Treadmill exercise negatively affects visual contribution to static postural stability.

This study was undertaken to explore the nature of impaired postural stability following physical exercise. Nine healthy subjects (aged 24 +/- 3 years) were subjected to 30 min of treadmill walking or running on two separate occasions. Walking and running speeds (1.9 to 2.2 m/s) were chosen to induce equal energy expenditure. During treadmill exercise, kinematic analysis of head movement was performed. Prior to and immediately following exercise, postural sway was evaluated as mean velocity of centre of pressure (VCOP), measured on a force plate during 30 s quiet stance with eyes open or eyes closed. The results indicate that exercise increased two-dimensional postural sway by 9 - 19 % in eyes open, but not in the eyes closed condition. The deteriorating effect of exercise was both evident in the sagittal and in the frontal plane, although the effect on the former was slightly more transient. Post-exercise sway values were significantly higher after running than after walking. Kinematic analysis of head movement confirmed larger vertical displacement and acceleration pattern in running compared to walking. It is concluded that exercise of moderate intensity deteriorates visual contribution to postural stability. The effect is evident as an initial destabilisation in the sagittal direction and a less transient loss of latero-lateral stability. Running tends to disturb postural stability more than walking, possibly due to more excessive head movement and disturbance of vestibular and visual information centres.

Carbohydrate availability affects ammonemia during exercise after beta 2-adrenergic blockade.

PURPOSE: Beta-adrenergic blockade increases blood ammonia concentration during exercise. The purpose of this study was to assess the role of decreased carbohydrate availability in this process. METHODS: Wistar rats (N = 47) were injected intravenously with a selective beta 2-adrenoceptor blocker (ICI 118,551), placebo, or beta 2-blocker + glucose 1 h before a treadmill exercise test. Blood samples were taken to measure the concentration of ammonia, glucose, lactic acid, free fatty acids (FFA), glycerol, branched-chain amino acids (BCAA), and muscle samples for determination of glycogen content. RESULTS: Beta 2-adrenergic blockade shortened running time to exhaustion (23 +/- 4.3 min compared to 44 +/- 5.2 min with placebo), increased blood ammonia levels (146.7 +/- 16.21 micromol x L(-1) compared to 47.5 +/- 0.92 micromol x L(-1) with placebo) and prevented exercise-induced glycogen breakdown in soleus and gastrocnemius muscles. Pre-exercise supplementation of glucose during beta 2-blockade restored exercise-induced glycogen breakdown and reduced blood ammonia concentration during exercise (66.5 +/- 5.65 mmol x L(-1)) but did not improve exercise capacity (26 +/- 3.2 min) when compared with beta2-blockade alone. CONCLUSION: The results suggest that the enhanced rise in blood ammonia concentration during exercise after beta-blockade is caused by impaired carbohydrate availability.

Effect of branched-chain amino acids (BCAA), glucose, and glucose plus BCAA on endurance performance in rats.

PURPOSE: The purpose of this study was to assess the effects of pre-exercise administration of branched-chain amino acids (BCAA), glucose, and glucose plus BCAA on time to exhaustion during treadmill exercise in rats. METHODS: Wistar rats were injected intraperitoneally with 1 mL of saline (0.9% NaCl), BCAA (30 mg), glucose (100 mg), or glucose plus BCAA 5 min before either 45 min of submaximal exercise (N = 32) or running to exhaustion (N = 24). After the submaximal exercise test, blood was collected for the measurement of ammonia, BCAA, free tryptophan (free TRP), glucose, free fatty acid, and lactic acid, and muscle samples were taken from the m. soleus for determination of glycogen content. RESULTS: Mean run time to exhaustion was significantly longer after BCAA administration (158+/-26 min) compared with that after saline (118+/-35 min)(P<0.05) but not compared with that after glucose administration (179+/-21 min). When glucose is administered before exercise, the supplementary administration of BCAA had no additional effect on performance (171+/-12 min). The data on blood ammonia, ratio of free TRP/BCAA, and muscle glycogen did not provide a clue for explaining the higher endurance performance after BCAA supplementation. CONCLUSION: The results support the hypothesis that the effect of BCAA administration on performance could be related to carbohydrate availability during exercise.

The influence of exercise and dehydration on postural stability.

