Synthetic leukotriene C4(LTC4) and leukotriene D4(LTD4) were examined on isolated human tracheal and bronchial smooth muscle. Both LTC4 and LTD4 produced slowly developing contraction of trachealis and bronchus which were submaximal (70-85% of the carbachol maximum) and were not blocked by 1.0 microM atropine, 5.0 microM mepyramine, or 5.6 microM indomethacin. The EC50's for LTC4 and LTD4 were 10.3 and 1.8 nM on trachealis and 1.8 and 1.7 nM on bronchus, respectively. LTD4 was in excess of 20 000 times more potent than acetylcholine on some bronchial and tracheal tissues. Similar differences in potency were obtained in some tissues when LTC4 and LTD4 were compared with histamine. Tissues pretreated for 30 min with 2.0-4.0 microM FPL-55712 were less reactive to LTC4 and LTD4 than untreated control tissues. Established contractions to LTC4 and LTD4 persisted despite washing with fresh Krebs solution, were partially reversed by FPL-55712 (0.5-10 microM) and the Ca2+ channel blocker D-600 (5-10 microM), but were completely reversed by the catecholamine adrenaline (1.0 microM) and by high concentrations of FPL-55712 (greater than 20 microM). The marked potency of the leukotrienes on human tracheal and bronchial smooth muscle suggests an important role for these lipoxygenase products in respiratory disease.

This study was aimed at validating the usefulness of a length based pediatric emergency tape (Broselow) in an Indian population. The secondary objective was to validate age based weight estimation formulae (Nelson, Argalls, APLS) for emergency needs (doses, sizes). This cross sectional study was done at a tertiary teaching hospital on a sample of 500 children attending outpatient clinic. Inclusion criteria was age between 1 month to 12 years. Children who were unstable, uncooperative or critically ill requiring emergency care and those measuring more than 145 cm in length or weighing more than 35 kg weight were excluded from the study. Measurement of actual weights, calculation of weight, adrenaline dose, fluid bolus and endotracheal tube size was done by all four methods. Results indicated good positive correlation between actual measured weights and weights estimated using Broselow Tape (r = 0.974), APLS (r = 0.902), Argalls modification (r = 0.902), and combined Nelson formulae (0.935). However, specific Nelson formulas for 7-12 yr and 3-12 mo were especially poor in correlation. Bland-Altman Plots comparing actual weight showed least mean bias for Broselow Tape estimations in < 15 kg group (0.080 +/- 0.96 kg) and maximum bias with Nelsons formula for 7 to12 yr (5.204 +/- 4.272 kg). For adrenaline doses and fluid bolus calculations, Broselow estimations were valid estimates. Broselow tape did underestimate endotracheal tube size (mean bias -0.53 +/- 0.18). To conclude, length based pediatric emergency tape (Broselow) correlates well with overall emergency decision making process in our setting. This is especially validated in the age group 0.1 to 6.7 yr weighing less than 15 kg.

1. Intracellular recording of membrane potential was made from acinar cells of the isolated mouse parotid gland superfused with physiological salt solutions.2. The mean acinar resting membrane potential was - 68.5 mV during superfusion with Krebs-Henseleit solution. Shift of the superfusion solution to one containing ACh or adrenaline (10(-5)M) always caused a transient hyperpolarization (about 10-15 mV).3. The membrane potential was mainly dependent on the extracellular K concentration ([K](o)). Increasing [K](o) tenfold decreased the membrane potential by 50 mV. This depolarization was not mediated by ACh release from depolarized nerve endings, since it was seen in the presence of atropine (1.4 x 10(-6)M) and not caused by the accompanying reduction in [Na](o) to 40 mM caused only a small depolarization (less than 10 mV).4. When the superfusion solution was shifted, during intracellular recording, from a normal Krebs-Henseleit solution ([K] = 4.7 mM) to a K-free solution, a hyperpolarization of about 8 mV was measured. Reintroduction of the normal K-containing solution after a longer period of K deprivation (30-70 min) resulted in a short-lasting pronounced hyperpolarization (about 20 mV) which could be blocked by Strophanthin-G (10(-3)M).5. In contrast to previous reports, the present findings indicate that the membrane potential of salivary acinar cells is similar, with respect to magnitude and K-dependence, to that of cells of more thoroughly investigated tissues, such as muscle and nerve, and that the membrane Na-K pump is electrogenic, at least when the cells have been loaded with Na.

