Plasma vasopressin,renin activity,and aldosterone responses to maximal exercise in active college females

Summary The effect of maximal treadmill exercise on plasma concentrations of vasopressin (AVP); renin activity (PRA); and aldosterone (ALDO) was studied in nine female college basketball players before and after a 5-month basketball season. Pre-season plasma AVP increased (p<0.05) from a pre-exercise concentration of 3.8±0.5 to 15.8±4.8 pg · ml⁻¹ following exercise. Post-season, the pre-exercise plasma AVP level averaged 1.5±0.5 pg · ml⁻¹ and increased to 16.7±5.9 pg · ml⁻¹ after the exercise test. PRA increased (p<0.05) from a pre-exercise value of 1.6±0.6 to 6.8±1.7 ngAI · ml⁻¹ · hr⁻¹ 5 min after the end of exercise during the pre-season test. In the post-season, the pre-exercise PRA was comparable (2.4±0.6 ngAI · ml⁻¹ · hr⁻¹), as was the elevation found after maximal exercise (8.3±1.9 ngAI · ml⁻¹ · hr⁻¹). Pre-season plasma ALDO increased (p<0.05) from 102.9±30.8 pg · ml⁻¹ in the pre-exercise period to 453.8±54.8 pg · ml⁻¹ after the exercise test. In the post-season the values were 108.9±19.4 and 365.9±64.4 pg · ml⁻¹, respectively. Thus, maximal exercise in females produced significant increases in plasma AVP, renin activity, and ALDO that are comparable to those reported previously for male subjects. Moreover, this response is remarkably reproducible as demonstrated by the results of the two tests performed 5 months apart.     

Effect of short-term endurance training on exercise capacity,haemodynamics and atrial natriuretic peptide secretion in heart transplant recipients

Exercise tolerance of heart transplant patients is often limited. Central and peripheral factors have been proposed to explain such exercise limitation but, to date, the leading factors remain to be determined. We examined how a short-term endurance exercise training programme may improve exercise capacity after heart transplantation, and whether atrial natriuretic peptide (ANP) release may contribute to the beneficial effects of exercise training by minimizing ischaemia and/or cardiac and circulatory congestion through its vasodilatation and haemoconcentration properties. Seven heart transplant recipients performed a square-wave endurance exercise test before and after 6 weeks of supervised training, while monitoring haemodynamic parameters, ANP and catecholamine concentrations. After training, the maximal tolerated power and the total mechanical work load increased from 130.4 (SEM 6.5) to 150.0 (SEM 6.0) W (P < 0.05) and from 2.05 (SEM 0.1) to 3.58 (SEM 0.14) kJ · kg⁻¹ (P < 0.001). Resting heart rate decreased from 100.0 (SEM 3.4) to 92.4 (SEM 3.5) beats · min⁻¹ (P < 0.05) but resting and exercise induced increases in cardiac output, stroke volume, right atrial, pulmonary capillary wedge, systemic and pulmonary artery pressures were not significantly changed by training. Exercise-induced decrease of systemic vascular resistance was similar before and after training. After training arterio-venous differences in oxygen content were similar but maximal lactate concentrations decreased from 6.20 (SEM 0.55) to 4.88 (SEM 0.6) mmol · 1⁻¹ (P < 0.05) during exercise. Similarly, maximal exercise noradrenaline concentration tended to decrease from 2060 (SEM 327) to 1168 (SEM 227) pg · ml⁻¹. A significant correlation was observed between lactate and catecholamines concentrations. The ANP concentration at rest and the exercise-induced ANP concentration did not change throughout the experiment [104.8 (SEM 13.1) pg · ml⁻¹ vs 116.0 (SEM 13.5) pg · ml⁻¹ and 200.0 (SEM 23.0) pg · ml⁻¹ vs 206.5 (SEM 25.9) pg · ml⁻¹ respectively]. The results of this study suggested that the significant improvement in exercise capacity observed after this short-term endurance training period may have arisen mainly through peripheral mechanisms, associated with the possible decrease in plasma catecholamine concentrations and reversal of muscle deconditioning and/or prednisone-induced myopathy.     

