Effects of Growth hormone on rat skeletal muscle after hindlimb suspension

To examine the effects of growth hormone (GH) on the preferential atrophy of the soleus muscle (SOL) occurring after hindlimb suspension (HS), two groups of male rats received daily injections of 2 IU · kg ^–1 body mass of recombinant human growth hormone (rhGH). Rats were either suspended by the tail for 21 days (HS-GH, n = 5) or nonsuspended (CGH, n=5). The effects of rhGH treatment on SOL and extensor digitorum longus muscles (EDL) were compared in two groups of animals receiving daily injections of saline, either suspended by the tail (HS-SA, n = 5) or nonsuspended (C-SA, n = 5). The results showed that the SOL hypertrophy in response to rhGH administration was mostly observed in C rats (+33%, P<0.01). This increase in muscle mass was correlated with a concomitant increase in the size of type I fibres (+21%, P<0.05). Although SOL mass decreased during HS in rhGH treated animals (–44%, P<0.001), the mean normalized mass of this muscle did not significantly differ between C-SA and HS-GH groups. A statistically significant increase in the absolute mass of EDL occurred with rhGH treatment in CGH (+12%, P<0.05). The HS-induced decrease in the percentage distribution of type I fibres in SOL was unaffected by the rhGH treatment. In addition, a decrease in the citrate synthase activity in the whole SOL was observed in the two groups of tail-suspended rats (–31%, P<0.05; –21%, P<0.05 in SA and GH animals, respectively). The activity of 3-hydroxyacyl coenzyme A dehydrogenase was enhanced by the rhGH treatment (P<0.05) with similar magnitude in both C (+25%) and HS rats (+24%). Therefore, GH prevented only slightly the atrophy of SOL, occurring after 21 days of HS. The effects of rhGH treatment appeared most effective in C rats, suggesting that HS impaired the growth-promoting effects of this hormone on skeletal muscle.     

Influence of age on the immediate cardiovascular response to orthostatic manoeuvre

The dynamics of cardiovascular changes following standing up from the supine position were investigated in 41 healthy men aged 20–59 years, classified into three groups: (22–26 years, n = 14), (33–49 years, n = 13) and (51–59 years, n = 14). The protocols consisted of a sequence repeated twice lying down-standing up-lying down. The initial period supine was for 20 min and then the subjects remained in each position for 8 min. Stroke volume, cardiac output (CO), ejection time (ET), pre-ejection period and heart rate (HR) were continuously calculated using automated impedance cardiography and electrocardiography. Blood pressure was measured by the auscultation method. The patterns of HR and haemodynamic orthostatic response were shown to be highly reproducible. Most of the indices characterizing the amplitude and rate of cardiovascular changes following standing up showed a tendency towards attenuation with age. However, only the indices of HR, CO and ET responses correlated significantly with age. The strongest relationships with age were observed in the sudden increase in HR (n = – 0.61, P < 0.01), the transient increase in CO (r = – 0.45, P < 0.001), and the rapid decrease in ET (r = 0.42, P < 0.01) after standing up. A few indices of HR and haemodynamic response also showed weak correlations with the subjects' heights and body masses.     

Extracellular fluid volume and central circulation after long lasting exercise and dehydration in conscious dogs

Summary Two aspects of the recovery period after endurance exercise were investigated: a) the fluid distribution between the intra- and extravascular parts of the extracellular fluid volume (ECFV) induced by exercise dehydration, b) the cardiovascular response pattern [blood pressure (BP), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), and central venous pressure (CVP)] to the heat load which results from the preceding exercise.Seven conscious dogs performed endurance exercise in a cool environment (16°C) on a horizontal treadmill till 4% of the body weight was lost. It was found that about 70% of the total fluid loss of the body came from intracellular water. During exercise sodium and chloride concentrations rose by 6 mMol and 7 mMol respectively (P<0.005) and remained elevated throughout the early recovery period indicating a fluid loss of about 100–200 ml out of the ECFV. Direct measurements of the ECFV as sulfate space confirmed these values. Since the plasma volume remained unchanged, this fluid loss was carried totally by the interstitial fluid volume.Immediately after exercise body temperature was elevated by 1.5°C and returned towards control within 90 min. Cardiac output was above control level for 2 h after the end of exercise, at first due to an increased HR and thereafter to an elevated stroke volume (SV) (P<0.02). CVP and TPR were below control levels for at least 2 h (P<0.01). A linear correlation was found between CVP and TPR.A close correlation existed between the body temperature and the cardiovascular parameters. It can be concluded that even long after exercise the cardiovascular system has to serve thermoregulatory needs.This study was supported by the Bundesinstitut für Sportwissenschaften Köln andthe Deutsche Forschungsgemeinschaft     

