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Biomedical subjects

O M Sejersted

Publications and source records attributed to O M Sejersted.

At least 55 records · Page 3Linked to original sources
PubMed1997

Cellular and subcellular expression of the monocarboxylate transporter MCT1 in rat heart. A high-resolution immunogold analysis.

An antibody to the C-terminus of the monocarboxylate transporter MCT1 was used to study the precise cellular and subcellular distribution of this transporter in rat heart. Postembedding immunogold procedures revealed that the labeling in the heart was restricted to cardiomyocytes and concentrated along the plasma membrane, including the transverse tubules. Gold particles occurred with highest densities in intercalated disks, where they avoided desmosomes and gap junctions. Labeling was also associated with plasmalemmal invaginations having ultrastructural features typical of caveolae. Internal membrane compartments were unlabeled. Quantitative analyses following postembedding labeling showed that the distribution of gold particles across the plasma membrane was nearly symmetrical, indicating that the C-terminus of the transporter is situated very close to the cell membrane. In preembedding immunogold experiments, the gold particles were localized at the external aspect of the plasma membrane, suggesting that the C-terminus is extracellular. From the present data, it can be concluded that even under basal conditions the majority of the MCT1 molecules in heart is present in the myocyte plasma membrane, implying that there is a constitutive functional expression of this transporter. It follows that the increased transmembrane flux of lactate during exercise or in pathological conditions such as ischemia must be a result of altered substrate gradients rather than of translocation of MCT1 molecules to the plasma membrane.

Animals↗
PubMed1996

Fuzzy space and control of Na+, K(+)-pump rate in heart and skeletal muscle.

Since intracellular Na+ activity (aiNa) is one important determinant of Na+ K(+)-pump rate as well as excitability and the finely tuned contractility, it is surprising that the relation between aNa and pump rate reported by different authors has kQ5 varying between 10 and 40 mmol L-1. Other data also point to a variable relation between pump rate and aiNa. During stimulation of isolated rat soleus muscles at 2 Hz, ouabain-sensitive 86Rb uptake was increased in spite of the intracellular Na+ remaining unaltered. In isolated cardiomyocytes, a transient Na+. K(+)-pump current was observed upon activation by extracellular K+ in spite of good control of aiNa. Na(+)-loaded, isolated, sheep cardiac Purkinje fibres initially hyperpolarized over a period of up to 1 min upon activation of the Na+, K+ pump with no detectable change of aiNa. These examples are compatible with the existence of a micro-environment close to the membrane where diffusion is slower than in the rest of the cytosol, so that local aiNa may fluctuate or gradients may develop as visualized by Wendt-Gallitelli at al. (1993). We conclude that the reported relationships between Na+, K+, pump rate and aiNa in intact cells probably underestimate the true affinity of the Na+, K+ pump for Na+ due to a functional diffusion barrier beneath the sarcolemma, and also because of incomplete cell dialysis in whole-cell voltage clamp experiments. The Na+, K+ pump seems to be preferentially supplied with Na+ from the outside through neighbouring channels and transporters.

Animals↗
PubMed1996

The effect of acute vs chronic treatment with beta-adrenoceptor blockade on exercise performance, haemodynamic and metabolic parameters in healthy men and women.