The aim of this study was to investigate the effects of exercise-induced and thermal dehydration on postural balance. Eight male subjects cycled for 2 h at a power output equal to 57-63% VO2max on two different occasions: once without drinking (NF) and once with intake of 1.9 l of a carbohydrate-electrolyte solution (FR). Before and after the exercise test, the velocity of the centre of pressure (COP) excursion was measured on a force platform during 30-s bipedal standing in normal position, feet side by side, and tandem position, feet heel to toe. On another occasion, eight subjects underwent seven consecutive sauna sessions (85 degrees C, 50% rh) of 15 min duration with no fluid replacement (S) to induce thermal dehydration. Mean fluid loss was 2.7 (+/- 0.4)%, 0.5 (+/- 0.5)% and 3.0 (+/- 0.6)% of body mass after NF, FR and S, respectively. Mean velocity of COP excursion after the exercise test was significantly higher in the NF than in the FR trial (p < 0.05). Postural stability was not influenced by S. In conclusion, prolonged exercise without fluid ingestion seems to negatively affect postural stability, whereas no effect is observed after exercise with fluid replacement or after thermal dehydration.

Inhaled salbutamol decreases blood ammonia levels during exercise in normal subjects.

The present study examines the effect of salbutamol, a beta2-adrenoreceptor agonist, on blood ammonia levels during an incremental cycle exercise test in healthy non-asthmatic subjects. Blood ammonia levels were lower after inhalation of 400 mcg of salbutamol than after placebo during submaximal exercise: 33+/-2 micromol x l(-1) v.s. 48+/-9 micromol x l(-1) at 220 W and 39+/-2 micromol x l(-1) v.s. 50+/-4 micromol x l(-1) at 260 W. At peak exercise there were no significant differences. The results suggest that beta2-adrenoreceptors are involved in the regulation of blood ammonia during exercise.

Pre-exercise branched-chain amino acid administration increases endurance performance in rats.

This study investigated the effects of pre-exercise branched-chain amino acid (BCAA) administration on blood ammonia levels and on time to exhaustion during treadmill exercise in rats. Adult female Wistar rats were trained on a motor driven treadmill. After a 24-h fast, rats were injected intraperitoneally (i.p.) with 1 mL of placebo or BCAA (30 mg), 5 min before performing 30 min of submaximal exercise (N = 18) or running to exhaustion (N = 12). In both cases, rats were sacrificed immediately following exercise, and blood was collected for the measurement of glucose, nonesterified fatty acid (NEFA), lactic acid, BCAA, ammonia, and free-tryptophan (free-TRP) levels. Control values were obtained from sedentary rats that were subjected to identical treatments and procedures (N = 30). Plasma BCAA levels increased threefold within 5 min after BCAA administration. Mean run time to exhaustion was significantly longer (P < 0.01) after BCAA administration (99 +/- 9 min) compared with placebo (76 +/- 4 min). During exercise, blood ammonia levels were significantly higher (P < 0.01) in the BCAA treated compared with those in the placebo treated rats both in the 30-min exercise bout (113 +/- 25 mumol.L-1 (BCAA) vs 89 +/- 16 mumol.L-1) and following exercise to exhaustion (186 +/- 44 mumol.L-1 (BCAA) vs 123 +/- 19 mumol.L-1). These data demonstrate that BCAA administration in rats results in enhanced endurance performance and an increase in blood ammonia during exercise.

Gender differences in blood ammonia response during exercise.

In order to test for possible gender differences in blood ammonia accumulation during exercise, groups of young, physically active women (n = 8) and men (n = 8) performed an incremental load (until exhaustion) and a constant load (30 min at 75% VO2 peak) treadmill exercise test. The groups were matched for physical activity habits. VO2 peak was significantly higher in males (55.8 +/- 2.6 ml/kg/min) than in females (44.5 +/- 2.8 ml/kg/min). During the incremental exercise test to exhaustion blood ammonia concentration progressively increased with increasing workload in both groups. Blood ammonia concentration was significantly higher in males at 70, 80 and 90% of VO2 peak. Peak blood ammonia concentration was higher in males than in females (155 +/- 35 vs 136 +/- 67 mumol/l, respectively), but the difference did not reach the level of statistical significance. During the constant load exercise test blood ammonia concentration increased in both groups. At the end of the exercise test blood ammonia concentration was significantly higher in males than in females (137 +/- 42 vs 91 +/- 24 mumol/l, respectively). In conclusion, the blood ammonia concentration during submaximal exercise is dependent on gender, the males showing higher ammonia concentrations compared to females at the same relative workload (percent of VO2 peak).

