Increase in Serum Ionized Calcium during Exercise

1977 ◽  
Vol 53 (6) ◽  
pp. 579-586 ◽  
Author(s):  
S. Pors Nielsen ◽  
T. Falch Christiansen ◽  
O. Hartling ◽  
J. Trap-Jensen
Keyword(s):  
Blood Lactate ◽  
Venous Blood ◽  
Recovery Period ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Normal Subjects ◽  
Ionized Calcium ◽  
Serum Ionized Calcium

1. Normal subjects showed an average increase in serum ionized calcium (Ca2+) concentration of 0·11 mmol/l in peripheral venous blood 10 min after onset of bicycle exercise at 70% of maximum aerobic capacity. The corresponding mean rise in serum total calcium concentration was 0·21 mmol/l. 2. The change in serum Ca2+ as result of acidification was studied in 20 normal subjects by carbon dioxide equilibration in vitro followed by measurement of serum Ca2+. The log serum Ca2+ was inversely proportional to serum pH. 3. The Δlog serum Ca2+/ΔpH in vitro was similar to the Δlog serum Caa+/ΔpH in vivo during exercise, this ratio, however, being somewhat greater during the first minute of exercise. 4. Serum Ca2+ returned to normal values about 20 min after stopping exercise as the pH returned to normal, but the fall immediately after stopping exercise was more pronounced than that due to the change in pH, as predicted from the studies in vitro. 5. Blood lactate concentration rose from 0·86 to 8·41 mmol/l after 10 min exercise, but the rise in blood lactate during exercise was slower than the rise in serum Ca2+. Also the fall during the recovery period was delayed compared with the fall in serum Ca2+. 6. It is suggested that the rise in serum Ca2+ during severe muscular exercise might be important for the physiological adaptations during work, and for bone metabolism.

Effects of cocaine on incremental treadmill exercise in horses

1993 ◽  
Vol 75 (6) ◽  
pp. 2727-2733 ◽  
Author(s):  
K. H. McKeever ◽  
K. W. Hinchcliff ◽  
D. F. Gerken ◽  
R. A. Sams
Keyword(s):  
Right Ventricular ◽  
Blood Lactate ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Ventricular Pressure ◽  
Mixed Venous Blood ◽  
Work Intensity ◽  
Venous Blood Lactate ◽  
Mixed Venous

Four mature horses were used to test the effects of two doses (50 and 200 mg) of intravenously administered cocaine on hemodynamics and selected indexes of performance [maximal heart rate (HRmax), treadmill velocity at HRmax, treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l, maximal mixed venous blood lactate concentration, maximal treadmill work intensity, and test duration] measured during an incremental treadmill test. Both doses of cocaine increased HRmax approximately 7% (P < 0.05). Mean arterial pressure was 30 mmHg greater (P < 0.05) during the 4- to 7-m/s steps of the exercise test in the 200-mg trial. Neither dose of cocaine had an effect on the responses to exertion of right atrial pressure, right ventricular pressure, or maximal change in right ventricular pressure over time. Maximal mixed venous blood lactate concentration increased 41% (P < 0.05) with the 50-mg dose and 75% (P < 0.05) with the 200-mg dose during exercise. Administration of cocaine resulted in decreases (P < 0.05) in the treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l from 6.9 +/- 0.5 and 6.8 +/- 0.9 m/s during the control trials to 4.4 +/- 0.1 m/s during the 200-mg cocaine trial. Cocaine did not alter maximal treadmill work intensity (P > 0.05); however, time to exhaustion increased by approximately 92 s (15%; P < 0.05) during the 200-mg trial.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Arterialized and venous blood lactate concentration difference during different exercise intensities

2017 ◽  
Vol 15 (1) ◽  
pp. 22-26 ◽  
Author(s):  
Leandro C. Felippe ◽  
Guilherme A. Ferreira ◽  
Fernando De-Oliveira ◽  
Flavio O. Pires ◽  
Adriano E. Lima-Silva
Keyword(s):  
Blood Lactate ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Concentration Difference ◽  
Venous Blood Lactate