1. Variable results have been reported on the effect of beta-adrenoceptor blockers on maximal oxygen uptake (VO2 max) and exercise endurance. This may in part be due to different subject populations, but it could also be due to an adaption of metabolic and haemodynamic responses to exercise during chronic treatment with beta-adrenoceptor blockers. The present study was therefore carried out to examine the effect of acute and chronic administration of the non-selective beta-adrenoceptor blocker propranolol on both peak VO2 and exercise performance in the same subjects. Since the effect of beta-adrenoceptor blockade has not been properly investigated in women, eight healthy women were compared with seven men. Progressive bicycle exercise to exhaustion was performed after propranolol 0.15 mg kg-1 i.v. (acute) or 80 mg three times daily for 2 weeks (chronic) or placebo given according to a double-blind crossover design. 2. Mean (s.e. mean) peak VO2, was significantly reduced from 42.3 (1.6) ml min-1 kg-1 during placebo to 40.3 (1.2, P < 0.05) ml min-1 kg-1 after acute and 39.1 (1.2, P < 0.001) ml min-1 kg-1 after chronic propranolol treatment. No significant difference in peak VO2 between the two propranolol treatment regimens was observed (mean difference 1.2, 95% CI -0.1 to 2.4 ml min-1 kg-1). There was no treatment interaction with gender. 3. Cumulative work, 163 (9.3) kJ, was significantly reduced by acute, 148 (7.7, P < 0.001) kJ, and chronic, 147 (7.6, P < 0.001) kJ, administration of propranolol since the time to exhaustion was reduced by 5.3% and 5.3%, respectively. There was no significant difference between the two regimens of propranolol (mean difference 0.2, 95% CI -6.7 to 7.0 kJ) or between the sexes. Maximal knee extensor and handgrip strengths were not affected by propranolol. 4. Whereas sex did not influence ventilatory, haemodynamic or metabolic parameters, some differences were observed between acute and chronic propranolol treatment. During submaximal exercise oxygen uptake was reduced by approximately 2% and RER values increased by 0.04-0.05 after chronic treatment in contrast to no effect of acute propranolol treatment. Heart rate and systolic blood pressure were reduced significantly more after chronic compared with acute propranolol treatment; peak heart rate being 186 (2.2), 147 (2.3) and 134 (2.3) beats min-1, and peak systolic blood pressure being 189 (7), 171 (4) and 161 (4) mmHg after placebo, acute and chronic propranolol administration, respectively. Also the exercise induced rise in potassium and lactate levels were modified differentially; the rise in potassium concentration was less after chronic compared with acute propranolol treatment and lactate levels were reduced only after chronic administration of propranolol. In contrast, ventilation, which was unchanged after propranolol during submaximal exercise, was reduced to similar extent at exhaustion from 108 (6.4) to 97 (7.2) and 96 (5.9) l min-1 after acute and chronic propranolol administration, respectively. Diastolic blood pressure and subjective perception of fatigue were similar across the treatment regimens. 5. The study has demonstrated that acute and chronic administration of propranolol result in different haemodynamic and metabolic response to exercise, although endurance and peak oxygen consumption were reduced to the same extent. The response to propranolol was not significantly different between men and women.

Adrenergic beta-Antagonists↗
PubMed1996

K+ balance during exercise and role of beta-adrenergic stimulation.

Infusion of the beta 2-adrenoceptor agonist terbutaline will cause an activation of the Na(+)-K+ pump that leads to lowering of plasma K+ concentration and intracellular Na+ concentration. The present study examines whether these changes will affect the K+ homeostasis during subsequent exercise. Two-legged knee-extension exercise was carried out at low (40 W) and high (75 W) power for 8 min in six healthy, male subjects before (control) and during intravenous infusion of terbutaline (priming dose 500 micrograms, sustained dose 4.1 micrograms/min). Catheters in the femoral vein and artery allowed blood sampling and continuous recording of femoral venous plasma K+ concentration ([K+]fv) by means of a pliable, K(+)-sensitive electrode. Leg blood flow was measured by bolus injections of indocyanine green. Terbutaline decreased arterial K+ concentration by 0.83 mmol/l. The femoral veno-arterial concentration difference for K+ and loss rates of K+ were not significantly affected by terbutaline, but leg blood flow during steady-state exercise increased by approximately 0.5 l/min (P < 0.05). However, at cessation of exercise terbutaline significantly attenuated the rate of fall of [K+]fv at high power from 63 +/- 6 to 38 +/- 6 micromol. l-1.s-1, indicating a reduced reuptake rate of K+. The loss rate of K+ from the leg peaked after around 40 s of exercise, pointing to a rapid activation of reuptake rate of K+. We conclude that, during terbutaline infusion, the reuptake rate of K+ in exercising muscles is attenuated.

Adrenergic beta-Agonists↗
PubMed1995

Intramuscular pressures for monitoring different tasks and muscle conditions.

Intramuscular fluid pressure (IMP) can easily be measured in man and animals. It follows the law of Laplace which means that it is determined by the tension of the muscle fibers, the recording depth and by fiber geometry (fiber curvature or pennation angle). Thick, bulging muscles create high IMPs (up to 1000 mmHg) and force transmission to tendons becomes inefficient. High resting or postexercise IMPs are indicative of a compartment syndrome due to muscle swelling within a low-compliance osseofascial boundary. IMP increases linearly with force (torque) independent of the mode or speed of contraction (isometric, eccentric, concentric). IMP is also a much better predictor of muscle force than the EMG signal. During prolonged low-force isometric contractions, cyclic variations in IMP are seen. Since IMP influences muscle blood flow through the muscle pump, autoregulating vascular elements, and compression of the intramuscular vasculature, alterations in IMP have important implications for muscle function.

