Heart rate and plasma catecholamines during 24 h of everyday life in trained and untrained men.

Physical training decreases resting heart rate as well as heart rate and catecholamine responses to ordinary physical activity and mental stress. These effects have been speculated to diminish cardiac morbidity. However, the sparing of heartbeats and catecholamine production might be outweighed by exaggerated responses during training sessions. To elucidate this issue, heart rate was measured continuously and plasma catecholamine concentrations were measured frequently during 24 h of ordinary living conditions in seven endurance-trained athletes (T) and eight sedentary or untrained (UT) young males. T subjects had lower heart rates than UT subjects during sleep and during nontraining awake periods. However, because of the increase during training, the total 24-h heartbeat number did not differ between groups (107,737 +/- 3,819 for T vs. 113,249 +/- 6,879 for UT, P = 0.731). Neither during sleep nor during awake nontraining periods were catecholamine levels lower in T than in UT subjects. Peak catecholamine levels during exercise in T were much higher than peak levels in UT subjects, and 24-h average epinephrine and norepinephrine concentrations were twice as high. We concluded that in highly trained athletes the total number of heartbeats per day is not decreased and the catecholamine production is, in fact, increased.     

Special feature for the Olympics: effects of exercise on the immune system: overtraining effects on immunity and performance in athletes

Overtraining is a process of excessive exercise training in high-performance athletes that may lead to overtraining syndrome. Overtraining syndrome is a neuroendocrine disorder characterized by poor performance in competition, inability to maintain training loads, persistent fatigue, reduced catecholamine excretion, frequent illness, disturbed sleep and alterations in mood state. Although high-performance athletes are generally not clinically immune deficient, there is evidence that several immune parameters are suppressed during prolonged periods of intense exercise training. These include decreases in neutrophil function, serum and salivary immunoglobulin concentrations and natural killer cell number and possibly cytotoxic activity in peripheral blood. Moreover, the incidence of symptoms of upper respiratory tract infection increases during periods of endurance training. However, all of these changes appear to result from prolonged periods of intense exercise training, rather than from the effects of overtraining syndrome itself. At present, there is no single objective marker to identify overtraining syndrome. It is best identified by a combination of markers, such as decreases in urinary norepinephrine output, maximal heart rate and blood lactate levels, impaired sport performance and work output at 110% of individual anaerobic threshold, and daily self-analysis by the athlete (e.g. high fatigue and stress ratings). The mechanisms underlying overtraining syndrome have not been clearly identified, but are likely to involve autonomic dysfunction and possibly increased cytokine production resulting from the physical stress of intense daily training with inadequate recovery.     

Adrenergic response to intense muscular activity in sedentary subjects as a function of emotivity and training]

Seven male sedentary human subjects were studied during intense muscular work (80% of maximal oxygen uptake) performed either for 15 min or until exhaustion (mean duration: 47 +/- 2 min). Plasma catecholamines were estimated before and after the experiment by means of an original fluorimetric assay. Epinephrine or norepinephrine were individually isolated from plasma and assayed in single extracts by a highly sensitive fluorimetric method. Epinephrine and norepinephrine levels as low as 15 ng per liter were detectable by this procedure in human plasma. The adrenergic pattern was found to be greatly different from one subject to another and related to emotivity: the effect of this factor was revealed by the predominance of epinephrine in plasma at rest or under exercise (ratio NA/A less than 1). In nonemotive subjects (ratio NA/A greater than 1 at rest) plasma epinephrine and norepinephrine increased progressively during exercise. Increments after exercise were higher for norepinephrine changes; however, the fact that epinephrine concentrations correlated significantly with norepinephrine suggests a simulataneous and coordinated stimulation of adrenal glands and orthosympathetic nervous system. In emotive subjects (ratio NA/A less than 1 at rest) the apprehension of muscular work promoted a difference in catecholamine responses: norepinephrine release was not affected by subject's anxiety, while epinephrine secretion, already elevated before the test, reached a high degree of magnitude in the first minutes of muscular work, remaining nearly constant until exhaustion. Physical training of nonemotive subjects, during 2 months with two intense exercises by a week, reduced strongly norepinephrine release after exhaustive muscular work. In the same conditions, the adrenal-medullary response was not significantly modified when compared with untrained subjects. Our results suggest that the adrenergic behaviour during exercise is a function of effort intensity to be supplied; catecholamines seem to be important factors in regulating body homeostasy during muscular work in man. In addition, emotive subjects exhibit amplified adrenal-medullary response, which may be related to psychological stimuli.     

