Sustained noradrenaline sulphate response in long-distance runners and untrained subjects up to 2 h after exhausting exercise

Summary We investigated the response of plasma and platelet free catecholamine ([CA]) and sulphated catecholamine ([CA-S]) concentrations after an incremental treadmill test to exhaustion and during recovery. In triathletes (n = 9) plasma and platelet [CA] and [CA-S] were measured before, immediately after and 0.5 and 24 h after exercise. In long-distance runners (n = 9) and in controls (n = 10) plasma [CA] and [CA-S] were determined 2 h instead of 24 h after exercise. Platelet [CA] and [CA-S] remained unchanged throughout the study. Plasma [CA] increased after exercise in all groups (P<0.05) and returned to pre-exercise values within 0.5 h of recovery. Plasma sulphoconjugated noradrenaline concentration ([NA-S]) was elevated after exercise in the triathletes, long-distance runners and in controls [9.96 (SEM 0.84) nmol·1^–1, 11.8 (SEM 1.19) nmol·1^–1, 9.53 (SEM 1.10) nmol·l^–1, respectively;P<0.05] compared with resting values [7.13 (SEM 1.04) nmol·l^–1, 6.19 (SEM 0.56) nmol·l^–1, 6.76 (SEM 0.67) nmol·1^–1, respectively] and remained elevated after 0.5 h of recovery [9.94 (SEM1.14) nmol·l^–1, 10.96 (SEM 0.80) nmol·l^–1, 8.95 (SEM 0.99) nmol·l^–1, respectively;P<0.05]. In the long-distance runners and controls plasma [NA-S] remained elevated during 2 h of recovery [9.96 (SEM 0.76) nmol·l^–1, 9.03 (SEM 0.88) nmol·l^–1, respectively]. These results would indicate that plasma [NA-S] increases after sympathetic nervous system activation by an exhausting incremental exercise test and remain elevated up to 2 h after exercise.     

Effect of acute mild hypoxia during exercise on plasma free and sulphoconjugated catecholamines

Catecholamine (CA) response to hypoxic exercise has been investigated during severe hypoxia. However, altitude training is commonly performed during mild hypoxia at submaximal exercise intensities. In the present study we tested whether submaximal exercise during mild hypoxia compared to normoxia leads to a greater increase of plasma concentrations of CA and whether plasma concentration of catecholamine sulphates change in parallel with the CA response. A group of 14 subjects [maximal oxygen uptake, 62.6 (SD 5.2) ml · min^–1 · kg^–1 body mass] performed two cycle ergometer tests of 1-h duration at the same absolute exercise intensities [191 (SD 6) W] during normoxia (NORM) and mild hypoxia (HYP) followed by 30 min of recovery during normoxia. Mean plasma concentrations of noradrenaline ([NA]), adrenaline ([A]), and noradrenaline sulphate ([NA-S]) were elevated (P < 0.01) after HYP and NORM compared with mean resting values and were higher after HYP [20.9 (SEM 3.1), 2.2 (SEM 0.24), 8.12 (SEM 1.5) nmol · 1^–1, respectively] than after NORM [(13.7 (SEM 0.9), 1.5 (SEM 0.14), 6.8 (SEM 0.7) nmol · 1^–1, respectively P < 0.01]. The higher plasma [NA-S] after HYP (P < 0.05) were still measurable after 30 min of recovery. From our study it was concluded that exercise at the same absolute submaximal exercise intensity during mild hypoxia increased plasma CA to a higher extent than during normoxia. Plasma [NA-S] response paralleled the plasma [NA] response at the end of exercise but, in contrast to plasma [NA], remained elevated until 30 min after exercise.     

The responses of the catecholamines and β-endorphin to brief maximal exercise in man

Summary The responses to brief maximal exercise of 10 male subjects have been studied. During 30 s of exercise on a non-motorised treadmill, the mean power output (mean±SD) was 424.8±41.9 W, peak power 653.3±103.0 W and the distance covered was 167.3±9.7 m. In response to the exercise blood lactate concentrations increased from 0.60±0.26 to 13.46±1.71 mmol·l^–1 (p<0.001) and blood glucose concentrations from 4.25±0.45 to 5.59±0.67 mmol·l^–1 (p<0.001). The severe nature of the exercise is indicated by the fall in blood pH from 7.38±0.02 to 7.16±0.07 (p<0.001) and the estimated decrease in plasma volume of 11.5±3.4% (p<0.001). The plasma catecholamine concentrations increased from 2.2±0.6 to 13.4±6.4 nmol·l^–1 (p<0.001) and 0.2±0.2 to 1.4±0.6 nmol·l^–1 (p<0.001) for noradrenaline (NA) and adrenaline (AD) respectively. The plasma concentration of the opioid-endorphin increased in response to the exercise from <5.0 to 10.2±3.9 p mol·l^–1. The post-exercise AD concentrations correlated with those for lactate as well as with changes in pH and the decrease in plasma volume. Post-exercise-endorphin levels correlated with the peak speed attained during the sprint and the subjects peak power to weight ratio. These results suggest that the increases in plasma adrenaline are related to those factors that reflect the stress of the exercise and the contribution of anaerobic metabolism. In common with other situations that impose stress,-endorphin concentrations are also increased in response to brief maximal exercise.     