Electromyography↗
PubMed1995

Changes in Na+, K(+)-adenosinetriphosphatase, citrate synthase and K+ in sheep skeletal muscle during immobilization and remobilization.

The K+ balance and muscle activity seem to interact in a complex way with regard to regulating the muscle density of Na(+)-K+ pumps. The effect of immobilization was examined in ten sheep that had low muscle K+ content. Three additional sheep served as untreated controls. After being brought from pasture to sheep stalls one hindlimb was immobilized in a plaster splint for 9 weeks, and in five of the animals remobilization was carried out for a further 9 weeks. The weight bearing of the leg in plaster was recorded by a force plate. Open muscle biopsies from the vastus lateralis muscle were obtained before the study, after 9 weeks of immobilization, and after another 9 weeks of remobilization. The Na(+)-K+ pump density was measured as [3H]-ouabain binding to intact tissue, and citrate synthase activity was measured in tissue homogenate. The tissue content of K+ was measured in fat-free dried tissue. Muscle K+ content increased linearly by almost 70% through the 18-week period independent of intervention. Immobilization reduced thigh circumference by 8% (P < 0.05). A slight decrease in the area of type I fibres at 9 weeks and a slight increase at 18-weeks was found. The [3H]-ouabain binding was reduced by 39% and 22% in the immobilized and control legs, respectively, whereas citrate synthase activity was reduced by about 30% in both legs after 9 weeks of immobilization. During remobilization both the [3H]-ouabain binding and the citrate synthase activity increased to the same level as in the control animals. The plaster cast significantly reduced mass bearing of the immobilized leg, and a corresponding reduction in muscle activity must be assumed to have occurred in both legs as judged from citrate synthase activity. We concluded from this study that the reduction in the [3H]-ouabain binding during immobilization independent of an increase in muscle K+ content points to muscle activity as a strong stimulus for control of Na(+)-K+ pump density.

Animals↗
PubMed1995

K+ balance of the quadriceps muscle during dynamic exercise with and without beta-adrenoceptor blockade.

The effect of propranolol (0.15 mg/kg body wt) on K+ fluxes was investigated in seven healthy males performing 8-min two-legged knee-extension exercise at two different powers. K+ concentration was measured in the femoral vein by a K(+)-selective electrode, and leg blood flow was measured by the dye-dilution technique. During control bouts, rates of change in femoral venous K+ concentration were 38 +/- 10 and 53 +/- 8 mumol.l-1.s-1 at onset of exercise (K+ efflux) and -14 +/- 3 and -34 +/- 3 mumol.l-1.s-1 at cessation of exercise (K+ reuptake) at low and high powers, respectively. This mismatch between K+ efflux and reuptake rates fits with the steady-state K+ loss rate of 0.14 +/- 0.04 and 0.32 +/- 0.09 mmol/min. Propranolol raised K+ efflux rate, did not modify K+ reuptake rate or steady-state K+ loss, but caused transiently increased K+ loss rate at the onset of exercise, thus accentuating the rise of arterial K+ concentration. In conclusion, the continuous muscle K+ loss during steady-state exercise with a small muscle mass is not due to lack of catecholamine stimulation, but beta-adrenoceptor blockade increased the Na(+)-K+ pump lag so that the initial K+ loss at onset of exercise was increased.

Adrenergic beta-Antagonists↗
PubMed1994

K+ shifts of skeletal muscle during stepwise bicycle exercise with and without beta-adrenoceptor blockade.

1. K+ efflux rate and control of K+ reuptake rate in exercising muscle cells was examined in six healthy female volunteers. 2. A K(+)-selective electrode in the femoral vein continuously monitored K+ concentration ([K+]fv) during bicycling. Power was increased stepwise 5-6 times by 30-40 W every fourth minute until exhaustion before and after I.V. administration of propranolol. Leg blood flow was measured by bolus injections of Cardiogreen. 3. [K+]fv increased from about 4.3 to 6.8 mmol l-1 at exhaustion both before and after propranolol administration, but after drug infusion endurance was reduced from 22.2 +/- 0.6 to 19.7 +/- 1.1 min, so [K+]fv rose more rapidly. 4. The exercise-induced efflux rate of K+ from the muscle cells was estimated to be about 11 mumol kg-1s-1 at exhaustion both before and after propranolol administration. 5. As an indicator of rate of net loss of K+ from the leg, veno-arterial concentration differences ([K+]fv-a) during first, fourth and fifth power increments were high after 15 and 40 s, but declined toward the end of each power step. Propranolol accentuated [K+]fv-a only after 15 and 40 s of the first and fourth increments. 6. The exercise-induced increase in reuptake rate of K+ in the muscle, estimated at exhaustion, was not significantly changed by propranolol and was about 10 mumol kg-1s-1, corresponding to about 15% of maximum Na(+)-K+ pump capacity in man. 7. Extracellular accumulation and loss of K+ from muscle during bicycle exercise is due to Na(+)-K+ pump lag. The higher [K+]fv during propranolol is mainly due to impaired redistribution outside the exercising muscles. In addition at low powers, beta-adrenoceptor blockade caused a transiently increased net loss due to an accentuated Na(+)-K+ pump lag.

