Changes in carotid blood flow and electrocardiogram in humans during and after walking on a treadmill

Blood flow velocity in the common carotid artery and the electrocardiogram were measured simultaneously by telemetry in seven male subjects during 20-min walking on a treadmill at an exercise intensity corresponding to a mean oxygen uptake of 26.0 (SD 2.9) ml · kg ^–1 · min ^–1. The mean cardiac cycle was shortened from 0.814 (SD 0.103) s to 0.452 (SD 0.054) s during this exercise. Of this shortening, 73% was due to shortening of the diastolic period and 27% to shortening of the systolic period. In the relatively small shortening of the mean systolic period [from 0.377 (SD 0.043) s to 0.268 (SD 0.029) s], the isovolumetric contraction time was shortened by 56%. During exercise, the heart rate (f _c) increased by 79.4% [from 74.3 (SD 9.3) beats · min ^–1 to 133.3 (SD 14.8) beats · min ^–1], and the peak blood velocity (S₁) in the common carotid artery increased by 56.1% [from 0.82 (SD 0.10) m · s^–1 to 1.28 (SD 0.11) m · s^–1]. After exercise, the S₁ decreased rapidly to the resting level. The f _c decreased more slowly, still being higher than the initial resting level 5 min after exercise. The diastolic velocity wave and the end-diastolic foot decreased during exercise. The blood flow rate in the carotid artery increased transiently by 13.5% at the beginning of exercise [from 5.62 (SD 0.63) ml · s^–1 to 6.38 (SD 0.85) ml · s^–1] and by 26.5% at the end of the exercise period [from 5.62 (SD 0.63) ml · s^–1 to 7.11 (SD 1.34) ml · s^–1]. The increase of blood flow in the carotid artery at the onset of exercise may have been mainly related to cerebral activation, and partly to an increase of blood flow to the skin of the head. The physiological significance for cerebral function of the increase of blood flow in the artery after the end of exercise is unknown.     

The physical demands of riding in National Hunt races

Heart rate (f _c) and post-competition blood lactate concentration ([La⁺]) were studied in seven male professional National Hunt jockeys over 30 races. Thef _c response for individual races followed a similar pattern for all subjects. The mean peakf _c recorded during competition was 184 beats·min^–1 (range 162–198 beats·min^–1) with averagef _c during the races ranging from 136 to 188 beats·min^–1. During consecutive races the recoveryf _c did not return to resting values. The mean [La⁺] was 7.1 mmol·l^–1 (range 3.5–15.0 mmol·l^–1). The conclusions of this study suggest that riding in National Hunt races is a physically demanding occupation. The muscular activity in this profession requires a high metabolic drive and produces a significant cardiorespiratory response.     

Validity of heart rate and ratings of perceived exertion as indices of exercise intensity in a group of children while swimming

Summary The purpose of this study was to investigate the validity of heart rate (f _c) and ratings of perceived exertion (RPE) as indices of exercise intensity in a group of children while swimming. Six healthy male swimmers, aged 10–12, swam tethered using the breast-stroke in a flume. The resistance started at 1.0 kg and increased in 1.0 kg steps up to the point of their exhaustion. The subjects swam for 5 min during each period, with a rest of 10–20 min until they had returned to their resting f _c level. The last exercise intensity was with the maximal mass the subjects could support for 2 min. The last min of oxygen consumption (VO₂) and 30 s of f _c were measured during each exercise period. The subjects gave their RPE assessment at the end of exercise.The individual relationships between f _c and VO₂, and percentage maximal oxygen consumption (% VO_2max, were linear with a high correlation r=0.962–0.996 and r=0.962–0.996, respectively. Therefore, it was concluded that f _c was valid as an index of the exercise intensity of children while swimming. Compared to the results found in adults using a similar protocol, the children's f _c were 8.3–26.9 beats·min^–1 higher than those of the adults at the given % VO_2max. The present study showed two different patterns in the relationship between VO₂ and RPE in individuals. In two subjects the RPE increased linearly with VO₂ while in the other four subjects the increase was discontinuous. If f _c and RPE were to be applied to the setting and evaluation of exercise intensity during swimming, it would seem that f _c would be a more useful guide than RPE for some children.     