Effect of muscle mass on lactate formation during exercise in humans

To elucidate the mechanisms of lactate formation during submaximal exercise, eight men were studied during one- (1-LE) and two-leg (2-LE) exercise (approximately 11-min cycling) using the catheterization technique and muscle biopsies (quadriceps femoris muscle). The absolute exercise intensity and thus the energy demand for the exercising limb was the same [mean 114 (SEM 7) W] during both 1-LE and 2-LE. At the end of exercise partial pressure of O₂ and O₂ saturation in femoral venous blood were lower and arterial adrenaline and noradrenaline were higher during 2-LE than during 1-LE. Mean arterial blood lactate concentration increased to 10.8 (SEM 0.8) (2-LE) and 5.2 (SEM 0.4) mmol · 1^–1 (1-LE) after 10 min of exercise. The intramuscular metabolic response to exercise was attenuated during 1-LE [mean, lactate = 49 (SEM 9); glucose 6-P = 3.3 (SEM 0.3); nicotinamide adenine dinucleotide, reduced = 0.17 (SEM 0.02); adenosine 5-diphosphate 2.7 (SEM 0.1) mmol · kg dry mass^–1] compared to 2-LE [76 (SEM 6); 6.1 (SEM 0.7); 0.21 (SEM 0.02); 3.0 (SEM 0.1) mmol · kg dry mass^–1, respectively]. To elucidate whether the lower plasma adrenaline concentration could contribute to the attenuated metabolic response, additional experiments were performed on four of the eight subjects with infusion of adrenaline during 1-LE (1-LEE). Average plasma adrenaline concentration was increased during 1-LEE and reached 2–4 times higher levels than during 2-LE. Post-exercise muscle lactate and glucose 6-P contents were higher during 1-LEE than during 1-LE and were similar to those during 2-LE. Also, leg lactate release was elevated during 1-LEE versus 1-LE. It was concluded that during submaximal dynamic exercise the intramuscular metabolic response not only depended on the muscle power output, but also on the total muscle mass engaged. Plasma adrenaline concentrations and muscle oxygenation were found to be dependent upon the working muscle mass and both may have affected the metabolic response during exercise.     

Effect of physical training on the responses of serum adrenocorticotropic hormone during prolonged exhausting exercise

Summary The purpose of this study was to investigate the effects of physical training on the responses of serum adrenocorticotropic hormone (ACTH) and cortisol concentration during low-intensity prolonged exercise. Five subjects who had fasted for 12 h cycled at the same absolute intensity that elicited 50% of pre-training maximal oxygen uptake ( O_2max), either until exhaustion or for up to 3 h, before and after 7 weeks of vigorous physical training [mean daily energy consumption during training exercise, 531 kcal (2230 kJ)]. In the pre-training test, serum ACTH and cortisol concentrations did not increase during the early part of the exercise. Increases in concentrations of both hormones occurred in all subjects when blood glucose concentration decreased during the later phase of the exercise. The mean values and SEM of serum ACTH and cortisol concentrations at the end of the exercise were 356 ng · l^–1, SEM 79 and 438 g · l^–1, SEM 36, respectively. After the physical training, O_2max of the subjects improved significantly from the mean value of 50.2 ml · kg^–1 · min^–1, SEM 2.5 to 57.3 ml · kg^–1 · min^–1, SEM 2.0 (P < 0.05). In the post-training test, exercise time to exhaustion was prolonged in three subjects. Comparing the pre- and post training values observed after the same length of time that the subjects had exercised in the pre-training test, the post-training values of serum ACTH (44 ng · l^–1, SEM 3) and cortisol (167 g · l^–1, SEM 30) concentration were less than the pre-training value (P < 0.05). However, after the subjects stopped exercising in the post-training test, the serum ACTH (214 ng · l^–1, SEM 49) and cortisol (275 g · l^–1, SEM 50) concentrations were not significantly different from those measured after the subjects stopped exercising in the pre-training test (P > 0.10). In conclusion, high-intensity physical training reduced the responses of both hormones during prolonged exercise, propbably because of a delayed decrease of blood glucose concentration after physical training, while the level of the blood glucose concentration which induces ACTH and cortisol secretion did not change.     