Naloxone-provoked vaso-vagal response to head-up tilt in men

A double-blind paired protocol was used to evaluate, in eight male volunteers, the effects of the endogenous opiate antagonist naloxone (NAL; 0.05 mg· kg^–1) on cardiovascular responses to 50° head-up tilt-induced central hypovolaemia. Progressive central hypovolaemia was characterized by a phase of normotensive-tachycardia followed by an episode of hypotensive-bradycardia. The NAL shortened the former from 20 (8–40) to 5 (3–10) min (median and range; (P < 0.02). Control head-up tilt increased the means of thoracic electrical impedance [from 35.8 (SEM 2.1) to 40.0 (SEM 1.8) ; P < 0.01 of heart rate [HR; from 67 (SEM 5) to 96 (SEM 8) beats · min^–1, P < 0.02], of total peripheral resistance [TPR; from 25.5 (SEM 3.2) to 50.4 (SEM 10.5)mmHg min 1^–1,P < 0.05] and of mean arterial pressure [MAP; from 96 (SEM 2) to 101 (SEM 2)mmHg, P < 0.02]. Decreases were observed in stroke volume [from 65 (SEM 12) to 38 (SEM 9) ml, P < 0.01], in cardiac output [from 3.7 (SEM 0.7) to 2.5 (SEM 0.5) 1 · mint, P < 0.01], in pulse pressure [from 55 (SEM 4) to 37 (SEM 3)mmHg, P < 0.01] and in central venous oxygen saturation [from 73 (SEM 2) to 59 (SEM 4)%, P < 0.01]. During NAL, mean HR increased from 70 (SEM 3); n.s. compared to control) to only 86 (SEM 9) beats · min^–1 (P < 0.02 compared to control) and MAP remained stable. The episode of hypotensive-bradycardia appeared as mean control HR decreased to 77 (SEM 7)beats · min^–1, TPR to 31.4(SEM 7.7)mmHg · min · 1^–1 and MAP to 60 (SEM 5)mmHg (P < 0.01), and the volunteers were tilted supine. Cardiovascular effects of naloxone on central hypovolaemia included a reduced elevation of HR and blood pressures and provocation of the episode of hypotensive-bradycardia.     

Effect of sex and age on brain monoamines and spatial learning in rats

The concentrations of noradrenaline (NA), dopamine (DA), serotonin (5-HT), and their metabolites were measured in the prefrontal cortex, caudate-putamen, and hippocampus in young (3 months) and aged (27–31 months) Wistar rats of both sexes. Age-related changes were found in prefrontal NA and HVA/DA ratio, striatal DA and DOPAC/DA ratio, and striatal and hippocampal 5-HT and 5-HIAA/5-HT ratio. Age and sex dependent changes were found in striatal DA and DOPAC/DA ratio, and hippocampal MHPG-SO₄/NA ratio. The aged rats were tested in spatial discrimination and reversal tasks in a T maze. The effects of α₂-agonist medetomidine (3 μg/kg) on the task performance were assessed in relation to individual variation in monoamine metabolism. Medetomidine impaired spatial discrimination learning of the aged rats by interacting with the hippocampal 5-HT turnover. Medetomidine improved reversal learning through an interaction with the striatal DA turnover and reduced the number of perseverative errors after reversal, mainly due to its interaction with the prefrontal NA turnover. It is concluded that the memory enhancing effect of drugs acting through the brain monoamine systems is highly dependent on the stage of degeneration of these systems that show considerable individual variation in aged animals.     