The influence of superovulation preparations on the levels of catecholamines in eminentia mediana, the pituitary and pineal gland of the sheep.

The influence of hormonal superovulation preparations of FSH (450 IU) or PMSG (1500 IU), on the levels of catecholamines (dopamine, norepinephrine and epinephrine) was studied in the oestrus period using radioenzymatic methods. The administration of FSH caused a significant increase in the concentrations of norepinephrine (NE) and epinephrine (EPI) in eminentia mediana (EM) of sheep (p<0.001 and p<0.01, respectively). The pituitary gland exhibited an increase in the level of norepinephrine after administration PMSG while no marked changes were recorded for epinephrine and dopamine (DA). The administration of FSH affected the increase in pituitary epinephrine (p<0.01). The hormonal stimulation by FSH resulted in a marked decrease of dopamine (p<0.05) as well as in a significant increase of norepinephrine (p<0.05) and epinephrine (p<0.05) in the epiphysis. The comparison of the effect of hormonal preparations on the changes in catecholamine levels showed that the effect of FSH was observed mostly in eminentia mediana and the pituitary gland while that of PMSG was recorded in the epiphysis.     

Effects of clentiazem (TA-3090) and nifedipine on basal circulating catecholamine levels and on stimulation-evoked adrenal catecholamine secretion in anesthetized dogs.

The effects of TA-3090 (clentiazem) and nifedipine on basal sympathoadrenal activity and on the adrenal medullary response during splanchnic nerve stimulation were studied in dogs anesthetized with sodium pentobarbital. Plasma concentrations of epinephrine and norepinephrine were measured in aortic and adrenal venous blood before and after acute administration of the drugs, as well as during left splanchnic nerve stimulation before and after administration of drugs. Following intravenous injections, TA-3090 (30, 100, and 300 micrograms/kg) did not affect basal circulating catecholamine levels, whereas nifedipine (10, 30, and 100 micrograms/kg) markedly increased aortic epinephrine and norepinephrine concentrations in a dose-dependent manner in correlation with progressive decreases in mean arterial pressure. The changes in aortic epinephrine and norepinephrine concentrations were inversely related to those in mean arterial pressure (r = 0.603, p < 0.01; r = 0.536, p < 0.01; respectively). In response to direct splanchnic nerve stimulation (2 Hz, 2 ms, 1 min, 12 V), adrenal venous epinephrine and norepinephrine concentrations significantly increased, with a high degree of reproducibility. The catecholamine responses to splanchnic nerve stimulation were not affected by either TA-3090 or nifedipine at any dose tested. The present results suggest that the increases in circulating catecholamine levels following nifedipine administration are due to baroreflex activation secondary to the drug-induced hypotension. The study indicates that both TA-3090 and nifedipine did not significantly affect L-type Ca2+ channels related to catecholamine release in the adrenal medulla under the present experimental conditions.     

Maternal plasma catecholamines in the rhesus macaque during late gestation: effect of photoperiod and timed melatonin infusion.