Effects of acute cardioselective and non-selective beta-adrenergic blockade on plasma ammonia levels in exercising dogs.

The aim of this study was to assess plasma ammonia levels during acute treadmill exercise in dogs after intravenous administration of a single dose of different cardioselective (atenolol) and non-selective (sotalol and propranolol) beta-adrenergic blocking drugs. The experiments were performed on 6 male mongrel dogs (20-25 kg) trained to run on a motor driven treadmill. After administration of saline or atenolol, there was no significant increase in plasma ammonia during exercise; propranolol and sotalol however, both non-selective beta-blockers, produced a significant increase in plasma ammonia. Plasma levels of alanine and glutamine were not altered during exercise compared with resting values, and were not modified by the administration of beta-blockers. It is not clear whether the different effects on exercise induced hyperammonemia are due to different effects on muscle ammonia formation or on the ammonia clearance by the liver.

Cardiorespiratory variables during a continuous ramp exercise protocol in normal young adults.

The purpose of the present study was to determine whether the cardiorespiratory variables measured during an exercise test with a continuously increasing workload (ramp) protocol are reproducible and to compare them to the values obtained with a step-wise incremental (James) protocol. Twenty normal adolescents and young adults performed two exercise tests on a cycle-ergometer, one with each protocol, and twelve of these subjects additionally performed a second identical ramp test. The results show that the cardiorespiratory variables measured during exercise with ramp protocol are reproducible and that peak values are not different from those obtained with step-wise incremental exercise protocol, except for a higher peak power. At intermediate equivalent workloads, there were significant correlations between cardiorespiratory variables measured in steady-state conditions with the incremental protocol and those obtained in non-steady-state conditions with the ramp protocol.

Effects of acute non-selective beta-adrenergic blockade on plasma ammonia levels in exercising dogs.

The purpose of the present study was to document exercise induced hyperammoniemia after blockade of the beta-adrenoceptors and to investigate the effect of administration of branched-chain amino acids (BCAA) and glucose in these conditions. Seven dogs, chronically instrumented with a catheter in the deep jugular vein and a Doppler probe around the carotid artery were trained to perform a ten-minute treadmill exercise test. Administration of propranolol i.v. prior to exercise increases plasma ammonia at peak exercise compared with placebo (78 +/- 7.9 vs 25 +/- 5.1 mumol/l; p < 0.05). This effect of propranolol on plasma ammonia during exercise is enhanced by the administration of BCAA (108 +/- 15 vs 78 +/- 7.9 mumol/l; p < 0.05), and diminished by the administration of glucose (42 +/- 7.7 vs 78 +/- 7.9 mumol/l; p < 0.05). These results suggest that increased metabolisation of BCAA is involved in the ammonia formation after beta-adrenergic blockade.

Blood ammonia response to treadmill and bicycle exercise in man.

Nine male healthy and physically active volunteers performed four different exercise tests: an incremental load exercise test to exhaustion and a constant load exercise test of 15 min at 65% VO2max, both on the bicycle ergometer and on the treadmill. During the incremental exercise test, blood ammonia levels were significantly higher on the bicycle ergometer as compared to the treadmill at the same submaximal VO2 (p < 0.05 at 80% of VO2max) and at the VO2max, which was identical in the two modes of exercise. Plasma lactate levels were also significantly higher on bicycle ergometer at high submaximal exercise intensity but not at VO2max. During the constant load exercise test blood ammonia levels increased continuously and showed no differences between cycling and running, in contrast to plasma lactate accumulation, which was higher on the bicycle ergometer. The finding that blood ammonia accumulation during exercise is critically dependent upon the test procedure has to be taken into account whenever blood ammonia measurements are used in the physiological monitoring of athletes.

The antiserotonin agent pizotifen does not increase endurance performance in humans.

