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Biomedical subjects

O M Sejersted

Publications and source records attributed to O M Sejersted.

At least 19 recordsLinked to original sources
PubMed1992

Enzymatic microdetermination of plasma and serum free fatty acids.

A simple and sensitive enzymatic method for determination of plasma and serum fatty acids (FAs) is described. The method is based on acylation of long chain FAs by a bacterial acyl-CoA synthetase (ACS) producing equivalent amounts of acyl-CoA and AMP. AMP production was measured using the coupled reaction of myokinase (MK), pyruvate kinase (PK) and lactate dehydrogenase (LDH) allowing fluorinate detection of NADH. Two moles of NAD were produced per mole of FA acylated. Concentrations of substrates and enzymes were kept as low as possible maintaining the ACS reaction as rate limiting. Addition of fat-free human serum albumin (HSA) to standards reduced initial reaction rates but did not affect end-point fluorescence levels. Triton X-100 partly counteracted the inhibition by HSA. To keep albumin concentration low, plasma or serum samples were diluted by 1:400. Duplicate measurements of plasma or serum FA concentrations between 0 and 2 mmol l-1 can then be performed on 5 microliters samples with intra- and inter-assay variation coefficients of 1.7 and 4% respectively.

Acyl Coenzyme A↗
PubMed1992

Effect of supramaximal exercise on excess postexercise O2 consumption.

This study was undertaken to determine the effect of high intensity exercise on the time course and magnitude of excess postexercise O2 consumption (EPOC). Six healthy male subjects performed three intermittent 2-min exercise bouts on a cycle ergometer at 108% of VO2max with 3-min rest periods (3 x 2 min). O2 uptake, blood lactate, plasma catecholamines, and rectal temperature were measured while the subjects rested in bed for 14 h postexercise, and the results were compared with those of an identical control experiment without exercise. In addition, they were studied on two separate days for 2 h after only two (2 x 2 min) or one (1 x 2 min) exercise bout. O2 uptake was significantly increased for 4 h after 3 x 2 min exercise, for 60 min after 2 x 2 min, and for 30 min after 1 x 2 min exercise. EPOC was 5.6 +/- 0.41 (1 x 2 min), 6.7 +/- 0.41 (2 x 2 min), and 16.3 +/- 3.01 (3 x 2 min), respectively. Over the first hour postexercise, EPOC was linearly related to the change in blood lactate and plasma norepinephrine. However, after exhaustive supramaximal exercise O2 consumption was significantly increased for 4 h, whereas blood lactate and plasma norepinephrine concentrations were significantly increased for only 2 h.

Adult↗
PubMed1991

Effect of intensity of exercise on excess postexercise O2 consumption.

After exercise, there is an increase in O2 consumption termed the excess postexercise O2 consumption (EPOC). In this study, we have examined the effect of exercise intensity on the time course and magnitude of EPOC. Six healthy male subjects exercised on separate days for 80 minutes at 29%, 50%, and 75% of maximal O2 uptake (VO2max) on a cycle ergometer. O2 uptake, R value, and rectal temperature were measured while the subjects rested in bed for 14 hours postexercise, and the results were compared with those of an identical control experiment without exercise. An increase in O2 uptake lasting for 0.3 +/- 0.1 hour (29% exercise), 3.3 +/- 0.7 hour (50%) and 10.5 +/- 1.6 hour (75%) was observed. EPOC was 1.3 +/- 0.46 I(29%), 5.7 +/- 1.7 I (50%), and 30.1 +/- 6.4 I (75%). There was an exponential relationship between exercise intensity and total EPOC, both during the first 2 hours and the next 5 hours of recovery. Hence, prolonged exercise at intensities above 40% to 50% of VO2max is required in order to trigger the metabolic processes that are responsible for the prolonged EPOC component extending beyond 2 hours postexercise.

Adult↗
PubMed1991

Frequency dependent myocardial potassium fluxes during beta adrenergic stimulation of intact pig hearts.