This study tested the hypothesis that changes in photoperiod alter plasma catecholamine concentrations in the rhesus monkey during late gestation. Twelve chronically catheterized pregnant rhesus macaques were acclimated to a 12-h photoperiod (lights-on, 0700-1900 h). Under the control L:D cycle, blood samples were collected at 3-h intervals over 24 h for catecholamine analysis. Plasma concentrations (mean +/- SEM, pg/ml) ranged from 678 +/- 90 to 928 +/- 142 for norepinephrine; 230 +/- 22 to 631 +/- 141 for epinephrine; and 282 +/- 70 to 1090 +/- 362 for dopamine. A diurnal rhythm was observed in epinephrine with peak concentrations during lights-on (0900-1800 h; p less than 0.05, compared to lights-off). After the first sampling protocol, the animals were divided equally between two groups: phase shift, in which lights-on was shifted 11 h (2000-0800 h) and constant light, with lights on continuously. After the phase shift, a parallel shift in the plasma epinephrine rhythm was noted, with peak levels observed between 2200 and 0700 h (p less than 0.05). Constant light abolished the rhythm in epinephrine, with an overall reduction in mean basal levels of all three catecholamines. Daily melatonin infusions (0.2 micrograms/kg/h, 1900-0630 h) under constant light failed to restore the epinephrine rhythm or to return basal catecholamine concentrations to control photoperiod levels. These data suggest that photoperiod entrains the rhythm in epinephrine secretion, but the rhythm is ablated under constant conditions. Further, melatonin does not appear to play a role in the regulation of catecholamine secretion in the pregnant rhesus macaque.     

Genomic analysis reveals association of specific SNPs with athletic performance and susceptibility to injuries in professional soccer players

The development of specific and individualized training programs is a possible way to improve athletic performance and minimize injuries in professional athletes. The information regarding the sport's physical demands and the athletes’ physical profile have been, so far, considered as exhaustive for the design of effective training programs. However, it is currently emerging that the genetic profile has to be also taken into consideration. By merging medical and genetic data, it is thus possible to identify the athlete's specific attitude to respond to training, diet, and physical stress. In this context, we performed a study in which 30 professional soccer players, subjected to standard sport medical evaluation and practices, were also screened for genetic polymorphism in five key genes (ACTN3, COL5A1, MCT1, VEGF, and HFE). This genetic analysis represents the central point of a multidisciplinary method that can be adopted by elite soccer teams to obtain an improvement in athletic performance and a concomitant reduction of injuries by tailoring training and nutritional programs. The genetic fingerprinting of single athletes led to the identification of two performance-enhancing polymorphisms (ACTN3 18705C>T, VEGF-634C>G) significantly enriched. Moreover, we derived a genetic model based on the gene set analyzed, which was tentatively used to reduce athletes’ predisposition to injuries, by dictating a personalized nutrition and training program. The potential usefulness of this approach is concordant with data showing that this team has been classified as the healthiest and least injured team in Europe while covering the highest distance/match with the highest number of high-intensity actions/match.     

Influence of age on orthostatic changes in plasma renin activity and urinary catecholamines in man.

The authors studied plasma renin activity (PRA), urinary epinephrine, norepinephrine and dopamine excretion and their mutual relationships in 54 healthy subjects under basal (recumbent) conditions and age-related orthostatic changes in these parameters. The test subjects were divided into six 10-years groups, according to their year of birth (1901-1910 to 1951-1960). In the oldest groups (1901-1910 and 1911-1920), both basal PRA values and norephrine and epinephrine excretion and their postural increase were smaller than in younger subjects. Conversely, urinary dopamine excretion and the dopamine/norepinephrine and epinephrine ratio rose with advancing age. There were no significant differences between the plasma sodium and potassium concentrations in the various groups. Urinary aldosterone excretion was slightly higher in the oldest group than in the others, but was still within the control value limits. The intravenous administration of Inderal reduced both resting PRA values and the orthostatic increase in the youngest age groups, so that their PRA approached the values in older subjects. Higher norepinephrine and epinephrine excretion and the lower dopamine/norepinephrine and epinephrine in young subjects may play a role in their higher PRA, especially in the orthostatic reaction. Diminution of sympathetic activity, with lower norepinephrine and epinephrine excretion and relatively high dopamine excretion, may have a direct bearing on the lower PRA values in older subjects. The diminished capacity of older subjects for catecholamine mobilization and raised renin secretion during an orthostatis stress may be related to the higher incidence of orthostatic forms of hypotension in old age.     

