Sympathetic response to maximal bicycle exercise before and after leg strength training

Summary Plasma catecholamine concentrations at rest and in response to maximal exercise on the cycle ergometer (278±15 watts, 6 min duration) have been measured on seven young active male subjects (19±1 years old; 80±3 kg; 176±3 cm) prior to and after a eight week leg strength training program (5RM, squat and leg press exercise). Strength training resulted in a significant increase in performance on squat (103±3 to 140±5 kg) and leg press exercise (180±9 to 247±15 kg) associated with a small significant increase in lean body mass (64.5±2.2 to 66.3±2.1 kg) and no change in maximal oxygen consumption (47.5±1.3 to 46.9±1.2 ml · kg^–1 · min^–1). Plasma norepinephrine (NE) and epinephrine (E) concentrations (pg · mL^–1) were not significantly different before and after training at rest (NE: 172±19 vs 187±30; E: 33±10 vs 76±16) or in response to maximal exercise (NE: 3976±660 vs 4163±1081; E: 1072±322 vs 1321±508). Plasma lactate concentrations during recovery were similar before and after training (147±5 vs 147±15 mg · dL^–1). Under the assumption that the central command is reduced for a given absolute workload on the bicycle ergometer following leg strength training, these observations support the hypothesis that the sympathetic response to exercise is under the control of information from muscle chemoreceptors.Supported by grants from NSERC, Government of Canada and FRSQ, Government of Quebec     

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.     

Vascular fluid shifts and endocrine responses to exercise in the heat

Summary This study examines the relationships between vascular changes and endocrine responses to prolonged exercise in the heat, associated with dehydration and rehydration by fluids of different osmolarity. Five subjects were exposed, in a 34 C environment for 4 h of intermittent exercise on a cycle ergometer at 85±12 Watts (SD). Fluid regulatory hormones and cortisol were analysed in 3 experimental sessions: one without any fluid supplement (NO FLUID), and two with progressive rehydration, either by spring water (WATER) or isotonic solution (ISO), given after 70 min of exercise. Results were expressed in terms of differences between the mean values observed at the end of the exercise and the first hour values taken as references.Dehydration (NO FLUID) elicited a 4.0±0.8% (SE) decrease in plasma volume (PV) and an increase in osmolarity (8.4±3.1 mosmol · l^–1). Concomitantly, plasma aldosterone (PA), renin activity (PRA), arginin vasopressin (AVP) and cortisol (PC) levels increased greatly in response to exercise in the heat (PA: 37.2+-10.8 ng. 100 ml^–1; PRA: 13.4±2.5 ng · ml^–1 · h^–1; AVP: 3.8±1.3 pg · ml^–1; PC: 12.2±2.7 g · 100 ml^–1). Rehydration with water led to decreased osmolarity (–8.2±2.1 mosmol · l^–1) with no significant changes in PV. With ISO, PV increased by 6.0±1.3% and the decrease in osmolarity was –5.8±1.8 mosmol · l^–1. With both modes of rehydration, the increases in PRA, AVP and cortisol were blunted; only ISO prevented the rise in PA.These data indicate that prolonged exercise in moderate heat is extremely effective in increasing cortisol and fluid-electrolyte regulatory hormones in dehydrated subjects. Progressive rehydration with water or isotonic solution, in the absence of osmotic and volemic stimuli, prevents the hormonal increases.     

