Vasoactive neuroendocrine responses associated with tolerance to lower body negative pressure in humans

The purpose of this investigation was to test the hypothesis that peripheral vasoconstriction and orthostatic tolerance are associated with increased circulating plasma concentrations of noradrenaline, vasopressin and renin–angiotensin. Sixteen men were categorized as having high (HT, n=9) or low (LT, n=7) tolerance to lower body negative pressure (LBNP) based on whether the endpoint of their pre‐syncopal‐limited LBNP (peak LBNP) exposure exceeded ?60 mmHg. The two groups were matched for age, height, weight, leg volume, blood volume and maximal oxygen uptake, as well as baseline blood volume and plasma concentrations of vasoactive hormones. Peak LBNP induced similar reductions in mean arterial pressure in both groups. The reduction in legarterial pulse volume (measured by impedance rheography), an index of peripheral vascular constriction, from baseline to peak LBNP was greater (P<0·05) in the HT group (?0·041 ± 0·005 ml 100 ml^?1) compared to the reduction in the LT group (?0·025 ± 0·003 ml 100 ml^?1). Greater peak LBNP in the HT group was associated with higher (P<0·05) average elevations in plasma concentrations of vasopressin (pVP, Δ=+7·2 ± 2·0 pg ml^?1) and plasma renin–angiotensin (PRA, Δ=+2·9 ± 1·3 ng Ang II ml^?1 h^?1) compared to average elevations of pVP (+2·2 ± 1·0 pg ml^?1) and PRA (+0·1 ± 0·1 ng Ang II ml^?1 h^?1) in the LT group. Plasma noradrenaline concentrations were increased (P<0·05) from baseline to peak LBNP in both HT and LT groups, with no statistically distinguishable difference between groups. These data suggest that the renin–angiotensin and vasopressin systems may contribute to sustaining arterial pressure and orthostatic tolerance by their vasoconstrictive actions.     

Differing responses of cortisol to oCRF during endonasal and oral treatment with DDAVP

Abstract. Arginine vasopressin (AVP) exerts a potentiating effect on the responses of cortisol and ACTH to ovine CRF (oCRF). A stimulation test using AVP plus oCRF to assess ACTH reserve has been proposed. In central diabetes insipidus, long-term substitution therapy is commonly undertaken with desmopressin (DDAVP), an analogue of the natural hormone which has a greater antidiuretic action but whose effects on the ACTH-cortisol axis are still controversial. The aim of our study was to evaluate the variations in the responses of ACTH and cortisol to oCRF in various phases of the treatment of central diabetes insipidus: no treatment, endonasal treatment with DDAVP solution and oral treatment with DDAVP in tablet form. Seven patients suffering from central diabetes insipidus underwent testing with oCRF during the various phases of treatment. In the absence of DDAVP treatment, normal responses were registered for cortisol (basal 164·1 ± 29·4 ng ml^?1, peak 396·1 ± 37·9 ng ml^?1; P < 0·05) and ACTH (basal 20·4 ± 3·9 pg ml^?1, peak 86·3 ± 20·9 pg ml^?1; P < 0·05) in all patients. During oral treatment with DDAVP, no variation in cortisol response to oCRF was seen. By contrast, when DDAVP was administered endonasally, a significant reduction in cortisol responsiveness to oCRF (secretory area: 2429 ± 548 ng ml^?1 120 min) was noted in comparison with that found during the other two tests (no treatment: 3070 ± 704 ng ml^?1 120 min; oral DDAVP: 3419 ± 650 ng ml^?1 120 min; P < 0·05) performed. There is no clear explanation for this phenomenon, but an interesting hypothesis is that DDAVP acts as a weak agonist which exerts only a slight stimulatory effect on the corticotropic hypophyseal cells but which is able to compete with the natural hormone for receptor binding.     

