Effect of exercise training on aortic collagen content in spontaneously hypertensive rats (SHR)

Summary We investigated the effects of exercise training on the amount of aortic collagen and systolic blood pressure in spontaneously hypertensive rats (SHR). Ten-week old SHR were trained either by forced treadmill running (26.8 m·min^–1 h·day^–1, five times a week, 0% incline) or by voluntary running in revolving wheels (7,800 m·day^–1 at peak) for 8 weeks. Succinate dehydrogenase (SDH) activity measured as a marker of an endurance training effect was 13% higher (P<0.01) in the soleus of forced-exercised animals than in that of sedentary ones. (6.56±0.17 mol·g^–1·min^–1; mean ± SEM), whereas SDH activity in that of voluntarily-exercised group was found to be at the same level as in sedentary animals. The systolic blood pressure after training increased by 26.4 in sedentary, 21.1 in voluntarily-exercised, and 33.9 mm Hg in forced-exercised rats, when compared with the value of each group at the beginning of the training programm. A significant difference was observed in the increment of blood pressure only between the voluntarily- and forced-exercised groups (P<0.05). The amount of aortic collagen in voluntarily-trained rats (96.5±2.0 mg·g tissue^–1, 39.8±0.7 mg·100 mg protein^–1) was significantly less than that in forced-trained rats (P<0.05). These results suggest that voluntary, mild exercise training may be more effective in the reduction of collagen accumulation in the aorta associated with the suppression of blood pressure increase than forced, vigorous exercise training in SHR.     

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.     

Hormonal regulation of potassium shifts during graded exhausting exercise

Summary Serum potassium, aldosterone and insulin, and plasma adrenaline, noradrenaline and cyclic adenosine 3:5-monophosphate (cAMP) concentrations were measured during graded exhausting exercise and during the following 30 min recovery period in six untrained young men. During exercise there was an increase in concentration of serum potassium (4.74 mmol·1^–1, SEM 0.12 at the end of exercise vs 3.80 mmol·1^–1, SEM 0.05 basal,P<0.001), plasma adrenaline (2.14 nmol·1^–1, SEM 0.05 at the end of exercise vs 0.30 nmol·1^–1, SEM 0.02 basal,P<0.001), plasma noradrenaline (1.10 nmol·1^–1, SEM 0.64 at the end of exercise vs 1.50 nmol·1^–1, SEM 0.05 basal,P< 0.001), serum aldosterone (0.92 nmol·1^–1, SEM 0.14 at the end of exercise vs 0.36 nmol·1^–1, SEM 0.05 basal,P<0.01), and plasma cAMP (35.4 nmol·1^–1, SEM 2.3 at the end of exercise vs 21.4 nmol·1^–1, SEM 4.5 basal,P<0.05). While concentrations of serum potassium, plasma adrenaline and cAMP returned to their basal levels immediately after exercise, those of plasma noradrenaline and serum aldosterone remained elevated 30 min later (1.90 nmol·1^–1, SEM 0.01,P<0.01; and 0.85 nmol·1^–1, SEM 0.12,P<0.01, respectively). Serum insulin concentration did not change during exercise (6.47 mlU·1^–1, SEM 0.58 at the end of exercise vs 5.47 mlU·1^–1, SEM 0.41 basal, NS) but increased significantly (P<0.02) at the end of the recovery period (7.12 mlU·1^–1, SEM 0.65). Serum potassium increases with exhausting exercise appeared to be caused not only by its release from contracting muscles but also by an -adrenergic stimulation produced by adrenaline and noradrenaline. On the other hand, the increased levels of plasma noradrenaline maintained during the recovery period may have served to avoid excessive hypokalaemia through the stimulation of muscle -receptors. Thus, catecholamines may play an important role in the regulation of serum potassium concentrations during and after exercise. Any disturbance of these adrenergic effects may lead either to an excessive increase or to a decrease of kalaemia, with the consequent risk of arrhythmias linked to exercise.     