Blood Lactate Levels in Free-Swimming Rainbow Trout (Salmo gairdneri) Before and After Strenuous Exercise Resulting in Fatigue

1976 ◽  
Vol 33 (1) ◽  
pp. 173-176 ◽  
Author(s):  
William R. Driedzic ◽  
Joe W. Kiceniuk
Keyword(s):  
Rainbow Trout ◽  
Blood Lactate ◽  
White Muscle ◽  
Recovery Period ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Strenuous Exercise ◽  
Salmo Gairdneri ◽  
Before And After ◽  
Lactate Levels

Rainbow trout (Salmo gairdneri) were exercised to fatigue in a series of 60-min stepwise increasing velocity increments. There was no increase in blood lactate concentration, serially sampled during swimming by means of indwelling dorsal and ventral aortic catheters, at velocities as high as 93% of critical velocity of individuals. The data show that under these conditions the rate of production of lactate by white muscle, at less than critical velocities, is minimal or that the rate of elimination of lactate from white muscle is equal to its rate of utilization elsewhere. Immediately following fatigue blood lactate level increases rapidly. During the recovery period there appears to be a net uptake of lactate by the gills.

scholarly journals Do patients with thromboembolic disease have circulating platelet aggregates?

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 205-209 ◽  
Author(s):  
FH Kohanna ◽  
MH Smith ◽  
EW Salzman
Keyword(s):  
Platelet Rich Plasma ◽  
Venous Blood ◽  
Adenosine Diphosphate ◽  
Normal Subjects ◽  
Thromboembolic Disease ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Lower Ratio

Reports of circulating platelet aggregates (ie, microemboli) in thromboembolism and other vascular disorders are based on a method (Wu and Hoak , 1974) in which venous blood is collected via scalp vein needle and tubing into either formaldehyde, which fixes aggregates, or EDTA, which disperses them. The ratio of platelet counts in platelet- rich plasma (PRP) from the two blood samples after centrifugation is interpreted as a measure of platelet aggregates in the circulation in vivo. We compared this standard Wu and Hoak technique with a modified one, in which blood was drawn directly into a syringe, and with a third method that avoided centrifugation by counting single platelets in whole blood. Both modified techniques could detect aggregates generated in vitro with adenosine diphosphate (ADP). In 12 normal subjects, the three methods were equivalent, but in 37 patients with thromboembolic disorders, the standard Wu and Hoak method gave a lower ratio than the other methods. Similar results were found in a subset of eight patients with myocardial infarction. Heparin treatment of patients did not influence the results. The data suggest that formation of platelet aggregates occurred during venipuncture. Platelets may be hyperactive in patients with thromboembolic disease and may form aggregates in vitro during collection, but the concept of chronic microembolism in such patients should be reassessed.

Effect of Whole-Body Vibration Therapy on Performance Recovery

2015 ◽  
Vol 10 (3) ◽  
pp. 388-395 ◽  
Author(s):  
Nuttaset Manimmanakorn ◽  
Jenny J. Ross ◽  
Apiwan Manimmanakorn ◽  
Samuel J.E. Lucas ◽  
Michael J. Hamlin
Keyword(s):  
Blood Lactate ◽  
Muscle Soreness ◽  
Recovery Period ◽  
Whole Body Vibration ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Quadriceps Strength ◽  
Whole Body ◽  
Active Recovery ◽  
Recovery Protocols