STUDY OBJECTIVE: The aim was to determine the frequency dependent myocardial potassium fluxes of intact pig hearts at control inotropy and during beta adrenergic stimulation. DESIGN - Atrial pacing rate was suddenly raised and decreased by 50 beats.min-1 at control inotropy and during infusion of isoprenaline, 2.5 nmol.min-1, into the left coronary artery. EXPERIMENTAL MATERIAL: Nine anaesthetised pigs (21-33 kg) were instrumented for electric pacing of the right atrium and metabolic and haemodynamic recordings. MEASUREMENTS AND MAIN RESULTS: Myocardial potassium balance was measured by PVC-valinomycin electrodes in the left atrial cavity and in a shunt (with flow meter) diverting blood from the coronary sinus to the right atrium. Isoprenaline raised net myocardial potassium flux following the change in pacing rate from 19(14-23) to 38(32-46) mumol.100 g-1.min-1 (median, 95% confidence interval, difference: p = 0.03). The corresponding myocardial potassium flux per beat increased from 0.38(0.29-0.45) to 0.80(0.63-0.97) mumol.100 g-1 (p = 0.03). Accumulated potassium flux increased from 9(8-11) to 17(11-27) mumol.100 g-1, respectively (p = 0.03). CONCLUSIONS: In intact hearts beta adrenergic stimulation doubles the frequency dependent myocardial potassium flux. This component constitutes 22-25% of the ouabain inhibitable potassium flux at both levels of inotropy.

Animals↗
PubMed1991

Strenuous prolonged exercise elevates resting metabolic rate and causes reduced mechanical efficiency.

Resting O2 consumption, net mechanical efficiency during cycling exercise and excess postexercise O2 consumption (EPOC) was measured in 15 army cadets after 3 or 4 days of continuous simulated combat exercises (estimated energy demand: 40 MJ day-1), no organized sleep and virtually no food intake (stress experiment). They exercised for 30 minutes at a work load corresponding to about 50% of maximal O2 uptake. An identical test using the same absolute work load was repeated when the cadets were completely recovered from the combat course (control experiment). Resting O2 consumption increased by 15% from 279 +/- 7 ml min-1 (control) to 320 +/- 8 ml min-1 (stress, P less than 0.001). Mechanical efficiency decreased from 24.6 +/- 0.4% (control) to 20.9 +/- 0.2% (stress, P less than 0.001). EPOC1h increased from 0.58 +/- 0.41 l (control) to 2.24 +/- 0.2% (stress, P less than 0.05). Glucose infusion during exercise (0.20 g kg-1 body weight) had no effect on mechanical efficiency or EPOC. About 1/5 of the increase in exercise O2 uptake can be explained by a substrate shift from carbohydrates to fat, as evidenced by a reduction in R-value during exercise from 0.90 +/- 0.012 (control) to 0.80 +/- 0.010 (stress). Hence, after severe physical stress combined with sleep deprivation and food restriction, O2 uptake is increased both at rest and during submaximal exercise.

Adult↗
PubMed1991

Effect of exercise on recovery changes in plasma levels of FFA, glycerol, glucose and catecholamines.

The prolonged effects of acute exercise on the plasma concentrations of FFA, glycerol, glucose and catecholamines were examined. Twelve young men performed exhaustive prolonged exercise on a cycle ergometer (80 minutes at 70-75% of VO2 max), and in separate experiments they exercised for shorter durations (20, 40 and 80 minutes) and at lesser intensities (29, 50 and 75% of VO2 max). Carbohydrate-rich meals were given 2, 7 and 12 hours after exercise. Blood samples were taken while the subjects rested in bed during a 12-14-hour recovery period. Control experiments without exercise were also performed. In some subjects the plasma concentration of FFA after exhaustive exercise was increased to levels considered to be potentially hazardous, and the mean plasma level of FFA was increased for 6 hours and that of glycerol was increased for 2.5 hours after exercise. The plasma concentration of glucose was generally reduced for 12 hours after exhaustive exercise. Plasma catecholamines were increased for 2 hours after exhaustive exercise. We observed a preprandial increase in FFA and glycerol concentrations during recovery from exercise which was related to the duration and intensity of exercise. These findings indicate that the rates of FA utilization and TG-FA substrate cycling were increased in the recovery period after exercise, and that the magnitude of both depends on the duration and intensity of exercise.