Effects of physical exercise and anti-G suit inflation on atrial natriuretic factor plasma level

Summary The purpose of this study was to measure the effect of enhanced venous return on atrial natriuretic factor (ANF) secretion during exercise and upright posture and the consequences on renin angiotensin aldosterone system (RAAS) activity. Six healthy male subjects were submitted to four different procedures. All procedures were performed in the same position, i.e. riding on a support with legs hanging. Two procedures were performed at rest: the subjects were studied after a 25-min rest in this position, with and without the lower limb fitted with an anti-G suit inflated to 60 mmHg. Two procedures were carried out with physical exercise; arm-cranking was performed in the same position with and without the anti-G suit inflated to 60 mmHg. Venous blood was collected before and after each procedure in order to measure plasma ANF, plasma aldosterone concentration (PAC), plasma renin activity (PRA), corticotrophin (ACTH) and catecholamine level. The data mean ±SEM showed that the ANF plasma level decreased significantly (p<0.05) from 32.5±4 to 28±6 pg · ml⁻¹ after a 20-min rest in the upright posture, whereas this effect was absolished with anti-G suit inflation. Physical exercise with and without the anti-G suit increased the ANF level above control values (60±13.6 pg · ml⁻¹ and 53±13 pg · ml⁻¹): anti-G suit inflation had no significant effect. PRA increased after rest in an upright posture and during physical exercise; anti-G suit inflation abolished this increase in both conditions. PAC was not influenced by postural change but significantly increased in all exercise tests. ACTH increased to the same extent in both exercise tests. The plasma catecholamine level increased during upright posture and both physical exercise procedures. These results indiate that enhanced venous return during anti-G suit inflation increases ANF secretion at rest in an upright posture and that physical exercise greatly increases plasma ANF level independently of the anti-G suit inflation. They suggest that ANF release during exercise could be influenced by factors other than haemodynamic stimuli. The comparison between ANF and PRA changes during arm-cranking indicates that PRA is influenced more than ANF by blood volume displacement. The ANF increase during exercise does not inhibit aldosterone secretion.     

Effects of inducing physiological hyperglucagonemia on metabolic responses to exercise

The purpose of the present study was to assess the effects of exogenously increasing the circulating levels of glucagon on the metabolic responses to exercise in rats. A total of six groups of rats were infused (iv) either with glucagon (20 or 50 ng·kg⁻¹·min⁻¹) or saline (0.9% NaCl), either in the resting state or during a bout of running exercise (45 min, 26 m·min⁻¹, 0% grade). Blood samples were taken at the end of the 45-min experiment. Animals infused with glucagon at 50 ng·kg⁻¹·min⁻¹ showed significantly (P<0.01) higher mean plasma glucagon concentrations than animals infused with saline or glucagon at 20 ng·kg⁻¹·min⁻¹. In addition, exercise resulted in significantly (P<0.05) higher mean plasma glucagon concentrations, compared to rest, in all groups. In spite of these differences in glucagon concentrations, there were no significant (P>0.05) effects of exercise and glucagon infusion on mean hepatic glycogen, plasma glucose, insulin, C-peptide, β-hydroxybutyrate, or catecholamine concentrations. Although exercise resulted in a significant (P<0.01) increase in plasma glycerol and free fatty acid concentrations and a significant (P<0.05) decrease in glycogen in the soleus muscle, these responses were not affected by the glucagon infusion. These results suggest that the liver is non-responsive to physiological hyperglucagonemia in a short-term (45 min) exercise situation. Electronic Publication     

Optimal glycaemic control in unrestrained diabetic dogs using programmed compound squarewave insulin infusions