The hormonal responses to repetitive brief maximal exercise in humans

Summary The responses of nine men and nine women to brief repetitive maximal exercise have been studied. The exercise involved a 6-s sprint on a non-motorised treadmill repeated 10 times with 30 s recovery between each sprint. The total work done during the ten sprints was 37,693±3,956 J by the men and 26,555±4,589 J by the women (M > F,P<0.01). This difference in performance was not associated with higher blood lactate concentrations in the men (13.96± 1.70 mmol·^–1) than the women (13.09±3.04 mmol·l^–1). An 18-fold increase in plasma adrenaline (AD) occurred with the peak concentration observed after five sprints. The peak AD concentration in the men was larger than that seen in the women (9.2 +- 7.3 and 3.7 ± 2.4 nmol · l^–1 respectively,P<0.05). The maximum noradrenaline (NA) concentration occurred after ten sprints in the men (31.6±10.9 nmol·l^–1) and after five sprints in the women (27.4 ± 20.8 nmol · l^–1). Plasma cardiodilatin (CDN) and atrial natriuretic peptide (ANP) concentrations were elevated in response to the exercise. The peak ANP concentration occurred immediately postexercise and the response of the women (10.8 ± 4.5 pmol · l^–1 was greater than that of the men (5.1 ± 2.6 pmol · l^–1,P<0.05). The peak CDN concentrations were 163 ± 61 pmol · l^–1 for the women and 135 ± 61 pmol · l^–1 for the men. No increases in calcitonin gene related peptide (CGRP) were detected in response to the exercise. These results indicate differences between men and women in performance and hormonal responses. There was no evidence for a role of CGRP in the control of the cardiovascular system after brief intermittent maximal exercise.     

Effects of muscarinic blockade on the thermic effect of oral or intravenous carbohydrate

Summary Muscarinic blockade by atropine has been shown to decrease the thermic effect of a mixed meal, but not of intravenous glucose. To further delineate the mechanisms involved in the atropine-induced inhibition of thermogenesis after a meal, plasma substrate and hormone concentrations, energy expenditure (EE) and substrate oxidation rates were measured before and during a continuous glucose infusion (44.4 mol·kg^–1·min^–1) with or without atropine. After 2 h of glucose infusion, a 20-g oral fructose load was administered while the glucose infusion was continued. Plasma insulin concentrations attained a plateau at 596 (SEM 100) pmol·l^–1 after 120 min of glucose infusion and were not affected by muscarinic blockade; plasma glucose concentrations peaked at 13.3 (SEM 0.5) mmol·l^–1 at 90 min and decreased progressively thereafter; no difference was observed with or without atropine. Plasma free fatty acid and glucagon concentrations, with or without atropine, were both decreased to 201 (SEM 18) mol·l^–1 and 74 (SEM 4) ng·l^–1, respectively, after 2 h of glucose infusion, and were not further suppressed after oral fructose. Carbohydrate oxidation rates (CHO_ox) increased to 20.8 (SEM 1.4) mol·kg^–1·min^–1 and lipid oxidation rates (L_ox) decreased to 1.5 (SEM 0.3) mol·kg^–1·min^–1 between 90 and 120 min after the beginning of glucose infusion and were not affected by atropine. Glucose-induced thermogenesis was similar with [6.5% (SEM 1.4%) of basal EE] or without [6.0% (SEM 1.0%), NS) muscarinic blockade during the 30 min preceding fructose ingestion. During the second half-hour after fructose ingestion, atropine infusion inhibited markedly the stimulation of CHO_ox [+2.8 (SEM 1.0) mol·kg^–1·min^–1 vs +6.9 (SEM 1.0) mol·kg^–1·min^–1, saline, P<0.02] and the suppression of L_ox [–0.8 (SEM 0.2) mol·kg^–1·min^–1 vs –1.4 (SEM 0.2) mol·kg^–1·min^–1, saline, P<0.05]. Carbohydrate-induced thermogenesis during the second half-hour after fructose ingestion, increased to 13.0% (SEM 2.0%) without atropine and was suppressed to 7.7% (SEM 1.9%) (P< 0.05, vs saline) with atropine. It was concluded that muscarinic blockade suppressed the increase of thermogenesis observed after oral fructose, but not during intravenous glucose infusion and that this suppression occurred independently of alterations of plasma insulin concentrations.     