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

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

Plasma renin activity,aldosterone and catecholamine levels when swimming and running

Summary The purpose of this study was to determine the response of plasma renin activity (PRA), plasma aldosterone concentration (PAC) and catecholamines to two graded exercises differing by posture. Seven male subjects (19–25 years) performed successively a running rest on a treadmill and a swimming test in a 50-m swimming pool. Each exercise was increased in severity in 5-min steps with intervals of 1 min. Oxygen consumption, heart rate and blood lactate, measured every 5 min, showed a similar progression in energy expenditure until exhaustion, but there was a shorter time to exhaustion in the last step of the running test. PRA, PAC and catecholamines were increased after both types of exercise. The PRA increase was higher after the running test (20.9 ng AngI · ml^–1 · h^–1) than after swimming (8.66 ng AngI · ml^–1 · h^–1). The PAC increase was slightly greater after running (123 pg · ml^–1) than swimming (102 pg · ml^–1), buth the difference was not significant. Plasma catecholamine was higher after the swimming test. These results suggest that the volume shift induced by the supine position and water pressure during swimming decreased the PRA response. The association after swimming compared to running of a decreased PRA and an enhanced catecholamine response rule out a strict dependence of renin release under the effect of plasma catecholamines and is evidence of the major role of neural pathways for renin secretion during physical exercise.     

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.     

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.     

Left ventricular performance during prolonged exercise and early recovery in healthy subjects

The effect of semi-supine long lasting exercise to exhaustion [61 (SD 10) min] on left ventricular systolic performance was studied by echocardiography in 16 young healthy volunteers. During the incremental phase of exercise, the ejection fraction increased from 65.2 (SD 4.1)% to 80.1 (SD 4.8)% (P<0.0001), then it levelled off up to the end of exercise [81.7 (SD 4.4)%,P<0.0001 vs rest]. During recovery, the ejection fraction rapidly and steadily decreased to a value similar to that at rest [66.1 (SD 5.0)%, n.s.). A similar pattern was shown by the systolic blood pressure/end-systolic volume coefficient, which rose from 3.2 (SD 0.8) mmHg · ml^–1 to 7.5 (SD 2.7) mmHg · ml^–1 (P < 0.0001) in the initial phase and subsequently did not change until the end of exercise [7.0 (SD 2.2) mmHg · ml^–1,P<0.0001 vs rest], to fall sharply after the cessation of exercise [2.9 (SD 1.1) mmHg · ml^–1 at the 10th min, n.s. vs rest]. Exercise and recovery indices of left ventricular performance were not correlated with exercise duration, maximal heart rate and increase in free fatty acids. The present results indicated that, after the initial increase, left ventricular performance remained elevated during prolonged high intensity exercise and that conclusions on exercise cardiac performance drawn from postexercise data can be misleading.     

Blood volume changes and arginine vasotocin (AVT) blood concentration in conscious fresh water and salt water adapted ducks

Blood volume changes consisting in the removal and reinfusion respectively, of 10% of the estimated blood volume (23.2 ml on average) were induced to determine their effects on the blood concentration of arginine vasotocin (AVT), the antidiuretic hormone (ADH) of birds, in fresh water adapted ducks (water ducks) with blood osmolalities and ADH concentrations similar to those of normally hydrated mammals, and in salt water adapted ducks (salt ducks) with chronically elevated blood osmolalities and ADH concentrations. The investigations were carried out in steady state conditions, when infusion of 1 ml·min^–1 of isotonic saline was matched by the excretion in water ducks and when infusion of 0.4 ml·min^–1 of 1,000 mosmolal saline was matched by the salt gland excretion in the salt ducks.After blood removal, AVT blood concentration (mean ±SE) increased from 6.5±0.4 to 8.4±0.6 pg·ml^–1 in water ducks and from 18.1±1.6 to 22.6±1.9 pg·ml^–1 in salt ducks. The respective blood osmolalities of 297.4±1.4 and 318.6±3.3 mOsm·kg^–1 did not change. Reinfusion of the blood after steady-state conditions had been reattained decreased blood AVT from 7.9±0.7 to 6.7±0.5 pg·ml^–1 in water ducks. In the salt ducks AVT concentration had already returned to the control level before blood reinfusion which induced no further reduction. The blood osmolalities remained unchanged in both groups.During blood removal and reinfusion, the excretion rate of the kidneys in water ducks and the salt glands in salt ducks were temporarily reduced and enhanced respectively, the effect being not symmetrical for salt gland secretion.For water ducks, the volume sensitivity of AVT release was found comparable to that of mammals, when related to the induced blood volume changes, the responses to blood removal and reinfusion being approximately equal in absolute terms. In the salt ducks, the volume sensitivity of AVT release was clearly expressed during blood removal but insignificant during blood reinfusion.Supported by the Alexander v. Humboldt-StiftungSupported by the Deutsche Forschungsgemeinschaft     

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.     