III. Determination of plasma catecholamines and free 3, 4-dihydroxyphenylacetic acid in continuously collected human plasma by high performance liquid chromatography with electrochemical detection

We have presented a sensitive and relatively simple and inexpensive method for continuous sampling and determination of plasma catecholamines and a major dopamine metabolite, DOPAC. This method provides the basis for determination of the short-term magnitude of catecholamine response as well as the time course of such a response following several physical or psychological interventions. Resting levels of plasma catecholamines--norepinephrine 292 pg/ml, epinephrine 81 pg/ml and dopamine 29 pg/ml--are comparable to those obtained by other methods. Dopamine and free DOPAC were unaffected by physical or psychological interventions while norepinephrine was considerably increased by isometric handgrip, knee bends, and cold pressor and epinephrine increased during knee bends, mental arithmetic, cold pressor, and blood pressure measurement.     

Unexpected changes in urinary catecholamines and vanillylmandelic acid following rape assault

Although psychological changes are recognized to occur in rape assault survivors there is no information on the biochemical changes in these victims. This study compares urinary catecholamines and metabolites in 17 rape victims to two female control groups (one of which engaged in normal sexual intercourse and the other did not). We found, in the rape victims, unexpected changes in the excretion pattern of catecholamines and metabolites as compared to the various control groups. The most significant difference was the dramatic increase in urinary conjugated dopamine (P less than 0.01) in the rape victims which remained elevated for over 24 hr. Urinary vanillylmandelic acid (VMA) rose significantly in rape assault victims when compared to the normal control group. The VMA levels in rape victims were significantly lower, however, than in the women who had undergone (normal) sexual intercourse (P less than 0.01). Urinary free epinephrine showed a marked decline and remained depressed for over 24 hr in the rape assault victims (P less than 0.01) compared to normal controls. Some possible reasons for these patterns in catecholamines and metabolite excretion are suggested. These changes may be of importance in the poststress syndrome that occurs following the rape assault. In summary, a different profile of catecholamine and metabolite excretion patterns was found in rape compared to normal sexual intercourse. The enhanced dopamine excretion is contrary to the expected change of enhanced epinephrine secretion in severe stress.     

Age-related augmentation of plasma catecholamines during dynamic exercise in healthy males

Although plasma norepinephrine (NE) increases with age in response to a variety of submaximal adrenergic stimuli, the effect of age on plasma catecholamine levels during maximal aerobic effort and during submaximal work at a fixed percent of peak O2 consumption (VO2) is unknown. We therefore measured NE, epinephrine (E), and VO2 at rest and during graded maximal treadmill exercise in 24 healthy male volunteers (ages 22-77 yr) from the Baltimore Longitudinal Study of Aging who were rigorously screened to exclude the presence of cardiovascular disease. At rest neither heart rate (HR) nor VO2 were age related. Resting NE (pg/ml) was not age related, but resting E (pg/ml) was higher in male subjects 68-77 yr old (group III) than in those aged 22-37 (group I) or 44-55 yr (group II), P less than 0.01. Maximal HR (beats/min) showed a strong inverse relationship to age (203.5 - 0.65 age, r = -0.80, P less than 0.001). Peak VO2 in milliliters per kilogram total body weight per minute decreased with age (47.7 - 0.23 age, r = -0.71, P less than 0.001). At maximal effort both NE (P less than 0.01) and E (P less than 0.05) were higher in group III than in either of the younger groups. At submaximal work levels NE and E also increased with age, and when normalized for relative effort at loads between 45 and 80% of peak VO2 both NE and E were higher in the group III male subjects, although statistical significance was reached for NE (P less than 0.01) but not for E (P = 0.09).(ABSTRACT TRUNCATED AT 250 WORDS)     