A glycaemic control identical with the normal has been achieved in unrestrained totally depancreatised dogs using a portable open-loop insulin delivery system. The device consisted of a battery power pack with a flow-rate controller, an insulin reservoir and a peristaltic pump from which pulses of insulin were delivered every 90 seconds into the inferior vena cava through an exteriorised indwelling catheter. Insulin was infused at the basal rate of 0.45±0.03 mUkg⁻¹ min⁻¹ (Mean±s.e.m.) in the postabsorptive state resulting in peripheral IRI and plasma glucose levels of 12±1 μU ml⁻¹ and 86±7 mg dl⁻¹. In the postprandial period the infusion rate was enhanced sevenfold to the rate of 3.16±0.21 mU kg⁻¹min⁻¹ for 7h and then reduced to 1.05±0.07 mU kg⁻¹ min⁻¹ for an additional 2.25 h. A weight-maintaining constant diet was provided and the resulting glycaemic profiles were similar to age, sex and weight-matched healthy controls. Fasting peripheral insulin levels in the infused diabetic dogs were not significantly different from non-diabetic controls (10±1μUml⁻¹). However, in the postprandial period of enhanced delivery, insulin levels in the diabetic dogs were 3.1 times higher than the controls. With the compound square waveforms of preprogrammed insulin infusion found appropriate in this study unaccountable low or high plasma glucose levels did not occur but hyperinsulinism accompanied the glycaemic normalisation following a mixed meal.     

Effect of glucose on plasma glucagon and free fatty acids during prolonged exercise

Summary The effects of glucose ingestion on the changes in blood glucose, FFA, insulin and glucagon levels induced by a prolonged exercise at about 50% of maximal oxygen uptake were investigated. Healthy volunteers were submitted to the following procedures: 1. a control test at rest consisting of the ingestion of 100 g glucose, 2. an exercise test without, or 3. with ingestion of 100 g of glucose. Exercise without glucose induced a progressive decrease in blood glucose and plasma insulin; plasma glucagon rose significantly from the 60th min onward (+45 pg/ml), the maximal increase being recorded during the 4th h of exercise (+135 pg/ml); plasma FFA rose significantly from the 60th min onward and reached their maximal values during the 4th h of exercise (2177±144 ΜEq/l, m±SE). Exercise with glucose ingestion blunted almost completely the normal insulin response to glucose. Under these conditions, exercise did not increase plasma glucagon before the 210th min; similarly, the exercise-induced increase in plasma FFA was markedly delayed and reduced by about 60%. It is suggested that glucose availability reduces exercise-induced glucagon secretion and, possibly consequently, FFA mobilization. Chercheur Qualifié of the Fonds National Belge de la Recherche Scientifique     

Levels of serum creatine kinase and myoglobin in women after two isometric exercise conditions

Summary The purpose of this study was to measure serum creatine kinase (CK) activity and serum myoglobin (MG) concentrations in women after two unilateral isometric knee extension exercises. Forty maximal voluntary contractions (MVC) were held for 10 s, with either a 5 s (10∶5) or 20 s 10∶20 exercise (349.4±66.1 mU · ml⁻¹) and 6 h and MG values were measured pre, 0, 3, 6, and 18 h post exercise. For CK, the highest post exercise values were observed at 6 h following the 10∶20 exercise (349.4±66.1 mU · ml⁻¹) and 6 h following the 10∶5 exercise (194.1±18.6 mU · ml⁻¹). For MG, the highest values were found 3 h after the 10∶20 exercise (148.9±61.7 ng · ml⁻¹) and 6 h after the 10∶5 exercise (67.3±10.9 ng · ml⁻¹). Serum CK and MG levels were significantly greater (p<0.01) after the 10∶20 exercise bout. The data demonstrate that CK and MG values for women increase significantly after isometric exercise. Since greater tension levels were maintained during the 10∶20 exercise it is hypothesized that increased serum CK and MG values after isometric exercise may be related to the tension generated by the contracting muscle.     