Acute hormonal responses following different velocities of eccentric exercise

The aim of this study was to compare the acute hormonal responses following two different eccentric exercise velocities. Seventeen healthy, untrained, young women were randomly placed into two groups to perform five sets of six maximal isokinetic eccentric actions at slow (30° s^?1) and fast (210° s^?1) velocities with 60‐s rest between sets. Growth hormone, cortisol, free and total testosterone were assessed by blood samples collected at baseline, immediately postexercise, 5, 15 and 30 min following eccentric exercise. Changes in hormonal responses over time were compared between groups, using a mixed model followed by a Tukey's post hoc test. The main findings of the present study were that the slow group showed higher growth hormone values immediately (5·08 ± 2·85 ng ml^?1, P = 0·011), 5 (5·54 ± 3·01 ng ml^?1, P = 0·004) and 15 min (4·30 ± 2·87 ng ml^?1, P = 0·021) posteccentric exercise compared with the fast group (1·39 ± 2·41 ng ml^?1, 1·34 ± 1·97 ng ml^?1 and 1·24 ± 1·87 ng ml^?1, respectively), and other hormonal responses were not different between groups (P>0·05). In conclusion, slow eccentric exercise velocity enhances more the growth hormone(GH) response than fast eccentric exercise velocity without cortisol and testosterone increases.     

Angiotensin II attenuates reflex decrease in heart rate and sympathetic activity in man

Summary. Circulatory variables and hormone concentrations in arterial plasma were measured in six normal subjects during angiotensin II (ANG II) step-up infusion of 0·25 and 1·00 ng kg^-1× min. During the 1·00 ng kg^-1× min infusion ANG II plasma concentrations increased from 11 ± 2 to 48 ± 6 pg ml^-1; i.e., similar to those obtained during acute hypotensive hypovolemia in man. Mean arterial pressure increased (P<0·05) from a resting value of 89±3 to 97±5 mmHg. Heart rate and catecholamine concentrations did not change. Plasma aldosterone increased (P<0·05) from 36 ± 4 to 77 ± 10 pg ml^-1 during the infusion. Plasma concentrations of vasopressin, adrenalin and pancreatic polypeptide did not change during the investigation. During the 0·25 and 1·00 ng kg^-1× min infusion subcutaneous blood flow decreased (P= 0·06) to 67 ±20 and 66 ±26%, respectively, of control. It is concluded that: (1) ANG II in physiological doses in man may augment the sympathetic activity on the circulatory system since compensatory decreases in heart rate or in plasma catecholamines were not observed during the increased arterial pressure; (2) ANG II does not induce a general decrease in vagal tone as plasma pancreatic polypeptide concentrations were unchanged; (3) the obtained plasma concentrations of ANG II do not stimulate the release of vasopressin to plasma; and (4) the threshold for reducing the subcutaneous blood flow is reached within relatively small increments in plasma ANG II.     

Association between biosynthesis of nitric oxide and changes in immunological and vascular parameters in patients treated with interleukin-2

Abstract Hypotension is a dose-limiting side effect of interleukin-2 (IL-2) therapy. This may be due to increased biosynthesis of the potent vasodilator nitric oxide (NO) induced by cytokines such as tumour necrosis factor-α (TNF-α) and interferon-γ (IFN-γ), which are known to be generated during IL-2 therapy. We describe the relationship between NO biosynthesis and changes in immunological and vascular parameters during IL-2 therapy in 13 patients with metastatic cancer. Plasma concentrations of neopterin and nitrite plus nitrate (NO_x) were higher in cancer patients prior to treatment compared with normal subjects (neopterin; 10·8±1·4 vs. 2·0±0·4 ng ml^-1, P<0·001: NO_x; 45±6 vs. 28±2 μM, P<0·005). Pretreatment TNF-α and IFN-γ plasma concentrations were not significantly different in cancer patients from those in controls. During infusion of IL-2 (18 times 10⁶ international units m^-2 per day for 5 days) these parameters increased, reaching maximal concentrations at day 3 for IFN-γ and day 5 for TNF-α, neopterin and NO_x. The maximal induced NO_x correlated with maximal TNF-α (r = 0·60, P<0·04), IFN-γ (r = 0·63, P<0·02) and neopterin (r = 0·66, P<0·01). As plasma NO_x concentrations increased, systolic blood pressure fell, reaching a minimum at day 3 despite a continued rise in NO_x concentrations. These changes were accompanied by a continuous increase in pulse rate throughout the infusion period. These findings indicate that induction of NO biosynthesis contributes to hypotension induced during IL-2 therapy. Inhibitors of NO synthase may be useful in limiting toxicity, thus allowing administration of higher and possibly more efficacious doses of this cytokine in the treatment of cancer.     