Lactate kinetics during passive and partially active recovery in endurance and sprint athletes

We investigated the effects of passive and partially active recovery on lactate removal after exhausting cycle ergometer exercise in endurance and sprint athletes. A group of 14 men, 7 endurance-trained (ET) and 7 sprint-trained (ST), performed two maximal incremental exercise tests followed by either passive recovery (20 min seated on cycle ergometer followed by 40 min more of seated rest) or partially active recovery [20 min of pedalling at 40% maximal oxygen uptake ( O_2max) followed by 40 min of seated rest]. Venous blood samples were drawn at 5 min and 1 min prior to exercise, at the end of exercise, and during recovery at 1, 2, 3, 4, 5, 6, 8, 10, 15, 20, 30, 40, 50, 60 min post-exercise. The time course of changes in lactate concentration during the recovery phases were fitted by a bi-exponential time function to assess the velocity constant of the slowly decreasing component (₂) expressing the rate of blood lactate removal. The results showed that at the end of maximal exercise and during the 1st min of recovery, ET showed higher blood lactate concentrations than ST. Furthermore, ET reached significantly higher maximal exercise intensities [5.1 (SEM 0.5) W · kg^–1 vs 4.0 (SEM 0.3) W · kg^–1,P < 0.05] and O_2max [68.4 (SEM 1.1) ml · kg^–1 · min^–1 vs 55.5 (SEM 5.1) ml · kg^–1 · min^–1,P < 0.01]. There was no significant difference between the two groups during passive recovery for ₂ During partially active recovery, ₂ was higher than during passive recovery for both groups (P < 0.001), but ET recovered faster and sooner than ST (P < 0.05). Compared to passive recovery, the ₂ measured during partially active recovery was increased threefold in ET and only 1.5-fold in ST. We concluded that partially active recovery potentiates the enhanced ability to remove blood lactate induced by endurance training.     

Immediate physiological responses of healthy volunteers to different types of music: cardiovascular,hormonal and mental changes

A group of 20 healthy volunteers [10 women, 10 men; median age 25 (20–33) years] were examined by means of pulsed wave Doppler echocardiography, blood sample analysis and psychological testing before and after listening to three different examples of music: a waltz by J. Strauss, a modern classic by H. W. Henze, and meditative music by R. Shankar. To assess small haemodynamic changes, mitral flow, which reflects left ventricular diastolic behaviour, was measured by Doppler ultrasound. Heart rate, arterial blood pressure and plasma concentrations of adrenocorticotropic hormone, cortisol, prolactin, adrenaline, noradrenaline, atrial natriuretic peptide (ANP) and tissue plasminogen activator (t-PA) were determined simultaneously. Transmitral flow profile is characterized by early E-wave and late atrial induced A-wave. Velocity-time integrals were measured and the atrial filling fraction was calculated. The mental state was measured by using a psychological score (Zerssen) with low values (minimum 0) for enthusiastic and high values (maximum 56) for depressive patterns. Music by J. Strauss resulted in an increase of atrial filling fraction (AFF; 29% vs 26%;P<0.05) and ANP (63 pg·ml^–1 vs 60 pg·ml^–1;P<0.05). The mental state was improved (Zerssen: 6.5 vs 11 points;P<0.05). After the music of H. W. Henze prolactin values were lowered (7.7 ng·ml^–1 vs 9.1 ng·ml^–1;P<0.01). The music of R. Shankar led to a decrease of cortisol concentrations (57 ng·ml^–1 vs 65 ng·ml^–1;P<0.001), noradrenaline concentrations (209 g·l^–1 vs 256 g·l^–1;P<0.01) andt-PAantigen concentrations (1.1 ng·ml^–1 vs 1.4 ng·ml^–1;P<0.05). Heart rate and blood pressure remained unchanged during the whole experiment. We concluded that different types of music induced changes of left ventricular diastolic function and plasma hormone concentrations. After rhythmic music (Strauss) AFF and ANP increased significantly, the mental state being improved. Meditative music (Shankar) lowered plasma cortisol, noradrenaline and t-PA concentrations; the observed increase of early left ventricular filling was not statistically significant. Prolactin concentrations decreased after modern music (Henze). Thus, it would seem to be possible to detect cardiovascular changes following different types of music by Doppler ultrasound and hormone analysis, meditative music having promising therapeutic implications in the treatment of conditions of stress.This paper contains data from J. Vollert's work for his doctoral degree.     