Sympathetic control of the forearm blood flow in man during brief isometric contractions

Summary Experiments were performed to assess the possible neurally mediated constriction in active skeletal muscle during isometric hand-grip contractions. Forearm blood flow was measured by venous occlusion plethysmography on 5 volunteers who exerted a series of repeated contractions of 4 s duration every 12 s at 60% of their maximum strength of fatigue. The blood flows increased initially, but then remained constant at 20–24 ml·min⁻¹·100 ml⁻¹ throughout the exercise even though mean arterial blood pressure reached 21–23 kPa (160–170 mm Hg). When the same exercise was performed after arterial infusion of phentolamine, forearm blood flow increased steadily to near maximal levels of 38.7±1.4 ml·min⁻¹·100 ml⁻¹. Venous catecholamines, principally norepinephrine, increased throughout exercise, reaching peak values of 983±258 pg·ml⁻¹ at fatigue. Of the vasoactive substances measured, the concentration of K⁺ and osmolarity in venous plasma also increased initially and reached a steady-state during the exercise but ATP increased steadily throughout the exercise. These data indicate a continually increasing α-adrenergic constriction to the vascular beds in active muscles in the human forearm during isometric exercise, that is only partially counteracted by vasoactive metabolites.     

Effects of angiotensin II on arterial pressure,renin and aldosterone during exercise

Summary To evaluate the effect of isotonic exercise on the response to angiotensin II, angiotensin II in saline solution was infused intravenously (7.5 ng · kg⁻¹ · min⁻¹) in seven normal sodium replete male volunteers before, during and after a graded uninterrupted exercise test on the bicycle ergometer until exhaustion. The subjects performed a similar exercise test on another day under randomized conditions when saline solution only was infused. At rest in recumbency angiotensin II infusion increased plasma angiotensin II from 17 to 162 pg · ml⁻¹ (P<0.001). When the tests with and without angiotensin II are compared, the difference in plasma angiotensin II throughout the experiment ranged from 86 to 145 pg · ml⁻¹. The difference in mean intra-arterial pressure averaged 17 mmHg at recumbent rest, 12 mmHg in the sitting position, 9 mmHg at 10% of peak work rate and declined progressively throughout the exercise test to become non-significant at the higher levels of activity. Plasma renin activity rose with increasing levels of activity but angiotensin II significantly reduced the increase. Plasma aldosterone, only measured at rest and at peak exercise, was higher during angiotensin II infusion; the difference in plasma aldosterone was significant at rest, but not at peak exercise. In conclusion, the exercise-induced elevation of angiotensin II does not appear to be an important factor in the increase of blood pressure. It is suggested that the vasodilating mechanisms in the working muscles and the vasoconstricting mechanisms in the non-working vascular beds are powerful and dominant during isotonic exercise and attenuate the opposing or additive vasoconstrictor effects of angiotensin II. The negative feedback effect of angiotensin II on renal renin secretion, however, is not inhibited by exercise.     

Beta-endorphin infusion alters pancreatic hormone and glucose levels during exercise in rats

β-Endorphin (BE) infusion at rest can influence insulin and glucagon levels and thus may affect glucose availability during exercise. To clarify the effect of BE on levels of insulin, glucagon and glucose during exercise, 72 untrained male Sprague-Dawley rats were infused i.v. with either: (1) BE (bolus 0.05?mg?·?kg^?1 +0.05?mg?·?kg^?1?·?h^?1, n?=?24); (2) naloxone (N, bolus 0.8?mg?·?kg^?1?+?0.4?mg?·?kg^?1, n?=?24); or (3) volume-matched saline (S, n?=?24). Six rats from each group were killed after 0, 60, 90 or 120 min of running at 22?m?·?min^?1, at 0% gradient. BE infusion resulted in higher plasma glucose levels at 60?min [5.93 (0.32)?mM] and 90?min [4.16 (0.29)?mM] of exercise compared to S [4.62 (0.27) and 3.41 (0.26?mM] and N [4.97 (0.38) and 3.44 (0.25)?mM]. Insulin levels decreased to a greater extent with BE [21.5 (0.9) and 18.3 (0.6) uIU?·?ml^?1] at 60 and 90?min compared to S [24.5 (0.5) and 20.6 (0.6)?uIU?·?ml^?1] and N [24.5 (0.4) and 21.6 (0.7)?uIU?· ml^?1] groups. Plasma C-peptide declined to a greater extent at 60 and 90?min of exercise with BE infusion compared to both S and N. BE infusion increased glucagon at all times during exercise compared to S and N. These data suggest that BE infusion during exercise influences plasma glucose by augmenting glucagon levels and attenuating insulin release.     