The acute effect of 30 min of moderate exercise on high density lipoprotein cholesterol in untrained middle-aged men

Summary Fifteen middle-aged, untrained (defined as no regular exercise) men (mean age 49.9 years, range 42–67) cycled on a cycle ergometer at 50 rpm for 30 min at an intensity producing 60% predicted maximum heart rate [(f _c,max), wheref _{c, max} = 220 - age]. Total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and triglyceride (Tg) concentrations were measured from fasting fingertip capillary blood samples collected at rest, after 15 and 30 min of exercise, and at 15 min post-exercise. The mean HDL-C level increased significantly from the resting level of 0.85 mmol · l^–1 to 0.97 mmol · 1^–1 (P<0.05) after 15 min of exercise, increased further to 1.08 mmol · 1^–1 (P<0.01) after 30 min of exercise and remained elevated at 1.07 mmol · 1^–1 (P<0.01) at 15 min post-exercise. These increases represented changes above the mean resting level of 14.1%, 27.1% and 25.9% respectively. The HDL-C/LDL-C ratio increased significantly from a resting ratio of 0.20 to 0.26 after 30 min of exercise (P < 0.01) and to 0.24 at 15 min post-exercise (P<0.05). The mean Tg level increased significantly from a resting level of 0.88 mmol · 1^–1 to 1.05 mmol · 1^–1 after 15 min, and to 1.06 mmol · I^–1 after 30 min of exercise (P<0.05 at each time). The TC/HDL-C ratio decreased significantly (P=0.05) after 30 min of exercise and at 15 min post-exercise by 18.8% and 14%, respectively. No significant changes were observed in the levels of TC or LDL-C over time. These results indicate that 30 min of moderate exercise elicits significant changes in HDL-C concentration during and up to 15 min after the exercise in untrained middle-aged men with low mean resting levels of HDL-C (0.85 mmol · 1^–1).     

Does functional alteration of the gonadotropic axis occur in endurance trained athletes during and after exercise?

In men, the hypothalamic-pituitary-testicular axis controls the secretion of testosterone which, in this sex, is a major anabolic hormone. Physical exercise modulates testosterone concentration, affecting the whole axis by poorly understood mechanisms. We have reported in this preliminary study the short and longterm effects of exercise on the function of the gonadotropic axis in trained compared to untrained subjects. Environmental factors known to interfere with pituitary function were minimized. Four marathon and four sedentary men, were studied during 5 days successively using different combinations of two factors: duration and intensity of running tests. Day 0 (DO) was a rest day, and the exercises were: D1 and D2 brief (20 min), light (50% maximal heart rate, HR_max, D1) or intense (80% HR_max, D2), D3 and D4 prolonged (120 min) and light (50% HR_max, D3) or intense (80% HR_max, D4). Testosterone (free and total) and luteinizing hormone (LH) concentrations were measured before, during and after exercise. The baseline concentrations of plasma testosterone were lower in the long distance runners than in the sedentary group [41.8 (SEM 5.5) vs 64.5 (SEM 7.9) pmol · 1^–1, respectively;P < 0.05]. This phenomenon was centrally mediated as LH concentration was apparentlyinappropriately low [3.4 (SEM 0.4) vs 4.3 (SEM 1.0) UI · 1^–1;P > 0.05]. Light to moderate exercise did not modify testosterone and LH concentrations. Conversely, intense and prolonged exercise increased testosterone concentration [73.2 (SEM 9.0) vs 92 (SEM 11.0) pmol · 1^–1 in the long distance runners and sedentary group, respectively;P < 0.05] and lowered LH concentrations [2.1 (SEM 0.3) vs 3.4 (SEM 0.3) UI · 1^–1 in the long distance runners and sedentary group, respectively;P <0.05 compared to DO, at the same time]. In our conditions of exercise, negative feedback of testosterone upon LH persisted, as positive feedback of low testosterone concentrations was apparently lacking (inappropriately low LH concentration with regard to low basal testosterone concentration).     