Purpose:To compare whole-body vibration (WBV) with traditional recovery protocols after a high-intensity training bout.Methods:In a randomized crossover study, 16 athletes performed 6 × 30-s Wingate sprints before completing either an active recovery (10 min of cycling and stretching) or WBV for 10 min in a series of exercises on a vibration platform. Muscle hemodynamics (assessed via near-infrared spectroscopy) were measured before and during exercise and into the 10-min recovery period. Blood lactate concentration, vertical jump, quadriceps strength, flexibility, rating of perceived exertion (RPE), muscle soreness, and performance during a single 30-s Wingate test were assessed at baseline and 30 and 60 min postexercise. A subset of participants (n = 6) completed a 3rd identical trial (1 wk later) using a passive 10-min recovery period (sitting).Results:There were no clear effects between the recovery protocols for blood lactate concentration, quadriceps strength, jump height, flexibility, RPE, muscle soreness, or single Wingate performance across all measured recovery time points. However, the WBV recovery protocol substantially increased the tissue-oxygenation index compared with the active (11.2% ± 2.4% [mean ± 95% CI], effect size [ES] = 3.1, and –7.3% ± 4.1%, ES = –2.1 for the 10 min postexercise and postrecovery, respectively) and passive recovery conditions (4.1% ± 2.2%, ES = 1.3, 10 min postexercise only).Conclusion:Although WBV during recovery increased muscle oxygenation, it had little effect in improving subsequent performance compared with a normal active recovery.

scholarly journals Lactate Arterial-Central Venous Gradient among COVID-19 Patients in ICU: A Potential Tool in the Clinical Practice

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Giuseppe Nardi ◽  
Gianfranco Sanson ◽  
Lucia Tassinari ◽  
Giovanna Guiotto ◽  
Antonella Potalivo ◽  
...  
Keyword(s):  
Blood Lactate ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Mitochondrial Metabolism ◽  
Lung Cells ◽  
Central Venous ◽  
Central Venous Blood ◽  
Arterial Blood ◽  
Anti Inflammatory

Objective. In physiological conditions, arterial blood lactate concentration is equal to or lower than central venous blood lactate concentration. A reversal in this rate (i.e., higher lactate concentration in central venous blood), which could reflect a derangement in the mitochondrial metabolism of lung cells induced by inflammation, has been previously reported in patients with ARDS but has been never explored in COVID-19 patients. The aim of this study was to explore if the COVID-19-induced lung cell damage was mirrored by an arterial lactatemia higher than the central venous one; then if the administration of anti-inflammatory therapy (i.e., canakinumab 300 mg subcutaneous) could normalize such abnormal lactate a-cv difference. Methods. A prospective cohort study was conducted, started on March 25, 2020, for a duration of 10 days, enrolling 21 patients affected by severe COVID-19 pneumonia undergoing mechanical ventilation consecutively admitted to the ICU of the Rimini Hospital, Italy. Arterial and central venous blood samples were contemporarily collected to calculate the difference between arterial and central venous lactate (Delta a-cv lactate) concentrations within 24 h from tracheal intubation (T0) and 24 hours after canakinumab administration (T1). Results. At T0, 19 of 21 (90.5%) patients showed a pathologic Delta a-cv lactate (median 0.15 mmol/L; IQR 0.07–0.25). In the 13 patients undergoing canakinumab administration, at T1, Delta a-cv lactate decreased in 92.3% of cases, the decrease being statistically significant (T0: median 0.24, IQR 0.09–0.31 mmol/L; T1: median −0.01, IQR −0.08–0.04 mmol/L; p=0.002). Conclusion. A reversed Delta a-cv lactate might be interpreted as one of the effects of COVID-19-related cytokine storm, which could reflect a derangement in the mitochondrial metabolism of lung cells induced by severe inflammation or other uncoupling mediators. In addition, Delta a-cv lactate decrease might also reflect the anti-inflammatory activity of canakinumab. Our preliminary findings need to be confirmed by larger outcome studies.