The clearance of plasma adrenaline and noradrenaline by human adipose tissue suggests the expression of the catecholamine-degrading enzyme monoamine oxidases and of catecholamine transport systems in adipocytes. In the present study, we identified and characterized the monoamine oxidases and an extraneuronal noradrenaline transporter expressed in human adipocytes. Enzyme assays using the monoamine oxidase A/B substrate [14C]tyramine showed that abdominal and mammary human adipocytes contain one of the highest monoamine oxidase activities in the body. Characterization of the enzyme isoforms by inhibition profiles of [14C]tyramine oxidation and Western and Northern blot analyses showed that mRNAs and proteins related to both monoamine oxidases A and B were expressed in adipocytes. Quantification of each enzyme isoform performed by enzyme assay and Western blot showed that monoamine oxidase A was predominant, representing 70-80% of the total enzyme activity. In uptake experiments, the monoamine oxidase substrate [3H]noradrenaline was transported into white adipocytes (Vmax 0.81+/-0.3 nmol/30 min/100 mg of lipid, Km 235+/-104 microM). The inhibition of [3H]noradrenaline uptake by specific inhibitors indicated that white human adipocytes contain an extraneuronal-type noradrenaline transporter. Competition studies of [14C]tyramine oxidation showed that noradrenaline is metabolized by monoamine oxidases in intact cells. In conclusion, the concomitant expression of monoamine oxidases and of a noradrenaline transporter in human white adipocytes supports the role of the adipose tissue in the clearance of peripheral catecholamines. These results suggest that adipocytes should be considered as a previously unknown potential target of drugs acting on monoamine oxidases and noradrenaline transporters.

1. (-)-Atenolol was used as a tool to assess the function of beta 1- and beta 2-adrenoceptors in human heart. Right atrial and left ventricular preparations from patients undergoing open heart surgery were set up to contract isometrically. Membrane particles were prepared for beta-adrenoceptor labelling with [3H]-(-)-bupranolol and adenylate cyclase assays. 2. The positive inotropic effects of (-)-noradrenaline were antagonized to a similar extent by (-)-atenolol in atrial and ventricular preparations. (-)-Atenolol consistently antagonized the effects of (-)-adrenaline to a lesser extent than those of (-)-noradrenaline in atrial preparations. In ventricular preparations (-)-atenolol antagonized the effects of low concentrations of (-)-adrenaline to a lesser extent than those of high concentrations. 3. pKB values (M) of (-)-atenolol, estimated with non-linear analysis from the blockade of the positive inotropic effects of the catecholamines, were 7.4 for beta 1-adrenoceptors and 6.0 for beta 2-adrenoceptors. 4. (-)-Atenolol inhibited the binding of [3H]-(-)-bupranolol to ventricular beta 1-adrenoceptors with a pKD (M) of 5.9 and to ventricular beta 2-adrenoceptors with a pKD of 4.6. 5. (-)-Atenolol inhibited the catecholamine-induced adenylate cyclase stimulation in the atrium and ventricle with pKB values of 5.8-6.4 for beta 1- and pKB values of 4.7-5.7 for beta 2-adrenoceptors. The binding and cyclase assays suggest a partial affinity loss for (-)-atenolol inherent to membrane preparations. 6. beta 1-Adrenoceptors mediate the maximum positive inotropic effects of (-)-noradrenaline in both the atrium and ventricle of man. beta 2-Adrenoceptors appear to be capable of mediating maximal positive inotropic effects of (-)-adrenaline in atrium. In contrast, ventricular beta 2-adrenoceptors mediated only submaximal effects of (-)-adrenaline.

Glomus cells, at least in the carotid body of cats, contain catechol and indolamines. Cells containing adrenaline, noradrenaline, and 5-hydroxytryptamine were identified.