Physical conditioning in rats influences the central and peripheral catecholamine responses to sustained exercise

We have investigated the effect of treadmill running in rats (25m · min^–1 using a 3 % gradient; for 1 h or 2 h) on the cortical extracellular concentrations of noradrenaline (NA) and its main metabolites — 3,4-dihydroxyphenylglycol and 3-methoxy-4-hydroxyphenylglycol-and the plasma adrenaline (A) and NA concentrations in relation to prior physical conditioning (1 or 2-h running -day-¹ for 12 days). Cortical microdialysates and peripheral blood were collected during 1-h resting, 1-h or 2-h running and for 1 h after exercise. Catecholamines and their metabolites were quantitated using high performance liquid chromatography with electrochemical detection. Treadmill running stimulated concomitantly peripheral catecholamine secretion and central noradrenergic activity, i.e. NA turnover and release. The effect extended into the recovery period even more as the duration of the run increased. Prior physical conditioning greatly influenced the central and peripheral catecholamine responses: the 1-h trained rats experienced the 2-h run as a stressful new event eliciting great long-lasting catecholamine responses, whereas the 2-h trained rats exhibited a progressive sustained catecholamine increase with an earlier onset of the central NA release. The data are discussed in relation to the psychological and intellectual effects of exercise and physical fitness in humans. In addition, the positive correlation found between the central noradrenergic activation and peripheral A secretion confirmed and extended our previous observations in exercising men and gave support to the hypothesis that the elevation of circulating A can be a relevant factor mediating — directly or indirectly — the exercise-induced central effects.     

Autonomic mechanisms underpinning the stress response in borderline hypertensive rats

This study investigates blood pressure (BP) and heart rate (HR) short-term variability and spontaneous baroreflex functioning in adult borderline hypertensive rats and normotensive control animals kept on normal-salt diet. Arterial pulse pressure was recorded by radio telemetry. Systolic BP, diastolic BP and HR variabilities and baroreflex were assessed by spectral analysis and the sequence method, respectively. In all experimental conditions (baseline and stress), borderline hypertensive rats exhibited higher BP, increased baroreflex sensitivity and resetting, relative to control animals. Acute shaker stress (single exposure to 200 cycles min-1 shaking platform) increased BP in both strains, while chronic shaker stress (3-day exposure to shaking platform) increased systolic BP in borderline hypertensive rats alone. Low- and high-frequency HR variability increased only in control animals in response to acute and chronic shaker (single exposure to restrainer) stress. Acute restraint stress increased BP, HR, low- and high-frequency variability of BP and HR in both strains to a greater extent than acute shaker stress. Only normotensive rats exhibited a reduced ratio of low- to high-frequency HR variability, pointing to domination of vagal cardiac control. In borderline hypertensive rats, but not in control animals, chronic restraint stress (9-day exposure to restrainer) increased low- and high-frequency BP and HR variability and their ratio, indicating a shift towards sympathetic cardiovascular control. It is concluded that maintenance of BP in borderline hypertensive rats in basal conditions and during stress is associated with enhanced baroreflex sensitivity and resetting. Imbalance in sympathovagal control was evident only during exposure of borderline hypertensive rats to stressors.     

Cardiac drift during prolonged exercise with echocardiographic evidence of reduced diastolic function of the heart

This study examined whether, in 16 male subjects, a continuous increase in heart rate (HR) during 4 h of ergometry cycling relates to cardiac fatigue or cardiomyocyte damage. Serum cardiac troponin T (cTnT) was determined and echocardiographic assessment was carried out prior to and after 2 h of exercise, within 15 min of completing exercise and after 24 h. Left ventricular contractile function (end-systolic blood pressure–volume relationship [SBP/ESV]) and diastolic filling (ratio of early to late peak left ventricular filling velocities [E:A]) were calculated. During exercise HR was 132±5 beats min^–1 after 2 h and increased to 141±5 beats min^–1 (mean ± SD; P<0.05), but there was no evidence of altered LV contractile function (SBP/ESV 39.0±5.1 mmHg cm^–1 to 36.5±5.2 mmHg cm^–1 and SBP/ESV was not correlated to maximal oxygen uptake (r²=0.363). In contrast, E:A decreased (1.82±0.32 to 1.48±0.30; P<0.05) and returned towards baseline after 24 h (1.78±0.28), and individual changes were correlated to maximal oxygen uptake (r²=0.61; P<0.05). Low levels of cTnT were detected in two subjects after 4 h of exercise that had normalised by 24 h of recovery. During prolonged exercise cardiovascular drift occurred with echocardiographic signs of a reduced diastolic function of the heart, especially in those subjects with a high maximal oxygen uptake.     