Influence of moderate cold exposure on blood lactate during incremental exercise

Summary This study examined the effect of exposure of the whole body to moderate cold on blood lactate produced during incremental exercise. Nine subjects were tested in a climatic chamber, the room temperature being controlled either at 30°C or at 10°C. The protocol consisted of exercise increasing in intensity in 35 W increments every 3 min until exhaustion. Oxygen consumption (VO₂) was measured during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for the measurement of blood glucose, free fatty acid (FFA), noradrenaline (NA) and adrenaline (A) concentrations and, during the last 15 s of each exercise intensity, for the determination of blood lactate concentration [la^–]_b. TheVO₂ was identical under both environments. At 10°C, as compared to 30°C, the lactate anaerobic threshold (Th_{an, la} ^–) occurred at an exercise intensity 15 W higher and [Th_{an, la} ^–]_b was lower for submaximal intensities above the Th_{an, la} ^– Regardless of ambient temperature, glycaemia, A and NA concentrations were higher at exhaustion while FFA was unchanged. At exhaustion the NA concentration was greater at 10°C [15.60 (SEM 3.15) nmol·l^–1] than at 30°C [8.64 (SEM 2.37) nmol·l^–1]. We concluded that exposure to moderate cold influences the blood lactate produced during incremental exercise. These results suggested that vasoconstriction was partly responsible for the lower [la^–]_b observed for submaximal high intensities during severe cold exposure.     

The interaction between short-term exercise training and a diuretic-induced hypovolemic stimulus

Nine healthy untrained males [mean (SEM) age, 20.2 (1) years; peak oxygen uptake (VO_2max, 48.2 (2) ml · kg^–1 · min^–1] took part in a study to examine whether short-term exercise training (cycle exercise 2 h · day^–1 for 3 days at 60% ), which normally results in an expansion of plasma volume (PV), can counteract a diuretic-induced hypovolemic stimulus (100 mg triamterene + 50 mg hydrochlorothiazide day^–1 for 5 days concurrent with exercise training) and restore PV to control levels. Resting and exercise responses (90 min, 60% ) in the diuretic plus exercise training condition (D + E) were compared to a control (C) and a diuretic (D) condition in which no exercise was performed. Following the short-term training, PV was still decreased (P < 0.05) below C by –8.3 (3)% in D + E and was similar (P > 0.05) to the reduction in D [–12.4 (2)%]. The reduced PV in response to the diuretic was associated with similar (P > 0.05) elevations in resting aldosterone (ALDO) and norepinephrine (NOREPI) levels (ng · 100 ml^–1) in D [101 (12), 61 (4)] and D + E [85 (16), 60 (10)] above (P < 0.05) C [22 (5), 37 (4)]. During exercise, ALDO levels were increased (P < 0.05) by 66 (5) and 70 (10) ng · 100 ml^–1 in D and D + E, respectively, and the increase was greater (P < 0.05) than C [44 (8) ng · 100 ml^–1]. The rise in NOREPI during exercise was lower (P < 0.05) in D + E [164 (44) ng · 100 ml^–1] than in D [244 (24) ng · 100 ml^–1] with levels similar to C [176 (25) ng · 100 ml^–1]. Thus, the ALDO response to the diuretic was heightened at rest and during exercise but was not additionally affected by the short-term training session. Results suggest that 3 days of exercise training are unable to counteract the hypovolemic effects of a diuretic and restore PV to control levels despite chronic elevations in NOREPI and ALDO.     

Effect of anaerobic and aerobic exercise of equal duration and work expenditure on plasma growth hormone levels

Summary Growth hormone (GH) and lactic acid levels were measured in five normal males before, during and after two different types of exercise of nearly equal total duration and work expenditure. Exercise I (aerobic) consisted of continuous cycling at 100 W for 20 min. Exercise II (anaerobic) was intermittent cycling for one minute at 285 W followed by two minutes of rest, this cycle being repeated seven times. Significant differences (P<0.01) were observed in lactic acid levels at the end of exercise protocols (20 min) between the aerobic (I) and anaerobic (II) exercises (1.96±0.33 mM·l^–1 vs 9.22±0.41 mM·l^–1, respectively). GH levels were higher in anaerobic exercise (II) than in aerobic (I) at the end of the exercise (20 min) (2.65±0.95 g·l^–1 vs 0.8±0.4 g·l^–1;P<0.10) and into the recovery period (30 min) (7.25±6.20 g·l^–1 vs 2.5±2.9 g·l^–1;P<0.05, respectively).     