This study investigated the effect of the serotonin receptor antagonist pizotifen on endurance performance during treadmill exercise in humans. Eight healthy men exercised to exhaustion on a treadmill at an intensity corresponding to 70% of their maximal oxygen uptake (VO2max). Pizotifen was administered orally in a 1-mg dose 5 h before the start of exercise. The study was double blind, using a randomized, placebo-controlled crossover design. Oxygen uptake, heart rate, and ratings of perceived exertion were measured and blood samples taken for determination of concentrations of lactate, glucose, amino acids, ammonia, and haematocrit. Measurements were made at intervals of 30 min during the run and at exhaustion. There was no significant difference between the placebo and the pizotifen trials for any of the variables except for the plasma free-tryptophane: branched chain amino acid ratio which was somewhat lower after pizotifen at postexercise. Pizotifen did not increase exercise time to exhaustion, which was even shorter after pizotifen than after placebo in seven out of the eight subjects; the difference between pizotifen and placebo did not reach the level of statistical significance [109.4 (SD 6.7) min after pizotifen versus 119.8 (SD 12.5) min after placebo]. The results do not support the hypothesis that there is a central component to fatigue which is mediated by the serotoninergic neurones.

Effect of adrenergic receptor blockade on plasma testosterone response to exercise in conscious dogs.

The aim of this study was 1) to establish the relationship between testosterone (T) levels and the intensity and duration of exercise in conscious dogs, and 2) to investigate the involvement of the sympathetic system in the response of plasma T to acute exercise. The experiments were performed on 14 male mongrel dogs (20-25 kg) trained to run on a motor driven treadmill. Testosterone (T), cortisol, epinephrine, norepinephrine, lactate and haematocrit were measured in arterial blood samples. A brief intensive exercise (leading to exhaustion within 5 or 20 min) induced a marked increase in plasma T, while during more prolonged (60 min) exercise plasma T showed an initial increase followed by a secondary decrease. Blockade of the beta adrenergic receptors with propranolol (Inderal 0.5 mg/kg i.v.) did not modify the changes of plasma T during exercise, but blockade of alpha adrenergic receptors with phentolamine (Regitine 0.5 mg/kg) lowered the exercise induced rise in plasma T.

Effect of specific test procedures on plasma lactate concentration and peak oxygen uptake in endurance athletes.

Plasma lactate accumulation during submaximal work and VO2peak were determined on the bicycle ergometer and on the treadmill in all round trained control subjects (n = 9) and in specifically trained athletes such as distance runners (n = 9) and racing cyclists (n = 8). Plasma lactate concentration at equivalent levels of oxygen uptake was lower during treadmill exercise than during bicycle exercise in the controls and in the runners, but the difference between the two work modalities was more pronounced in the runners. In contrast to the runners, the cyclists had a higher plasma lactate concentration on the treadmill. VO2peak values on the two ergometers were similar in the controls, while the specifically trained athletes reached the highest value when they were tested with the exercise test which is specific to the training conducted. In the runners VO2peak was 14% higher on the treadmill than on the bicycle ergometer and in the cyclists VO2peak was 11% higher on the bicycle ergometer. It is concluded that the difference in plasma lactate concentration during submaximal work and in VO2peak between treadmill and bicycle exercise can be affected by the training conditions of the subjects.

[Alpha-adrenergic control of coronary circulation and left ventricular function during exertion]. / Alfa-adrenerge controle van de coronaire doorbloeding en linker ventrikel functie tijdens inspanning.