Determinants of post-ischaemic reactive hyperaemia in patients with diabetes mellitus type II

Dysfunction of resistance arteries is thought to be an early reversible stage in the development of atherosclerosis. Dynamics of post-ischaemic reactive hyperaemia are believed to constitute a useful tool for monitoring resistance vessel function. Patient characteristics influencing reactive hyperaemia, however, need to be defined more precisely. Since reactive hyperaemia is a dynamic process, yielding submaximal peak values after 5 min of ischaemia, this period was chosen to investigate the determinants of reactive hyperaemia in 100 type II diabetic patients as well as in 61 control subjects. Reactive hyperaemia was measured by venous-occlusion plethysmography; clinical and laboratory data were acquired by routine methods. Statistical comparison was performed with SYSTAT 5·0 for Apple Macintosh. Overall, no significant differences between diabetic patients and controls were observed by group comparison. In control subjects, only gender showed an influence on peak reactive hyperaemia (females 40·5 ± 15·3; males 51·8 ± 17·7 ml min^–1 100 ml^–1, P<0·01). In diabetic patients, in addition to gender, actual blood glucose (r=0·377, P<0·05) and meal intake (non-fasting 42·8 ± 19·2; fasting 51·2 ± 19·5 ml min^–1 100 ml^–1, P<0·05) were found to influence reactive hyperaemia. Further investigation revealed a loss of the correlation between peak reactive hyperaemia and actual blood glucose observed in the fasting state (P<0·001) in non-fasting diabetic patients, indicating an influence of meal intake on resistance vessel reactivity. Our results suggest that, in diabetic subjects, in addition to gender actual blood glucose and the postprandial situation impacts on peak reactive hyperaemia.     

The impact of short duration,high intensity exercise on cardiac troponin release

The aim of this study was to assess the appearance of cardiac troponins (cTnI and/or cTnT) after a short bout (30 s) of ‘all‐out’ intense exercise and to determine the stability of any exercise‐related cTnI release in response to repeated bouts of high intensity exercise separated by 7 days recovery. Eighteen apparently healthy, physically active, male university students completed two all‐out 30 s cycle sprint, separated by 7 days. cTnI, blood lactate and catecholamine concentrations were measured before, immediately after and 24 h after each bout. Cycle performance, heart rate and blood pressure responses to exercise were also recorded. Cycle performance was modestly elevated in the second trial [6·5% increase in peak power output (PPO)]; there was no difference in the cardiovascular, lactate or catecholamine response to the two cycle trials. cTnI was not significantly elevated from baseline through recovery (Trial 1: 0·06 ± 0·04 ng ml^?1, 0·05 ± 0·04 ng ml^?1, 0·03 ± 0·02 ng ml^?1; Trial 2: 0·02 ± 0·04 ng ml^?1, 0·04 ± 0·03 ng ml^?1, 0·05 ± 0·06 ng ml^?1) in either trial. Very small within subject changes were not significantly correlated between the two trials (r = 0·06; P>0·05). Subsequently, short duration, high intensity exercise does not elicit a clinically relevant response in cTnI and any small alterations likely reflect the underlying biological variability of cTnI measurement within the participants.     

Effects of physical exercise on insulin absorption in insulin-dependent diabetics. A comparison between human and porcine insulin

Summary. Nine insulin-dependent diabetics with undetectable plasma C-peptide (<0·05 nmol 1^-1) and without insulin antibodies (insulin binding to IgG<0·05 Ul^-1) received subcutaneous injections of 10 U ¹²⁵I-labelled soluble human or porcine insulin in the thigh on 2 consecutive days. Disappearance rates of ¹²⁵I were monitored continuously by external counting and plasma insulin levels were determined during rest for 30 min, bicycle exercise of moderate intensity for 40 min, and 60 min recovery. Subcutaneous blood flow was measured concomitantly in the contralateral thigh by the ¹³³Xenon clearance technique. During the initial period of rest human insulin was absorbed approximately 40% faster than its porcine analogue (first order rate constants 0·37±0·06 vs 0·27±0·06% min^-1, P<0·05) and the increment of the area under the plasma insulin curve was greater after hum-ii than after porcine insulin (184±46 vs 112±42 mUl^-1 min, P<0·05). Exercise enhanced the absorption rates for both ¹²⁵I-insulins to 0·50±0·06 and 0·48±0·10% min^-1 for human and porcine insulin, respectively (P<0·05). This increase was less pronounced for human compared to porcine insulin (49±19 vs 105±40%, P=0·06). During exercise plasma insulin rose to 37±5 mUl^-1 after human and 30±5 mUl^-1 after porcine insulin and the areas under the plasma insulin curves were similar. During the recovery phase the absorption rates decreased slightly compared to the exercise value for both insulins. The blood glucose lowering effect was similar for the two insulins. Subcutaneous blood flow was not significantly altered by exercise in either group. It is concluded that during rest human soluble insulin is more rapidly absorbed than porcine insulin. Physical exercise tends to increase porcine insulin absorption more and eliminates the basal difference in the absorption kinetics between human and porcine insulin. The increased insulin absorption during exercise is not coupled to corresponding changes in the subcutaneous blood flow.     