Arterial diameter during central volume depletion in humans

The luminal diameter of the radial artery was followed by high frequency ultrasound during 50° head-up tilt-induced central volume depletion in ten healthy subjects of whom six were tilted twice and pretreated with the serotonin receptor antagonist methysergide or placebo following a double-blind randomized design. Eight subjects without active treatment experienced presyncopal symptoms after 16–45 (mean 32 min). Central volume depletion was indicated by an increase in mean thoracic electrical impedance [from 31.5 (SEM 1.6) to 33.4 (SEM 1.7) P < 0.05]. Cardiac output decreased [from 4.1 (SEM 0.3) to 2.2 (SEM 0.3) l · min^–1] and heart rate [HR, from 64 (SEM 3) to 100 (SEM 7) beats · min^–1], mean arterial pressure {MAP, from 77 (SEM 4) to 89 (SEM 2) mmHg [10.3 (SEM 0.53 to 11.9 (SEM 0.27) kPa]} and total peripheral resistance {TPR, from 19 (SEM 2) to 34 (SEM 4) mmHg · min · l^–] [2.5 (SEM 0.27) to 4.5 (SEM 0.53) kPa · min^–1]} increased; but with the appearance of presyncopal symptoms, HR, MAP and TPR were reduced to 65 (SEM 8) beats · min^–1, 46 (SEM 4) mmHg [6.1(SEM 0.53) kPa] and 18 (SEM 3) mmHg · min · l^–1 [2.4 (SEM 0.4) kPa · min^–1 · l^–], respectively (P < 0.05). Vascular resistance was reflected in the arterial diameter which decreased from 2.42 (SEM 0.17) to 2.27 (SEM 0.14) mm during head-up tilt and increased to 2.71 (SEM 0.14) mm with the appearance of presyncopal symptoms (P < 0.05). Methysergide reduced the resting radial (15 ± 2%) and temporal artery diameters (10 ± 3%) (P < 0.05); however, it affected neither tilt-tolerance nor the central cardiovascular response to tilt. The results suggested a serotonergic influence on arterial tone at rest, and demonstrated that vessels as large as the radial artery participated in vascular control during central volume depletion independent of such a serotonergic influence.     

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.     

Effect of moderate exercise on rat T-cells

Summary The aim of this study was a detailed examination of the effects of moderate exercise on T-cells in adult male Wistar rats. The T-cell populations were compared in sedentary rats (C, n = 5) and in rats trained for 4 weeks on a treadmill (30–60 min·day^–1, 6 days·week^–1, 20–30 m·min^–1) and sacrificed at rest (Trest, n=5). In the T-rest rats, there were higher percentages of CD4+CD8–, CD4– CD8 + and CD4 – CD8 –thymocytes (P<0.05, P<0.05 and P<0.01 respectively) and of CD4–CD8 + splenocytes (P< 0.01), and a lower percentage of CD4–CD8+ cells in the lymph nodes (P<0.01). Compared with T-rest or C rats, trained rats (n = 5) or untrained rats (n = 5) sacrificed immediately after a running session (60 min, 30 m·min^–1) had a higher percentage of mononucleated cells CD4 + CD8 -in the blood (P<0.05 and P<0.01). Lastly, compared with C rats, rats (n=5) sacrificed immediately after their 5th day of training (30–60 min·day^–1) presented a higher total splenocyte population (P<0.05) and greater in vitro production of T-cell growth factor (interleukin 2 + interleucin 4) by splenocytes in response to a mitogen (P<0.01). These results would indicate that moderate endurance training modifies the cellular composition of lymphoid organs, without impairing the in vitro functions of T-cells.     

