Lactate, glycerol, and catecholamine in the venous blood after 400-m and 3,000-m runs were determined in eight sprint runners, eight long distance runners, and seven untrained students. In 400-m sprinting, average values of velocity, peak blood lactate, and adrenaline were significantly higher in the sprint group than in the long distance and untrained groups. The mean velocity of 400-m sprinting was significantly correlated with peak blood lactate in the untrained (r = 0.76, P less than 0.05) and long distance (r = 0.71, P less than 0.05) groups, but not in the sprint group. In the 3,000-m run, on the other hand, average values of velocity and glycerol were significantly higher in the long distance group than in the sprint and untrained groups, but there are no significant differences in lactate levels between the three groups. These results suggest that 1) performance in 400-m sprinting may depend mainly upon an energy supply from glycolysis in the long distance and untrained group, but in the sprinters is influenced not only by glycolysis, but also by other factors such as content of ATP or force per unit muscle cross-sectional area; 2) peak blood lactate obtained after 400-m sprinting may be used as a useful indication of anaerobic work capacity in the long distance and untrained groups, but not in the sprinters. 3) high speed in the 3,000-m run could be maintained in the long distance runners by means of a greater energy supply from lipid metabolism as compared with sprinters or untrained subjects.

Interrelations between age and plasma renin, aldosterone and cortisol levels, urinary catecholamiens, plasma and blood volumes, exchangeable body sodium and blood pressure wwere studied in 28 young (19 to 29 years), 16 middle-aged (32 to 58 years) and 15 elderly (60 to 74 years) healthy subjects. Supine and upright plasma renin and supine aldosterone levels decreased while urinary noradrenaline excretion rate increased progressively with aging (r= greater than 0.34; p less than 0.05), with significant differences in mean values between young and elderly subjects (p less than 0.02). There was also an age-related decrease in upright plasma aldosterone concentration, although this was no statistically significant. Furthermore, mean plasma cortisol concentrations increased in response to upright posture in elderly ( + 50%; p less than 0.02), but not in young ( --10%) or middle-aged ( --8%) subjects. Blood pressure correlated with age ( r =0.35; p less than 0.05) or noradrenaline excretion rate ( r= 0.34) in the entire study population and with blood volume in the elderly ( r = 0.68), but not in the young or middle-aged study. Groups. There were no significant age-related differences in the body sodium/volume state, basal plasma cortisol levels or urinary adrenaline excretion rate, and plasma renin or aldosterone levels did not correlate with these parameters or with blood pressure. It is concluded that the influence of age on plasma renin or aldosterone levels, plasma cortisol responsiveness to upright posture, and urinary noradrenaline excretion should be taken into consideration, whenever these factors have to be interpreted in patients with arterial hypertension or other clinical disorders. Further more, these data are conssitent with the possiblity that in normal man increases in supine blood pressure with aging may be related at least partly to concomitant changes in free peripheral noradrenaline.

Ten days of total energy deprivation evoked the following endocrine changes in 12 healthy, normal-weight males: early and marked reductions and increments in the blood levels of T3 and reverse T3, respectively, with rapid returns to pre-starvation levels after refeeding; a slight and late decrease in the blood levels of T4; a minute reduction of the blood levels of TSH; a pronounced increase in the blood levels of growth hormone, but a return towards pre-exposure levels even before discontinuation of starving; a minor and gradual enhancement of the blood levels of cortisol, and an increase in nocturnal urinary adrenaline excretion. It is assumed that these changes reflect a complex regulatory mechanism, the purpose of which is to secure adequate energy supply to vital organs.

A strip of fundus from a rat's stomach was suspended in Krebs solution containing 5-hydroxytryptamine. Movements of the muscle were recorded by means of a frontal writing lever giving a magnification of sixteen-times. The strip relaxed when isoprenaline, adrenaline or noradrenaline was added to the organ-bath in concentrations of 0.2 to 2 ng/ml. The preparation was most sensitive to isoprenaline and least sensitive to noradrenaline. The components of a mixture of two catechol amines could be assayed by superfusing the rat stomach and a chick rectum in the same stream of fluid.