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     

One- and two-dimensional echocardiography in bodybuilders using anabolic steroids

Summary The object of this study was to investigate the possible concentric increase in the left ventricular (LV) wall thickness by intensive strength training and to differentiate between the specific effect of the strength training itself and the influence of anabolic drugs. In this study 21 top-level bodybuilders [users of anabolic steroids (A): n=14; non-users (N): n=7] underwent one-dimensional and two-dimensional echocardiography as well as a cycle ergometer test. In both groups blood pressure at rest and during ergometric exercise was within the normal range. In spite of the same amount of time being spent on training, A showed significantly better power results than N. Total heart volume (A=11.3±0.9 ml · kg^–1; N=11.9±0.9 ml · kg^–1) and LV muscle mass were almost identical in A and N and correlated significantly with body weight and lean body mass respectively. The body dimension-related diastolic LV diameter was significantly lower in A (0.567±0.062 mm · kg^–1) than in N (0.639±0.040 mm · kg^–1). An increase in the LV posterior wall (p<0.01) and septum thickness (ns) resulted in increased LV wall thickness:diameter (p<0.01) and LV muscle mass:volume (p<0.05) ratios in A (0.458±0.590; 1.38± 0.25 g · ml^–1) in comparison to N (0.356±0.077; 1.16±0.17 g · ml^–1). The septal:posterior wall thickness ratio was similar for both groups. Systolic LV function did not differ between A and N, while the isovolumetric relaxation time was prolonged in A (A=43.2±19.8 ms; N=28.6±9.9 ms; p<0.05), without correlating to wall thickness. Clearly thickened LV walls (>13 mm) were observed only in bodybuilders regularly using anabolic steroids (n=11). The study suggests that the intake of anabolic steroids combined with intense bodybuilding may induce a minor concentric increase in the ventricular wall thickness along with a minor impairment of diastolic function.     

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.     

Limb vasodilatory capacity and venous capacitance of trained runners and untrained males

Aerobically trained athletes possess enhanced vasodilatory capacity and venous capacitance in their exercising muscles. However, whether they also possess these characteristics in their non-specific exercising muscles is undetermined. This study examined vasodilatory capacity and venous capacitance of specific (legs) and non-specific exercising muscles (arms) of ten trained runners and ten active but untrained males aged 18–35 years. Venous occlusion plethysmography determined baseline and peak blood flow after 5 min of reactive hyperaemia. Forearm and leg venous capacitance were determined as the difference between baseline and 2 min of venous occlusion at 50 mmHg. During reactive hyperaemia, trained runners had higher leg (48.4±5.3 ml·100 ml tissue^–1·min^–1) and arm (40.8±2.1 ml·100 ml tissue^–1·min^–1) vasodilatory capacity compared to the untrained (leg: 37.3±2.5 ml·100 ml tissue^–1·min^–1; arm: 34.2±2.2 ml·100 ml tissue^–1·min^–1; P<0.05), and higher calf vascular conductance (0.51±0.06 ml·100 ml tissue^–1·min^–1·mmHg^–1 versus 0.35±0.03 ml·100 ml tissue^–1·min^–1·mmHg^–1; P<0.05). The trained also had higher venous capacitance in both arms (3.5±0.2 ml 100·ml^–1) and legs (4.8±0.1 ml·100 ml^–1) compared to the untrained (3.0±0.2 ml 100·ml^–1; 4.2±0.2 ml·100 ml^–1; P<0.05). These findings show that vasculature adaptations to running occur in both specific and non-specific exercising muscles.     