Erythropoietic adaptations to endurance training

Summary Erythropoietic adaptations involving the oxygen dissociation curve (ODC) and erythropoietin production have been implicated in the etiology of reduced blood haemoglobin concentrations in sportspersons (known as sports anaemia). A significant increase in the half-saturation pressure indicating a right-shift in the ODC was measured in 34 male [25.8–27.4 mmHg (3.44–3.65 kPa)] and 16 female (25.8–27.7 mmHg (3.44–3.69 kPa)] trained distance runners (P<0.01 for both genders) after completing a standard 42-km marathon. Erythrocyte 2,3-diphosphoglycerate concentrations measured concurrently were unaltered by exercise, although consistently higher in the female compared to the male athletes (P<0.05). The serum erythropoietin (EPO) concentrations of 15 male triathletes (26.3 U · ml^–1) were significantly lower than those of 45 male distance runners (31.6 U · ml^–1 ;P<0.05). However, the mean serum EPO concentrations of male and female athletes engaged in a variety of sports were not different from those of sedentary control subjects of both sexes (26.5–35.3 U · ml^–1). Furthermore, the serum EPO concentrations were unaltered after prolonged strenuous exercise in 20 male marathon runners. These data suggest that the haematological status of these endurance athletes is in fact normal and that the observed shift in the ODC, while providing a physiological advantage during exercise, has no measurable effect on the erythropoietic drive.     

Effect of heat stress on muscle blood flow during dynamic handgrip exercise

Summary During exercise in a hot environment, blood flow in the exercising muscles may be reduced in favour of the cutaneous circulation. The aim of our study was to examine whether an acute heat exposure (65–70°C) in sauna conditions reduces the blood flow in forearm muscles during handgrip exercise in comparison to tests at thermoneutrality (25° C). Nine healthy men performed dynamic handgrip exercise of the right hand by rhythmically squeezing a water-filled rubber tube at 13% (light), and at 34% (moderate) of maximal voluntary contraction. The left arm served as a control. The muscle blood flow was estimated as the difference in plethysmographic blood flow between the exercising and the control forearm. Skin blood flow was estimated by laser Doppler flowmetry in both forearms. Oesophageal temperature averaged 36.92 (SEM 0.08) ° C at thermo-neutrality, and 37.74 (SEM 0.07) ° C (P<0.01) at the end of the heat stress. The corresponding values for heart rate were 58 (SEM 2) and 99 (SEM 5) beats -min^–1 (P<0.01), respectively. At 25° C, handgrip exercise increased blood flow in the exercising forearm above the control forarm by 6.0 (SEM 0.8) ml · 100 ml^–1 · min^–1 during light exercise, and by 17.9 (SEM 2.5) ml · 100 ml^–1 · min^–1 during moderate exercise. In the heat, the increases were significantly higher: 12.5 (SEM 2:2) ml · 100 ml^–1 · min^–1 at the light exercise level (P<0.01), and 32.2 (SEM 5.9) ml · 100 ml^–1·min^–1 (P<0.05) at the moderate exercise level. Skin blood flow was not significantly different in any of the test conditions between the two forearms. These results suggested that hyperthermia of the observed magnitude did not reduce blood flow in active muscles during light or moderate levels of dynamic handgrip exercise.     

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.     

Endurance training attenuates exercise-induced oxidative stress in erythrocytes in rat

The aim of this study was to investigate whether endurance training reduces exercise-induced oxidative stress in erythrocytes. Male rats (n=54) were divided into trained (n=28) and untrained (n=26) groups. Both groups were further divided equally into two groups where the rats were studied at rest and immediately after exhaustive exercise. Endurance training consisted of treadmill running 1.5 h·day^–1, 5 days a week for 8 weeks, reaching the speed of 2.1 km·h^–1 at the fourth week. For acute exhaustive exercise, graded treadmill running was conducted reaching the speed of 2.1 km·h^–1 at the 95th min, 10% uphill, and was continued until exhaustion. Acute exhaustive exercise increased the erythrocyte malondialdehyde level in sedentary but not in trained rats compared with the corresponding sedentary rest and trained rest groups, respectively. While acute exhaustive exercise decreased the erythrocyte superoxide dismutase activity in sedentary rats, it increased the activity of this enzyme in trained rats. On the other hand, acute exhaustive exercise increased the erythrocyte glutathione peroxidase activity in sedentary rats; however, it did not affect this enzyme activity in trained rats. Erythrocyte glutathione peroxidase activity was higher in trained groups compared with untrained sedentary group. Neither acute exhaustive exercise nor treadmill training affected the erythrocyte total glutathione level. Treadmill training increased the endurance time in trained rats compared with sedentary rats. The results of this study suggest that endurance training may be useful to prevent acute exhaustive exercise-induced oxidative stress in erythrocytes by up-regulating some of the antioxidant enzyme activities and may have implications in exercising humans.     