1. The pharmacological characteristics of the alpha-adrenoceptor population in the rabbit isolated saphenous vein has been examined with (-)-noradrenaline (NA), as principal agonist, and a number of antagonists with selectivity for either alpha 1- or alpha 2-adrenoceptors. 2. The rank order of potency of various agonists is consistent with a population of alpha 2-adrenoceptors; UK-14304 greater than (-)-noradrenaline = (-)-adrenaline greater than B-HT 920 = cirazoline greater than phenylephrine greater than amidephrine, but the rank order of pA2 values for the antagonists against (-)-noradrenaline: BDF-6143 greater than rauwolscine = prazosin greater than CH-38083 = YM-12617 greater than Wy-26703 = phentolamine greater than corynanthine, is indicative of a mixed population of alpha 1- and alpha 2-adrenoceptors or, alternatively, a new subtype with characteristics of both the alpha 1- and alpha 2-subtypes. 3. Further evidence for two discrete populations of alpha-adrenoceptors is provided by, (a) the potent but non-competitive effect of prazosin against (-)-noradrenaline, (b) the presence of a component of the contractions elicited by NA and phenylephrine which is resistant to the selective alpha 2-adrenoceptor antagonists rauwolscine and CH-38083: these responses were inhibited by the selective alpha 1-adrenoceptor antagonists prazosin and YM-12617, but not by the selective alpha 2-adrenoceptor antagonist BDF-6143 and, (c) the relative potency of the yohimbine diastereoisomers rauwolscine and corynanthine against NA, phenylephrine and UK-14304. 4. In spite of the overwhelming evidence for a population of postjunctional alpha 2-adrenoceptors, prazosin was similarly effective against all agonists and failed to discriminate between those with putative selectivity for alpha 1- and alpha 2-adrenoceptors. This suggests an interaction of the effects of agonists at the two alpha-adrenoceptor subtypes. 5. An attempt has been made to reconcile a number of paradoxical observations with regard to the identification of postjunctional alpha 2-adrenoceptors in vitro, and it is suggested that in many of the isolated blood vessels presently available for examination both subtypes reside on the same smooth muscle cell. The pharmacological consequences of multiple subtypes of receptors mediating the same response is considered.

The action potential duration (APD) of isolated guinea pig papillary muscle is directly related to the medium glucose concentration regardless of the gas mixture with which it is in equilibrium. The APD can be maintained at control value for many hours by a glucose concentration of 50 mM in the complete absence of oxygen. Following reduction of the APD by incubation of the muscle in medium containing 5 mM glucose, adjustment of the glucose concentration to 50 mM will cause restoration of normal APD. Phlorizin has been shown to competitively interfere with the effect of glucose on the APD and insulin to prevent or reverse the effect of phlorizin. Nonmetabolizable sugars cannot produce glucose-like effects on the APD. Adrenaline, noradrenaline, and isopropylnoradrenaline increased the reduced APD of papillary muscles incubated in the absence of oxygen in a medium containing 5 mM glucose coincident with an increase in contractile force. The effect of isopropylnoradrenaline was blocked by acetylcholine and propranolol. In the presence of iodoacetate and 2-deoxyglucose, isopropylnoradrenaline increased contractile force but not the reduced APD. Aminophylline was found to produce changes in the reduced APD similar to those caused by the sympathomimetic amines. The findings clearly support the hypothesis that anaerobic metabolism utilizing either glycogen or exogenous glucose is capable of maintaining normal transmembrane electrical activity in guinea pig papillary muscle.

We investigated properties of catecholamine-sensitive adenylate cyclase in membranes from human right atria. Basal adenylate cyclase was activated by Mg2+-ions and guanyl nucleotides [Gpp(NH)p, GTP] in a concentration-dependent manner; guanyl nucleotide activation was strongly dependent on the presence of Mg2+-ions. Catecholamines stimulated adenylate cyclase activity in the following order of potency: (-)-isoprenaline greater than (-)-adrenaline = (-)-noradrenaline greater than phenylephrine, indicating that, in human right atrium, beta 1-adrenoceptors predominate. The beta 1-agonist dobutamine and the beta 2-agonists fenoterol and procaterol activated adenylate cyclase with an intrinsic activity of 0.5-0.7 (isoprenaline = 1.0). Adenylate cyclase activation by dobutamine or procaterol was not additive with the activation induced by isoprenaline. On the contrary, combination of dobutamine (100 microM) and procaterol (10 microM) resulted in activation of adenylate cyclase which was not different from that evoked by saturating concentration of isoprenaline (10 microM), indicating that dobutamine (beta 1) and procaterol (beta 2) produce adenylate cyclase activation through stimulation of different beta-adrenoceptor subtypes. The beta 2-selective antagonist ICI 118,551 was much more potent in inhibiting procaterol-than isoprenaline-stimulated adenylate cyclase activity, whereas the beta 1-selective antagonist betaxolol inhibited isoprenaline-stimulated activity more potently. We conclude that in human right atrium, both beta 1- and beta 2-adrenoceptors are functionally coupled to the adenylate cyclase system.