Sympathetic activation is responsible for a striking inotropic and chronotropic response as well as for important coronary hyperemia during exercise. However the exact role of the coronary and myocardial alpha adrenergic receptors during sympathetic activation is not well defined. It is well accepted that coronary artery smooth muscle contains both alpha-1 and alpha-2 adrenergic receptors which elicit a vasoconstrictor response upon neurogenic and humoral stimulation. It seems however paradoxical that coronary vasoconstriction should occur in conditions of increased myocardial oxygen consumption such as during exercise. On the other hand, presynaptic alpha-2 receptors have been identified at the sympathetic nerve endings which, when stimulated by the locally released norepinephrine, will attenuate further norepinephrine release through a negative feed-back mechanism. A possible regulatory role of this mechanism for the left ventricular and coronary flow response during exercise has not been established. The major goal of this work was to define the exact role of alpha adrenergic receptors for the regulation of cardiac function and coronary circulation during exercise. Left ventricular function, coronary circulation, myocardial metabolism and catecholamine release were analysed during standardized treadmill exercise in conscious chronically instrumented dogs, prior to and following the administration of different alpha receptor blockers with different affinities for the different subtypes of alpha receptors. Three series of experiments were conducted to clarify: 1. the role of postsynaptic alpha receptors for the regulation of coronary blood flow during exercise, 2. the role of presynaptic alpha receptors for the regulation of left ventricular function during exercise, and 3. the role of postsynaptic alpha receptors for the regulation of transmural myocardial blood flow distribution during exercise. Dogs were instrumented with a solid state pressure transducer in the left ventricular cavity, a Doppler flow probe around the left circumflex coronary artery, and silastic catheters in aorta, left atrium and coronary sinus. 2-3 weeks after surgery the dogs were subjected to standard treadmill exercise. Simultaneous and continuous measurements were performed of heart rate, left ventricular systolic and end diastolic pressure, LV dP/dt/P, mean arterial pressure, late diastolic coronary vascular resistance, regional myocardial blood flow, myocardial oxygen consumption and plasma catecholamines. In the first series of experiments, coronary blood flow and myocardial oxygen consumption were analyzed in 15 conscious dogs at rest and during exercise prior to and following IV administration of phentolamine (1 mg/kg) or prazosin (0.5 mg/kg).(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of diltiazem and atenolol on exercise performance in man.

The effects of diltiazem and atenolol on exercise performance were studied in 9 healthy and physically fit volunteers according to a double-blind cross-over design. All subjects performed, with an interval of 1 week, 3 exercise tests on a treadmill with stepwise increase of the workload until exhaustion. Two hours prior to each exercise test they received in a randomised order placebo, diltiazem 120 mg or atenolol 100 mg. Running time and VO2peak were not influenced by diltiazem, while running time was significantly reduced (-10%) after atenolol. The reduction of VO2peak (-9%) after atenolol did not reach statistical significance. Both diltiazem and atenolol significantly decreased heart rate at peak effort but the decrease was much more pronounced after atenolol (-52 b.min-1) than after diltiazem (-6 b.min-1). At submaximal level VO2 was not influenced by diltiazem, but significantly lowered (-6%) after atenolol. Submaximal heart rate was decreased and plasma lactate concentration was increased by both diltiazem and atenolol, but the effect of atenolol was more pronounced. The study shows that maximal work performance of young healthy subjects is not affected by diltiazem 120 mg, in contrast to atenolol 100 mg which decreases maximal work performance in the same subjects.

Cardiorespiratory response to bicycle and rowing ergometer exercise in oarsmen.

Maximal aerobic power and related variables during submaximal work were determined on the bicycle and on the rowing ergometer in 9 oarsmen and in 9 control subjects. During submaximal work, heart rate and pulmonary ventilation were similar with the two exercise procedures in each group, but the oarsmen had lower values than the control subjects. Oxygen uptake at a given workload was higher on the rowing ergometer than on the bicycle ergometer for both the oarsmen and the control subjects. During maximal exercise, the control subjects reached significantly lower values on the rowing ergometer than on the bicycle ergometer for maximal oxygen uptake and maximal oxygen pulse. The oarsmen however attained practically the same values on the two ergometers, with a rank difference correlation coefficient of 0.94. The difference between the results obtained in control subjects and in oarsmen supports the concept of training specificity.

alpha-Adrenergic control of oxygen delivery to myocardium during exercise in conscious dogs.

alpha-Adrenergic control of the oxygen delivery to the myocardium during exercise was investigated in eight conscious dogs instrumented for chronic measurements of coronary blood flow, left ventricular (LV) pressure, aortic blood pressure, and heart rate and sampling of arterial and coronary sinus blood. After alpha-adrenergic receptor blockade a standard exercise load elicited a significantly greater increase in heart rate, rate of change of LV pressure (LV dP/dt), LV dP/dt/P, and coronary blood flow than was elicited in the unblocked state. In contrast to the response pattern during control exercise, there was no significant change in coronary sinus oxygen tension (PO2), myocardial arteriovenous oxygen difference, and myocardial oxygen delivery-to-oxygen consumption ratio. It is concluded that the normal relationship between myocardial oxygen supply and oxygen demand is modified during exercise after alpha-adrenergic blockade, whereby oxygen delivery is better matched to oxygen consumption. These results indicate that the increase in coronary blood flow and oxygen delivery to the myocardium during normal exercise is limited by alpha-adrenergic vasoconstriction.