Effect of very low calorie diet on body composition and exercise response in sedentary women

Summary The effect of very low calorie diet (VLCD) on fat-free mass (FFM) and physiological response to exercise is a topic of current interest. Ten moderately obese women (aged 23–57 years) received VLCD (1695 kJ·day^–1) for 6 weeks. FFM, estimated by four conventional techniques, and heart rate (f _c), blood lactate (la_b), mean arterial pressure (MAP), respiratory exchange ratio (R) and rating of perceived exertion (RPE) were measured during a submaximal cycle ergometry test 1 week bevore, in the 2nd and 6th week, and 1 week after VLCD treatment. Strength and muscular endurance of the quadriceps and hamstrings were tested by isokinetic dynamometry. The 11.5-kg reduction in body mass was approximately 63% fat and 37% FFM. The latter was attributed largely to the loss of water associated with glycogen. Whilst exercise f _c increased by 9–14 beats·min^–1 (P<0.01), there were substantial decreases (P<0.01) in submaximal MAP (1.07–1.73 kPa), lab (0.75–1.00 mmol·1^–1 and R (0.07–0.09) during VLCD. R and f _c returned to normal levels after VLCD. Gross strength decreased (P<0.01) by 9 and 13% at 1.05 rad·s^–1 and 3.14 rad·s^s–1, respectively. Strength expressed relative to body mass (Nm·kg^–1) increased (P<0.01) at the lower contraction velocity, but there was no change at the faster velocity. Muscular endurance also decreased (P<0.01) by 62 and 82% for the hamstrings and quadriceps, respectively: We concluded that the strength decrease was a natural adaptation to the reduction in body mass as the ratio of strength to FFM was maintained. Despite the physiological alterations, subjects could tolerate short-term, steady-state exercise during VLCD, with only slight increases in RPE. However, greater fatigue is associated with long duration strength training exercises during VLCD.     

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.     

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.     

Exhausting handgrip exercise reduces the blood flow in the active calf muscle exercising at low intensity

The calf and forearm blood flows (Q _calf and Q _forearm respectively), blood pressure, heart rate and oxygen uptake of six men and women were studied during combined leg and handgrip exercise to determine whether a reduction of exercise-induced hyperaemia would occur in the active leg when exhausting rhythmic handgrip exercise at 50% maximal voluntary contraction (MVC) was superimposed upon rhythmic plantar flexion lasting for 10 min at 10% MVC (P₁₀) prior to this combined exercise. The Q _calf and Q _forearm were measured by venous occlusion plethysmography during 5-s rests interposed during every minute of P₁₀ exercise and immediately after combined exercise. The muscle sympathetic nerve activity (MSNA) changes were also recorded during leg exercise alone and combined exercise. During plantar flexion performed 60 times · min^–1 with a load equal to 10% MVC (P₁₀), Q _calf was maintained at a constant level, which was significantly higher than the resting value (P < 0.001). When rhythmic handgrip contraction at 50% MVC (H₅₀) and P₁₀ were performed simultaneously, the combined exercise was concluded due to forearm exhaustion after a mean of 51.2 (SEM 5.5) s. At exhaustion, Q _calf had decreased significantly from 20.6 (SEM 3.0) ml · 100 ml^–1 · min^–1 (10th min during P₁₀ exercise) to 15.3 (SEM) ml · 100 ml^–1 · min^–1 (P = 0.001), whereas Q _forearm had increased significantly (0.001 < P < 0.01) from 8.6 (SEM 1.9) ml · 100 ml^–1 · min^–1 (10th min of P₁₀ exercise) to 26.2 (SEM 3.2) ml · 100 ml^–1 · min^–1. The mean blood pressure remained at an almost constant level during the 3rd to 10th min of P₁₀ exercise and increased markedly when H₅₀ was added. The calf vascular conductance during combined exercise decreased significantly (0.001 < P < 0.01) compared with that at the 10th min of P₁₀ alone. Although the MSNA (expressed as burst rate) remained unchanged during P₁₀ exercise for 10 min, it increased markedly when exhausting H₅₀ and P₁₀ exercise were performed simultaneously. These findings indicated that superimposition of exhausting handgrip exercise at 50% MVC caused a vasoconstriction in the exercising calf due to increased MSNA, which counteracted the vasodilatation in this active muscle.     