1. Single guinea-pig ventricular cells were voltage clamped using the patch clamp method combined with the pipette-perfusion technique. The voltage-dependent current systems were mostly blocked, and the background membrane conductance was measured by applying ramp pulses. 2. beta-Adrenergic effectors and related substances such as adrenaline, isoprenaline, forskolin or internal application of cyclic AMP induced a current component which showed a reversal potential near the expected Cl- equilibrium potential as well as an outward rectification in the I-V relation. It is suggested that the activation of this Cl- current was due to phosphorylation of the channel protein or related structure by the cyclic AMP-dependent protein kinase. Coincidentally with the activation of the Cl- current, the membrane capacitance of the cell decreased reversibly. 3. Acetylcholine (ACh) depressed the responses induced by beta-adrenergic stimulation and forskolin, but failed to interfere with the one induced by cyclic AMP. 4. The dose dependence of the Cl- current activation by isoprenaline or forskolin was fitted by the Hill equation, with a coefficient of 1.9 and a half-maximum concentration K 1/2 = 13 nM for isoprenaline, and with a Hill coefficient of 3 and a K 1/2 = 1.2 microM for forskolin. In the presence of 5.5 microM-ACh the dose-response relation shifted to higher doses; K 1/2 was 65 nM for isoprenaline and 3.6 microM for forskolin. 5. Washing out ACh in the presence of isoprenaline frequently caused transient overshoots of the response. When a saturating concentration of isoprenaline was used, this rebound was not observed. 6. The internal application of cyclic GMP enhanced the response of the Cl- current induced by isoprenaline or adrenaline. 7. When cyclic AMP was applied internally, the response was small in most cells. When the cell was superfused with 20 microM-IBMX (3-isobutyl-1-methylxanthine), the Cl- current was consistently induced by the application of cyclic AMP. It is suggested that phosphodiesterase activity strongly buffered the influx of cyclic AMP through the patch pipette tip. 8. We suggest that the compensatory interaction between the beta-adrenergic stimulation and the muscarinic inhibition is at the membrane level, most probably via GTP-binding proteins in activating adenylate cyclase.

The effect of transient hypertension on blood-brain barrier (BBB) permeability, particularly on extravasation of immunoglobulin G (IgG), has not been fully understood. In the present experiment, we investigated the time course of endogenous albumin and IgG extravasation through BBB and the localization of extravasated IgG in brain parenchyma during adrenaline(AD)-induced transient hypertension in the rat by using Evans blue fluorescence, immunohistochemistry, and Western blot. The results showed that a bolus injection of AD (10 microg/kg) induced a transient elevation of arterial pressure lasting about 1 min. The endogenous albumin and IgG entered the brain parenchyma via BBB only when hypertension occurred. Electron microscopically, the IgG-like immunoreactivities were predominantly seen in the cytoplasm of endothelia of capillaries, pericytes, extracellular space of parenchyma, and the cytoplasm of glial cells. The results suggest that circulating IgG or antibodies might contact the structures of brain parenchyma through passage of BBB when its permeability is temporally changed by transient hypertension. This phenomenon implies a possible mechanism of pathogenesis for immune-mediated diseases in the brain.

Plasma adrenaline, noradrenaline, and dopamine concentrations and plasma renin activity were measured in the supine position and after standing for 10 minutes in 14 patients with sustained benign essential hypertension and in five patients with labile hypertension. Results were compared with values obtained in 11 normotensive control subjects. In controls plasma noradrenaline concentrations increased with age, while plasma adrenaline values tended to decrease with age. No significant difference in mean plasma noradrenaline was found between hypertensive and control subjects, but plasma noradrenaline seemed slightly increased in a proportion of hypertensive patients aged less than 50. Plasma adrenaline was considerably raised in both supine and standing positions in eight patients with sustained hypertension and in two with labile hypertension. Dopamine concentrations and plasma renin activity were similar in all groups studied. The finding of significantly raised plasma adrenaline concentrations in a large proportion of hypertensive patients supports the hypothesis that the activity of the sympathetic nervous system is increased in essential hypertension. Measurement of plasma adrenaline seems to be a more sensitive index of this activity than that of plasma noradrenaline.

Little is known of the ability of the human newborn infant to mount an endocrine and metabolic response to surgical trauma. Blood concentrations of glucose, lactate, pyruvate, alanine, hydroxybutyrate, acetoacetate, and glycerol together with plasma concentrations of insulin, glucagon, adrenaline, and nonadrenaline were measured in 33 infants (26 term, 7 preterm) subjected to surgery during the neonatal period. The results show that newborn infants can indeed mount a substantial endocrine and metabolic stress response, the main features of which are hyperglycemia and hyperlactatemia associated with the release of catecholamines and the inhibition of insulin secretion. There are specific differences between preterm and term neonates and between neonates anesthetised by different anesthetic techniques in the pattern of this response.