Adrenergic responses to cognitive activity in a cold environment

Adrenergic responses during physical stress such as cold exposure have been reported to differ from those responses observed during cognitive activity. Both the separate and the combined effects of cold and cognitive activity on catecholamine activity were examined in six male subjects. Alterations in plasma epinephrine and norepinephrine showed different patterns as a function of exposure to a 4 degrees C cold environment, a cognitive performance assessment battery (PAB), and the two conditions combined. Plasma epinephrine was not altered by exposure to cold and only slightly increased by PAB performance when given at 23 degrees C. However, epinephrine was substantially elevated by exposure to combined cold and PAB. Heart rate changes paralleled observed changes in epinephrine. Norepinephrine release was predominantly increased by cold exposure and was not altered by PAB performance.     

Effect of metabolic control on urinary excretion and plasma levels of catecholamines in diabetics.

Urinary excretion and plasma levels of catecholamines were determined in 20 normal and 39 diabetic subjects to evaluate the sympathetic activity. Diabetic patients were divided into 4 groups according to the metabolic control. Sympathetic activity showed no differences between normal and subjects with chemical diabetes (group I, n = 5). In insulin-treated diabetics in good metabolic control (group II, n = 11) only urinary excretion of free norepinephrine was significantly higher than normals (p less than .05). In insulin-treated diabetics in poor metabolic control (group III, n = 16) urinary excretion and plasma levels of norepinephrine showed a marked increase over groups I and II (p less than .001). In insulin-treated diabetics with ketosis (group IV, n = 7) urinary excretion and plasma levels of both norepinephrine and epinephrine showed the highest values (p less than .001 and less than .1). Finally, in groups III and IV, after achieving improved metabolic control, a significant decrease of urinary excretion and plasma levels of catecholamines was observed. The results confirm that there is an increased rate of catecholamine release in poorly controlled diabeties and suggest a close correlation between sympathetic activity and metabolic derangement in diabetes.     

Effect of chronic cadmium treatment on rat adrenal catecholamines.

Daily intraperitoneal injection of cadmium chloride (1 mg/kg) for 45 days significantly increased adrenal weights and augmented the levels of adrenal norepinephrine and epinephrine as well as the activity of adrenal tyrosine hydroxylase. Discontinuation of the heavy metal treatment for 28 days, in rats previously injected with cadmium for 45 days, restored the activity of tyrosine hydroxylase as well as the amount of norepinephrine and epinephrine. In contrast, adrenal weights were restored only partially following the withdrawal of cadmium treatment. Evidence indicates that the changes in adrenal catecholamine metabolism may be the result of stress induced by chronic exposure to this heavy metal. In addition, some of the untoward effects such as hyperglycemia and arterial hypertension seen during cadmium toxicity might be related to increased synthesis of epinephrine in adrenal glands.     

Quantitative correlation between cardiovascular and plasma epinephrine response to mental stress

To investigate the quantitative correlations between cardiovascular and endogenous catecholamine response to mental stress, we gave a mental arithmetic test to 20 young healthy men. A direct and non-invasive haemodynamic measurement was performed by serial M-mode echocardiography. Heart rate, blood pressure, cardiac output, stroke volume, ejection fraction, left ventricular end-systolic pressure-volume ratio and plasma epinephrine increased over the baseline period during the test. The peripheral resistance and left ventricular end-systolic volume decreased, whereas left ventricular end-diastolic volume and plasma norepinephrine were unaltered. Furthermore, the degree of change in each haemodynamic parameter showing significant reaction, was well correlated with that of the increase in plasma epinephrine. The data suggest that acute mental stress induces endogenous epinephrine secretion resulting in a beta-adrenergic activated state in the cardiovascular system, namely, positive chronotropism, positive inotropism and vasodilatation.     