Adult↗
PubMed1994

[Can processes connected to muscular activity explain development of chronic pain?].

The pathogenetic mechanisms of chronic muscle pain are not known, but may be related to incomplete recovery between bouts of work. During monotonous repetitive static muscle contraction, fatigue develops gradually, parallel to an increase in oxidative metabolism combined with a change in Ca(2+)-homeostasis in a few muscle fibres. Ischemia or high lactate probably do not contribute to fatigue in this state. We review some recent results on muscle fatigue during a low force static work situation and also discuss the significance of K+ released from muscle as an important extracellular messenger.

Calcium↗
PubMed1994

Effect of exercise intensity on potassium balance in muscle and blood of man.

1. The rise of plasma [K+] during high intensity exercise is due to an initially rapid loss of K+ from the exercising muscle to the circulation. The K+ loss is primarily governed by the balance between K+ efflux rate from the muscle cells and the reuptake rate. It has been assumed that the reuptake rate is proportional to [K+] in the femoral vein ([K+]fv) during short-lasting uphill running, but this may not hold true for other types and durations of exercise. 2. In four subjects, initial rates of increase and decay of [K+]fv at start and end of bicycle exercise were quantified by means of K(+)-sensitive electrodes inserted into the femoral vein. Responses to exercise intensities between 90 and 440 W were examined. Both the initial rate of rise and the rate of decay of [K+]fv were linearly related to power. 3. In six subjects, exercising at 60, 85 and 110% of maximal oxygen uptake, blood was obtained from the femoral artery and vein. The veno-arterial concentration difference for K+ across the exercising leg decayed with half-times of about 3 min at all exercise levels and became not significantly different from zero at low powers. This fits with a good match between K+ efflux and reuptake rates at the cellular level. 4. Arterial plasma [K+] ([K+]a) rose faster with increasing exercise intensity, reaching peak values of 5.7 +/- 0.1, 6.0 +/- 0.2 and 8.0 +/- 0.2 mmol l-1. [K+]a fell again over the subsequent 5 min at the lowest intensity in spite of significant loss of muscle K+. Hence, released K+ was redistributed to other compartments outside the vascular bed. 5. While K+ loss increased linearly with increasing power, [K+]a showed a curvilinear relationship. Thus redistribution of K+ is less efficient at high intensities. [K+]a correlated better with relative work load than with absolute work load. 6. Reuptake of K+ after the end of the high intensity bout of exercise caused [K+]a to fall with a half-time of 31 s. The rate of K+ reuptake in the exercising muscle was not proportional to [K+]a or [K+]fv. However, at the level of the muscle cell, the rate of K+ reuptake was probably inversely related to intracellular [K+].

Adult↗
PubMed1994

Atrial natriuretic peptide in plasma after prolonged physical strain, energy deficiency and sleep deprivation.

Plasma concentrations of atrial natriuretic peptide (ANP) were investigated daily in 16 male cadets during a 6-day military training course with continuous heavy physical activities, sleep and energy deficiency (course I). At the end of another similar course (course II) 15 cadets were studied during 30-min cycle exercise at 50% maximal oxygen uptake with and without glucose infusion. A small, but not significant increase was found in the plasma concentrations of ANP during course I from 9.6 (SEM 1.1) pmol.l-1 in the control experiment to 11.1 (SEM 0.5) pmol.l-1 on day 5. During course II a small but significant increase was found from 7.8 (SEM 0.5) pmol.l-1 in the control experiment to 9.1 (SEM 0.5) pmol.l-1 at the end of the course. Plasma osmolality and chloride concentration decreased during the course. During the exercise test a significant increase was seen in ANP concentration from 8.2 (SEM 0.8) to 13.1 (SEM 2.0) pmol.l-1 in the control experiment and from 9.4 (SEM 0.7) to 13.5 (SEM 1.2) pmol.l-1 during the course. This response was attenuated by glucose infusion, an effect which may have been due to an exercise induced increase in plasma chloride concentration being abolished. In contrast, the potassium concentration response to exercise was increased during the course but unaffected by glucose infusion. In conclusion, the large increases in endogenous plasma catecholamine concentration shown to take place during previous courses were not reflected in the plasma concentrations of ANP, indicating only a moderate cardiac stress or no cardiac work overload during such courses.

