Biomedical subjects

N Maassen

Publications and source records attributed to N Maassen.

26 records · Page 2Linked to original sources

PubMed1989

Effect of consecutive exercise bouts on plasma potassium concentration during exercise and recovery.

During and after two similar incremental treadmill tests, one with increasing, the other with initially decreasing blood acidosis, plasma potassium was measured in 11 volunteers. Independent of increasing or decreasing hydrogen ion, lactate, or bicarbonate concentrations, plasma potassium rose in relation to muscular stress with nearly equal concentrations for comparable exercise intensities in both tests. During the first 3 min of recovery, plasma potassium fell rapidly in spite of nearly unchanged blood acidosis and significantly decreasing bicarbonate concentration. After the 5th min of recovery, plasma potassium concentration was even slightly below pre-exercise values despite severe metabolic acidosis. It was concluded that there was little or no effect of plasma hydrogen ion, lactate, or bicarbonate on plasma potassium concentration during and after exercise. We propose that plasma potassium is primarily regulated by intracellular effects of inorganic phosphate, pH, and temperature on (Na+-K+)-ATPase. We suggest that these results reflect a model of grand mal seizure-induced lactic acidosis. The noted low blood potassium concentrations despite the presence of severe metabolic acidosis secondary to epileptic seizure is thus suggested to reflect the "normal" post-exercise state of potassium concentration.

Acidosis, Lactic↗

PubMed1988

Hemoglobin oxygen affinity in patients suffering from arterial occlusive disease of the legs.

Parameters characterizing the hemoglobin oxygen affinity were determined in blood of 12 male patients suffering from arterial occlusive disease (AOD) of the legs and compared with data obtained earlier from healthy human subjects (controls). Due to a COHb content of 4.8% +/- 2.2% in the cigarette-smoking AOD patients, the standard oxygen dissociation curve (ODC) was left-shifted, the half-saturation pressure (P50) amounted to 24.8 +/- 1.7 mmHg (3.30 +/- 0.23 kPa), although the 2,3-diphosphoglycerate concentration was increased to 15.3 +/- 1.7 mumol/g Hb. Correcting the effects of elevated COHb shifts the P50 to 26.3 mmHg (3.5 kPa) and increases the steepness of the ODC (Hill's "n") from 2.79 +/- 0.27 to about 2.99, which is significantly different from controls. The Bohr coefficients after acidification of blood with lactic acid (BCLac) show high values at low oxygen saturations of hemoglobin (-0.50 +/- 0.04 in AOD patients, -0.32 +/- 0.04 in controls; P less than 0.05 at 10% SO2). The cause of the alterations in hemoglobin oxygen affinity may be a reduced mean erythrocyte age, but also the influence of unknown factors generated, e.g., from anaerobic muscle metabolism in AOD.

Arterial Occlusive Diseases↗

PubMed1988

Training induced effects on blood volume, erythrocyte turnover and haemoglobin oxygen binding properties.

The effect of three weeks ergometer training (Tr) 5 times a week for 45 min at 70% VO2max by 6 subjects on erythrocyte turnover and haemoglobin O2 affinity has been studied. Increased reticulocytosis could be observed from the second day after beginning Tr until a few days after its end, probably caused by increased erythropoietin release by the kidney. Erythrocyte destruction was most pronounced in the first and markedly reduced in the third week of Tr. Elevated glutamate oxalacetate transaminase activity and creatine as well as lowered mean corpuscular haemoglobin indicate a younger erythrocyte population in the first week of recovery. Total blood volume increased during the course of Tr by 700 ml, mainly caused by a raised plasma volume (74%). Red cell volume increased later with maximal values one week after Tr (+280 ml). In this week the standard oxygen dissociation curve was most shifted to the right (P50 increased from 3.77 +/- 0.05 kPa to 3.99 +/- 0.07 kPa) and the Bohr coefficients had their lowest values. Both effects are completely explainable by the haemoglobin O2 binding properties of young erythrocytes. After training, all parameters of physical performance (VO2max, maximal workload, heart rate during rest and exercise) were markedly improved, indicating fast adaptation mechanisms. The increased erythrocyte turnover, including higher erythropoiesis, seems to be one important part of these effects.

Adult↗

PubMed1988

Exercise versus immersion: antagonistic effects on water and electrolyte metabolism during swimming.

Changes in blood composition, renal function, aldosterone and antidiuretic hormone (ADH) concentrations were investigated in 10 untrained male subjects when swimming (60 min at a heart rate of about 155 beats.min-1, water temperature 28 degrees C) and during the subsequent 3 h in a sitting position. Many specific effects of either exercise or immersion were abolished or attenuated; no significant changes in plasma aldosterone, [ADH], [K+], [Cl-], or of urinary volume, glomerular filtration rate, free water or osmolar clearance were observed. The urine was diluted resulting in lowered [Na+]. In blood some quantities which are only slightly influenced by immersion increased during swimming ([Na+], [Lac-], [H+], osmolality, [creatinine]). Exercise induced plasma volume loss, calculated from increasing [Hb], was small (110 ml), probably because interstitial fluid enters the vascular space during the initial phase of immersion. One might anticipate that the training effects on fluid and electrolyte metabolism and circulation are different when swimming and when performing endurance sports on land.

Adult↗

PubMed1987

Blood osmolality in vitro: dependence on base addition, buffer value, and temperature.