OBJECTIVE

To investigate whether levosimendan diminishes the incidence of heart failure after cardiac surgery.

METHODS

Prospective, randomized, placebo-controlled clinical study.

METHODS

Cardiac surgery operating room and postanesthesia care unit in a university hospital.

METHODS

Two hundred patients assigned to undergo heart valve or combined heart valve and coronary artery bypass grafting surgery.

METHODS

Patients were randomized to receive a 24-hr infusion of placebo or levosimendan administered as a 24 μg/kg bolus over 30-mins and thereafter at a dose of 0.2 μg/kg/min.

RESULTS

Heart failure was defined as cardiac index<2.0 L/min/m or failure to wean from cardiopulmonary bypass necessitating inotrope administration for at least 2 hrs postoperatively. Heart failure was less frequent in the levosimendan compared to the placebo group: 15 patients (15%) in the levosimendan and 59 patients (58%) in the placebo group experienced heart failure postoperatively (risk ratio 0.26; 95% confidence interval 0.16-0.43; p<.001). Accordingly, a rescue inotrope (adrenaline) was needed less frequently in the levosimendan compared to the placebo group (risk ratio 0.11; 95% confidence interval 0.01-0.89), p=.005. Intra-aortic balloon pump was utilized in one patient (1%) in the levosimendan and in nine patients (9%) in the placebo group (risk ratio 0.11; 95% confidence interval 0.01-0.87), p=.018. The hospital and the 6-month mortality were comparable between groups. There were no significant differences in major organ failures postoperatively. Eighty-three patients were hypotensive and needed noradrenaline in the levosimendan compared to 52 patients in the placebo group, p<.001. The cardiac enzymes (creatine kinase MB isoenzyme mass) indicating myocardial damage were lower in the levosimendan group on the first postoperative day, p=.011.

CONCLUSIONS

In the present study, levosimendan infusion reduced the incidence of heart failure in cardiac surgery patients but was associated with arterial hypotension and increased requirement of vasopressor agents postoperatively. Improved mortality or morbidity was not demonstrated.

1. A scheme is presented which summarizes the activation and deactivation of the membrane currents which underlie pacemaking in the natural pacemaker of the heart. 2. Experimental evidence (mostly obtained using the voltage-clamp technique) for the properties of the time-dependent membrane currents in pacemaking tissue of the frog and the rabbit is discussed. 3. The mode of the inhibitory action of acetylcholine on pacemaker cells is considered. In the amphibian pacemaker cell, acetylcholine probably reduces slow inward current (as it certainly does in amphibian atrium) but in mammalian sino-atrial node it seems that such action, if present at all, is much less marked. In the pacemakers of both amphibian and mammal, acetylcholine greatly increases outward potassium current and there is recent evidence that it may do so by opening up a special acetylcholine-activated potassium channel. 4. Adrenaline greatly increases the slow inward current in pacemaker as in other cardiac tissues. This increase, together with (in mammal at least) an increased change of an additional pacemaking current, overrides an adrenaline-induced increase in outward current and leads to acceleration of the pacemaking rate. 5. The Appendix contains a brief consideration of the experimental and theoretical basis for the method of exponential separation of outward current components in the presence of the extracellular potassium accumulation that inevitably accompanies the flow of outward membrane current.

1. A method was developed for the isolation of essentially pure myosin light chains from perfused rat heart. The phosphorylation of the P-light chains was estimated by hydrolysis and measurement of phosphate released, by electrophoresis in 8 M-urea and by 32P incorporation in perfusion with [32P]Pi. 2. In control perfusions there was 0.5-0.6 mol of phosphate/mol of P-light chain. This was not changed by perfusion with 5 microM-adrenaline for 10-40s. Perfusion for 1 min with medium containing 7.5 mM-CaCl2, or for 30s with medium containing 118 mM-KCl, also did not change the phosphorylation of P-light chains. 3. It is concluded that phosphorylation of P-light chains is not important in mediating the action of inotropic agents in the heart.