Continuous measurement of blood pressure, heart rate and left ventricular performance during and after isometric exercise in head-out water immersion

Experiments were performed to determine the changes in blood pressure (BP), heart rate (HR) and left ventricular function during and after isometric knee extension during thermoneutral (35°C) head-out water immersion (HWI) or in air. Seven healthy male subjects mean age 24 (SD 3) years kept their knees extended (60% maximal voluntary extension) until they reached exhaustion. The mean BP at rest was 80 (SD 10) and 78 (SD 8) mmHg [10.7 (SD 1.33) and 10.4 (SD 1.07) kPa] in air and during HWI, respectively, (NS). They increased progressively (P < 0.01) during contraction and reached maximal values of 148 (SD 22) and 143 (SD 26) mmHg [19.7 (SD 2.93) and 19.1 (SD 3.47) kPa] in air and in HWI, respectively, (NS). The mean HR at rest was 74 (SD 8) and 70 (SD 11) beats·min^–1 in air and in HWI, respectively, (NS). They also increased progressively (P < 0.01) and reached 126 (SD 14) and 118 (SD 17) beats·min^–1 in air and in HWI, respectively, (NS). The changes in BP and HR during contraction in HWI tended to be smaller than those in air (NS). Left ventricular end diastolic diameters (dd) at rest in HWI were greater than those in air and were maintained at higher values during and after isometric contraction. In contrast, dd decreased during isometric contraction in air (P < 0.01). The change of left ventricular systolic diameters (d _s) in HWI was no different to those in air. From these findings, isometric exercise in thermoneutral HWI would seem to be characterized by a greater d _d than in air and this could be useful for patients with deconditioning effects such as orthostatic hypotension.     

Antagonistic effect of naloxone on the hypertensive response of intraventricularly administered histamine

Intracerebroventricular (i.c.v.) injections of histamine (HA) to Vetbutal-anaesthetized rats elicited a biphasic pressor response: a fall of blood pressure (BP) in the first minute, followed by a rise in BP. The heart rate (HR) response was also biphasic: bradycardia in the first minute, followed by tachycardia. The H₁-receptor agonist 2-pyridylethylamine (PEA) increased the fall in BP in the first minute in comparison with the HA group, and then elicited a rise in BP that was, however, much lower than that produced by HA. Throughout the experiment PEA produced essentially only a bradycardia. The H₂-receptor agonist dimaprit elicited a single-phase pressor response, i.e. a rise in BP and did not elicit tachycardia. Intraventricular pretreatment of rats with naloxone greatly reduced the initial response (phase 1) in the first minute in HA groups by 77–83% and PEA groups by 83–100%. Naloxone given in small doses also reduced the fall in HR by 71–100% in those groups. The experimental results permit a conclusion that the phase 1 response, i.e. the fall in BP, results from excitation of H₁-receptors. Thus we may propose that H₁-receptors are involved in the action of naloxone. Naloxone in a dose of 0.1 g inhibited the hypertensive responses of HA after 25–30 min. The reduction reached 71%. Naloxone reduced the small rise in BP induced by PEA (10 g) but totally blocked the rise in BP induced by dimaprit (50 g). This blockade indicates that the central opioid system may transmit the total stimulating response (rise in BP) of H₂ receptors induced by dimaprit. Participation of central opioid receptors in HA-stimulated responses has already been demonstrated in corticosterone secretion [1].The study was supported by the Polish Academy of Sciences, grant No. 06.03.     

Effects of different strength training regimes on moment and power generation during dynamic knee extensions

This study examined the effect of different training regimes on moment and power generation during maximal knee extensions at low to very high extension velocities (0–1000°·s^–1 individual range). A group of 24 soccer players performed 12 weeks of progressively adjusted strength training of the knee extensors at either high resistance (HR,n=7), low resistance (LR,n=6), loaded kicking movements (FU,n=6), while one group served as controls (n=5). Moment and power generation of the knee extensors were determined before and after the training period with a nonisokinetic measuring method recently described. Following HR training, knee extension moment increased 9%–10% at knee angular velocities 0 (isometric) and 30° · s^–1 (P<0.05), peak moment increased 20% at 240–300°·s^–1 (P<0.05), while power generation increased 5%–29% at 240–480° · s^–1 (P<0.01). In addition, in the HR group maximal recorded power increased 45% (P<0.01). After FU training a 7%–13% increase in moment and power was observed at 30–180° · s^–1 (P<0.05). Following LR training, peak moment increased 9% at 120° · s^–1 (P<0.05). Improvements in knee extension moment and power were generally related to the angular velocities employed during training. However, as evaluated using the present measuring method, moment and power increased not only at very low but also at high knee angular velocities following the high-resistance strength training.     