Exercise and the oxidation and storage of glucose,maize-syrup solids and sucrose determined from breath13CO2

In order to determine which of maize syrup solids, glucose and sucrose were more readily oxidised during exercise and least readily oxidised afterwards, the rates of oxidation of three almost identical isoenergetic solutions of carbohydrates (330 ml of 18.5% w/v solutions of glucose, maize syrup solids and sucrose, 989–1050 kJ total energy) naturally enriched with¹³C were examined at rest and during and after 1 h uphill walking at 75% maximum oxygen uptake ( ) in nine subjects [mean (SEM) , 45.4 (0.9) ml·kg^–1-min^–1]. Rates of production of expired¹³CO₂ were used to estimate rates of oxidation of each exogenous substrate. Energy expenditure and the contributions from total carbohydrate and fat oxidation were calculated from whole-body gas exchange. At rest, aize syrup solids were oxidised less than sucrose during the 1st h [glucose 2.7 (0.2) g · h^–1, maize syrup solids 1.9 (0.3) g · h^–1, sucrose 3.7 (0.2) g · h^–1; maize syrup solids vs sucroseP < 0.01], but this difference disappeared after a further 3 h at rest [glucose 8.3 (0.5) g · h^–1, maize syrup solids 7.7 (0.5) g · h^–1, sucrose 8.1 (0.4) g · h-1]. During exercise, all the carbohydrates were oxidised to the same extent [glucose 23.0 (2.8) g · h^–1, maize syrup solids 23.9 (3.4) g · h^–1, sucrose 27.5 (2.6) g · h^–1) but during 4 h of recovery after exercise, maize syrup solids were oxidised least [glucose 4.6 (0.1) g · h^–1, maize syrup solids 3.7 (0.1) g · h^–1, sucrose 6.4 (0.1) g · h^–1;P < 0.05] suggesting that it may be stored to a greater extent. The results suggest that 18.5% glucose, maize syrup solids and sucrose solutions were equally well oxidised during exercise. During recovery from exercise maize syrup solids were oxidised less than glucose, which in turn was oxidised less than sucrose.     

Energy expenditure and cardiorespiratory responses at the transition between walking and running

We investigated whether the spontaneous transition between walking and running during moving with increasing speed corresponds to the speed at which walking becomes less economical than running. Seven active male subjects [mean age, 23.7 (SEM 0.7) years, mean maximal oxygen uptake ( ), 57.5 (SEM 3.3) ml·kg ^–1·min ^–1, mean ventilatory threshold (VTh), 37.5 (SEM 3) ml·kg ^–1 ·min ^–1] participated in this study. Each subject performed four exercise tests separated by 1-week intervals: test 1, and VTh were determined; test 2, the speed at which the transition between walking and running spontaneously occurs (ST) during increasing speed (increases of 0.5 km·h ^–1 every 4 min from 5 km·h ^–1) was determined; test 3, the subjects were constrained to walk for 4 min at ST, at ST ± 0.5 km·h ^–1 and at ST ± 1 km·h ^–1; and test 4, the subjects were constrained to run for 4 min at ST, at ST±0.5 km·-h ^–1 and at ST±1 km·h ^–1. During exercise, oxygen uptake ( ), heart rate (HR), ventilation ( ), ventilatory equivalents for oxygen and carbon dioxide (% MathType!MTEF!2!1!+-% feaafiart1ev1aaatCvAUfeBSjuyZL2yd9gzLbvyNv2CaerbuLwBLn% hiov2DGi1BTfMBaeXatLxBI9gBaerbd9wDYLwzYbItLDharqqtubsr% 4rNCHbGeaGqiVu0Je9sqqrpepC0xbbL8F4rqqrFfpeea0xe9Lq-Jc9% vqaqpepm0xbba9pwe9Q8fs0-yqaqpepae9pg0FirpepeKkFr0xfr-x% fr-xb9adbaqaaeGaciGaaiaabeqaamaabaabaaGcbaGabmOvayaaca% WaaSbaaSqaaiaabweaaeqaaOGaai4laiqadAfagaGaamaaBaaaleaa% caqGYaaabeaakiaacYcacaqGGaGaaeiiaiqadAfagaGaamaaBaaale% aacaqGfbaabeaakiaac+caceWGwbGbaiaacaqGdbGaae4tamaaBaaa% leaacaaIYaaabeaaaaa!4240!\[\dot V_{\text{E}} /\dot V_{\text{2}} ,{\text{ }}\dot V_{\text{E}} /\dot V{\text{CO}}_2 \]), respiratory exchange ratio (R), stride length (SL), and stride frequency (SF) were measured. The results showed that: ST occurred at 2.16 (SEM 0.04) m·s ^–1; , HR and speed at ST were significantly lower than the values measured at VTh (P< 0.001, P< 0.001 and P< 0.05, respectively); changed significantly with speed (P< 0.001) but was greater during running than walking below ST (ST minus 1 km·h ^–1, P< 0.001; ST minus 0.5 km·h ^–1, P< 0.05) with the converse above ST (ST.plus 1 km·h ^–1, P<0.05), whereas at ST the values of were very close [23.9 (SEM 1.1) vs 23.7 (SEM 0.8) ml·kg ^–1 · min ^–1 not significant, respectively, for walking and running]; SL was significantly greater during walking than running (P<0.001) and SF lower (P<0.001); and HR and were significantly greater during running than walking below ST (ST minus 1 km·h ^–1, P<0.01; ST minus 0.5 km·h ^–1, P{<0.05) with the converse above ST (ST plus 1 km·h ^–1, P·< 0.05), whereas no difference appeared for and R between the two types of locomotion. We concluded from this study that ST corresponded to the speed at which the energy expenditure of running became lower than the energy expenditure of walking but that the mechanism of the link needed further investigation.     