Increased serum angiotensin converting enzyme activity in type T insulin—dependent diabetes mellitus: its relation to metabolic control and diabetic complications

Abstract. Serum angiotensin-converting enzyme (ACE) was measured in 150 insulin-dependent diabetes mellitus (IDDM) patients and 72 healthy subjects by radioassay, using [³H]-hippuryl-glycyl-glycine as a substrate. Mean (SD) serum ACE activity in diabetic patients was 120 ± 33 nmol ml^?1 min^?1 (range 46–215) and was significantly increased by 56% compared to control values (77 ± 23 nmol ml^?1 min^?1, range 46–125, P < 0·001). ACE activity > 125 nmol ml^?1 min^?1 was observed in 60 of 150 IDDM patients. 96 IDDM patients were normoalbuminuric (< 22 mg 24 h^?1) and 49 patients were micro- or macroalbuminuric (range 22–6010 mg 24 h^?1). Micro- and macroalbuminuric IDDM patients were found to have significantly greater ACE activity values than normoalbuminuric patients (128 ± 36 vs. 115 ± 30 nmol ml^?1 min^?1, P = 0·025). Metabolically well-controlled IDDM patients (glycosylated haemoglobin ≤ 8%) had lower ACE activity values than the patients with glycosylated haemoglobin greater than 8% (109 ± 20 vs. 127 ± 32 nmol ml^?1 min^?1, P < 0·02). A significant correlation between degree of metabolic control and ACE activity was found (r = 0.435, P < 0·001) so that an increase in one glycosylated quartile unit is accompanied by an increase in ACE activity of 10·5 nmol ml^?1 min^?1. Thus ACE activity in the serum of IDDM patients was increased by 56% in 40% of the patients. It was increased in IDDM patients without complications and in patients with retinopathy or nephropathy. In diabetic patients with nephropathy, ACE activity was greater than in diabetic patients without nephropathy. ACE activity was positively correlated with metabolic control. The role of increased ACE activity in the development of diabetic nephropathy remains to be established.     

Plasma and urinary leukotrienes in sickle cell disease: possible role in the inflammatory process

Abstract. Sickle cell (HbSS) disease is associated with rheological and inflammatory stresses within the microcirculation. In order to determine the role of leukotrienes in the inflammatory processes in HbSS patients, we analysed plasma and urine levels of leukotrienes (LT); LTB₄, LTC₄, LTD₄, and LTE₄ as indicators of their in vivo metabolism. Plasma and urine level samples of 15 HbSS patients in steady-state and age-matched healthy, homozygous (HbAA) controls were extracted for leukotrienes and quantitated by HPLC. Control plasma level of leukotrienes (mean ± SEM, ng ml^-1) were: LTB₄, 8·95 ± 0·26; LTC₄, 7·24 ± 0·21; LTD₄, 11·42 ± 0·40; and LTE₄, 14·51 ± 0·50. Corresponding values for HbSS patients were: LTB₄, 6·15 ± 0·42; LTC₄, 13·61 ± 1·45; LTD₄, 6·44 ± 0·51 and LTE₄, 4·97 ± 0·37. The differences were significant at P < 0·05. Urine levels (mean ± SEM, ng mmol^-1 creatinine), for controls were: LTB₄, 10·60 ± 0·35; LTC₄, 360·0 ± 9·82. Values for HbSS urine were: LTB₄, 27·50 ± 3·33; LTC₄, 356·0 ± 17·87; LTD₄, 69·90 ± 14·51. LTD₄ was not detected in control urine. These results suggest that sickle cell patients may exhibit impaired ability to catabolize LTC₄ in plasma during steady state conditions. This altered metabolism may contribute to the persistent stress of the microcirculation, and is probably related to the abnormal microvascular rheology of sickle blood cells.     