Adult↗
PubMed1991

Effect of feeding and fasting on excess postexercise oxygen consumption.

This study was undertaken to determine the effect of fasting on the magnitude and time course of the excess postexercise O2 consumption (EPOC). Six lean untrained subjects were studied in the fasted state for 7 h after a previous strenuous exercise bout (80 min at 75% of maximal O2 uptake) and in a control experiment. The results were compared with identical control and exercise experiments where the subjects were fed a 4.5-MJ test meal after 2 h of rest. EPOC was calculated as the difference in O2 uptake between the corresponding control and exercise experiments. The total EPOC (0-7 h postexercise) was 20.9 +/- 4.5 (fasting) and 21.1 +/- 3.6 liters (food, NS). A significant prolonged EPOC component was observed in the fasted and in the fed state. The thermic effect of food (TEF) was calculated from O2 consumption and respiratory exchange ratio as the difference in energy expenditure between the corresponding food and fasting experiments. The total TEF (0-5 h postprandial) was 321 +/- 32.0 (control) and 280 +/- 37.7 kJ/5 h (exercise, NS). It is concluded that the prolonged component of EPOC is present in the fasting state. Furthermore, no major interaction effects between food intake and exercise on the postexercise O2 consumption could be detected.

Adult↗
PubMed1990

Triglyceride/fatty acid cycling is increased after exercise.

After exercise, there is a prolonged increase in O2 consumption termed the excess postexercise O2 consumption (EPOC). In this study, we have assessed the relative contribution of the triglyceride/fatty acid (TG/FA) substrate cycle to EPOC. Six healthy, young men exercised for 2 hours at 51% of maximal O2 uptake. The total energy expenditure and the rate of FA oxidation were estimated from measurements of O2 uptake, respiratory exchange ratio, and urinary nitrogen excretion while the subjects rested in bed for 3.5 hours postexercise. During the last part of the recovery period, the rate of FA mobilization was determined by infusion of glycerol. The rate of TG/FA cycling was calculated from the difference between the rate of FA mobilization and oxidation. An identical control study without exercise was also performed. The total EPOC during the recovery period was 7.82 +/- 1.51 L O2 (a 15% +/- 3% increase above the control O2 consumption). The rate of FA oxidation increased from 252 +/- 36 mumol/min (control) to 360 +/- 27 mumol/min (3 hours postexercise). The rate of FA mobilization increased from 666 +/- 108 mumol/min (control) to 1833 +/- 456 mumol/min (3 hours postexercise). TG/FA cycling was found to increase from 414 +/- 90 mumol FA/min (control) to 1473 +/- 435 mumol FA/min (3 hours postexercise). The energy cost of these rates of TG/FA cycling was found to be 0.09 +/- 0.02 kJ/min (control) and 0.31 +/- 0.09 kJ/min (3 hours postexercise). It is concluded that the energy cost of the increased TG/FA cycling rate may account for as much as half of the delayed component of EPOC.

Adult↗
PubMed1990

Increased erythrocyte magnesium in never treated essential hypertension.

In the present study we aimed at evaluating the intracellular concentrations of magnesium, potassium and sodium in 50-year-old, otherwise healthy white men with never treated, essential hypertension (n = 12) and in normotensive control subjects (n = 12) matched for age, sex, race, height, weight and smoking habits. Intraerythrocyte magnesium was significantly increased in the hypertensive group (P less than .001) and correlated positively and significantly to blood pressure in the total group (P less than .01). The intracellular potassium to sodium ratio tended to be lower in the hypertensive group (P less than .05). Thus, the present study supports increased intracellular magnesium probably unrelated to intracellular potassium-sodium imbalance in never treated, essential hypertension.

Blood Pressure↗
PubMed1990

Isoprenaline augments total myocardial K+ influx of the in-situ beating porcine heart.