The binding of the alpha 2-adrenoceptor ligands [3H]yohimbine and [3H]idazoxan to rabbit kidney and forebrain membranes was compared. The maximum number of [3H]yohimbine binding sites was higher than the number of [3H]idazoxan binding sites in forebrain and lower in kidney. Large differences were observed in the ability of noradrenaline, adrenaline, idazoxan, rauwolscine, yohimbine and WY 26392 to displace [3H]yohimbine and [3H]idazoxan from their binding sites. These data suggest that [3H]idazoxan and [3H]yohimbine bind to different sites on rabbit tissue membranes.

(-)-Pindolol antagonized competitively and to a similar extent the positive inotropic effects of both (-)-noradrenaline and (-)-adrenaline in human ventricular preparations. An equilibrium dissociation constant KD (-log mol 1(-1) = pKD) of 9.2-9.3 was estimated regardless of disease present or agonist used. (-)-Pindolol antagonized competitively the positive inotropic effects of (-)-adrenaline more than those of (-)-noradrenaline in human atrial preparations. pKD values of (-)-pindolol were 9.6 against (-)-adrenaline and 9.1 against (-)-noradrenaline. The results are consistent with a moderate selectivity of (-)-pindolol for beta 2-compared to beta 1-adrenoceptors in human atrium. (-)-Pindolol competed with [3H]-(-)-bupranolol with a pKD of 9.4 for beta-adrenoceptors of human ventricle. Positive inotropic effects of (-)-pindolol were not detected on human atrium or ventricle in a concentration range of 1-1000 nmol 1(-1). The affinity of (-)-pindolol estimated for human myocardial beta-adrenoceptors, its moderate beta 2-selectivity and its lack of intrinsic activity for contractile force agreed with similar characteristics in other species. (-)-Pindolol caused marked positive chronotropic effects in kitten right atria with an intrinsic activity of 0.5 with respect to catecholamines. On kitten left atria it caused only weak positive inotropic effects with an intrinsic activity of 0.1. (-)-Pindolol (0.6-6000 nmol-1) did not cause positive inotropic effects in kitten papillary muscle. The concentration-effect curve for (-)-pindolol on kitten right and left atria was biphasic. Its positive chronotropic and inotropic effects were not blocked by methysergide, suggesting that 5-hydroxytryptamine (5-HT)-receptors were not involved. Low concentrations of antagonists selective for beta 1- and beta 2-adrenoceptors blocked the high sensitivity component but not the low sensitivity component of the positive chronotropic and inotropic effects. The biphasic nature of the positive chronotropic effects of (-)-pindolol in kitten agreed with previous observations made on guinea-pig right atria and support the concept that 3 receptors in the sinoatrial pacemaker contribute to these chronotropic effects: beta 1, beta 2 and a low-affinity receptor for (-)-pindolol which is neither beta 1 nor beta 2. The partial agonistic activity of (-)-pindolol in the heart appears to be mainly (kitten) or completely (man) restricted to the sinoatrial pacemaker.

Adrenaline-containing neurons in the C1 group of the ventrolateral rostral medullary reticular formation which project to the thoracic spinal cord were identified by a combined retrograde transport immunocytochemical technique. No other medullary catecholamine neurons, including the A1 and A2 noradrenaline cells, project to thoracic spinal cord. These data, taken with results of other studies of spinal catecholamine innervation, suggest a segmental segregation of projections to spinal cord by dopaminergic, noradrenergic, and adrenergic neurons.