Postprandial impairment of resistance vessel function in insulin treated patients with diabetes mellitus type‐2

Reduced postischaemic reactive hyperaemia, is considered a marker of impaired resistance vessel function. Acute postprandial hyperlipidaemia has been shown to induce vascular dysfunction. In the present study, the impact of postprandial hyperglycaemia on resistance vessel reactivity was investigated in insulin treated type‐2 diabetic patients. The study was performed in 16 insulin treated type‐2 diabetics (eight male/eight female, age 47 ± 3 years, HbA1c 7·2 ± 0·2) and 16 controls. Reactive hyperaemia was measured in the forearm by venous occlusion plethysmography after 5 min of ischaemia in the fasting state and 90 min after a test meal. In diabetics, blood glucose increased from 8·7 ± 1·1 to 15·3 ± 1·0 mmol l^?1 (P<0·001) postprandially. This resulted in (i) a significant increase of resting blood flow (3·4 ± 0·3 to 4·8 ± 0·4 ml min^?1 100 ml^?1, P<0·01) and (ii) in a reduced peak reactive hyperaemia (52·3 ± 7·4 to 36·8 ± 4·3 ml min^?1 100 ml^?1, P<0·005). In controls, a similar effect of the meal on resting flow was observed but reactive hyperaemia was unaltered. In the absence of a test meal, basal flow as well as peak reactive hyperaemia remained unchanged in diabetic as well as in non‐diabetic subjects. Our data provide evidence that in the postprandial state resistance vessel reactivity becomes reduced in insulin treated type‐2 diabetic patients.     

Altered skeletal muscle glucose transport and blood lipid levels in habitual cigarette smokers

We determined whether habitual cigarette smoking alters insulin-stimulated glucose transport and GLUT4 protein expression in skeletal muscle. Vastus lateralis muscle was obtained from 10 habitual cigarette smokers and 10 control subjects using an open muscle biopsy procedure. Basal 3-O-methylglucose transport was twofold higher (P > 0·01) in muscle from habitual smokers (0·05 ± 0·08 vs. 1·04 ± 0·19 μmol ml^?1 h^?1; controls vs. smokers respectively). Insulin (600 pmol l^?1) increased glucose transport 2·6-fold (P > 0·05) in muscle from control subjects, whereas no significant increase was noted in habitual smokers. Skeletal muscle GLUT4 protein expression was similar between the groups. FFA levels were elevated in the smokers (264 ± 49 vs. 748 ± 138 μmol l^?1 for control subjects vs. smokers; P < 0·05), and serum triglyceride levels were increased in the smokers (0·9 ± 0·2 vs. 2·3 ± 0·6 mmol l^?1 for control subjects vs. smokers; P < 0·05). Skeletal muscle carnitine palmitil (acyl) transferase activity was similar between the groups, indicating that FFA transport into the mitochondria was unaltered by cigarette smoking. In conclusion, cigarette smoking appears to have a profound effect on glucose transport in skeletal muscle. Basal glucose transport is markedly elevated, whereas insulin-stimulated glucose transport is impaired. These changes cannot be explained by altered protein expression of GLUT4, but may be related to increased serum FFA and triglyceride levels. These findings highlight the importance of identifying habitual cigarette smokers in studies aimed at assessing factors that lead to alterations in lipid and glucose homeostasis in people with non-insulin-dependent diabetes mellitus (NIDDM).     

Endothelin‐1: increased plasma clearance,pulmonary affinity and renal vasoconstriction in young smokers

Pulmonary and renal haemodynamics and elimination of endothelin‐1 (ET‐1) were studied in six young smokers in response to 20 min intravenous infusion of ET‐1 (4 pmol kg^–1 min^–1) after smoking. At 20 min of ET‐1 infusion fractional ET‐1 extractions in the lungs and kidneys were 60 ± 2 and 60 ± 7%, respectively. Cardiac output and renal blood flow (RBF) fell by 18 ± 4% (P<0·05) and 34 ± 5% (P<0·01). Mean systemic arterial pressure increased (P<0·05) whereas pulmonary pressures were unchanged. Compared with previously published data in non‐smokers ( 38 , 39 ) basal arterial ET‐1 and ET‐1‐values during ET‐1 infusion were lower with a more rapid return to basal value. Smokers had higher pulmonary extraction of ET‐1 at the same pulmonary arterial concentration (P<0·05). RBF reduction was more pronounced (P<0·05). Systemic vascular resistance increased while pulmonary vascular resistance did not increase as in non‐smokers. Increased plasma clearance and more efficient pulmonary elimination of ET‐1 lowers the arterial level in young smokers. In addition ET‐1 evokes more pronounced renal vasoconstriction in these individuals.     