A single session of resistance exercise enhances insulin sensitivity for at least 24 h in healthy men

The aim of the present study was to determine whether a single session of resistance exercise improves whole-body insulin sensitivity in healthy men for up to 24 h. Twelve male subjects (23±1 years) were studied over a period of 4 days during which they consumed a standardized diet, providing 0.16±0.01 MJ·kg^–1·day^–1 containing 15±0.1 energy% (En%) protein, 29±0.1 En% fat and 55±0.3 En% carbohydrate. Insulin sensitivity was determined 24 h before and 24 h after a single resistance exercise session (8 sets of 10 repetitions at 75% of 1 repetition maximum for two leg exercise tasks) using an intravenous insulin tolerance test. Insulin sensitivity index was calculated by the decline in arterial blood glucose concentration following intravenous administration of a single bolus of human insulin (0.075 IU·kg^–1 fat free mass). Basal glucose and insulin concentrations were not changed up to 24 h after the resistance exercise. However, a substantial 13±5% improvement in whole-body insulin sensitivity was observed, 24 h after the resistance exercise (P<0.05). This study shows that even a single session of resistance exercise improves whole-body insulin sensitivity for up to 24 h in healthy men, which is consistent with earlier observations following endurance exercise tasks.     

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.     

Sodium citrate and anaerobic performance: implications of dosage

Summary The use of sodium bicarbonate to improve anaerobic performance is well known but other buffering agents have been used with some success. Sodium citrate is one such substance which has been used but without the normal gastro-intestinal discomfort usually associated with sodium bicarbonate ingestion. The effects of five doses of sodium citrate (0.1 g·kg^–1 body mass, 0.2 g·kg^–1 body mass, 0.3 g·kg^–1 body mass, 0.4 g·kg^–1 body mass and 0.5 g·kg^–1 body mass) on anaerobic performance were studied in order to determine the minimal and most productive dose required for performance enhancement. A maximal test was performed for 1^–1, min on a cycle ergometer. Total work and peak power were measured at the end of the exercise period. Blood was drawn 1.5 h prior to the test session and measured for pH, partial pressure of carbon dioxide and concentrations of bicarbonate, base excess and lactate. In all but the control and placebo trials subjects then ingested one of five doses of sodium citrate which was contained in 400 ml of flavoured drink. Blood was again taken 90 min later and this was repeated after the completion of the exercise test. The greatest amount of work was completed in the trial with citrate given at 0.5 g·kg^–1 body mass (44.63 kJ, SD 1.5) and this was also true for peak power (1306 W, SD 75). The post-exercise blood lactate concentration was also highest during this trial 15.9 mmol·1^–1, SD 1.1. Post-exercise pH decreased significantly in all trials (P<0.0001) while the administration of the sodium citrate in all doses above 0.1 g·kg^–1 body mass significantly increased resting pH values. Blood bicarbonate concentrations also increased with dose in an almost linear fashion with the administration of sodium citrate. Bicarbonate increases were all significant, P<0.05 (citrate 0.1 g·kg^–1 body mass), P<0.01 (citrate 0.2 g·kg^–1 body mass, 0.3 g·kg^–1 body mass and 0.4 g·kg^–1 body mass) and P<0.005 (citrate 0.5 g·kg^–1 body mass). The administration of sodium citrate also significantly increased base excess values (citrate 0.1 g·kg^–1 body mass,P<0.01; 0.2 g·kg^–1body mass, P<0.001; 0.3 g·kg^–1 body mass, P<0.001; 0.4 g·kg^–1 body mass, P<0.001; 0.5 g·kg^–1 body mass, P<0.0001) above control and placebo values. All post-exercise base excess values were significantly lower than basal or pre-exercise values (P<0.0001). It was concluded that sodium citrate was an effective ergogenic aid for anaerobic performance of approximately 60-s duration, with the most effective of those dosages tested being 0.5 g·kg^–1 body mass.     

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.     