Capillary-venous differences of free plasma catecholamines at rest and during graded exercise

Summary Levels of free plasma catecholamines were simultaneously determined in 10 cyclists using capillary blood from one ear lobe and venous blood from one cubital vein. Catecholamine concentrations were higher in the ear lobe blood than in the venous blood at rest and during graded exercise. Average differences amounted to 1.7 nmol · l^–1 (dopamine), 2.1 nmol · l^–1 (noradrenaline) and 1.9 nmol · l^–1 (adrenaline) at rest and increased only to 8.8 nmol · l^–1 for noradrenaline during exercise. We assume that higher concentrations of dopamine and adrenaline in the capillary blood point to a significant neuronal release of these catecholamines, similar to noradrenaline. Catecholamine concentrations in capillary blood may better reflect sympathetic drive and delivery of catecholamines to the circulation than the concentrations in venous blood.Supported by Bundesinstitut für Sportwissenschaften, Köln-Lövenich, FRG     

Plasma testosterone and catecholamine responses to physical exercise of different intensities in men

Summary Plasma testosterone, noradrenaline, and adrenaline concentrations during three bicycle ergometer tests of the same total work output (2160 J·kg^–1) but different intensity and duration were measured in healthy male subjects. Tests A and B consisted of three consecutive exercise bouts, lasting 6 min each, of either increasing (1.5, 2.0, 2.5 W·kg^–1) or constant (2.0, 2.0, 2.0 W·kg^–1) work loads, respectively. In test C the subjects performed two exercise bouts each lasting 4.5 min, with work loads of 4.0 W·kg^–1. All the exercise bouts were separated by 1-min periods of rest.Exercise B of constant low intensity resulted only in a small increase in plasma noradrenaline concentration. Exercise A of graded intensity caused an increase in both catecholamine levels, whereas, during the most intensive exercise C, significant elevations in plasma noradrenaline, adrenaline and testosterone concentrations occurred. A significant positive correlation was obtained between the mean value of plasma testosterone and that of adrenaline as well as noradrenaline during exercise.It is concluded that both plasma testosterone and catecholamine responses to physical effort depend more on work intensity than on work duration or total work output.This work was performed within the Scientific Exchange Programme between the Institute of Experimental Endocrinology, Slovak Academy of Sciences in Bratislava and Medical Research Centre, Polish Academy of Sciences, Warsaw/Project 10.4/     

Pathways of phosphate transport in chick jejunum

The effect of vitamin D₃ on intestinal phosphate (P_i) absorption was studied in everted sacs prepared from jejunum of either vitamin D-deficient (–D) or vitamin D-replete (+D) chicks. Vitamin D₃ stimulates the maximal velocity (V _max) of a mucosal active P_i transport mechanism from 125 to 314 nmol·min^–1·g^–1 tissue.K _m of this process remains virtually unchanged (–D: 0.15 mmol·l^–1; + D: 0.18 mmol·l^–1).Active P_i entry into the epithelium depends on extracellular Na⁺. Reduction of buffer Na⁺ reducesV _max in the + D group to 182 nmol·min^–1·g^–1 tissue but has no significant effect in the –D animals (V _max=105 nmol·min^–1·g^–1 tissue). In this group, the predominant effect of Na⁺ substitution is a shift ofK _m to 1.13 mmol·l^–1, whileK _m in the +D group is changed only to 0.53 mmol·l^–1.Transeptithelial P_i transport in the + D group involves the mucosal phosphate pump and hence an intracellular pathway, proceeding at a rate of 48 nmol·min^–1·g^–1 tissue. This is in contrast to –D P_i transfer (8 nmol·l^–1·g^–1 tissue) which is by a diffusional, Na⁺-insensitive, and presumably paracellular pathway.Transepithelial calcium transport (–D: 3.3 nmol·min^–1·g^–1; + D: 7.6 nmol·min^–1·g^–1 tissue) does not require the presence of extracellular Na⁺ and apparently involves pathways different from those of the P_i absorptive system.Presented in part at the Annual Meeting of the Austrian Biochemical Society, Salzburg, September 1978     

Catecholamines,lymphocyte subsets,and cyclic adenosine monophosphate production in mononuclear cells and CD4+ cells in response to submaximal resistance exercise