Adult↗
PubMed1994

Effect of beta-adrenoceptor blockade on post-exercise oxygen consumption.

In the recovery period after strenuous exercise, there is an increase in O2 uptake termed the excess post-exercise O2 consumption (EPOC), consisting of a rapid and a prolonged component. Mechanisms regulating the prolonged component of EPOC are not completely understood, but an effect of catecholamines has been suggested. The purpose of this study was to investigate the effect of beta-adrenoceptor blockade on EPOC. Six healthy young men were randomized to one control experiment and two exercise experiments, one with and one without nonselective beta-adrenoceptor blockade. In the exercise experiments, they exercised for 60 minutes at 78% +/- 3% (mean +/- SD) of maximal O2 uptake (VO2max) on a cycle ergometer followed by 6.5 hours' bedrest. In the beta-adrenoceptor blockade experiment, propranolol (0.1 mg.kg-1 body weight [BW]) was administered intravenously immediately after the exercise bout and again 3.5 hours after exercise. The control experiment was performed without exercise or beta-adrenoceptor blockade. EPOC was calculated as the difference in O2 uptake between the exercise and control experiments. A supplementary study on 15 subjects showed resting O2 uptake to be unaffected by propranolol. O2 uptake was significantly increased during the recovery period after exercise when no beta-adrenoceptor blocker was administered. After 6.5 hours of bedrest, the mean increase (+/- SE) in O2 uptake was 19 +/- 4 mL.min-1. In contrast, when propranolol was administered during recovery from exercise, O2 uptake was significantly increased for only the first 2 hours. Propranolol decreased total EPOC (+/- SE) by about one third, from 14.4 +/- 1.9 to 9.5 +/- 2.5 L.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1994

Na,K-pump concentration in hypertrophied human hearts.

Several studies have associated myocardial dysfunction with reduced myocardial Na,K-pump concentration, but whether impaired Na,K-pump capacity is a pathogenetic factor or an epiphenomenon related to accompanying cardiac hypertrophy is not established. We measured Na,K-pump concentrations in 10 hypertrophied and 11 normal weighted hearts obtained at autopsy using [3H]ouabain as ligand. Specific [3H] ouabain binding site concentration (OBC) in the left ventricle (LV) averaged 449 +/- 40 (pmol.g-1 wet weight; mean +/- SEM) in hypertrophied and 598 +/- 36 in normal weighted ventricles (P = 0.02). A trend towards lower LV OBC (-19%; P = 0.25) was found in hypertrophied hearts from patients with congestive heart failure as compared with non-failing hypertrophied hearts. In multivariate analysis with 18 variables including age and heart failure, only LV weight correlated independently with LV OBC (r = -0.61; P = 0.003). When OBC was related to either dry weight or to protein content, a 25-35% reduction was consistently found in hypertrophied LV, whereas RV OBC was similar in both groups. In conclusion, myocardial Na,K-pump concentration and thus the capacity to maintain homeostasis is reduced in LV, but not in RV, of hypertrophied hearts. Whether the moderately reduced myocardial Na,K-pump concentration is a pathogenetic factor in LV dysfunction remains to be determined.

Aged↗
PubMed1994

Plasma K+ changes during intense exercise in endurance-trained and sprint-trained subjects.

