and polycythemia. The data indicate that hemodynamic adjustments in normovolemic anemia and polycythemia are insufficient to maintain normal oxygen delivery.

Effects of khellin on coronary blood flow and related metabolic functions

1959 ◽  
Vol 196 (2) ◽  
pp. 391-393 ◽  
Author(s):  
Richard L. Farrand ◽  
Steven M. Horvath
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Coronary Blood Flow ◽  
Control Period ◽  
Systemic Arterial Pressure ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Fick Principle ◽  
Metabolic Functions ◽  
Pulmonary Arterial

Khellin, a drug employed as a coronary dilator, was tested to determine its effects on the cardiovascular system of the dog. Ten mongrel dogs were anesthetized with Nembutal and, after control observations were made, given an intravenous administration of 1 mg/kg body weight of khellin. Coronary blood flow and cardiac output samples were drawn during the control period and at 10, 40 and 80 minutes after administration of the drug Cardiac output was calculated by the direct Fick principle and coronary blood flow by the nitrous oxide method. There was a significant (5%) increase in the arterial oxygen content during the 10- and 40-minute intervals, but no change was observed at 80 minutes. An increase in arterial-mixed venous oxygen difference occurred at 40 and 80 minutes. No change in systemic arterial pressure or cardiac output was noted at any time. Coronary blood flow had decreased slightly at 80 minutes. A significant decrease in carbon dioxide content of the arterial, pulmonary arterial and coronary sinus blood was observed, possibly as a consequence of hyperventilation. Khellin appeared to alter the metabolism of the myocardial and splanchnic tissues.

Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension

1983 ◽  
Vol 59 (6) ◽  
pp. 938-944 ◽  
Author(s):  
Quentin J. Durward ◽  
A. Lorne Amacher ◽  
Rolando F. Del Maestro ◽  
William J. Sibbald
Keyword(s):  
Cardiac Output ◽  
Intracranial Hypertension ◽  
Cardiovascular Responses ◽  
Arterial Oxygen ◽  
Optimum Level ◽  
Moderate Degree ◽  
Content Type ◽  
Arterial Oxygen Content ◽  
Head Elevation ◽  
The Mean

✓ To establish if an optimum level of head elevation exists in patients with intracranial hypertension, the authors examined changes in intracranial pressure (ICP), systemic and pulmonary pressures, systemic flows, and intrapulmonary shunt fraction with the patient lying flat, and then with the head elevated at 15°, 30°, and 60°. Cerebral perfusion pressure (CPP) was calculated. The lowest mean ICP was found with elevation of the head to 15° (a fall of −4.5 ± 1.6 mm Hg, p < 0.001) and 30° (a fall of −6.1 ± 3.5 mm Hg, p < 0.001); the CPP and cardiac output were maintained. With elevation of the head to 60°, the mean ICP increased to −3.8 ± 9.3 mm Hg of baseline, while the CPP decreased −7.9 ± 9.3 mm Hg (p < 0.02), and the cardiac index also fell −0.25 ± 0.28 liters/min/sq m (p < 0.01). No significant change in filling pressures, arterial oxygen content, or heart rate was encountered at any level of head elevation. Therefore, a moderate degree (15° or 30°) of head elevation provides a consistent reduction of ICP without concomitant compromise of cardiac function. Lower (0°) or higher (60°) degrees of head elevation may be detrimental to the patient because of changes in the ICP, CPP, and cardiac output.

The role of α-adrenergic receptors in carbon monoxide hypoxia

1986 ◽  
Vol 64 (11) ◽  
pp. 1442-1446 ◽  
Author(s):  
S. M. Villeneuve ◽  
C. K. Chapler ◽  
C. E. King ◽  
S. M. Cain
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cardiac Output ◽  
Adrenergic Receptors ◽  
Muscle Blood Flow ◽  
Control Period ◽  
Arterial Oxygen ◽  
Adrenergic Blockade ◽  
Limb Blood Flow ◽  
Arterial Oxygen Content

The importance of α-adrenergic receptors in the cardiac output and peripheral circulatory responses to carbon monoxide (CO) hypoxia was studied in anesthetized dogs. Phenoxybenzamine (3 mg/kg i.v.) was injected to block α-receptor activity and the data obtained were then compared with those from a previous study of CO hypoxia in unblocked animals. Values for cardiac output, hindlimb blood flow, vascular resistance, and oxygen uptake were obtained prior to and at 30 and 60 min of CO hypoxia which reduced arterial oxygen content by approximately 50%. α-Adrenergic blockade resulted in a lower (p < 0.05) control value for cardiac output than observed in unblocked animals, but no differences were present between the two groups at 30 or 60 min of CO hypoxia. Similarly, limb blood flow was lower (p < 0.05) during the control period in the α-blocked group but rose to the same level as that in the unblocked animals at 60 min of COH. No change in limb blood flow occurred during CO hypoxia in the unblocked group. These findings demonstrated that during CO hypoxia (i) α-receptor mediated venoconstriction does not contribute to the cardiac output response and (ii) α-receptor mediated vasoconstriction probably does prevent a rise in hindlimb skeletal muscle blood flow.