We studied the distribution, within the rabbit medulla oblongata, of neuronal cell bodies containing either tyrosine hydroxylase or neuropeptide Y-like immunoreactivity. Both avidin-biotin and immunofluorescence procedures were used. Because the two primary antibodies were raised in different species it was possible to perform simultaneous colocalization studies with the immunofluorescence procedure. Tyrosine hydroxylase-containing neurons in the rostral medulla were demonstrated to contain a catecholamine by the colchicine-enhanced FAGLU (formaldehyde-glutaraldehyde) fluorescence histochemical procedure. These neurons are presumably adrenergic, corresponding to the C1 and C2 groups described in the rat. No C3 group was found in the rabbit. The distribution of tyrosine hydroxylase-containing neurons in the caudal medulla was in accordance with previous descriptions of the A1 and A2 groups based on the unenhanced FAGLU procedure. Neuropeptide Y-like immunoreactivity was observed in cell groups corresponding to those already described in the rat, but additional groups were discovered in the rabbit. Some neurons containing neuropeptide Y-like immunoreactivity were observed in nucleus raphe pallidus and these also contained serotonin (5-HT). In the nearby nucleus reticularis gigantocellularis there were occasional neurons that contained neuropeptide Y-like immunoreactivity without any colocalized 5-HT. Neuropeptide Y-like immunoreactivity was also observed in the dorsal motor nucleus of the vagus, rostral to the obex, and these neurons were demonstrated to be true vagal preganglionic cells by colocalization of neuropeptide Y-like immunoreactivity and Fast Blue retrogradely transported from the cervical vagus. We found that neuropeptide Y-like immunoreactivity was colocalized in approximately 75% of the tyrosine hydroxylase-containing neurons in the rostral medulla (C1 and C2 cells). A smaller proportion of the A1 cells also contained this peptide but it was absent from both the most caudal A1 cells and from the A2 cells. Some tyrosine hydroxylase-containing neurons occur in direct apposition to vagal preganglionic cells in both the dorsal motor nucleus of the vagus and the nucleus ambiguous. However, colocalization studies revealed that none of these neurons contained Fast Blue when this dye was retrogradely transported from the cervical vagus. Medullary catecholamine-synthesizing neurons apparently do not contribute axons to the vagus nerve. This finding is consistent with our own studies in the rat but is in contrast to studies in this species published by other workers.

We have studied the effect of a short period of exposure to the intense heat of a sauna bath on the electrocardiogram and plasma catecholamine, free fatty acid, and triglyceride concentrations in 17 subjects with apparently normal hearts and 18 persons with coronary heart disease. Similar observations were made on 11 of the 17 normal subjects and on 7 of the persons with coronary heart disease in response to exercise.Exposure to heat was associated with an increase in plasma adrenaline with no change in noradrenaline, free fatty acid, or triglyceride concentrations. Exercise was associated with the expected increase in both plasma noradrenaline and adrenaline concentrations. A heart rate up to 180 beats/min was observed in response to both heat and exercise. Apart from the ST-T changes inherent to sinus tachycardia, ST-T segment abnormalities were frequent in response to heat in both the subjects with normal and abnormal hearts, but little change occurred in the ST-T configuration when the subjects were exercised to produce comparable heart rates. Ectopic beats, sometimes numerous and multifocal, were observed in some subjects of both groups in response to heat, but not to exercise. It seems likely that the net unbalanced adrenaline component of the increased plasma catecholamine concentrations (which is also seen in certain emotional stress situations) is predominantly responsible for ischaemic-like manifestations of the electrocardiogram in susceptible subjects. The observations provide further validation for previously reported studies that it is the increased plasma noradrenaline in response to emotional stress that is associated with the release of free fatty acids and ultimate hypertriglyceridaemia, of probable importance in the aetiology of atheroma.

The role of the sympathetic nervous system and of arginine vasopressin (AVP) in the mediation of the central cardiovascular effects of angiotensin II (ANG II) and substance P (SP) was investigated. ANG II and SP caused dose-dependent blood pressure increases when injected into the lateral brain ventricle (i.c.v.) of conscious rats; ANG II was tenfold more potent than SP. Peripheral blockade of alpha-adrenoceptors with prazosin or blockade of the vasopressor action of AVP by the AVP antagonist d(CH2)5VDAVP both partially inhibited the pressor responses to central ANG II. Combined treatment with the two blockers produced almost complete inhibition of the central ANG I responses. Substance P injected i.c.v. produced increases in noradrenaline and adrenaline but not AVP in the plasma. Peripheral alpha-receptor blockade by prazosin reversed the central pressor effects of SP to depressor responses. The AVP antagonist did not alter the cardiovascular responses to SP. It is concluded that in conscious animals, stimulation of the sympathetic nervous system and release of AVP contribute to the central pressor action of ANG II to a similar extent and independently of each other. In contrast, the central pressor responses to SP appear to be exclusively mediated by the sympathetic nervous system without participation of AVP.