Atrial natriuretic peptide concentrations in umbilical cord plasma from pre-eclamptic women

Summary. Atrial natriuretic peptide (ANP) was measured in arterial and venous umbilical cord plasma at the time of delivery by cesarean section in pre-eclamptic (n= 7) and normal women (n= 6). In addition venous samples were obtained from pre-eclamptic (n= 7) and normal pregnant women (n= 7) near term. ANP plasma levels were higher in pregnant women with pre-eclampsia than in normal pregnant women (27·9±4·4 [mean±SEM] and 14·1 ±2·5 pmol 1^-1, respectively, P<0·05). Immediately after delivery plasma ANP in pre-eclamptic mothers was 66·7 ± 12·8 pmol 1^-1 compared to 13·9 ±2·2 pmol 1^-1 in normal mothers (P<0·01). However, in the pre-eclamptic group the levels of ANP in arterial and venous umbilical cord plasma (19·5 ±4·2 and 16·7±4·3 pmol 1^-1 respectively) were significantly (P<0·01) lower than ANP levels in arterial and venous cord plasma (39·6 ± 1·0 and 31·1±4·2 pmol 1^-1, respectively) from normal mothers. It is concluded that the increased ANP plasma level in pre-eclamptic women originates from a maternal source. In addition, since the ANP level is lower in cord plasma than in maternal plasma in pre-eclampsia, fetoplacental volume homeostasis may also be changed in pre-eclampsia.     

Interactions of stress hormones on lipid and carbohydrate metabolism in man with partial insulin deficiency

Abstract. The metabolic responses to 4-h infusions of adrenaline (3 μg kg^-1 h^-1) and cortisol (10 mg m^-2 h^-1 for 2 h followed by 5 mg m^-2 h^-1 for 2 h), separately and in combination, have been studied in six healthy subjects with concurrent somatostatin infusion (250 μg h^-1). A combined infusion of adrenaline, cortisol, glucagon (180 ng kg^-1 h^-1) and somatostatin has also been studied. Somatostatin plus adrenaline and somatostatin plus cortisol resulted in hyperglycaemia (at 240 min, somatostatin plus adrenaline 11·4 ± 0·4 mmol l^-1, P < 0·001; somatostatin plus cortisol 6·7 ± 0·3 mmol l^-1, P < 0·05; somatostatin alone 4·9 ± 0·4 mmol l^-1). No synergistic effect on blood glucose was seen with adrenaline and cortisol together. When glucagon was added, blood glucose rose more rapidly than without glucagon (9·3 ± 0·4 mmol l^-1v. 7·2 ± 0·5 mmol l^-1 at 45 min, P < 0·001), but plateau values were similar. Plasma NEFA levels were raised by somatostatin plus adrenaline (0·55 ± 0·04–1·82 ± 0·11 mmol l^-1 at 60 min). Somatostatin plus cortisol had no more effect on plasma NEFA than somatostatin alone. During the combined infusion of somatostatin plus adrenaline plus cortisol, a synergistic effect on plasma NEFA was observed (2·30 ± 0·11 mmol l^-1 at 60 min, P < 0·01 v. somatostatin plus adrenaline). This occurred despite a small escape of insulin secretion. The lipolytic actions of adrenaline are potentiated by elevated circulating cortisol levels in insulin-deficient man. Glucagon does not modify this response, but accelerates the development of hyperglycaemia.     