Effectiveness of lower-level voluntary exercise in disease prevention of mature rats

To evaluate the chronic effects of voluntary exercise at lower levels on primary cardiovascular risk factors, inactive strain male Fischer rats were housed either with or without free access to activity wheels under controlled environmental conditions. The average amount of exercise for the 35-week duration was 722 (SD 362) m·day^–1·rat^–1, which was among the lowest found in the existing reports. Nonetheless, the body mass gains of the exercising rats were markedly inhibited, being 13% less (P < 0.001) than those of the sedentary controls, despite a 22% increase in food consumption (P < 0.0001), suggesting a remarkable prevention of adiposity. A noticeable improvement of serum lipid profiles was also found; a 53% reduction in triglyceride concentrations (P < 0.01) and a 13% increase in high density lipoprotein cholesterol concentrations (P < 0.05). In addition, resting systolic blood pressure was lowered by 7% (P < 0.01). These results would suggest that even lower-level physical activity, if continued regularly, will attenuate the age-related development of cardiovascular risk factors associated with a sedentary lifestyle.     

Hypohydration effects on thermoregulation during moderate exercise in the cold

Hyperosmotic hypovolemia impairs vasoconstriction during sedentary cold exposure. The purpose of this study was to determine whether hypohydration alters thermoregulation and cardiovascular responses to exercise in cold air. On four occasions, eight males [35.1 (2.7) years, 175.5 (3.1) cm, 73.3 (2.6) kg, 57.2 (2.6) ml kg^–1 min^–1 maximal oxygen uptake (O_2max), 19.6 (2.4)% fat] walked, in t-shirt, shorts, and shoes, at 50% O_2max, for 60 min in either a 4°C (Cold) or a 25°C (Temperate) environment in both hypohydrated state (HYPO, –4% body mass) and euhydrated state (EU). During exercise–cold stress, rectal temperature (T_re), mean weighted skin temperature, heart rate (HR), cardiac output (CO), and stroke volume (SV) were measured every 20 min. Mean weighted skin temperature values were not different between HYPO and EU but were lower (P<0.05) in Cold versus Temperate trials. T_re was not different (P>0.05) between HYPO–Cold and EU–Cold. CO and SV were not different within hydration states and were not different between Cold and Temperate trials (P<0.05). HR was not different between HYPO–Cold and EU–Cold. These data demonstrate that moderate intensity exercise in the cold while hypohydrated does not alter metabolic heat production, skin temperatures and heat loss, nor does it increase thermoregulatory and cardiovascular strain.     

Threshold increases in plasma growth hormone in relation to plasma catecholamine and blood lactate concentrations during progressive exercise in endurance-trained athletes

Plasma human growth hormone ([HGH]), adrenaline ([A]), noradrenaline ([NA]) and blood lactate ([La^–]_b) concentrations were measured during progressive, multistage exercise on a cycle ergometer in 12 endurance-trained athletes [aged 32.0 (SEM 2.0) years]. Exercise intensities (3 min each) were increased by 50 W until the subjects felt exhausted. Venous blood samples were taken after each intensity. The [HGH] and catecholamine concentrations increased negligibly during exercise of low to moderate intensities revealing an abrupt rise at the load corresponding to the lactate threshold ([La^–]-T). Close correlations (P < 0.001) were found between [La^–]_b and plasma [HGH] (r = 0.64), [A] (r = 0.71) and [NA] (r = 0.81). The mean threshold exercise intensities for [HGH], [A] and [NA], detected by log-log transformation, [154 (SEM 19) W, 162 (SEM 15) W and 160 (SEM 17) W, respectively] were not significantly different from the [La^–]-T [161 (SEM 12) W]. The results indicated that the threshold rise in plasma [HGH] followed the patterns of plasma catecholamine and blood lactate accumulation during progressive exercise in the endurancetrained athletes.     