Heart rate overshoot at the beginning of muscle exercise

Summary A characteristic notch in the heart rate (f _c) on-response at the beginning of square-wave exercise is described in 7 very fit marathon runners and 12 sedentary young men, during cycle tests at 30% and 60% of maximal oxygen consumption (VO_2max). The (f _c) notch revealed af _c overshoot with respect to the (f _c) values predicted from exponential beat-by-beat fitted models. While at 30% of (VO_2max). all subjects showed af _c over-shoot, at 60% of (VO_2max). it occurred in the marathon runners but not in the sedentary subjects. The mean time of occurrence of thef _c overshoot from the onset of the exercise was 16.7 (SD 4.7) s and 12.2 (SD 3.2) s at 30% of (VO_2max). in the runners and the sedentary subjects respectively, and 23.8 (SD 8.8) s at 60% of (VO_2max). in the runners. The amplitude of the overshoot, with respect to rest, was 41 (SD 12) beats·min^–1and 31 (SD 4) beats·min^–1 at 30% of (VO_2max). in the runners and the sedentary subjects respectively, and 46 (SD 19) beats·min^–1 at 60% of (VO_2max). in the runners. The existence and the amplitude of thef _c overshoot may have been related to central command and muscle heart reflex mechanisms and thus may have been indicators of changes in the balance between sympathetic and parasympathetic activity occurring in fit and unfit subjects.     

Cardiac responses to maximal anisotonic isometric contractions during handgrip and leg extension

A group of 14-healthy men performed anisotonic isometric contractions (AIC), for 60 s, at an intensity of 100% maximal voluntary contraction force (MVC) during handgrip (HG) and leg extension (LE). Heart rate (f _c), stroke volume index (SVI) and cardiac output index (Q_cI) were measured during the last 10 s of both AIC by an impedance reography method. Force (F) exerted by the subjects was recorded continuously and reported as a relative force (F _r) (% MVC). The F generated during MVC was greater for LE than for HG (502.I N compared to 374.6 N, P < 0.001). The rate of decrease in F _r was significantly slower for LE than HG for the first 25 s of the exercise (phase 1 of AIC). The F _r developed by the subjects at the end of AIC was 40% MVC for both LE and HG. The increase in f _c was greater for LE (63 beats · min^–1) than for HG (52 beats · min^–1), P < 0.01. The SVI decreased significantly from the resting level by 17.0 ml · m^–2 and by 18.2 ml · m^–2 for LE and HG, respectively. The Q_cI increased insignificantly for HG by 0.091 · min^–1 · m^–2 andsignificantly forLE by 0.561 · min^–1 · m^–2 (P < 0.001). It was concluded that although both AIC caused a significant decrease in SVI, greater increases in f _c and Q_c were observed for LE than for HG. The greater f _c and Q_c reported during LE was probably related to the greater relative force exerted by LE during phase 1 of AIC. It seems, therefore that central command might have dominated for phase 1 of AIC but that the muscle reflex also contributed significantly to the control of the cardiac response to the high intensity AIC.     

Endurance training slows down the kinetics of heart rate increase in the transition from moderate to heavier submaximal exercise intensities