Blood osmolality (Osm) increases with PCO2 because of CO2 absorption. The influences of NaOH addition, equilibration temperature, and hemoglobin concentration on these respiratory changes of Osm were measured by freezing-point determination in true plasma. Addition of NaOH increases Osm by 2 mosmol X kg H2O-1 X mmol base-1 X l at constant PCO2 due to the osmotic effects of Na+ and produced bicarbonate. Respiratory compensation of the pH change further increases Osm. This contrasts to the respiratory compensation of the osmolar disturbance caused by fixed acid. Raising the equilibration temperature reduces Osm by 0.5 mosmol X kg H2O-1 X degrees C-1 at constant pH mainly caused by a lower absorption coefficient for CO2 and changed pK value for H2CO3. The slope of the linear regression lines between Osm and pH during CO2 equilibration increases with hemoglobin; the value of the quotient delta Osm/delta pH depends directly on the nonbicarbonate buffer value. The use of this quotient for the estimation of the mean nonbicarbonate buffer value of the whole body is suggested. The osmotic effects of therapeutic base infusion should be regarded with caution.

Acid-Base Equilibrium↗

PubMed1984

Relationship between work load, pedal frequency, and physical fitness.

The aim of this investigation was to study how the known dependence of working efficiency on pedaling frequency is influenced by the work load as well as by physical fitness. Oxygen uptake, CO2 output, ventilation, heart rate, and lactate concentration in capillary blood from the earlobe were determined at varying combinations of work loads and pedaling rates in road-racing cyclists and medical students. Respiratory exchange ratio, consumption of energy, gross efficiency, net efficiency, and delta efficiency (delta work rate/delta metabolic rate) were calculated. All parameters showed a nonlinear dependence on pedaling frequency. The lowest oxygen uptake and the highest efficiency shifted to higher frequencies with increasing work load. Delta efficiency increased with rising pedaling frequency. Differences of VO2 and efficiencies between trained and untrained subjects were only small. Most effects can be explained by variations in leg movement frequency and recruitment of muscle fibers. There is evidence that racing cyclists chose pedaling rates yielding optimal efficiency at any load.

Analysis of Variance↗

PubMed1983

Blood osmolality in vitro: dependence on PCO2, lactic acid concentration, and O2 saturation.

Changes of osmolality (Osm) were measured by freezing-point determination in true plasma of 10 healthy subjects. This was done after equilibration with CO2 (0.5-10.0%), after the addition of lactic acid (10 and 20 mmol/l), and after deoxygenation. The graph for the dependence of Osm on CO2 partial pressure (PCO2) in oxygenated blood resembles the classical CO2 absorption curve. The increase of Osm with PCO2 (approximately 0.2 mosmol . kg H2O-1 . Torr-1) is almost as great as the increase in dissolved CO2 plus bicarbonate (HCO-3). Addition of lactic acid shifts the curve upward by only 0.6 mosmol/mmol because of displacement of HCO-3. Deoxygenation has no significant effect at constant PCO2 despite an increase in [HCO-3]. This is probably due to the binding of 2,3-diphosphoglycerate to hemoglobin. It can be seen in the Osm-pH diagram that differences between CO2 and lactic acid titration largely disappear. For each lactic acid concentration there is a linear dependence corresponding to the linear [HCO-3]-pH relation in plasma. At constant pH, Osm increases after deoxygenation. The observed in vitro relation might explain part of the osmolality increase during physical exercise.

Adult↗

PubMedDate not supplied

Extracellular pH defense against lactic acid in normoxia and hypoxia before and after a Himalayan expedition.

The extracellular pH defense against the lactic acidosis resulting from exercise can be estimated from the ratios -delta[La].delta pH-1 (where delta[La] is change in lactic acid concentration and delta pH is change in pH) and delta[HCO3-].delta pH-1 (where delta[HCO3-] is change in bicarbonate concentration) in blood plasma. The difference between -delta[La].delta pH-1 and delta[HCO3-].delta pH-1 yields the capacity of available non-bicarbonate buffers (mainly hemoglobin). In turn, delta[HCO3-].delta pH-1 can be separated into a pure bicarbonate buffering (as calculated at constant carbon dioxide tension) and a hyperventilation effect. These quantities were measured in 12 mountaineers during incremental exercise tests before, and 7-8 days (group 1) or 11-12 days (group 2) after their return from a Himalayan expedition (2800-7600 m altitude) under conditions of normoxia and acute hypoxia. In normoxia -delta[La].delta pH-1 amounted to [mean (SEM)] 92 (6) mmol.l-1 before altitude, of which 19 (4), 48 (1) and 25 (3) mmol.l-1 were due to hyperventilation, bicarbonate and non-bicarbonate buffering, respectively. After altitude -delta[La].delta pH-1 was increased to 128 (12) mmol.l-1 (P < 0.01) in group 1 and decreased to 72 (5) mmol.l-1 in group 2 (P < 0.05), resulting mainly from apparent large changes of non-bicarbonate buffer capacity, which amounted to 49 (14) mmol.l-1 in group 1 and to 10 (2) mmol.l-1 in group 2. In acute hypoxia the apparent increase in non-bicarbonate buffers of group 1 was even larger [140 (18) mmol.l-1]. Since the hemoglobin mass was only modestly elevated after descent, other factors must play a role. It is proposed here that the transport of La- and H+ across cell membranes is differently influenced by high-altitude acclimatization.

Acclimatization↗