Plasma adrenocorticotrophin and cortisol responses to acute hypoxia at rest and during exercise

Summary Plasma adrenocorticotrophin (ACTH) and cortisol (F) concentrations were studied in six male subjects under normoxic (N) and acute hypoxic (H) conditions (altitude 3000 m) in a hypobaric chamber. Comparisons were made at rest, at 15, 30, and 60 min of exercise (65% ), and after a 10 min recovery period. Mean (±SE) resting plasma ACTH levels were significantly higher in H (18.6±5.7 pmol · l^–1) than in N (9.6±1.6 pmol · l^–1) but no difference in resting plasma cortisol was observed between the two conditions. Both plasma ACTH and F concentrations were significantly increased at 60 min of exercise and during the recovery period under normoxic conditions. Hypoxia did not affect the ACTH response to exercise but reduced cortisol elevation. The changes in plasma cortisol concentration from rest to exercise were significantly correlated to ACTH under normoxic (r=0.89,p<0.001) but not under hypoxic (r=0.43, NS) conditions. Plasma lactate concentration was higher at the end of exercise in hypoxia (p<0.01), and no correlation existed between plasma lactate and ACTH levels. These observations provide further evidence that at sea level the increase in plasma cortisol levels during exercise is the result of ACTH-induced steroidogenesis. The responses observed at rest and during exercise in hypoxia suggest that adrenal sensitivity for ACTH may be altered.     

Interleukin-6 response to exercise during acute and chronic hypoxia

Prolonged exercise is associated with increased plasma levels of the cytokine interleukin-6 (IL-6). Both circulating catecholamine levels and exercise intensity have been related to the exercise-derived IL-6. During hypoxia and acclimatization, changes in sympathetic activity is seen, and also a given workload becomes more intense in hypoxia. Therefore, hypoxia offers a unique opportunity to study the effect of catecholamines and intensity on exercise-derived IL-6. In the present study, eight Danish sea-level residents performed 60 min of cycle ergometer exercise at sea level (SL) (154 W, 45% maximal O₂ consumption, O₂max), in acute (AH) and chronic hypoxia (CH), at the same absolute (_abs) (AH_abs=154 W, 54% O₂max; CH_abs=154 W, 59% O₂max) and same relative (_rel) (AH_rel=130 W, 46% O₂max; CH_rel=120 W, 44% O₂max) workload. We hypothesized that the IL-6 response to exercise at the same absolute workload would be augmented during hypoxia compared with sea level, and that these changes would not correlate with changes in catecholamines. In AH_abs (2.35 pg·ml^–1) and CH_abs (3.34 pg·ml^–1) the IL-6 response to exercise was augmented (p<0.05) compared with that at sea level (0.78·ml^–1). In addition, after 60 min of bicycling at sea level, AH_rel (1.02 pg·ml^–1) and CH_rel (1.31 pg·ml^–1) resulted in similar IL-6 responses. The augmented IL-6 response during AH_abs and CH_abs did not match changes in circulating catecholamine levels when comparing all trials. We conclude that the plasma IL-6 concentration during exercise in hypoxia is intensity dependent, and that factors other than catecholamine levels are more important for its regulation.     