CARDIAC OUTPUT IN ACUTE EXPERIMENTAL METHEMOGLOBINEMIA

1960 ◽  
Vol 38 (12) ◽  
pp. 1411-1416 ◽  
Author(s):  
C. W. Gowdey
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Blood Viscosity ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Arterial Oxygen ◽  
Hematocrit Level ◽  
Arterial Oxygen Content ◽  
Anesthetized Dogs ◽  
Oxygen Difference

Methemoglobinemia induced in normal anesthetized dogs by intravenous infusions of aniline resulted in a decreased arterial oxygen content and a marked increase in cardiac output. Heart rate, arterial pressure, blood viscosity, and oxygen consumption increased, while total peripheral resistance and arteriovenous oxygen difference decreased. The elevation of cardiac output occurred in spite of the fact that the hematocrit level and blood viscosity increased. Ganglion-blocking doses of pentolinium bitartrate did not significantly alter the cardiovascular responses to the methemoglobinemia.

Respiratory and cardiovascular system

2012 ◽  
Keyword(s):  
Carbon Dioxide ◽  
Cardiac Output ◽  
Cardiovascular System ◽  
Oxygen Delivery ◽  
Pulmonary Ventilation ◽  
Venous Blood ◽  
Arterial Oxygen ◽  
Alveolar Air ◽  
Arterial Oxygen Content ◽  
Partial Pressures

Oxidative metabolism is essential for our cellular life. Although tissues such as skeletal muscle can operate for short periods anaerobically, human life does not continue for long in the absence of a ready supply of oxygen. Adequate oxygen delivery to tissues is essential for aerobic metabolism and disorders of delivery ultimately become life-threatening. The factors contributing to oxygen delivery are summarised in the oxygen flux equation: OXYGEN FLUX = CARDIAC OUTPUT × ARTERIAL OXYGEN CONTENT The cardiac output is the product of heart rate and stroke volume and amounts to about 5 litres per minute. The arterial oxygen content is the product of the blood’s haemoglobin concentration multiplied by the haemoglobin’s % saturation. The latter is determined by the partial pressure of oxygen in the blood. This is higher in arterial than in venous blood. A small, additional amount of oxygen is carried dissolved in the blood, the amount again determined by the oxygen partial pressure. The five litres of arterial blood delivered to the tissues each minute contain about 1000ml of oxygen. Only a quarter of this (250ml) is needed to support resting metabolism. There is therefore a large safety factor in oxygen delivery. This can be utilized, in concert with adaptive changes to cardiac output, vascular resistance and pulmonary ventilation, in situations such as muscular exercise, where oxygen demand increases dramatically, or at high altitude where inspired oxygen is low. Oxygen delivery depends on the cardiovascular system, respiratory system and the blood. In the lungs, blood in the alveoli is brought into close proximity with alveolar air so that oxygen can diffuse easily into the blood and carbon dioxide, a major waste product of metabolism, can diffuse into the alveolar air. Alveolar air is kept refreshed with atmospheric air by pulmonary ventilation which keeps the partial pressures of oxygen and carbon dioxide in alveolar air and pulmonary capillary blood in a constant equilibrium. This process ensures that pulmonary venous blood and systemic arterial blood have high oxygen and low carbon dioxide partial pressures. Once in the blood, almost all of the oxygen combines with haemoglobin and is transported by the cardiovascular system to the tissues.

CARDIAC OUTPUT IN ACUTE EXPERIMENTAL METHEMOGLOBINEMIA

1960 ◽  
Vol 38 (1) ◽  
pp. 1411-1416 ◽  
Author(s):  
C. W. Gowdey
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Blood Viscosity ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Arterial Oxygen ◽  
Hematocrit Level ◽  
Arterial Oxygen Content ◽  
Anesthetized Dogs ◽  
Oxygen Difference

Methemoglobinemia induced in normal anesthetized dogs by intravenous infusions of aniline resulted in a decreased arterial oxygen content and a marked increase in cardiac output. Heart rate, arterial pressure, blood viscosity, and oxygen consumption increased, while total peripheral resistance and arteriovenous oxygen difference decreased. The elevation of cardiac output occurred in spite of the fact that the hematocrit level and blood viscosity increased. Ganglion-blocking doses of pentolinium bitartrate did not significantly alter the cardiovascular responses to the methemoglobinemia.