The effect of different exercise‐testing protocols on atrial natriuretic peptide

The aim of this study was to examine and to compare alterations in the secretion of atrial natriuretic peptide (ANP) during different exercise‐testing protocols in moderately trained men. Fifteen healthy male physical education students were studied (mean age 22·3 ± 2·5 years, training experience 12·3 ± 2·5 years, height 1·80 ± 0·06 m, weight 77·4 ± 8·2 kg). Participants performed an initial graded maximal exercise testing on a treadmill for the determination of VO_2max (duration 7·45–9·3 min and VO_2max 55·05 ± 3·13 ml kg^?1 min^?1) and were examined with active recovery (AR), passive recovery (PR) and continuous running (CR) in random order. Blood samples for plasma ANP concentration were taken at rest (baseline measurement), immediately after the end of exercise as well as after 30 min in passive recovery time (PRT). The plasma ANP concentration was determined by radioimmunoassay (RIA). The results showed that ANP plasma values increased significantly from the rest period to maximal values. In the short‐term graded maximal exercise testing the ANP plasma values increased by 56·2% (44·8 ± 10·4 pg ml^?1 versus 102·3 ± 31·3 pg ml^?1, P<0.001) and in the CR testing the ANP levels increased by 29·2% (44·8 ± 10·4 pg ml^?1 versus 63·3 ± 19·8 pg ml^?1, P<0.001) compared to the baseline measurement. Moreover, the values of ANP decreased significantly (range 46·4–51·2%, P<0.001) in PRT after the end of the four different exercise modes. However, no significant difference was evident when ANP values at rest and after AR and PR were compared. It is concluded that the exercise testing protocol may affect the plasma ANP concentrations. Particularly, short‐term maximal exercise significantly increases ANP values, while the intermittent exercise form of active and passive recovery decreases ANP concentrations.     

Effects of a high‐fat meal on resistance vessel reactivity and on indicators of oxidative stress in healthy volunteers

High fat meals postprandially impair macrovascular endothelial function and a link to increased oxidative stress is suggested. Few information, on the other hand, exists on the effect of postprandial hyperlipidaemia on resistance vessel function. Under normal circumstances this vascular bed regulates tissue perfusion and, by controlling flow, impacts on macrovascular nitric oxide formation. The impact of a high fat meal (1200 kcal, 90 g fat, 46 g protein and 47 g carbohydrates) on postprandial resistance vessel reactivity and on indicators of oxidative stress was studied in 11 healthy subjects by venous‐occlusion plethysmography using another six subjects as time control group. Ingestion of the test meal resulted in a pronounced increase of serum triglycerides from 1·05 ± 0·61 mmol l^?1 in the fasting state to peak postprandial values of 1·94 ± 0·41 mmol l^?1 (P < 0·001) reached after 4 h and a return to baseline after 8 h. Fasting peak reactive hyperaemia (RH) was 19·6 ± 2·4 ml min^?1 (100 ml)^?1. Two hours after ingestion of the test meal peak RH was transiently reduced to 16·8 ± 2·2 ml min^?1 (100 ml)^?1 (P < 0·05). No alteration of resting forearm perfusion was observed. The time course of peak RH suggested a potential biphasic effect of the test meal with an early impairment and a late increase of RH. Ingestion of a lipid rich test meal did not exert any influence on either total plasma antioxidant capacity given in trolox equivalents (513 ± 26 μmol l^?1 at baseline) or on plasma peroxides measured as H₂O₂ equivalents (469 ± 117 μmol l^?1). Our results suggest that ingestion of a meal containing 90 g of fat results in a transient impairment of reactive hyperaemia in healthy subjects but these vascular alterations are not accompanied by signs of systemically increased oxidative stress.     

Forearm composition and muscle function in trained and untrained limbs

Summary. The influence of a period of training, which lasts for several years, on the proportions of muscle, fat and bone present in the human forearm has been investigated by comparing trained and untrained limbs of nine experienced male tennis players. Ten healthy but untrained males of similar age served as a control group. Computed tomography (CT) scans of the forearm were made at intervals along its length to identify fat, muscle and bone and to calculate the volumes occupied by each of these components. Total forearm volume was greater in the dominant limb compared with the contralateral side in both trained (by 135±59 cm³, mean±SD, P<0·001) and untrained subjects (by 41±45 cm³, P<0·02). Forearm muscle volume was also greater in dominant limbs of trained (by 117±52 cm³, P<0·001) and untrained by 35±41 cm³, P<0·025) subjects. Muscle accounted for 75·4±2·7% of the total volume in the dominant arm of trained subjects compared with 71·4±4·2% in the control group (P<0·05). There was a greater proportion of muscle (P<0·05) and a smaller proportion of fat (P<0·001) in the trained limb compared with the contralateral limb of the same subjects. No differences in proportions of fat, muscle and bone were observed in dominant and non-dominant limbs of the control subjects. Trained subjects were able to exert a greater isometric force with the dominant limb (549±76N) than with the non-dominant limb (496±48N; P<0·005). There was no difference in grip strength between the arms of the untrained group (dominant: 516±107N; non-dominant: 491±91N). The ratio of strength to muscle volume was, however, the same in dominant and non-dominant arms of both groups of subjects.     