Effects of dichloroacetate on exercise performance in healthy volunteers

Dichloroacetate (DCA), a stimulator of the pyruvate dehydrogenase complex, decreases lactate levels and peripheral resistance and increases cardiac output. This study was performed to examine the effects of DCA on exercise performance in humans. Eight healthy male volunteers (age 20–28 years) were tested by bicycle spiro-ergometry using a microprocessor-controlled gas analysis system after infusion of DCA (50 mg/kg body weight) or saline. Prior infusion of DCA significantly reduced the increase of lactate levels during exercise when compared with infusion of saline (1.40±0.21 vs 2.10±0.09 mmol·l^–1 at 50% of the expected maximal working capacity, P<0.05; 8.53±0.45 vs 9.92±0.59 mmol·l^–1 at maximal working capacity, P<0.05). Oxygen uptake increased significantly after DCA when compared with saline from 7.5±0.4 vs 7.4±0.5 to 27.2±1.5 vs 23.7±1.7 (P<0.05) at anaerobic threshold and to 35.6±1.7 vs 30.5±1.0 ml · kg^–1 min^–1 (P<0.05) at maximal exercise capacity. Following DCA infusion the workload at which the anaerobic threshold was reached was significantly higher (160±7 vs 120±5 W, P<0.05) and the maximal working capacity was significantly increased (230±9 vs 209±8 W, P<0.05). In summary, DCA reduced the increase of lactate levels during exercise and increased oxygen uptake at the anaerobic threshold and at maximal working capacity, which was significantly increased. These results warrant further studies on a potential therapeutic application of DCA in patients with reduced exercise capacity.     

Effect of high intensity interval training on 2,3-diphosphoglycerate at rest and after maximal exercise

Summary The purpose of this study was to examine the effect of intense interval training on erythrocyte 2,3-diphosphoglycerate (2,3-DPG) levels at rest and after maximal exercise. Eight normal men, mean ± SE=24.2±4.3 years, trained 4 days·week^–1 for a period of 8 weeks. Each training session consisted of eight maximal 30-s rides on a cycle ergometer, with 4 min active rest between rides. Prior to and after training the subjects performed a maximal 45-s ride on an isokinetic cycle ergometer at 90 rev·min^–1 and a graded leg exercise test (GLET) to exhaustion on a cycle ergometer. Blood samples were obtained from an antecubital vein before, during and after the GLET only. Training elicited significant increases in the amount of work done during the 45-s ride (P<0.05), and also in maximal oxygen uptake ( max: Pre=4.01±0.13; Post=4.29±0.07 l·min^–1;P<0.05) during exercise and total recovery (Pre=19.14±0.09; Post=21.45±0.10 l·30 min^–1;P<0.05) after the GLET. After training blood lactate was higher, base excess lower and pH lower during and following the GLET (P<0.05 for all variables). Training caused no significant differences in erythrocyte 2,3-DPG levels at rest (Pre=11.8±0.7; Post=12.1±0.7 mol·g^–1 hemoglobin (Hb);P>0.05), at exhaustion (Pre=12.0±0.8; Post=11.2±0.8 mol·g^–1 Hb;P>0.05) or during 30 min of recovery from the GLET. Additionally, acute exercise (pre-training GLET) did not effect any change in 2,3-DPG at exhaustion or during recovery from exercise compared to resting values. The higher max and total recovery values observed after training appear to be unrelated to 2,3-DPG levels. Under the present conditions, the role, if any, of 2,3-DPG in enhancing tissue oxygenation during increased metabolic demand remains obscure.Supported by grants from Miles Laboratories, Elkhart, Indiana, and the Ball State Graduate Student Research Fund     

Effect of exercise on systemic blood pressure and heart rate in horses

Summary Carotid loops were prepared in 3 horses several months prior to the experiments. Systemic blood pressure was recorded at rest and during exercise by insertion of a plastic cannula into the carotid artery. The pressure transducer was fixed at the neck of the animal. The blood pressure signal was transmitted by telemetry.When the horses were standing under the rider, the following results were obtained: heart rate 38±5 beats · min^–1, systolic pressure 115±15, disstolic pressure 83±10, mean pressure 97±12, and pulse pressure 32±9 mm Hg. During steady gallop at a mean speed of 548±90 m · min^–1, heart rate rose to 184±23 beats · min^–1, systolic pressure to 205±23, diastolic pressure to 116±12, mean pressure to 160±20 and pulse pressure to 89±19 mm Hg. These values remained stable throughout the exercise period of 5–6 min.When the horses were exercised at stepwise increasing speed from walk through trot to gallop, both the mean arterial blood pressure and the pulse pressure rose in proportion to the running speed.     

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.