Secretagogues of pancreatic enzyme secretion, the hormones pancreozymin, carbamylcholine, gastrin I, the octapeptide of pancreozymin, and caerulein as well as the Ca++ -ionophore A 23187 stimulate 45Ca efflux from isolated pancreatic cells. The non-secretagogic hormones adrenaline, isoproterenol, secretion, as well as dibutyryl cyclic adenosine 3',5'-monophosphate and dibutyryl cyclic guanosine 3',5'-monophosphate have no effect on 45Ca efflux. Atropine blocks the stimulatory effect of carbamylcholine on 45Ca efflux complately, but not that of pancreozymin. A graphical analysis of the Ca++ efflux curves reveals at least three phases: a first phase, probably derived from Ca++ bound to the plasma membrane; a second phase, possibly representing Ca++ efflux from cytosol of the cells; and a third phase, probably from mitochondria or other cellular particles. The Ca++ efflux of all phases is stimulated by pancreozymin and carbamylcholine. Ca++ efflux is not significantly effected by the presence or absence of Ca++ in the incubation medium. Metabolic inhibitors of ATP production. Antimycin A and dinitrophenol, which inhibit Ca++ uptake into mitochondria, stimulate Ca++ efflux from the isolated cells remarkably, but inhibit the slow phase of Ca++ influx, indicating the role of mitochondria as an intracellular Ca++ compartment. Measurements of the 45Ca++ influx at different Ca++ concentrations in the medium reveal saturation type kinetics, which are compatible with a carrier or channel model. The hormones mentioned above stimulate the rate of Ca++ translocation. The data suggest that secretagogues of pancreatic enzyme secretion act by increasing the rate of Ca++ transport most likely at the level of the cell membrane and that Ca++ exchange diffusion does not contribute to the 45Ca++ fluxes.

1. The post-ganglionic nerve fibres to the vas deferens of the guinea-pig and rat were interrupted in vivo by stripping one vas deferens of its serous coat; the other vas deferens was left intact as a control.2. Four to eight days later the stripped vas deferens did not contract in response to electrical transmural stimulation in vitro at 0.1 msec pulse duration. Pulses of 1.0 msec duration produced small contractions which were not abolished by local anaesthetic or adrenergic neurone-blocking drugs.3. Log dose-response curves to noradrenaline were, for stripped vasa deferentia, to the left of those for control vasa. The increase in sensitivity to noradrenaline at 8 days was about sixteenfold for rat vasa and about tenfold for guinea-pig vasa. Tyramine did not contract stripped vasa from guinea-pigs or rats.4. The noradrenaline and adrenaline content of guinea-pig and rat vasa was greatly reduced or abolished 8 days after the stripping operation.5. Fluorescent nerve terminals were usually absent when transverse sections of stripped vasa were examined by fluorescence microscopy after treatment by the formaldehyde condensation method for demonstrating catecholamines.6. It is concluded that post-ganglionic sympathetic denervation is achieved by stripping the vas deferens in vivo of its serous coat and mesenteric attachments.

Investigation of the subcellular and molecular components of insulin secretion has been made difficult by the small quantities of material available. The recent development of a transplantable rat islet cell tumour of high insulin content and state of differentiation suggested a system more amenable to analysis. To validate the tumour as a model of secretion we have studied its release of insulin. In acute experiments in vitro immunoreactive insulin release was increased by leucine, glucagon, theophylline and dibutyryl cyclic AMP, though not by glucose. Leucine (20 mmol/l) plus theophylline (5 mmol/l) caused an abrupt, sustained and rapidly reversible stimulation of two- to fivefold. The response was inhibited by antagonists of cellular oxidative phosphorylation (cyanide, 2,4-dinitrophenol, antimycin A), calcium flux (EGTA, verapamil, Mg2+), calmodulin (trifluoperazine), microtubules (vinblastine, colchicine) and by adrenaline and somatostatin. These findings suggest that the tumour secretes insulin by an exocytotic mechanism similar to that of normal islet tissue.