Summary To find out whether endurance training influences the kinetics of the increases in heart rate (f _c) during exercise driven by the sympathetic nervous system, the changes in the rate off _c adjustment to step increments in exercise intensities from 100 to 150 W were followed in seven healthy, previously sedentary men, subjected to 10-week training. The training programme consisted of 30-min cycle exercise at 50%–70% of maximal oxygen uptake ( O_2max) three times a week. Every week during the first 5 weeks of training, and then after the 10th week the subjects underwent the submaximal three-stage exercise test (50, 100 and 150 W) with continuousf _c recording. At the completion of the training programme, the subjects' O_2max had increased significantly(39.2 ml·min^–1·kg^–1, SD 4.7 vs 46 ml·min^–1·kg^–1, SD 5.6) and the steady-statef _c at rest and at all submaximal intensities were significantly reduced. The greatest decrease in steady-statef _c was found at 150 W (146 beats·min^–1, SD 10 vs 169 beats·min^–1, SD 9) but the difference between the steady-statef _c at 150 W and that at 100 W (f _c) did not decrease significantly (26 beats·min^–1, SD 7 vs 32 beats·min^–1, SD 6). The time constant () of thef _c increase from the steady-state at 100 W to steady-state at 150 W increased during training from 99.4 s, SD 6.6 to 123.7 s, SD 22.7 (P<0.01) and the acceleration index (A=0.63·f _c·^–1) decreased from 0.20 beats·min^–1·s^–1, SD 0.05 to 0.14 beats·min^–1·s^–1, SD 0.04 (P<0.02). The major part of the changes in and A occurred during the first 4 weeks of training. It was concluded that heart acceleration following incremental exercise intensities slowed down in the early phase of endurance training, most probably due to diminished sympathetic activation.     

Atrial natriuretic peptide response to endurance physical training in the rat

Summary The effect of an endurance physical training programme on the plasma and atrial natriuretic peptides (ANP) and on renal glomerular ANP receptors was evaluated in male normotensive Wistar rats. Maximal O₂ uptake was significantly greater in the endurance trained (117.1 Ml O₂ · kg^–1 · min^–1, SEM 6.18 versus the control rats 84.2 ml O₂ · kg^–1 · min^–1, SEM 4.88, P<0.01. In addition, various muscle oxidative enzymes were also significantly higher in endurance trained animals. An increase in resting plasma [ANP] was observed after 11 weeks of physical training (40.02 pg · ml^–1, SEM 7.07 vs 22.8 pg.ml^–1, SEM 3.83, P<0.05). Glomerular ANP receptor density was lower in trained rats (272 fmol · mg^–1 protein, SEM 3.1 vs 380 fmol · mg^–1 protein, SEM 6.1, P < 0.05), whereas atrial tissue [ANP] was not significantly different between controls and trained animals. However, in trained rats, circulating [ANP] was closely correlated with left atrial [ANP] (r = –0.92, P<0.05). Resting systolic blood pressure had not changed at the end of this physical training programme. It is considered that under physiological conditions ANP may be involved in long-term extracellular fluid volume homeostasis through the regulation of renal glomerular ANP receptors, and that the left atrium might play a significant role in this long term fluid volume control.     

Effects of exercise during normoxia and hypoxia on the growth hormone—insulin-like growth factor I axis

The response of plasma insulin-like growth factor I (IGF I) to exercise-induced increase of total human growth hormone concentration [hGH_tot] and of its molecular species [hGH_20kD] was investigated up to 48 h after an 1-h ergometer exercise at 60% of maximal capacity during normoxia (N) and hypoxia (H) (inspiratory partial pressure of oxygen = 92 mmHg (12.7 kPa);n = 8). Lactate and glucose concentrations were differently affected during both conditions showing higher levels under H. Despite similar maximal concentrations, the increase of human growth hormone (hGH) was faster during exercise during H than during N[hGH_tot after 30 min: 8.6 (SD 11.4) ng · ml^–1 (N); 16.2 (SD 11.6) ng · ml^–1 (H);P < 0.05]. The variations in plasma [hGH_20kD] were closely correlated to those of [hGH_tot], but its absolute concentration did not exceed 3% of the [hGH_tot]. Plasma IGF I concentration was significantly decreased 24 h after both experimental conditions [N from 319 (SD 71) ng · ml^-1 to 228 (SD 72) ng · ml^–1,P < 0.05; H from 253 (SD 47) to 200 (SD 47) ng · ml^–1,P < 0.01], and was still lower than basal levels 48 h after exercise during H [204 (SD 44) ng · ml^–1,P < 0.01]. Linear regression analysis yielded no significant correlation between increase in plasma [hGH_tot] or [hGH_20kD] during exercise and the plasma IGF I concentration after exercise. It was concluded that the exercise-associated elevated plasma [hGH] did not increase the hepatic IGF I production. From our study it would seem that the high energy demand during and after the long-lasting intensive exercise may have overridden an existing hGH stimulus on plasma IGH I, which was most obvious during hypoxia.     