Plasma lipid and lipoprotein profiles in pre- and post-menopausal middle-aged runners

Summary. Plasma lipid and lipoprotein profiles were compared in middle-aged trained and untrained women before and after menopause. Subjects were assigned to one of four groups: (1) pre-menopausal trained (Pre-T: n= 17, aged 42 ±5 years, body fat 19±5%, training distance 53 ±20 km week^-1, V?o_2max 49 ±4 ml kg^-1 min^-1, mean±SD); (2) pre-menopausal untrained (Pre-UT: n= 26, 42 ±5 years, 24 ±7%, 34 ±6 ml kg^-1 min^-1); (3) post-menopausal trained (Post-T: n= 16, 54 ±3 years, 20 ±4%, 43 ±19 km week^-1, 41 ±5 ml kg^-1 min^-1); and (4) post-menopausal untrained (Post-UT: n= 15, 55 ±3 years, 25 ±6%, 31 ±3 ml kg^-1 min^-1). There were no significant differences in total cholesterol (range 173–194 mg dl^-1), triglyceride (56–72 mg dl^-1), and HDL-cholesterol (HDLC: 76–85 mg dl^-1) among the four groups. LDL-cholesterol (LDLC) in the post-menopausal women (Post-T: 96 ±32 mg dl^-1; Post-UT: 104 ±23 mg dl^-1) tended to be higher than in the premenopausal women (Pre-T: 86 ± 25 mg dl^-1, Pre-UT: 81 ± 23 mg dl^-1). LDLC/HDLC ratio in Post-UT (1·42 ±0·38 unit) was higher than in the pre-menopausal women (Pre-T: 1·03±0·31 unit, P<0·01; Pre-UT: 1·10±0·38 unit, P<0·05), whereas the ratio in Post-T (1·20 ±0·38 unit) was not different from those of the pre-menopausal groups. These results suggest that endurance running protects against the increase in LDLC/HDLC ratio that frequently occurs after menopause.     

Body composition,maximal aerobic performance and inflammatory biomarkers in endurance-trained athletes

This study was designed to examine the relationships between body composition, cardiorespiratory fitness and simultaneously measured inflammatory parameters in endurance-trained athletes. In 20 well-trained rowers (19·0 ± 2·9 years; 185·6 ± 4·8 cm; 85·7 ± 10·8 kg; 17·1 ± 5·1% body fat; maximal oxygen consumption [VO₂max]: 63·9 ± 8·5 ml min⁻¹ kg⁻¹), body composition was measured by dual-energy X-ray absorptiometry and cardiorespiratory fitness by direct VO₂max test. Twelve inflammatory factors [interleukin (IL)-2, IL-4, IL-6, IL-8, IL-10, vascular endothelial growth factor, interferon-gamma (IFN-γ), tumour necrosis factor-alpha, IL-1α, IL-1β, monocyte chemoattractant protein-1 (MCP-1), epidermal growth factor (EGF)] were analysed from serum samples. Serum IFN-γ was related (P<0·05) to fat-free mass (FFM) (r = −0·56) and muscle mass (r = −0·50). The stepwise regression analysis showed that IFN-γ explained 27·5%, and IFN-γ and IL-6 together explained 39·8% of the variability of FFM, while IFN-γ explained 21·1%, and IFN-γ together with EGF explained 36·6% of the variability of muscle mass in male rowers. Serum IL-8 (r = −0·65) and VEGF (r = −0·48) correlated (P<0·05) with VO₂max kg⁻¹. Serum IL-8 explained 38·5% of the variability of VO₂max kg⁻¹. Significant correlations were also found among several inflammatory parameters, indicating that various inflammatory cytokines act on the body as an ensemble. In conclusion, this cross-sectional study in endurance-trained male rowers showed that FFM and muscle mass were negatively correlated with serum IFN-γ level, whereas cardiorespiratory fitness was negatively related to serum IL-8 level.