Substrate utilisation during exercise and shivering

It is generally assumed that exercise and shivering are analogous processes with regard to substrate utilisation and that, as a consequence, exercise can be used as a model for shivering. In the present study, substrate utilisation during exercise and shivering at the same oxygen consumption (V˙O₂) were compared. Following an overnight fast, eight male subjects undertook a 2-h immersion in cold water, designed to evoke three different intensities of shivering. At least 1 week later they undertook a 2-h period of bicycle ergometry during which the exercise intensity was varied to match the V˙O₂ recorded during shivering. During both activities hepatic glucose output (HGO), the rate of glucose utilisation (Rd), blood glucose, plasma insulin, free fatty acid (FFA) and beta-hydroxybutyrate (B-HBA) concentrations were measured. The V˙O₂ measured during the different levels of shivering averaged 0.49 l · min⁻¹ (level 1: low), 0.6 l · min⁻¹ (level 2: low-moderate), and 0.9 l · min⁻¹ (level 3: moderate), and corresponded closely to the levels measured during exercise. HGO and Rd were greater (P < 0.05) during exercise than during shivering at the same V˙O₂ (9.5% and 14.7%, respectively). The average (SD) HGO during level 3 exercise was 3.0 (0.91) mg · kg⁻¹ . min⁻¹ compared to 2.76 (1.0) mg · kg⁻¹ . min⁻¹ during shivering. The values for Rd were 3.06 (0.98) mg · kg⁻¹ · min⁻¹ during level 3 exercise and 2.68 (0.82) mg · kg⁻¹ · min⁻¹ during shivering. Blood glucose levels did not differ between conditions, averaging 5.4 (0.3) mmol . l⁻¹ over all levels of shivering and 5.2 (0.3) mmol · l⁻¹ during exercise. Plasma FFA and B-HBA were higher (P < 0.01) during shivering than during corresponding exercise (12.3% and 33.3%, respectively). FFA averaged 0.61 (0.2) mmol · l⁻¹ over all levels of shivering and 0.47 (0.16) mmol · l⁻¹ during exercise. The figures for B-HBA were 0.44 (0.13) mmol · l⁻¹ during all levels of shivering and 0.32 (0.1) mmol · l⁻¹ during exercise. Plasma insulin was higher (P < 0.05) during level 2 and 3 shivering compared to corresponding exercise; at these levels the average value for plasma insulin was 95.9 (21.9) pmol · l⁻¹ during shivering and 80.6 (16.1) pmol · l⁻¹ during exercise. On the basis of the present findings it is concluded that, with regard to substrate utilisation, shivering and exercise of up to 2 h duration should not be regarded as analogous processes. Accepted: 12 February 1997     

Circulating reverse triiodothyronine in humans during exercise

Summary Circulating thyroxine (T₄), triiodothyronine (T₃) and reverse triiodothyronine (rT₃) as well as blood lactate and glucose concentrations were measured in a group of 12 trained volunteer subjects prior to and after swimming 0.18 or 0.9 km, to determine if increase in metabolic activity was accompanied by diversion of T₄ monodeiodination from the active (T₄ to T₃) to the inactive (T₄ to rT₃) pathway. The resting T₄, T₃, and rT₃ levels were 8.5 Μg·100 ml⁻¹, 108 ng·100 ml⁻¹, and 57 ng·100 ml⁻¹, respectively, whereas after 0.18 km of swimming the corresponding levels were 9.5 Μg·100 ml⁻¹, 135 ng. 100 ml⁻¹ and 70 ng·100 ml⁻¹. After 0.9 km of swimming, T₄, T₃, and rT₃ levels were 9.0 Μg·100 ml⁻¹, 126 ng·100 ml⁻¹, and 66 ng·100 ml⁻¹, respectively. The swimming was accompanied by hemoconcentration and increase in blood lactate but not in glucose concentrations. In two other investigations thyroid hormones were measured prior to and after 60 or 90 min of moderate exercise on a bicycle ergometer. This exercise had no effect on circulating thyroid hormone levels. Free thyroxine (FT₄) concentration and thyroxine binding globulin (TBG) capacity were unaltered after exercise. In conclusion, brief strenuous swimming or moderate bicycle exercise had minor or no effect on thyroid hormone concentrations when consideration was given to the attendant hemoconcentration. Even when exercise induced small T₃ and rT₃ changes were noted, they were in the same direction (increase) thus demonstrating a lack of diversion of peripheral T₄ monodeiodination. Investigations partially supported by NIH grant AG-01613 and the Narveen Medical Research Foundation, St. Louis, Missouri, USA     