The occurrence of neuropeptide Y (NPY)-like immunoreactivity (LI) in the adrenal gland of several species as well as in tumor tissue and plasma from pheochromocytoma patients was investigated. NPY-LI was present in chromaffin cells of the adrenaline type in all species investigated except in the pig, as demonstrated by a colocalization of NPY-LI and the adrenaline-synthetizing enzyme phenylethanolamine N-methyltransferase (PNMT). NPY-LI in the adrenaline cells of the cat was clearly separated from the neurotensin-LI in the noradrenaline dopamine-beta-hydroxylase-positive, PNMT-negative cells. NPY-LI seems to co-exist with enkephalin-like material in the chromaffin cells. In addition, NPY-LI was present in nerves both within the adrenal cortex and medulla. The highest levels of NPY-LI were found in mouse and cat, while only a very low amount of NPY-LI was present in the pig adrenal. Characterization of the adrenal NPY-LI by reversed-phase high-performance liquid chromatography revealed that the main peak was similar to porcine NPY. In addition, two minor peaks of NPY-LI were present. High levels of NPY-LI were found in plasma and tumors from the pheochromocytoma patients. During manipulation of the tumors upon surgical removal, there was a marked increase in plasma NPY-LI in parallel with the raise in catecholamines and in blood pressure. At least two forms of NPY-LI were present in plasma and tumor extracts from pheochromocytoma patients with the main peak corresponding to porcine NPY. Since NPY exerts vasoconstrictor effects, it may be postulated that NPY contributes to the adrenal cardiovascular response and to the hypertension seen in pheochromocytoma patients.

BACKGROUND

Egg allergy is common and although resolution to uncooked egg has been demonstrated, there is lack of evidence to guide reintroduction of well-cooked egg.

OBJECTIVE

To examine the rate of resolution to well-cooked, compared with uncooked egg in children, and safety of egg challenges.

METHODS

A longitudinal study of egg-allergic children from 2004 to 2010, who underwent challenge with well-cooked and if negative, uncooked egg. Participants underwent repeat annual challenges and egg-specific IgE measurement.

RESULTS

One hundred and eighty-one open egg challenges were performed in 95 children whose median age of allergy onset was 12 months. Fifty-three of 95 (56%) had at least one annual repeat challenge. Pre-study historical reactions occurred to baked egg in five (5%), lightly cooked in 58 (61%) and uncooked in nine (9%); respiratory reactions occurred in 11 (12%) and seven (7%) had anaphylaxis; adrenaline was used during five reactions. There were 77 well-cooked and 104 uncooked egg challenges. Tolerance was gained twice as rapidly to well-cooked than uncooked egg (median 5.6 vs. 10.3 years; P<0.0001) and continued to 13 years; hazard ratio 2.23 (95% confidence interval 1.6-3.9). Nearly 1/3 had resolved allergy to well-cooked egg at 3 years and 2/3 at 6 years. Of 28/77 (37%) positive well-cooked egg challenges, 65% had cutaneous symptoms, 68% gastrointestinal and 39% rhinitis, with no other respiratory reactions. Adrenaline was not required. CONCLUSIONS AND CLINICAL RELEVANCE RESOLUTION: of egg allergy takes place over many years, with children outgrowing allergy to well-cooked egg approximately twice as quickly as they outgrow allergy to uncooked egg. There were no severe reactions to well-cooked egg challenge, and adrenaline was not required. Our data support initiation of home reintroduction of well-cooked egg from 2 to 3 years of age in children with previous mild reactions and no asthma. Resolution continues to occur in older children, so that despite an earlier positive challenge, attempts at reintroduction should be continued.

Several studies have shown increased sympathetic activity during acute exposure to hypobaric hypoxia. In a recent field study we found reduced plasma catecholamines during the first days after a stepwise ascent to high altitude. In the present study 14 subjects were exposed to a simulated ascent in a hypobaric chamber to test the hypothesis of a temporary reduction in autonomic activity. The altitude was increased stepwise to 4500 m over 3 days. Heart rate variability (HRV) was assessed continuously in seven subjects. Baroreceptor reflex sensitivity (BRS) was determined in eight subjects with the 'Transfer Function' method at baseline, at 4500 m and after returning to baseline. Resting plasma catecholamines and cardiovascular- and plasma catecholamine- responses to cold pressor- (CPT) and mental stress-test (MST) were assessed daily in all and 12 subjects, respectively. Data are mean +/- SEM. Compared with baseline at 4500 m there were lower total power (TP) (35 457 +/- 26 302 vs. 15 001 +/- 11 176 ms2), low frequency (LF) power (3112 +/- 809 vs. 1741 +/- 604 ms2), high frequency (HF) power (1466 +/- 520 vs. 459 +/- 189 ms2) and HF normalized units (46 +/- 0.007 vs. 44 +/- 0.006%), P < or = 0.001. Baroreceptor reflex sensitivity decreased (15.6 +/- 2.1 vs. 9.5 +/- 2.6 ms mmHg(-1), P = 0.015). Resting noradrenaline (NA) decreased (522 +/- 98 vs. 357 +/- 60 pmol L(-1), P = 0.027). The increase in systolic blood pressure (SBP) and NA during mental stress was less pronounced (21 +/- 4 vs. 10 +/- 2% and 25 +/- 9 vs. -2 +/- 8%, respectively, P < 0.05). The increase in SBP during cold pressor test decreased (16 +/- 3 vs. 1 +/- 6%, P = 0.03). Diastolic blood pressure, HR and adrenaline displayed similar tendencies. We conclude that a transient reduction in parasympathetic and sympathetic activity was demonstrated during stepwise exposure to high altitude.