Dietary intervention and training in swimmers

Summary To ascertain if muscle damage occurred in swimmers as a result of high-intensity training and to find if fluid and dietary manipulation could affect muscle damage, we studied 40 members of the University of Florida swimming team using creatine kinase (CK) and lactic dehydrogenase (LDH) as markers of muscle damage during a 6-month period of intensive training. During this time, training intensity, fluid intake during exercise and dietary supplementation were all modified one by one to examine their individual effects. During a control period of 4 weeks, all swimmers drank water before and during (120 min) workouts. CK in men at the end of this period averaged 315, SD 122 (normal < 170 IU · l^–1). Half of the swimmers were then given 500 ml of a glucose-electrolyte solution (GES) (Na 21 mmol · l^–1, Cl 13 mmol · l^–1, K 2.5 mmol · l^–1, PO₄ 5 mmol · l^–1 and glucose 6%) before workouts and twice at intervals during the workout, while half continued to drink the same volume of water. One week after division into fluid groups, the workout intensity was increased by about 10%. Another week later CK had increased to 500, SD 180 IU · l^–1 in swimmers drinking water, but fell to 280, SD 105 IU · l^–1 in those drinking GES (P < 0.05). The second phase of the study began after a 4-week control period during which all athletes drank water before and during workouts. The swimmers were divided into four matched groups. Group I drank water before and during workouts and 250 ml of a 16% sucrose solution after; group II drank water before and during exercise and 250 ml of a milk protein supplement (MPS) containing 15 g lactalbumin and 16% sugar afterwards; group III drank GES before and during and the sucrose drink after exercise; group IV drank GES before and during and the MPS drink after exercise. Then during a 6-week period, the intensity of exercise was progressively increased by 25%. CK increased 61% (P < 0.01) in group I men, while it fell 12% (P < 0.05) in groups II and III, and 41% (P < 0.01) in group IV. In women, CK in group I increased 18% (P < 0.05); in group II it decreased 3.5%, in group III was unchanged, and in group IV declined 12.6% (P < 0.05). The final phase of the study was performed on 8 olympic swimmers who performed identical workouts each Saturday for 4 weeks. The 1st week they ingested water before and during exercise and the 16% sucrose solution afterwards. The 2nd week the GES solution was consumed before and during exercise and the sucrose solution afterwards. The 3rd week water was consumed before and during and MPS afterward and the 4th week GES before and during and MPS afterwards. Determination of CK and LDH before, immediately after, and at intervals afterwards showed that CK and LDH increased less when GES was the test fluid during exercise than when water was consumed. Recovery, as judged by return of CK and LDH to control values was more rapid when MPS was the post-exercise fluid than when the sucrose solution was given.     

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.     

The effect of reactive oxidant generation in acute exercise-induced proteinuria in trained and untrained rats

Exercise-induced proteinuria is a common consequence of physical activity, although its mechanism is not clear. We investigated whether free radicals generated during exercise play a role in post-exercise proteinuria in sedentary and treadmill-running trained rats, separately. Sedentary and trained rats were randomly divided into four sub-groups: control, antioxidant treatment, exhaustive exercise and an exhaustive exercise plus antioxidant treatment group. Antioxidant therapy was applied by intragastric catheter for 4 weeks with vitamin C (ascorbic acid, 50 mg·kg^–1·day^–1) and vitamin E (-tocopherol, 20 mg·kg^–1·day^–1). Twenty-four-hour urine samples were used for measuring protein levels and protein electrophoresis. Thiobarbituric acid (TBARS) and glutathione (GSH) levels, superoxide dismutase (SOD) and catalase (CAT) activities were assayed in blood and tissues. Increased urinary protein levels and mixed type proteinuria in electrophoresis were identified after exhaustive exercise in sedentary rats. Erythrocyte, kidney and muscle TBARS levels were significantly elevated in this group. Antioxidant treatment prevented the increase in urinary protein levels, TBARS levels and the occurrence of mixed type proteinuria after exhaustive exercise in sedentary rats. Exhaustive exercise in trained rats resulted in elevation of urine protein levels and mixed type proteinuria although kidney TBARS levels were not changed compared to those of the trained controls. Antioxidant therapy in trained and exhausted-trained animals resulted in decreased TBARS levels in the kidney but it did not affect urinary-increased protein levels or electrophoresis in exhausted animals. This findings suggest that the exercise-induced oxidant stress may contribute to post-exercise proteinuria in sedentary rats. However, this mechanism may not be responsible for proteinuria in trained rats.