To determine the total rate of K+ flux into myocardial cells of the in-situ beating heart and how this influx is affected by beta-adrenoceptor stimulation, we measured 42K+ content in myocardial biopsies taken at intervals after an intra-atrial infusion of 42K+ before and during an i.v. isoprenaline infusion (20 micrograms min-1) in six anaesthetized, open-chest pigs. Determination of the total K+ influx during beta-adrenoceptor stimulation was initiated 10 min after the start of isoprenaline infusion, when the transient net myocardial K+ uptake had subsided. Total K+ influx increased from a control value of 414 +/- 42 to 1086 +/- 246 mumol 100 g-1 min-1 during isoprenaline infusion. A quantitatively smaller increase in K+ influx carried by the Na(+)-K+ pump has previously been demonstrated during isoprenaline infusion. Left ventricular dP/dt rose from 1350 +/- 146 to 4833 +/- 150 mmHg s-1, stroke volume remained unchanged, but heart rate and peak left ventricular systolic pressure rose as expected, by 52 +/- 4 and 32 +/- 4% respectively during isoprenaline stimulation. All haemodynamic parameters, total plasma K+ concentration and plasma 42K+ activity remained stable throughout each experimental period. The number of ouabain binding sites was 65.5 +/- 1.0 before and 66.9 +/- 1.6 nmol 100 g-1 during isoprenaline infusion (difference n.s.). The present data indicate that not only the K+ influx carried by the ouabain-sensitive Na(+)-K+ pump but also the influx through ouabain-insensitive pathways is increased during beta-adrenoceptor stimulation of the in-situ beating pig heart.

Animals↗
PubMed1990

Plasma potassium changes with high intensity exercise.

1. Exercise seems to change the extracellular potassium concentration far beyond the narrow limits seen in resting subjects. To examine alterations in plasma potassium concentration during exercise, twenty healthy, well-trained men ran on the treadmill at 6 deg inclination with catheters inserted in the femoral vein and artery. 2. During 1 min exhausting exercise plasma potassium concentration rose in parallel in the vein and artery, reaching peak post-exercise values of 8.34 +/- 0.23 mmol l-1 and 8.17 +/- 0.29 mmol l-1. After 3 min recovery the potassium concentration was 0.50 +/- 0.05 mmol l-1 below pre-exercise values. Both the rise of plasma potassium concentration during exercise and the decline during recovery followed exponential time courses with a half-time of 25 s. 3. Exercise at reduced intensity showed that the peak post-exercise potassium concentration was linearly related to the exercise intensity. Individual resting, peak and nadir values were proportionally related. 4. The increased potassium concentration during exercise can be explained in full by the electrical activity in the exercising muscles. Repeated 1 min exhausting exercise bouts revealed no relationship between potassium concentration and plasma pH nor glycogen break-down. 5. All of the observations fit a simple model of potassium efflux from active muscle and elimination from blood with the following characteristics: the efflux increases (decreases) stepwise at the onset (end) of exercise, and the efflux rate during exercise increases with exercise intensity. Potassium is eliminated from blood by a proportional regulator which may be the Na(+)-K+ pump of the exercising muscle. Extracellular potassium is indirectly linked to the pump stimulus, and the rate of reuptake is proportional to the extracellular accumulation. Thus no limited maximal power for potassium uptake was found. The post-exercise undershoot of 0.5 mmol l-1 can be explained by a higher gain of the pump after exercise. 6. The large, rapid changes in the plasma potassium concentration during and after exercise is due to the first order kinetics of the reuptake mechanism rather than to a limited power to take up potassium.

Adolescent↗
PubMed1990

Gradual increase in leg oxygen uptake during repeated submaximal contractions in humans.

We examine whether muscle oxygen consumption (VO2) increases gradually during repeated submaximal isometric contractions. Six subjects made two-legged isometric quadriceps contractions at 30% maximal voluntary contraction for 6 s with 4 s of rest between until exhaustion (58 +/- 8 min). Blood samples were taken from the femoral vein and artery, and blood velocity was recorded by ultrasound-Doppler technique in the femoral artery. Blood flow was calculated from velocity and artery diameter values. Leg VO2 increased sixfold within the 1st min of exercise. A further doubling of the VO2 was seen during the remainder of the exercise, reaching 307 +/- 22 ml/min at exhaustion. This latter increase was due to a 54% increase in blood flow and a 34% increase in oxygen extraction. After 20 min of recovery VO2 was still 75% higher than preexercise values. The results show a twofold increase in energy demand of the working muscle during repeated constant-force isometric contractions. The increased energy cost of contraction is probably localized at the cellular level, and it parallels fatigue determined as decreased force-generating capacity.