A comparative assessment of two techniques for investigating initial cardiovascular reflexes under acute orthostatic stress

The physiological differences between active and passive changes in posture have been previously established. This study determined the extent of the differences in the initial cardiovascular responses to the passive head-up tilt (HUT) and the active squat-stand test (SST). Eleven females and 13 males underwent one +75° HUT and one SST. Beat-to-beat diastolic blood pressure (DBP), systolic blood pressure (SBP), mean arterial pressure (MAP) and heart rate (HR) were determined non-invasively. Data were recorded 10 s prior to (control) and 30 s after tilt or stand (event). Blood pressure and HR responses were analysed by calculating the deviation from control at 10 s (T10), 20 s (T20) and 30 s (T30) after the onset of each test. The DBP response (reflecting changes in systemic vascular resistance) at T10 was –10 (2) mmHg [mean (SEM)] for the HUT and –25 (2) mmHg for the SST (P<0.01). DBP returned to control levels by T30 for the HUT, but remained depressed for the SST. MAP responses directly reflected these changes in DBP. HR significantly increased from control values (P<0.001) for the HUT [+14 (1) bpm] and the SST [+16 (1) bpm], and remained elevated for the entire 30-s period for both tests. This study demonstrates that although the magnitude of the initial blood pressure decrease is greater for the active SST compared with the passive HUT, the reflex compensatory response is no different, making the SST a greater challenge for the cardiovascular reflexes.     

Tubuloglomerular feedback and autoregulation of glomerular filtration rate in Wistar-Kyoto spontaneously hypertensive rats

Experiments were done in Wistar-Kyoto spontaneously hypertensive rats (SHR) to examine the efficiency of autoregulatory adjustments of kidney and nephron filtration rate (GFR) to acute changes in blood pressure (BP) over a broad blood pressure range. When BP of the SHR was reduced from 158±7 to 118 ±3 mm Hg by aortic clamping, kidney-GFR remained unchanged from 1.19±0.11 to 1.17±013 ml·min^–1·g^–1 kidney weight (KW), respectively. Single nephron GFR (SNGFR) measured at early distal tubule sites was similarly unchanged with the same BP change, 27.9±1.5 vs. 24.9±2.1 nl·min^–1·g^–1 KW (P>0.10). Proximal and distal estimates of SNGFR were significantly different from each other at high BP (7 nl·min^–1·g^–1,P<0.025), but were not different at low BP (2.0 nl·ml^–1·g^–1,P>0.10). Studies assessing tubuloglomerular feedback activity were done with orthograde perfusion of the loop of Henle using recollections of early proximal flow rate (EPFR) as an index of change of glomerular filtration rate. A change in perfusion rate from 0 to 45 nl·min^–1 induced a reduction in early proximal flow rate of 40.5 ±4.5%. Juxtaglomerular renin activity of superficial nephrons was 36.2±4.3 in the SHR, a value insignificantly different from 23.7±4.4 ng Angiotensin II amide·0.1 ml^–1·h^–1. 5 glomeruli^–1 in normal controls (P>0.05). The SHR appears to behave as a normal animal with respect to tubologlomerular feedback and autoregulatory renal vascular adjustments. Like normal rat models, the SHR demonstrated dependence on maintenance of distal filtrate delivery to achieve single nephron GFR autoregulation.Financial support for these studies and for Dr. Ploth were made available by funds from the Deutsche Forschungsgemeinschaft     

Exercise‐induced sympathetic activation is correlated with cerebral hemisphere laterality,but not handedness

To investigate whether sympathetic responses are correlated with central laterality or handedness, muscle sympathetic nerve activity (MSNA), heart rate (HR) and blood pressure (BP) were compared between right (RA) and left arm (LA) grip exercise with volitional maximum effort (MVHG) for 2 min and post‐exercise arterial occlusion (PEAO) in right‐ and left‐handed volunteers. MVHG and PEAO led to a greater increase in MSNA in RA than in LA exercise (180 vs. 150%, P=0.004; 140 vs. 85%, P=0.005). MVHG elevated HR to a significantly lesser extent in RA than in LA (35 vs. 46%, P=0.030), and the difference was maintained during PEAO. The BP rise during MVHG and PEAO was the same in RA and in LA. Muscle sympathetic nerve activity, HR and BP responses during MVHG and PEAO showed no difference between the dominant and non‐dominant arm. These results suggested that the effects of central motor command and metaboreflex on sympathetic outflow to the vasculature and the heart may be selectively modulated partly by hemispherical laterality.