Left ventricular catecholamines during acute myocardial infarction in the dog

To determine whether changes in left ventricular catecholamine content occur during the first 30 to 90 min of acute myocardial infarction, myocardial catecholamine (radioenzymatic assay) over the interval was studied in the dog. In nine pentobarbital-anesthetized opened-chest dogs without coronary ligation, myocardial catecholamine at 2.5 h after pentobarbital (i) consisted mainly of norepinephrine (87% total catecholamine), (ii) showed a base to apex gradient in norepinephrine (1.44 +/- 0.10 vs. 1.03 +/- 0.10 micrograms/g, p less than 0.05) and dopamine (0.20 +/- 0.03 vs. 0.12 +/- 0.02 micrograms/g, p less than 0.05) but not epinephrine (0.017 vs. 0.016 micrograms/g), and (iii) showed no difference in norepinephrine, dopamine, or epinephrine across basal, mid, and apical left ventricular transverse planes spanning the vascular territories of the two coronary arteries. In 18 pentobarbital-anesthetized dogs with coronary ligation, (i) norepinephrine, measured in 14 regions across the mid left ventricle after 90 min ischemia in four dogs, was less in the ischemic center of the occluded bed than normal myocardium (1.01 +/- 0.04 vs. 1.29 +/- 0.04 micrograms/g, p less than 0.05), and (ii) norepinephrine was unchanged in normal myocardium of 14 dogs at 30, 60, 90 min, and 48 h but decreased in ischemic myocardium by 31% at 60 min (0.89 +/- 0.10 vs. 1.29 +/- 0.08 micrograms/g, p less than 0.025) and 79% at 48 h (0.27 +/- 0.04 vs. 1.26 +/- 0.08 micrograms/g, p less than 0.001). Thus, norepinephrine depletion from ischemic but not normal myocardium is detectable by 60 min during acute myocardial infarction.     

Plasma free and sulfoconjugated catecholamine responses to varying exercise intensity

Plasma free catecholamines rise during exercise, but sulfoconjugated catecholamines reportedly fall. This study examined the relationship between exercise intensity and circulating levels of sulfoconjugated norepinephrine, epinephrine, and dopamine. Seven exercise-trained men biked at approximately 30, 60, and 90% of their individual maximal oxygen consumption (VO2max) for 8 min. The 90% VO2max period resulted in significantly increased plasma free norepinephrine (rest, 219 +/- 85; exercise, 2,738 +/- 1,149 pg/ml; P less than or equal to 0.01) and epinephrine (rest, 49 +/- 49; exercise, 555 +/- 516 pg/ml; P less than or equal to 0.05). These changes were accompanied by consistent increases in sulfoconjugated norepinephrine at both the 60% (rest, 852 +/- 292; exercise, 1,431 +/- 639; P less than or equal to 0.05) and 90% (rest, 859 +/- 311; exercise, 2,223 +/- 1,015; P less than or equal to 0.05) VO2max periods. Plasma sulfoconjugated epinephrine and dopamine displayed erratic changes at the three exercise intensities. These findings suggest that sulfoconjugated norepinephrine rises during high-intensity exercise.     

Age dependence of the levels of plasma norepinephrine, aldosterone, renin activity and urinary vanillylmandelic acid in normal and essential hypertensives

In the present study the upper reference limits (URLs) for resting plasma norepinephrine, epinephrine, serum aldosterone, plasma renin activity, aldosterone/renin activity ratio, as well as urinary vanillylmandelic acid in healthy Egyptian normotensive subjects over a range of ages (5-60 yr) were established. There was a significant age effect on plasma norepinephrine, UVMA, serum aldosterone and PRA, whereas a single URL for plasma epinephrine level is satisfactory. In uncomplicated untreated essential hypertensive subjects (5-60 yr), the average prevalence of elevation in the plasma norepinephrine, epinephrine and urinary vanillylmandelic acid above their corresponding URLs was 85.10, 62.15 and 83.20%, respectively. This suggests that elevation in plasma catecholamine concentrations is more likely a common consequence than playing a possible role in the pathogenesis of hypertension, supported by insignificant correlation coefficients between the plasma catecholamine levels and resting systolic and diastolic blood pressure values (SBP & DBP) in all hypertensive age groups. Primary hyperaldosteronism was not detected among the normokalemic essential hypertensives at any age using aldosterone/plasma renin activity ratio as a primary screening method. In the present study, 7 statistically significant positive coefficient correlations are reported for SBP or DBP values with UVMA levels in hypertensive children and adolescents, serum aldosterone in old hypertensives, and PRA in adult hypertensives.     