Although the importance of sympathetic nervous activation in the pathogenesis of essential hypertension is well documented, the exact pathophysiology of the sympathetic nervous dysfunction present remains to be delineated. This review details three relatively new findings of disturbed sympathetic neurobiology in hypertension. Adrenaline cotransmission is present in the cardiac sympathetic nerves of patients with essential hypertension, as it is in patients with panic disorder, providing presumptive evidence of exposure to high levels of mental stress in hypertensive patients. In lean patients with hypertension there is also evidence of faulty noradrenaline reuptake into the sympathetic nerves of the heart, an abnormality amplifying the sympathetic neural signal by impairing removal of noradrenaline from the synaptic cleft. If both abnormalities are present in the sympathetic nerves of the kidneys also (which we did not test), there would most probably be a direct contribution to hypertension development. In the kidneys the causal chain between sympathetic overactivity and the development of hypertension is stronger than for the heart. In obesity-related hypertension there is evidence that renal sympathetic tone is high, based on approximately a doubling of the measured rate of spillover of noradrenaline into the renal veins. This increase in sympathetic outflow to the kidneys appears to be a necessary but apparently not a sufficient cause for the development of clinical hypertension, commonly being present also in overweight people with blood pressure in the normotensive range. High renal sympathetic tone in the latter, of course, may well still contribute to elevation of their pressure level, although not on such a scale as to cause clinical hypertension.

BACKGROUND

The aim of this study was to examine the associations between urinary levels of the stress hormones adrenaline, noradrenaline and cortisol during treatment with self reported stress, in order to investigate the mechanism for the previously observed negative association of anxiety and depression with the outcome of IVF/ICSI.

METHODS

In a multicentre prospective cohort study, women entering their first cycle of IVF/ICSI treatment were asked to participate. From each participant nocturnal urine samples were collected; pre-treatment, before oocyte retrieval and before embryo-transfer (ET), to assess hormonal concentrations. Additionally, two questionnaires were administered before the start of the treatment to measure anxiety and depression.

RESULTS

168 women completed the questionnaires and collected at least two urine specimens. A significant positive correlation between urinary adrenaline concentrations at baseline and ET and the scores on depression at baseline were found. In women with successful treatment, lower concentrations of adrenaline at oocyte retrieval and lower concentrations of adrenaline and noradrenaline at ET, compared with unsuccessful women, were found.

CONCLUSIONS

The significant positive association of adrenaline concentration with pregnancy and with depression suggested that this adrenal hormone could be one of the links in the complex relationship between psychosocial stress and outcome after IVF/ICSI.

While socio-epidemiologic studies documented impressive associations of indicators of chronic psychosocial stress with cardiovascular (c.v.) disease evidence on patho-physiologic processes is still limited. In this regard, the concept of heightened c.v. and hormonal reactivity (RE) to mental stress was proposed and explored. While this concept is a static one we suggest a more dynamic two-stage model of RE where recurrent high responsiveness (stage 1) in the long run results in attenuated, reduced maximal RE due to functional adaptation (stage 2). We present results of an indirect test of this hypothesis in a group of 68 healthy middle-aged men undergoing a modified Stroop Test: in men suffering from high chronic work stress in terms of effort-reward imbalance significantly reduced RE in heart rate, adrenaline and cortisol was found after adjusting for relevant confounders. In conclusion, results underscore the potential of linking sociological with physiological data in stress research.