We examined the effect of 30 min of submaximal resistance exercise on free and sulphoconjugated plasma catecholamine concentrations determined by high performance (-pressure) liquid chromatography separation, the distribution of circulating lymphocytes quantified by flow cytometry, and isoproterenol induced cyclic adenosine monophosphate (cAMP) production in mononuclear cells (MNL) and CD4⁺ cells. Venous blood samples were taken before, immediately after and 45 min after exercise. Resistance exercise increased free plasma adrenaline (A) and noradrenaline (NA) concentrations, whereas sulphoconjugated catecholamine concentrations remained unchanged. Exercise induced leucocytosis and lymphocytosis was predominantly manifested by an increase in the number of total lymphocytes, monocytes, CD3⁺, CD8⁺ cells and CD3^– CD16/CD56^– cells. Redistribution resulted in a decrease in the CD4^–: CD8⁺ ratio. The total number and distribution of lymphocytes returned to baseline after 45-min rest. An exercise-induced increase in the number of CD3^– CD16/CD56⁺ cells was significantly correlated with the increase in plasma NA (r = 0.66;P = 0.035), indicating a NA dependent process of redistribution. The cAMP-production in MNL was significantly elevated after resistance exercise, when cells were stimulated with 1 mol·1^–1 isoproterenol [pre-exercise 16.5 (SD 3.3); postexercise 21.6 (SD 9.8); 45 min postexercise 10.7 (SD 2.8)]. The cAMP production in CD4⁺ cells was not affected by exercise. Therefore, it is discussed whether redistribution is responsible for the exercise induced increase in cAMP production in MNL.     

Glucoregulation and hormonal changes during prolonged exercise in boys and girls

A group of 17 children, 8.5–11 years old, performed a 60-min cycle exercise at 60% of maximal oxygen uptake (VO_2max) 2 h after a standardized breakfast. They were 10 young boys (pubertal stage =1) and 7 young girls (pubertal stage 2) of similarVO_2max (respective values were 48.5 ml min^–1 kg^–1, SEM 1.8; 42.1 ml min^–1 kg^–1, SEM 2.4). Blood samples of 5 ml were withdrawn by heparinized catheter, the subjects being in a supine position, 30 min before the test, then after 0, 15, 30 and 60 min of exercise and following 30 min recovery. Haematocrit was immediately measured. Thereafter plasma was analysed for glucose, non-esterified fatty acid, glycerol, catecholamine (noradrenaline, adrenaline), insulin and glucagon concentrations. This study showed two main results. First, the onset of exercise induced a significant glucose decrease (of about 11,4%) in all the children. Secondly, both the glycaemic and the hormonal responses were obviously different according to the sex. In boys only, the initial glucose drop was significantly correlated to the pre-exercise insulin values. Whatever the time, the glycaemic levels and the catecholamine responses were lower in girls than in boys, whereas the insulin values remained higher. However, none of these two hormonal parameters seemed to be really responsible for the lower glucose values in girls. On the one hand, the great individual variability of noradrenaline and adrenaline and differences in their relative intensity at the end of the exercise between boys and girls might contribute to the lower catecholamine levels in girls. On the other hand, the lack of a significant relationship in girls between the glucose decrease after exercise and the pre-exercise insulin values might be explained by a relative insulin insensitivity concomitant with the earlier growth spurt in girls, as demonstrated in subjects at rest by other authors. Finally the mechanisms of all these gender differences remain to be clarified and might be accounted for by a different maturation level in boys and girls.     

Thermogenic effect of adrenaline: interaction with insulin

Summary The contribution of insulin (3.6 pmol sd kg body mass^–1·min^–1 to adrenaline-induced (0.164 nmol · kg fat free mass^–1·min^–1) thermogenesis was studied in ten postabsorptive healthy volunteers using two sequential protocols. Variables considered were oxygen consumption as well as carbon dioxide production, heart rate, blood pressure, plasma concentrations of glucose, insulin, glycerol, free fatty acids,-HO-butyrate and lactate. Adrenaline increased plasma concentrations of glucose, glycerol, free fatty acids, and-HO-butyrate, and heart rate and metabolic rate during normo-insulinaemia [61.3 (SEM 6.6) pmol·^–1]. Similar effects were observed during hyperinsulinaemia [167.9 (SEM 18.7) pmol·^–1], but the effect of adrenaline on oxygen consumption was reduced. On average, metabolic rate increased by 12.9% during normo-insulinaemia and by 8.9% during hyperinsulinaemia. We concluded that relative hyperinsulinaemia resulted in decreased adrenaline-induced thermogenesis and therefore increased whole body anabolism.