Cardiovascular responses of cardiac transplant patients to arm and leg exercise

This investigation compares the cardiovascular responses of normal (n=10) and cardiac transplant (n=14) subjects to peak arm and leg exercise. It also tests the hypothesis that the higher heart rate (f _c) in normal subjects during light (30 W) submaximal arm versus leg exercise is due to cardiac innervation. In cardiac transplant patients, power output, oxygen consumption ,f _c and rate pressure product were 54%, 28%, 7%, and 8% lower during peak arm than leg exercise, respectively. In normal subjects, power output, ,f _c and rate pressure product were 61%, 33%, 8%, and 11% lower during peak arm than leg exercise, respectively. In cardiac transplant patients there was no significant difference in absolutef _c during submaximal arm and leg exercise. In normal subjects, absolutef _c during arm and leg exercise was [mean (SD)] 97 (4) beats · min^–1 and 92 (4) beats · min^–1, respectively (P=0.07). Plasma noradrenaline was increased more during arm than leg exercise in both cardiac transplant and normal subjects. Maximal leg testing is useful when determining the capacity of cardiac transplant patients to perform arm work. The higher absolutef _c reported by other investigators for normal subjects during submaximal arm versus leg exercise may be mediated by cardiac innervation.     

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.     

Heart rate deflection related to lactate performance curve and plasma catecholamine response during incremental cycle ergometer exercise

The correlation between the behaviour of the heart rate/work performance (f _c W) curve and blood lactate ([la]_b) and plasma adrenaline/noradrenaline concentrations ([A]/[NA]) during incremental cycle ergometer exercise was investigated. A group of 21 male sports students was divided into two groups: group I, with a clear deflection of thef _c W curve; group II, without or with an inverse deflection of thef _c W curve. The aerobic threshold (Th_aer) and the lactate turn point (LTP) were defined. Between Th_aer and maximal work performance (f _c W _max) the behaviour of thef _c W curve as well as the behaviour of [la^–]_b and [A]. [NA] were described mathematically. Thef _c, systolic blood pressure (BP_S),W, [la^–]_b, [A] and [NA] at rest, Th_aer, LTP,f _c W _max, after 3 and 6 min of recovery (Re₃/Re₆) were calculated. A significant difference between the two groups could only be detected forf _c at LTP, Re₃ and Re₆ (P < 0.05). No significant, correlation could be found between individualf _c W-behaviour and individual time course of [la^–]_b, [A] and [NA]. However, a significant correlation was visible between [la^–/W-behaviour and individual catecholamine response. These results and the fact that the different flattening at the top of thef _c W curve was related to diminished stress-dependent myocardial function led us to the conclusion that it is possible that sympathetic drive is not directly involved in mechanisms of regulation between load dependentf _c and myocardial function. In addition, individualf _c W behaviour was independent of BP_S andW _max, or individual conditions of energy supply.     

Maximal heart rates and plasma lactate concentrations observed in middle-aged men and women during a maximal cycle ergometer test

Summary The purpose of this study was to investigate criteria for maximal effort in middle-aged men and women undertaking a maximal exercise test until they were exhausted if no measurements of oxygen uptake are made. A large group of 2164 men and 975 women, all active in sports and aged between 40 and 65 years, volunteered for a medical examination including a progressive exercise test to exhaustion on a cycle ergometer. In the 3rd min of recovery a venous blood sample was taken to determine the plasma lactate concentration ([la^–]_{p, 3min}). Lactate concentration and maximal heart rate (f _{c, max}) were lower in the women than in the men (P<0.001). Multiple regression analyses were performed to assess the contribution of sex to [la^–]_{p, 3 min}, independent of age and f _c max, It was found that [la^–]_{p,3 min} was about 2.5 mmol·l^–1 lower in women than in men of the same age and f _{c, max}. In our population 88% of the men and 85% of the women met a combination of the following f _{c, max} and [la^–]_{p, 3min} criteria: f _{c, max} equal to or greater than 220 minus age beats·min^–1 and/or [la^–]_{p, 3min} equal to or greater than 8 mmol·l^–1 in the men and f _{c, max} equal to or greater than 220 minus age beats·min^–1 and/or [la^–]_{p, 3min} equal to or greater than 5.5 mmol·1^–1 in the women.     