Active muscle releases K+, and the plasma K+ concentration is consequently raised during exercise. K+ is removed by the Na,K pump, and training may influence the number of pumps. The plasma K+ concentration was therefore studied in five endurance-trained (ET) and six sprint-trained (ST) subjects during and after 1 min of exhausting treadmill running. Non-exhausting bouts of exercise at either lower speed or of shorter duration were also carried out. Blood samples were taken from a catheter in the femoral vein before and at frequent intervals after exercise. The pre-exercise venous plasma [K+] was (mean +/- SEM) 3.68 +/- 0.10 mmol l-1 (ET) and 3.88 +/- 0.06 mmol l-1 (ST). One minute of exhausting exercise was sustained at 5.27 +/- 0.08 m s-1 (ET) and 5.59 +/- 0.06 m s-1 (ST) and caused the plasma K+ concentration to rise by 4.4 +/- 0.3 (ET) and 4.7 +/- 0.3 mmol l-1 (ST; ns) respectively. Three minutes after exercise the K+ concentration was 0.48 +/- 0.08 mmol l-1 (ST) and 0.50 +/- 0.07 mmol l-1 (ST) below the pre-exercise value. During the following 6 min of recovery, the value was unchanged for the ET subjects, while a 0.32 +/- 0.06 mmol l-1 rise was seen for the ST subjects. Exercise at reduced intensity or of reduced duration resulted in smaller changes in the K+ concentration both during exercise and in the post-exercise recovery, and for each subject the lowest post-exercise K+ concentration was therefore inversely related to the peak K+ concentration during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Electromyographic activation and proportion of fast versus slow twitch muscle fibers: a genetic disposition for psychogenic muscle tension?

17 right-handed males volunteered for an experiment that compared task-related patterns of electromyographic (EMG) activation with data from muscle biopsy on proportion of slow-twitch ((ST) aerobic) to fast-twitch ((FT) anaerobic) muscle fibers. The biopsy was taken from the right-leg gastrocnemius muscle after EMG measurement from that area of the leg muscle. EMG was also recorded from the left forearm flexor carpi radialis area. Recordings were obtained from pre- and post-task resting periods and during 150 s of video-task performance when the right hand operated a joy-stick. The results showed a highly significant tonic EMG activation in the leg muscle of subjects with predominance of ST fibers, and this relationship generalized to the EMG from the 'passive' forearm. The proportion of ST to FT fibers is genetically defined and not altered by exercise. Therefore, our results lend support to a genetic differentiation between individuals with high vs. low probability of unintended build-up of muscle tension during perceptual-motor task performance.

Adult↗
PubMed1993

Variable effects of beta-adrenoceptor blockade on muscle blood flow during exercise.

The role of beta-adrenoceptors in exercise-induced muscle hyperaemia was investigated. Exercise was performed with a small and a large muscle mass: knee extension (KE) and bicycle exercise (BE). Seven healthy subjects performed light and maximal KE and eight subjects performed stepwise dynamic BE to exhaustion before and after acute i.v. administration of propranolol (0.15 mg kg-1). Leg blood flow was measured by a bolus dye dilution technique. During KE at low and high power leg blood flow was reduced by 8.7 and 10.5% after propranolol was administered, mean arterial blood pressure (MAP) was reduced at low, but not at high power resulting in increased leg vascular resistance (LVR) during high intensity. During BE propranolol reduced leg blood flow and increased LVR at low power, but not at high power. At high BE intensity LVR did not change with increasing power and was slightly decreased after propranolol was administered. In this situation oxygen uptake was close to maximum and the concentration of catecholamines was 3-5 times higher compared with KE. There was no significant effect of propranolol on lactate release or arterial-femoral venous (a-fv) differences for adrenaline or noradrenaline. We conclude that beta-adrenoceptors modulate local vasodilation in skeletal muscles during exercise independently of local muscle energy demand, but that the effect is highly dependent on active muscle mass since alpha-adrenergic activity during maximal BE seemed to disguise any effect of propranolol on LVR.

Adrenergic beta-Antagonists↗
PubMed1993

Intravasal use of pliable K(+)-selective electrodes in the femoral vein of humans during exercise.

Continuous recording of plasma K+ concentration ([K+]) during exercise would be valuable in determining K+ fluxes associated with muscle activation. Pliable polyvinyl chloride electrodes were constructed by incorporation of valinomycin into a polyvinyl chloride membrane attached to the end of a catheter with a 1 mm outer diameter. Through an outer catheter the electrode was inserted into the femoral vein of human subjects. The setup allowed easy in vivo calibration, and rapid changes of femoral venous [K+] of < 0.1 mmol/l could easily be detected. Drift over 1 h amounted to < 3 mV and was corrected for by analysis of blood samples. Rapid changes in femoral venous [K+] occurred during and after dynamic exercise, short and prolonged isometric contractions, and repetitive isometric contractions of the quadriceps muscle. Combined with arterial blood sampling and flow measurements, the electrodes will allow good approximation of 1) cellular K+ efflux rate associated with increased electrical activity, 2) rate of intramuscular reuptake of K+ mediated by the Na(+)-K+ pump, and 3) rate of K+ loss to or uptake from the circulation by the muscle.

Exercise↗