A comparison of trihydroxyindole and HPLC/electrochemical methods for catecholamine measurement in adrenal chromaffin cells

Three commonly used methods for the determination of epinephrine and norepinephrine levels in adrenal medullary tissue were compared. Two variations of the trihydroxyindole procedure, which utilized oxidation at room temperature or 0°C, underestimated levels of total catecholamines in certain standard solutions and were unable to determine correctly their norepinephrine:epinephrine ratios. However, both the variability and the underestimation of the trihydroxyindole procedure carried out at room temperature were more pronounced than that of the trihydroxyindole assay at 0°C. In addition, we tested an isocratic HPLC method utilizing electrochemical detection which separates epinephrine from norepinephrine. The ability of this method to measure correctly total and individual catecholamine levels was superior to either trihydroxyindole procedure, as was its variability. When the three assay methods were used to measure total and individual catecholamine levels in cultured adrenal bovine chromaffin cells, both the trihydroxyindole (0°C) method and the HPLC method yielded values in agreement with those in the literature. However, the HPLC method produced data with lower error estimates. The trihydroxyindole (room temperature) assay was unable to reliably measure levels of epinephrine and norepinephrine in chromaffin cells.These comparisons of catecholamine assays demonstrated that there are circumstances under which the use of each is appropriate. In experiments where the epinephrine:norephinephrine ratio may be changing, the more accurate and precise HPLC assay may be essential, since the trihydroxyindole assays underestimate total catecholamines to varying degrees depending on this ratio. However, the HPLC method suffers from a requirement for technical sophistication for routine use. Therefore, in some laboratories and for repetitive measurement of many samples, the trihydroxyindole assay has a distinct advantage due to its easy utilization and ubiquitous materials. However, the superior results obtained with the trihydroxyindole (0°C) assay over the trihydroxyindole (room temperature) assay emphasizes the need to evaluate the trihydroxyindole procedure for the required purpose, especially if differential oxidation is used for estimation of individual catecholamine levels.     

Plasma epinephrine in chronically adrenodemedullated rats: lack of response to acute or chronic exercise.

Even if it is well established that epinephrine is a hormone originating from the adrenal medullae, the reappearance of circulating epinephrine has been reported in rats a few days after adrenodemedullation. To verify if the extra-adrenal tissue responsible for this epinephrine production can be stimulated, sham-operated or adrenodemedullated rats, either trained or kept sedentary, were submitted to an acute exercise stimulation test. Blood sampling was done before and after the test in precannulated rats for the determination of plasma epinephrine, norepinephrine, and corticosterone levels. Basal epinephrine levels were significantly reduced in trained and sedentary adrenodemedullated rats compared with their sham-operated counterparts. In response to exercise, there was no significant rise in epinephrine levels in both groups of adrenodemedullated rats. The norepinephrine levels in the basal state and in response to exercise were not altered by adrenodemedullation nor by physical conditioning. Basal corticosterone levels were similar between adrenodemedullated and sham-operated animals, either trained or kept sedentary. In response to exercise, corticosterone levels increased significantly in each group of rats but to a lesser extent in both groups of adrenodemedullated animals. These data indicate that the extra-adrenal epinephrine secretion that develops in the absence of adrenal medullae is not influenced by acute exercise nor by physical training.