Cardiovascular response to static handgrip in trained and untrained men

Summary The influence of aerobic capacity on the cardiovascular response to handgrip exercise, in relation to the muscle mass involved in the effort, was tested in 8 trained men (T) and 17 untrained men (U). The subjects performed handgrip exercises with the right-hand (RH), left-hand (LH) and both hands simultaneously (RLH) at an intensity of 25% of maximal voluntary contraction force. Maximal aerobic capacity was 4.3 l·min^–1 in T and 3.21·min^–1 in U (P<0.01). The endurance time for handgrip was longer in T than in U by 29% (P<0.05) for RH, 38% (P<0.001) for LH and 24% (P<0.001) for RLH. Heart rate (f _c) was significantly lower in T than in U before handgrip exercise, and showed smaller increases (P<0.01) at the point of exhaustion: 89 vs 106 beats·min^–1 for RH, 93 vs 100 beats·min^–1 for LH and 92 vs 108 beats·min^–1 for RLH. Stroke volume (SV) at rest was greater in T than in U and decreased significantly (P<0.05) during handgrip exercise in both groups of subjects. At the point of exhaustion SV was still greater in T than in U: 75 vs 57 ml for RH, 76 vs 54 ml for LH and 76 vs 56 ml for RLH. During the last seconds of handgrip exercise, the left ventricular ejection time was longer in T than in U. Increases in cardiac output (Q _c) and systolic blood pressure did not differ substantially between T and U, nor between the handgrip exercise tests. It was concluded that handgrip exercise caused similar increases inQ _c in both T and U but in T the increased level ofQ _c was an effect of greater SV and lowerf _c than in U. Doubling the muscle mass did not alter the cardiovascular response to handgrip exercise in either T or U.     

Stroke volume response to progressive exercise in athletes engaged in different types of training

Summary Using the impedance cardiography method, heart rate ( _c) matched changes on indexed stroke volume (SI) and cardiac output (CI) were compared in subjects engaged in different types of training. The subjects consisted of untrained controls (C), volleyball players (VB) who spent about half of their training time (360 min · week^–1) doing anaerobic conditioning exercises and who had a maximal oxygen uptake ( ) 41% higher than the controls, and distance runners (D) who spent all their training time (366 min·week^–1) doing aerobic conditioning exercises and who had a 26% higher than VB. The subjects performed progressive submaximal cycle ergometer exercise (10 W·min^–1) up to _c of 150 beats·min^–1. In group C, SI had increased significantly (P<0.05) at _c of 90 beats·min^–1 ( + 32%) and maintained this difference up to 110 beats·min^–1, only to return to resting values on reaching 130 beats·min^–1 with no further changes. In group VB, SI peaked (+ 54%) at _c of 110 beats·min^–1, reaching a value significantly higher than that of group C, but decreased progressively to 22010 of the resting value on reaching 150 beats·min^–1. In group D, SI peaked at _c of 130 beats·min^–1 (+ 54%), reaching a value significantly higher than that of group VB, and showed no significant reduction with respect to this peak value on reaching 150 beats·min^–1. As a consequence, the mean CI increase per _c unit was progressively higher in VB than in C (+46%) and in D than in VB (+ 105%). It was concluded that thef _c value at which SI ceased to increase during incremental exercise was closely related to the endurance component in the training programme.     