Adenosine Triphosphate↗
PubMed1990

Increased erythrocyte magnesium content in essential hypertension.

The present study aimed at testing the hypothesis of decreased erythrocyte magnesium content and magnesium deficiency in essential hypertension. Atomic absorption was used to measure the erythrocyte content of total magnesium in 50-year-old otherwise healthy white males with essential hypertension (n = 12, blood pressure (mean +/- SE) 155 +/- 4/109 +/- 2 mmHg) that had never been treated and in normotensive control subjects (n = 12, blood pressure 128 +/- 2/88 +/- 1 mmHg) matched for age, sex, race, height, weight and smoking habits. The erythrocyte magnesium content was significantly increased in the hypertensive group (2.266 +/- 0.063 vs 1.903 +/- 0.069 mmol/l erythrocytes, p less than 0.001). No significant difference between the groups was detected for serum concentration or the 24-h urinary excretion of magnesium. In conclusion, the present study indicates increased rather than decreased erythrocyte content of magnesium in 50-year-old white males with 'never-treated', essential hypertension. Magnesium deficiency is, therefore, unlikely in this subset of critically selected and matched hypertensive patients.

Erythrocytes↗
PubMed1989

Increased erythrocyte magnesium in untreated essential hypertension.

In the present study we tested the hypothesis of magnesium deficiency and intracellular magnesium depletion in essential hypertension. Atomic absorption was used to determine the erythrocyte content of magnesium in 50-year-old otherwise healthy white men with never-treated, essential hypertension (n = 12, supine blood pressure 155 +/- 4/109 +/- 2 mmHg) and in a group of particularly well-matched normotensive control subjects. The erythrocyte magnesium content was higher in the hypertensive group (P less than 0.001). No significant difference between the groups was detected for serum concentration or the 24-h urinary excretion of the magnesium. In conclusion, magnesium deficiency is unlikely in white middle-aged hypertensive men.

Blood Pressure↗
PubMed1989

In-vivo quantification of myocardial Na-K pump rate during beta-adrenergic stimulation of intact pig hearts.

Maintenance of adequate electrical activity of the heart depends critically on the ability of the Na-K pump to compensate for normal passive sodium and potassium fluxes. Using sudden injections of [3H]ouabain into the left coronary artery in anaesthetized open-chest pigs, we monitored transient changes in myocardial potassium balance by PVC-valinomycin mini-electrodes. When related to the number of pumps blocked and fractional inhibition, these data provided estimates of total Na-K pump capacity as well as actual pump rate and perturbations of the Na-K balance. Experiments were performed in hearts with and without intracoronary isoprenaline infusion (2.5 nmol min-1). After injection of 120 nmol [3H]ouabain into the left coronary artery, myocardial [3H]ouabain concentrations were 118 (74-178) and 103 (76-145) pmol g-1 and total concentrations of [3H]ouabain binding sites were 893 (752-1076) and 785 (691-877) pmol g-1 (median, 95% confidence interval) in isoprenaline-treated and control hearts respectively (differences not significant). The [3H]ouabain injection caused a net potassium release of 81 (56-132) and 43 (23-75) mumol 100 g-1 (median, 95% confidence interval) in isoprenaline-treated and control hearts respectively (n = 6-8; significance of difference, P = 0.03). Na-K pump rate estimated from mono-exponential release curves was 6363 (3942-10,858) K+ ions min-1 site-1 during beta-adrenoceptor stimulation and 2514 (1380-4322) in control (significance of difference, P = 0.03). This corresponds to 40 and 16%, respectively, of the maximum possible pump rate determined from ATP hydrolysis. Comparison of accumulated potassium release and relative Na-K pump rate indicates that catecholamines enhance the sensitivity of the Na-K pump for intracellular sodium.