1. Cats, virgin and 17 days pregnant, and guinea-pigs, virgin and 14-60 days pregnant, or treated for 1-8 days with oestradiol+progesterone, were used. The response of the uterus to adrenaline and noradrenaline was observed and, in pieces from the same tissues, the resting and active membrane potentials were recorded and the ionic content was determined.2. Adrenaline and noradrenaline relaxed the virgin cat uterus, adrenaline being 20-100 times more potent in vivo and about 10 times or less in vitro.3. Adrenaline and noradrenaline caused contraction of the early pregnant cat uterus, the ratio of potency being about 1.4. Adrenaline and noradrenaline had a biphasic effect on the guinea-pig uterus in all conditions. The ratio of potency was about 1.5. The mean membrane potential was 48 mV in virgin cat uterus and 64 mV on the seventeenth day of pregnancy.6. In guinea-pigs the average membrane potential increased from 38 mV in the virgin uterus to 58 mV on the thirtieth day of pregnancy. A similar increase was produced by eight daily injections of 5 mug oestradiol and, on the last 4 days, additional 1.5 mg progesterone.7. In the cat, no significant change in K and Na content was observed during pregnancy. The intracellular chloride content, however, rose from 51.5 m-moles/1. fibre water in the virgin uterus to 89 m-moles in the early pregnant uterus. As a result, the calculated chloride equilibrium potential changed from - 25 mV in virgin uterus to - 11 mV in pregnant uterus.8. In the guinea-pig no significant change in ion content was observed and the calculated potassium and chloride equilibrium potentials remained both unaltered during pregnancy.9. In contrast to guinea-pig uterus in all conditions, and to virgin cat uterus, early pregnant cat uterus was not spontaneously active and excess calcium caused no hyperpolarization.10. The reversal of the uterine response to adrenaline as a result of pregnancy is discussed in relation to the increase of the intracellular chloride content which was only observed in the cat.

Leaves and fruits of Phyllanthus emblica L. have been used for the anti-inflammatory and antipyretic treatment of rural populations in its growing areas in subtropical and tropical parts of China, India, Indonesia, and the Malay Peninsula. In the present study, leaves of Ph. emblica were extracted with ten different solvents (n-hexane, diethyl ether, methanol, tetrahydrofuran, acetic acid, dichloromethane, 1,4-dioxane, toluene, chloroform, and water). The inhibitory activity of the extracts against human polymorphonuclear leukocyte (PMN) and platelet functions was studied. Methanol, tetrahydrofuran, and 1,4-dioxane extracts (50 micrograms/ml) inhibited leukotriene B4-induced migration of human PMNs by 90% and N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP)-induced degranulation by 25-35%. The inhibitory activity on receptor-mediated migration and degranulation of human PMNs was associated with a high proportion of polar compounds in the extracts as assessed by normal phase thin layer chromatography. Diethyl ether extract (50 micrograms/ml) inhibited calcium ionophore A23187-induced leukotriene B4 release from human PMNs by 40%, thromboxane B2 production in platelets during blood clotting by 40% and adrenaline-induced platelet aggregation by 36%. Ellagic acid, gallic acid and rutin, all compounds isolated earlier from Ph. emblica, could not explain these inhibitory activities on PMNs or platelets by Ph. emblica extracts. These results show that the leaves of Ph. emblica have inhibitory activity on PMNs and platelets, which confirm the anti-inflammatory and antipyretic properties of this plant as suggested by its use in traditional medicine. The data suggest that the plant leaves contain as yet unidentified polar compound(s) with potent inhibitory activity on PMNs and chemically different apolar molecule(s) which inhibit both prostanoid and leukotriene synthesis.

Gender differences in the changes substrates of carbohydrate and lipid metabolism as well as in adrenaline, noradrenaline, growth hormone, insulin and cortisol were investigated in 24 women and 24 men during exhaustive endurance exercise. Training history and current performance capacity were taken into consideration in the design of the study. Since previous papers present conflicting results the purpose of the present study was to obtain further information regarding possible gender differences in lipid metabolism and its regulation by hormones. Non-endurance-trained women and men each ran 10 km on a treadmill at an intensity of 75% of VO2max; endurance-trained women and men ran 14 and 17 km, respectively, at an intensity of 80% of VO2max. Blood glucose levels in non-endurance-trained women were higher when compared to non-endurance-trained men. This might be explained by increased mobilization of free fatty acids from intramuscular fat depots during energy production in non-specifically trained women. In contrast, no substantial gender differences in endurance-trained persons were seen in lipid metabolism. The changes in substrates of lipid metabolism confirm the higher lipolytic activity and greater utilization of free fatty acids in endurance-trained persons. During endurance exercise, changes in adrenaline, noradrenaline, growth hormone, insulin and cortisol were not substantially affected by the sex of the subjects. This study does not present any conclusive results that endurance-trained persons show gender differences in lipid metabolism and major regulatory hormones.