Effects of a 24-h carbohydrate-poor diet on metabolic and hormonal responses during prolonged glucose-infused leg exercise

Summary Extant literature dealing with metabolic and hormonal adaptations to exercise following carbohydrate (CHO) reduced diets is not sufficiently precise to allow researchers to partial out the effects of reduced blood glucose levels from other general effects produced by low CHO diets. In order to shed light on this issue, a study was conducted to examine the effects of a 24-h CHO-poor diet on substrate and endocrine responses during prolonged (75 min; 60% ) glucose-infused leg exercise. Eight subjects exercised on a cycle ergometer in the two following conditions: 1) after a normal diet (CHO_N), and 2) after a 24-h low CHO diet (CHO_L). In both conditions, glucose was constantly infused intravenously (2.2 mg · kg⁻¹ · min⁻¹) from the 10th to the 75th min of exercise in relatively small amounts (10.4±0.8 g). No significant differences in blood glucose concentrations were found between the two conditions at rest and during exercise although a significant increase (p<0.01) in glucose level was observed in both conditions after 40 min of exercise. The CHO_L as compared to the CHO_N condition, was associated with significantly (p<0.05) lower resting concentrations of insulin, muscle glycogen (8.7 vs 10.6 g · kg⁻¹), and triacylglycerol, and greater concentrations of Β-hydroxybutyrate (0.5 vs 0.2 mmol · L⁻¹), and free fatty acids. During exercise, the CHO_L condition as compared to the CHO_N condition, was associated with significantly (p<0.05) lower insulin and R values, as well as greater free fatty acid (from min 20 to 60) and epinephrine (min 60 to 75) concentrations. Norepinephrine and glucagon concentrations also showed a net tendency (p<0.06) to be higher in the CHO_L condition. There were no significant differences at rest and during exercise in blood lactate and cortisol concentrations between the two conditions. These results demonstrate that blood glucose is not the sole determinant of the metabolic and hormonal responses during prolonged exercise following a low CHO intake and indicate that other factors may be involved in the regulatory mechanism.     

Angiotensin II induced reduction of peritubular capillary diameter in the rat kidney

Summary Large peritubular capillaries were infused consecutively (20 nl · min⁻¹) in random sequence with isotonic saline and angiotensin II (20–80 ng · ml⁻¹). The diameters of the infused capillaries were measured, without knowledge of the infusate used, from colour photographs of the infused area. Angiotensin II induced a significant (p<0.001) decrease in capillary diameter (Δ=−1.2±0.2 (SE) μm and Δ=−2.1±0.2 (SE) μm with 20 ng · ml⁻¹ and 80 ng · ml⁻¹ angiotensin II infusates, respectively). This decrease was shown to be independent of external tubular compression: separate experiments in which the surrounding tubules were collapsed by injection of oil blocks yielded similar results. The possibility that the observed reduction in diameter was caused by an angiotensin II induced change in capillary permeability to the staining solution was excluded, since the angiotensin II effect was unchanged when fluorescent dextran (mol. wt. 150000) was substituted for lissamin green. These experiments indicate that peritubular capillaries contract actively when infused with angiotensin II.     