Adrenergic beta-Agonists↗
PubMed1988

Biochemical correlates of fatigue. A brief review.

Muscle fatigue, defined as a decreased force generating capacity, develops gradually during exercise and is distinct from exhaustion, which occurs when the required force or exercise intensity can no longer be maintained. We have reviewed several biochemical and ionic changes reported to occur in exercising muscle, and analysed the possible effects these changes may have on the electrical and contractile properties of the muscle. There is no evidence that substrate depletion can account for the decreased force generating capacity, but this factor may be important for the rate of energy turnover and be a major determinant for endurance. Increased concentration of inorganic phosphate and hydrogen ions will depress the force generating capacity, but since fatigue can develop gradually without accumulation of these ions they can only be important when aerobic ATP production is insufficient to support the contractions. Evidence is presented showing that a disturbed balance of K+ alone might cause depolarisation block at high stimulation frequencies, but extracellular K+ accumulation does not increase gradually during prolonged dynamic or static exercise, and is therefore not closely related to fatigue. The repeated release of Ca2+ from the sarcoplasmic reticulum (SR) during muscular activity is suggested of Ca2+ by the mitochondria, increasing with stimulation frequency and duration and possibly also deteriorating mitochondrial function. We therefore speculate that decreased Ca2+ availability for release from SR might contribute to a gradual decline in force generating capacity during all types of exercise.

Energy Metabolism↗
PubMed1988

Na,K pump stimulation by intracellular Na in isolated, intact sheep cardiac Purkinje fibers.

Regulation of the Na,K pump in intact cells is strongly associated with the level of intracellular Na+. Experiments were carried out on intact, isolated sheep Purkinje strands at 37 degrees C. Membrane potential (Vm) was measured by an open-tipped glass electrode and intracellular Na+ activity (aNai) was calculated from the voltage difference between an Na+-selective microelectrode (ETH 227) and Vm. In some experiments, intracellular potassium (aiK) or chloride (aCli) was measured by a third separate microelectrode. Strands were loaded by Na,K pump inhibition produced by K+ removal and by increasing Na+ leak by removing Mg++ and lowering free Ca++ to 10(-8) M. Equilibrium with outside levels of Na+ was reached within 30-60 min. During sequential addition of 6 mM Mg++ and reduction of Na+ to 2.4 mM, the cells maintained a stable aNai ranging between 25 and 90 mM and Vm was -30.8 +/- 2.2 mV. The Na,K pump was reactivated with 30 mM Rb+ or K+. Vm increased over 50-60 s to -77.4 +/- 5.9 mV with Rb+ activation and to -66.0 +/- 7.7 mV with K+ activation. aiNa decreased in both cases to 0.5 +/- 0.2 mM in 5-15 min. The maximum rate of aiNa decline (maximum delta aNai/delta t) was the same with K+ and Rb+ at concentrations greater than 20 mM. The response was abolished by 10(-5) M acetylstrophantidin. Maximum delta aNai/delta t was independent of outside Na+, while aKi was negatively correlated with aNai (aKi = 88.4 - 0.86.aNai). aCli decreased by at most 3 mM during reactivation, which indicates that volume changes did not seriously affect aNai. This model provided a functional isolation of the Na,K pump, so that the relation between the pump rate (delta aNai/delta t) and aiNa could be examined. A Hill plot allowed calculation of Vmax ranging from 5.5 to 27 mM/min, which on average is equal to 25 pmol.cm-2.s-1.K 0.5 was 10.5 +/- 0.6 mM (the aNai that gives delta aNai/delta t = Vmax/2) and n equaled 1.94 +/- 0.13 (the Hill coefficient). These values were not different with K+ or Rb+ as an external activator. The number of ouabain-binding sites equaled 400 pmol.g-1, giving a maximum Na+ turnover of 300 s-1. The Na,K pump in intact Purkinje strands exhibited typical sigmoidal saturation kinetics with regard to aNai as described by the equation upsilon/Vmax = aNai(1.94)/(95.2 + aNai(1.94)). The maximum sensitivity of the Na,K pump to aiNa occurred at approximately 6 mM.

Adenosine Triphosphate↗