Role of adrenergic-dependent H+ release from red cells in acidosis induced by hypoxia in trout

1987 ◽  
Vol 252 (2) ◽  
pp. R269-R275 ◽  
Author(s):  
B. Fievet ◽  
R. Motais ◽  
S. Thomas
Keyword(s):  
Blood Lactate ◽  
Beta Blocker ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Second Phase ◽  
Beta Adrenergic ◽  
Blood Ph ◽  
Adrenergic Control ◽  
Net Uptake

The response to severe hypoxia is characterized in trout by a sudden drop in blood pH, which is of metabolic origin, and by an increase in the blood concentration of adrenaline. This acidification is biphasic in nature. The first phase of acidification is not associated with a rise in the blood lactate concentration and no longer occurs after pretreatment of the fish with a beta-blocker agent, propranolol. Thus an acid other than lactic acid is released into the blood at the onset of hypoxia and this release, which is under beta-adrenergic control, is responsible for the first phase of acidification. On the other hand the second phase of acidification is related to an increase in blood lactate and is not modified by a beta-blocker agent. We have also demonstrated that deep hypoxia promotes a rapid increase in red blood cell volume and that this cell enlargement is coincident with a large net uptake of Na+ and Cl-. In the presence of beta-blocking agents the Na+ uptake is blocked and the swelling of the cells is considerably inhibited. The residual swelling is clearly due to the chloride shift induced by both deoxygenation of hemoglobin and change in blood pH. In the light of data obtained in vitro on the effect of catecholamines on trout erythrocytes, it can be considered that the first phase of acidification occurring at the onset of hypoxia, and that is under beta-adrenergic control, is due essentially to the release of H+ by red blood cells in exchange with external sodium mediated by a beta-adrenergic-stimulated Na+-H+ exchanger.(ABSTRACT TRUNCATED AT 250 WORDS)

Correlation of Plasma Phenformin Concentration with Metabolic Effects in Normal Subjects

1980 ◽  
Vol 58 (2) ◽  
pp. 153-155 ◽  
Author(s):  
M. Nattrass ◽  
Karen Sizer ◽  
K. G. M. M. Alberti
Keyword(s):  
Blood Glucose ◽  
Plasma Concentration ◽  
Blood Lactate ◽  
Serum Insulin ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Normal Subjects ◽  
Metabolic Effects ◽  
Intermediary Metabolites ◽  
Pyruvate Ratio

1. Circulating concentrations of intermediary metabolites have been measured after administration of 50 mg of phenformin to normal subjects. 2. Phenformin caused a significant increase in blood lactate, alanine and the lactate/pyruvate ratio but did not affect blood glucose or serum insulin concentrations. 3. There was a significant correlation between the increase in blood lactate concentration after phenformin and the plasma concentration of the drug.

scholarly journals Do patients with thromboembolic disease have circulating platelet aggregates?

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 205-209 ◽  
Author(s):  
FH Kohanna ◽  
MH Smith ◽  
EW Salzman
Keyword(s):  
Platelet Rich Plasma ◽  
Venous Blood ◽  
Adenosine Diphosphate ◽  
Normal Subjects ◽  
Thromboembolic Disease ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Lower Ratio

Abstract Reports of circulating platelet aggregates (ie, microemboli) in thromboembolism and other vascular disorders are based on a method (Wu and Hoak , 1974) in which venous blood is collected via scalp vein needle and tubing into either formaldehyde, which fixes aggregates, or EDTA, which disperses them. The ratio of platelet counts in platelet- rich plasma (PRP) from the two blood samples after centrifugation is interpreted as a measure of platelet aggregates in the circulation in vivo. We compared this standard Wu and Hoak technique with a modified one, in which blood was drawn directly into a syringe, and with a third method that avoided centrifugation by counting single platelets in whole blood. Both modified techniques could detect aggregates generated in vitro with adenosine diphosphate (ADP). In 12 normal subjects, the three methods were equivalent, but in 37 patients with thromboembolic disorders, the standard Wu and Hoak method gave a lower ratio than the other methods. Similar results were found in a subset of eight patients with myocardial infarction. Heparin treatment of patients did not influence the results. The data suggest that formation of platelet aggregates occurred during venipuncture. Platelets may be hyperactive in patients with thromboembolic disease and may form aggregates in vitro during collection, but the concept of chronic microembolism in such patients should be reassessed.

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