Nervous control of pancreatic endocrine secretion in pigs

The increases in the concentrations of insulin and pancreatic glucagon in portal venous and arterial plasma in response to electrical stimulation of the vagus nerves were studied in anesthetized splanchnicotomized young pigs. The responses were frequence dependent; threshold frequency was below 1 Hz and maximum response was reached at 8–12 Hz. With maximal stimulation responses of magnitudes comparable to the responses to maximal arginine (glucagon) and glucose stimulation (insulin) were observed. However, both the insulin and the glucagon response were critically dependent on the blood glucose concentration during the stimulation: the glucagon response was inversely correlated to blood glucose, whereas the insulin response was positively correlated to blood glucose at concentrations above 4.5 mmol · 1^-1. Below this glucose concentration there was no detectable insulin response and above 8.0 mmol ·^-1 no glucagon response to vagal stimulation. A stimulated secretion of glucagon as well as insulin was maintained for up to 30 min stimulation, but insulin secretion tended to decrease, whereas glucagon secretion tended to increase. Above blood glucose concentrations of 4 mmol · 1^-1, blood glucose concentrations increased slightly in response to vagal stimulation, whereas no change was noted during stimulations performed at lower blood glucose concentrations.     

Plasma norepinephrine and heart rate dynamics during recovery from submaximal exercise in man

Summary The time course of heart rate (HR) and venous blood norepinephrine concentration [NE], as an expression of the sympathetic nervous activity (SNA), was studied in six sedentary young men during recovery from three periods of cycle ergometer exercise at 21%±2.8%, 43%±2.1% and 65%±2.3% of respectively (mean±SE). The HR decreased mono-exponentially withτ values of 13.6±1.6 s, 32.7±5.6 s and 55.8±8.1s respectively in the three periods of exercise. At the low exercise level no change in [NE] was found. At medium and high exercise intensity: (a) [NE] increased significantly at the 5th min of exercise (Δ[NE]=207.7±22.5 pg·ml⁻¹ and 521.3±58.3 pg·ml⁻¹ respectively); (b) after a time lag of 1 min [NE] decreased exponentially (τ=87 s and 101 s respectively); (c) in the 1st min HR decreased about 35 beats · min⁻¹; (d) from the 2nd to 5th min of recovery HR and [NE] were linearly related (100 pg·ml⁻¹ Δ[NE]5 beats ·min⁻¹). In the 1st min of recovery, independent of the exercise intensity, the adjustment of HR appears to have been due mainly to the prompt restoration of vagal tone. The further decrease in HR toward the resting value could then be attributed to the return of SNA to the pre-exercise level.     

Involvement of muscarinic cholinergic and α2-adrenergic mechanisms in growth hormone secretion during exercise in humans

The purpose of this study was to examine the role of muscarinic cholinergic and α₂-adrenergic mechanisms in growth hormone (GH) secretion during exercise in humans. The GH responses induced during moderate-intensity exercise (using a cycle ergometer at 60% maximal oxygen uptake, V˙O_2max, for 30 min) without treatment (control) and after the administration of a muscarinic cholinergic antagonist (atropine 1 mg) or after an α₂-adrenergic antagonist (yohimbine 15 mg) were compared in seven healthy men. Although, serum GH concentration had increased significantly after exercise in the control experiment [mean peak GH concentration 52.64 (SEM 18.60) ng · ml⁻¹], the increase was suppressed by the administration of either atropine [mean peak GH concentration 8.64 (SEM 7.47)  ng · ml⁻¹] or yohimbine [mean peak GH concentration 17.50 (SEM 7.89) ng · ml⁻¹]. The area under the curve of serum GH concentration against time was significantly lower in the experiment using these drugs [with atropine, mean area 458 (SEM 409) ng · ml⁻¹ · min], with yohimbine mean area 946 (SEM 435) ng · ml⁻¹ · min] than in the control experiment [mean area 3135 (SEM 1098) ng · ml⁻¹ · min]. These results suggest that muscarinic cholinergic and α₂-adrenergic mechanisms are involved in GH secretion during exercise in humans. Accepted: 9 March 2000     

Effects of improvement in aerobic power on resting insulin and glucose concentrations in children