The effect of training on responses of Β-endorphin and other pituitary hormones to insulin-induced hypoglycemia

Summary We studied whether the previously reported intensified -endorphin response to exercise after training might result from a training-induced general increase in anterior pituitary secretory capacity. Identical hypoglycemia was induced by insulin infusion in 7 untrained (Skeletal muscle enzyme activity, fiber composition and in relation to distance running performance 49±4 ml · (kg · min)^–1, mean and SE) and 8 physically trained (Skeletal muscle enzyme activity, fiber composition and in relation to distance running performance 65±4 ml · (kg · min)^–1) subjects. In response to hypoglycemia, levels of -endorphin and prolactin immunoreactivity in serum increased similarly in trained (from 41±2 pg · ml^–1 and 6±1 pg · ml^–1 before hypoglycemia to 103±11 pg · ml^–1 and 43±9 pg · ml^–1 during recovery, P<0.05) and untrained (from 35±7 pg · ml^–1 and 7±2 pg · ml^–1 to 113±18 pg · ml^–1 and 31±8 pg · ml^–1 P<0.05) subjects. Growth hormone (GH) was higher 90 min after glucose nadir in trained (61±13 mU · l^–1) than in untrained (25±6 mU · l^–1) subjects (P<0.05). Levels of thyrotropin (TSH) changed in neither of the groups. It is concluded that, in contrast to what has been formerly proposed, training does not result in a general increase in secretory capacity of the anterior pituitary gland. TSH responds to hypoglycemia neither in trained nor in untrained subjects. Finally, differences in -endorphin responses to exercise between trained and untrained subjects cannot be ascribed to differences in responsiveness to hypoglycemia.     

The monitoring of the menstrual status of female athletes by salivary steroid determination and ultrasonography

Summary This study was designed to evaluate whether traditional plasma hormone determinations can be adequately replaced by measurements of salivary hormones. Eleven young sportswomen with menstrual irregularities attributed to strenuous physical exercise participated in this study. Mean body weight expressed as a percentage of ideal body weight was 92%, SD 4%. Their mean weekly training distance was 35 km, SD 15. Basal plasma endocrinological measurements revealed a hypo-oestrogenic status (mean plasma oestradiol values: 22pg-ml^–1, SD 8.8), and a deficient luteal phase (mean plasma progesterone: 2.9 ng · ml^–1, SD 2.1). Preexercise salivary sex steroids were low. Salivary progesterone levels were 39.3 pg · ml^–1, SD 9.5 (normal ranges in saliva: 25–60 pg· ml^–1), salivary oestrone (E₁) was 12.2 pg · ml^–1, SD 2.3 (normal ranges in saliva: 7.5–25 pg·ml^–1), and salivary oestradiol (E₂) < 1.9 pg · ml^–1, SD 1.1 (normally 1.0–10.0 pg · ml^–1). After a 21-km run, all salivary steroids appeared to increase. Mean salivary testosterone levels increased by 15.2% and salivary progesterone by 14.8%. Mean salivary oestrogens also increased (E₁: + 13.9%; E₂: +21.1%). These findings confirm the results of earlier studies which found higher post-exercise plasma sex steroid levels. Since salivary measurements are believed to reflect non-protein-bound, thus free steroid levels, the results obtained by these techniques may provide a more realistic picture of the hormonal effects of physical exercise. In future, more accurate, cost-effective and easier techniques for salivary measurements may offer additional advantages.     

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 pyridostigmine on the exercise-heat response of man

Summary The effect of pyridostigmine on thermoregulatory responses was evaluated during exercise and heat stress. Eight heat acclimated, young adult male subjects received four doses of pyridostigmine (30 mg) or identical placebo tablets every 8 h, in a double blind, randomized, cross-over trial. A 30.3%, SD 4.6% inhibition of the circulating cholinesterase (ChE) activity was induced in the pyridostigmine-treated group. The subjects were exposed to 170-min exercise and heat-stress (dry bulb temperature, 33° C; relative humidity 60%) consisting of 60 min in a sitting position and two bouts of 50-min walking (1.39 m · s^–1, 5% gradient) which were separated by 10-min rest periods. No differences were found between treatments in the physiological responses and heat balance parameters at the end of exposure: heart rate (f _c) was 141 beats · min^–1, SD 16 and 150 beats · min^–1, SD 12, rectal temperature (T _re) was 38.5°C, SD 0.4° and 38.6°C, SD 0.3°, heat storage was 60 W · m^–2, SD 16 and 59 W · m^–2, SD 15 and sweat rate was 678 g · h^–1, SD 184 and 661 g · h^–1, SD 133, in the pyridostigmine and placebo treatments, respectively. The changes in T _re and f _c over the heat-exercise period were parallel in both study and control groups. Pyridostigmine caused a slight slowing of f _c (5 beats·min^–1) which was consistent throughout the entire exposure (P<0.001) but was of no clinical significance. The overall change in f_c was similar for both groups. We have concluded that pyridostigmine administration, in a dose sufficient to induce a moderate degree of ChE inhibition, does not significantly affect performance of exercise in the heat.     