Oxygen transport of colloidal fluorocarbon suspensions in asanguineous rabbits

1975 ◽  
Vol 229 (4) ◽  
pp. 1045-1049 ◽  
Author(s):  
F Gollan ◽  
M Aono ◽  
A Flores
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Oxygen Content ◽  
Peripheral Resistance ◽  
Arterial Oxygen ◽  
Oxygen Utilization ◽  
Arterial Oxygen Content ◽  
Arterial Blood ◽  
Hypervolemic Hemodilution

In anesthetized, oxygen-breathing rabbits, the entire blood volume was exchanged with a 20% colloidal fluorocarbon fluid suspension of high gas solubility. In contrast to the control animals with acute isovolemic and hypervolemic hemodilution, the fluorocarbon suspension prevented the decrease in arterial oxygen content below a hematocrit of 13%. However, the more pronounced effect of the fluorocarbon suspension on oxygen delivery occurred at higher hematocrits and was due to its efficiency as a plasma expander, since it increased the cardiac output even above the level of the hypervolemic hemodilution group. The fluorocarbon suspension also raised arterial blood pressure and total peripheral resistance due to its increased viscosity. Thus, in mild hemodilution, the fluorocarbon suspension kept oxygen utilization in the normal range by increasing cardiac output, and in extreme hemodilution it improved oxygen utilization by also raising the arterial oxygen content and arterial blood pressure. The survival time of the isovolemic control animals was 31.6 min, it was extended to 57.8 min in the hypervolemic control animals, and the rabbits with the fluorocarbon suspension lived for 124.8 min.

scholarly journals Effect of Exercise-Induced Reductions in Blood Volume on Cardiac Output and Oxygen Transport Capacity

2021 ◽  
Vol 12 ◽  
Author(s):  
Janis Schierbauer ◽  
Torben Hoffmeister ◽  
Gunnar Treff ◽  
Nadine B. Wachsmuth ◽  
Walter F. J. Schmidt
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Oxygen Saturation ◽  
Blood Volume ◽  
Oxygen Transport ◽  
Arterial Oxygen ◽  
Peripheral Oxygen Saturation ◽  
Heart Volume ◽  
Arterial Oxygen Content ◽  
Oxygen Transport Capacity

We wanted to demonstrate the relationship between blood volume, cardiac size, cardiac output and maximum oxygen uptake (V.O2max) and to quantify blood volume shifts during exercise and their impact on oxygen transport. Twenty-four healthy, non-smoking, heterogeneously trained male participants (27 ± 4.6 years) performed incremental cycle ergometer tests to determine V.O2max and changes in blood volume and cardiac output. Cardiac output was determined by an inert gas rebreathing procedure. Heart dimensions were determined by 3D echocardiography. Blood volume and hemoglobin mass were determined by using the optimized CO-rebreathing method. The V.O2max ranged between 47.5 and 74.1 mL⋅kg–1⋅min–1. Heart volume ranged between 7.7 and 17.9 mL⋅kg–1 and maximum cardiac output ranged between 252 and 434 mL⋅kg–1⋅min–1. The mean blood volume decreased by 8% (567 ± 187 mL, p = 0.001) until maximum exercise, leading to an increase in [Hb] by 1.3 ± 0.4 g⋅dL–1 while peripheral oxygen saturation decreased by 6.1 ± 2.4%. There were close correlations between resting blood volume and heart volume (r = 0.73, p = 0.002), maximum blood volume and maximum cardiac output (r = 0.68, p = 0.001), and maximum cardiac output and V.O2max (r = 0.76, p &lt; 0.001). An increase in maximum blood volume by 1,000 mL was associated with an increase in maximum stroke volume by 25 mL and in maximum cardiac output by 3.5 L⋅min–1. In conclusion, blood volume markedly decreased until maximal exhaustion, potentially affecting the stroke volume response during exercise. Simultaneously, hemoconcentrations maintained the arterial oxygen content and compensated for the potential loss in maximum cardiac output. Therefore, a large blood volume at rest is an important factor for achieving a high cardiac output during exercise and blood volume shifts compensate for the decrease in peripheral oxygen saturation, thereby maintaining a high arteriovenous oxygen difference.

Sign in / Sign up

Export Citation Format

Share Document