In this study we determined the influence of improving aerobic power (V˙O_2max) on basal plasma levels of insulin and glucose of 11- to 14-year-old children, while accounting for body fat, gender, pubertal status, and leisure-time physical activity (LTPA) levels. Blood samples were obtained from 349 children after an overnight fast and analyzed for plasma insulin and glucose. Height, mass, body mass index (BMI), and sum of skinfolds (Σ triceps + subscapular sites) were measured. LTPA levels and pubertal status were estimated from questionnaires, and V˙O_2max was predicted from a cycle ergometry test. Regardless of gender, insulin levels were significantly correlated (P = 0.0001) to BMI, skinfolds, pubertal stage, and predicted V˙O_2max, but were not related to LTPA levels. Fasting glucose levels were not correlated to measures of adiposity or exercise (LTPA score, V˙O_2max) for females; however, BMI and skinfolds were correlated for males (P < 0.006). The children then took part in an 8-week aerobic exercise program. The 60 children whose V˙O_2max improved (≥3 ml · kg⁻¹ · min⁻¹) had a greater reduction in circulating insulin than the 204 children whose V˙O_2max did not increase −16 (41) vs −1 (63) pmol · l⁻¹; P = 0.028. The greatest change occurred in those children with the highest initial resting insulin levels. Plasma glucose levels were slightly reduced only in those children with the highest insulin levels whose V˙O_2max improved (P < 0.0506). The results of this study indicate that in children, adiposity has the most significant influence on fasting insulin levels; however, increasing V˙O_2max via exercise can lower insulin levels in those children with initially high levels of the hormone. In addition, LTPA does not appear to be associated with fasting insulin status, unless it is sufficient to increase V˙O_2max. Accepted: 2 June 1999     

Acute phase proteins,humoral and cell mediated immunity in environmentally-induced hyperthermia in man

Summary The effects of repeated hyperthermia, caused by a Finnish sauna bath over 1 week, on the serum levels of some acute phase reactant proteins and on both humoral and cell-mediated immunity on twelve healthy young volunteers are presented. The mean rise in rectal temperature during each 30-min period in the bath was about 1.3‡ C. Heat exposure caused significant increases in the serum concentrations of two of the acute phase reactant proteins, α₁-antitrypsin (from a mean value of 1.8 (0.1) to 1.9 (0.2) g·l⁻¹,p<0.01) and transferrin (from a mean value of 36.9 (3.4) to 38.3 (4.4) Μmol·l⁻¹,p<0.05), but no changes occurred in immunoglobulins or cell-mediated immunity. These findings suggest that environmentally induced hyperthermia can initiate the acute phase reaction associated with fever. Supported by the Sigrid Jusélius Foundation     

Dynamic model of the short-term regulation of arterial pressure in the cat

The purpose of this study was to characterise the dynamics of the short-term control of arterial pressure in the cat with the aid of a model consisting of a nonlinear negative-feedback control system. The arterial system was described by a three element windkessel model (peripheral resistance, R, aortic characteristic impedance, R_c, and total arterial compliance, C). The resistance regulation was represented by a second-order system with static gain G_R, a damping factor σ and an undamped natural frequency ω_n. The resistance gain, G_R, and the windkessel parameters were obtained from measurements of aortic and venous pressures and cardiac output in two steady states. The parameters σ and ω_n were estimated from mean pressure and mean flow during the transient from control to the new steady state. Pressure reductions averaged 10 per cent and resistance changes averaged 12 per cent. Average windkessel model parameters in the control condition were: C=(25·9±6·1) 10⁻⁶ g⁻¹ cm⁴ s², R_c=(2·51±0·53) 10³ g cm⁻⁴ s⁻¹, R=(40·9±9·8) 10³ g cm⁻⁴ s⁻¹. Average estimates of parameters of the resistance regulator were: G_R=(4·14±2·38) 10⁻³ min ml⁻¹, ω_n = 1·0 ± 1·0 rad s⁻¹, σ=0·41±0·19. A satisfactory fit was found between model predicted and measured pressure. The results suggest that the dynamic short-term control of pressure is underdamped and oscillatory. The amplitude of these oscillations is affected by arterial compliance, suggesting an interaction between the arterial system and short-term resistance regulation.