Finger and forearm vasodilatatory changes after local cold acclimation

Summary To determine the vascular changes induced by local cold acclimation, post-ischaemia and exercise vasodilatation were studied in the finger and the forearm of five subjects cold-acclimated locally and five non-acclimated subjects. Peak blood flow was measured by venous occlusion plethysmography after 5 min of arterial occlusion (PBF_isc), after 5 min of sustained handgrip at 10% maximal voluntary contraction (PBF_exe), and after 5 min of both treatments simultaneously (PBF_isc+exe). Each test was performed at room temperature (25° C, SE 1 C) (non-cooled condition) and after 5 min of 5'C cold water immersion (cooled condition). After the cold acclimation period, the decrease in skin temperature was more limited in the cold-acclimated compared to the non-acclimated (P<0.01). The PBF_isc was significantly reduced in the cooled condition only in the cold-acclimated subjects (finger: 8.4 ml · 100 ml^–1 · min^–1, SE 1.1,P<0.01; forearm: 5.8 ml · 100 ml^–1 · min^–1, SE 1.5,P<0.01) compared to the non-cooled condition. Forearm PBF_exe was significantly decreased in the cooled condition only in the cold-acclimated subjects (non-cooled: 7.4 ml · 100 ml^–1 · min^–1, SE 1.2; cooled: 3.9 ml · 100 ml^–1 ·min^–1, SE 2.6,P<0.05) indicating that muscle blood flow was also reduced. The application of PBF_isc+exe elicited an increase in peak blood flow only in the forearm of the non-acclimated subjects (non-cooled: 10.4 ml· 100 ml^–1 · min^–1, SE 2.0; cooled: 14.3 ml · 100 ml^–1 · min^–1, SE 2.6,P<0.05) and conversely only in the finger of the cold-acclimated (non-cooled finger: 25.7 ml · 100 ml^–1 · min^–1, SE 4.4; cooled finger: 19.2 ml · 100 ml^–1 · min^–1, SE 3.3,P<0.01). Therefore, subjects cold-acclimated locally showed decreased vasodilatatory responses only when exposed to cold.     

Influence of acute maximal exercise on lecithin: cholesterol acyltransferase activity in healthy adults of differing aerobic performance

Summary To document the possible influence of a single episode of maximal aerobic stress on the serum lecithin: cholesterol acyltransferase (LCAT) activity in subjects with differing histories of training, two groups of healthy male adults [controls (C),n = 18, 28.6 years, SD 5.2, 50.1 ml · kg^–1 · min^–1 maximal O₂ uptake (VO_2max), SD 5.3; endurance trained athletes (T),n = 18, 31.4 years, SD 8.8, 65.0 ml · kg^–1 · min^–1 VO_2max, SD 2.8] were examined in a maximal aerobic stress test. In addition to the routine assessment of lipid status, LCAT activity was measured immediately before and after exercise. At rest nearly identical LCAT activity values were found in both groups: C 64.4 nmol · ml^–1 · h^–1, SD 16.7 vs T 65.0 nmol · ml^–1 · h^–1, SD 20.9. The post-exercise LCAT values induced by the maximal stress test increased significantly to (C) 95.7 nmol · ml^–1 · h^–1, SD 23.5, +48.6%,P<0.001; (T) 83.5 nmol · ml^–1 · h^–1, SD 24.3, +29.1%,P<0.01. Neither the pre nor the post-exercise individual LCAT activity values showed any significant correlation to the corresponding data on physical performance.