Ultra-weak photon emission during wrist curl and cycling exercises in trained healthy men

Human ultra-weak photon emission (UPE) is related to the activity of respiratory chain and oxygen consumption. Investigations on UPE and its response to exercise are almost non existent. Since human UPE is an indicator of reactive oxygen species (ROS) levels, we used exercises as a model to study UPE. To continue the research on the relationship between human UPE and exercise, it was decided to carry out measurements of UPE in response to different exercise modes with 20 healthy male subjects. The performed exercises were wrist curls with a dumbbell and indoor cycling. Regarding wrist curl exercises, 70% of the subjects for the first exercise and 65% for the second exercise did not show any significant changes in UPE. Also, the statistical analysis did not show significant changes of the UPE levels. In terms of cycling exercise, 85% of subjects did not show any significant increase of UPE. The gathered data showed that a majority of the subjects didn't show an increase of the UPE during both types of exercises. Our results imply that the UPE is not only affected by oxygen consumption, but also by the intensity, the type of exercise, and the physiology of the subject.     

Beta-endorphin and corticotropin release is dependent on a threshold intensity of running exercise in male endurance athletes

Relationship between the intensity of running exercise on a treadmill and the changes in the concentrations of beta-endorphin + beta-lipotropin (beta-E + beta-LPH) and adrenocorticotropic hormone (ACTH) in plasma were studied in 10 experienced male endurance athletes. At random order, the subjects run on a treadmill six exercises which required on an average (mean +/- S.E.) 50 +/- 0.8%, 58 +/- 0.8%, 69 +/- 1.1%, 80 +/- 0.7%, 92 +/- 1.0% and 98 +/- 0.5% of their maximal oxygen consumption. Plasma levels of beta-E + beta-LPH and ACTH did not show any significant changes during the 50-80%-tests. During the 92% test, the mean levels (+/- S.E.) of beta-E + beta-LPH and ACTH increased significantly (p less than 0.001), from 3.0 +/- 0.4 to 8.0 +/- 1.2 pmol/l and from 3.1 +/- 0.5 to 8.9 +/- 1.3 pmol/l, respectively, and during the 98% test, from 3.7 +/- 0.6 pmol/l to 20.4 +/- 1.5 pmol/l, and from 3.6 +/- 0.6 to 21.8 +/- 1.5 pmol/l, respectively. Increases in the plasma levels of beta-E + beta-LPH and ACTH were always accompanied by an increase in the blood lactate level. We conclude that intensive running with an anaerobic response causes an increase in the concentrations of beta-endorphin and ACTH in plasma in endurance athletes, whereas slight aerobic exercise did not elicit any response.     

Greater serum GH response to arm than to leg exercise performed at equivalent oxygen uptake

The aim of this study was to provide information concerning the mechanism of exercise-induced stimulation of growth hormone (GH) release in human subjects. For this reason serum GH as well as some hemodynamic variables and blood concentrations of noradrenaline (NA), insulin (IRI), lactate (LA), glucose (BG), and free fatty acids (FFA) were determined in seven healthy male subjects exercising on a bicycle ergometer with arms or legs and running on a treadmill at equivalent oxygen consumption levels. Significantly greater increases in serum GH concentration accompanied arm exercises than those observed during the leg exercises. This was accompanied by greater increases in heart rate, blood pressure, and plasma NA and blood lactate concentrations. Serum IRI decreased during both leg exercises and did not change during the arm exercise. There were no differences in BG and plasma FFA concentrations between the three types of exercise. The role of humoral and neural signals responsible for the greater GH response to arm exercise is discussed. The findings are consistent with the hypothesis that neural afferent signals sent by muscle "metabolic receptors" participate in the activation of GH release during physical exercise. It seems likely that the stimulation of these chemoreceptors is more pronounced when smaller muscle groups are engaged at a given work load. However, a contribution of efferent impulses derived from the brain motor centres to the control system of GH secretion during exercise is also possible.     

Footstrike is the major cause of hemolysis during running.

There is a wide body of literature reporting red cell hemolysis as occurring after various forms of exercise. Whereas the trauma associated with footstrike is thought to be the major cause of hemolysis after running, its significance compared with hemolysis that results from other circulatory stresses on the red blood cell has not been thoroughly addressed. To investigate the significance of footstrike, we measured the degree of hemolysis after 1 h of running. To control for the potential effects of oxidative and circulatory stresses on the red blood cell, the same subjects cycled for 1 h at equivalent oxygen uptake. Our subjects were 10 male triathletes, who each completed two separate 1-h sessions of running and cycling at 75% peak oxygen uptake, which were performed in random order 1 wk apart. Plasma free hemoglobin and serum haptoglobin concentrations were measured as indicators of hemolysis. We also measured methemoglobin as a percentage of total hemoglobin immediately postexercise as an indicator of red cell oxidative stress. Plasma free hemoglobin increased after both running (P < 0.01) and cycling (P < 0.01), but the increase was fourfold greater after running (P < 0.01). This was reflected by a significant fall in haptoglobin 1 h after the running trials, whereas no significant changes occurred after cycling at any sample point. Methemoglobin increased twofold after both running and cycling (P < 0.01), with no significant differences between modes of exercise. The present data indicate that, whereas general circulatory trauma to the red blood cells associated with 1 h of exercise at 75% maximal oxygen uptake may result in some exercise-induced hemolysis, footstrike is the major contributor to hemolysis during running.     

Effect of aerobic capacity on the T(2) increase in exercised skeletal muscle.

The increase in nuclear magnetic resonance transverse relaxation time (T(2)) of muscle water measured by magnetic resonance imaging after exercise has been correlated with work rate in human subjects. This study compared the T(2) increase in thigh muscles of trained (cycling VO(2 max) = 54.4 +/- 2.7 ml O(2). kg(-1). min(-1), mean +/- SE, n = 8, 4 female) vs. sedentary (31.7 +/- 0.9 ml O(2). kg(-1). min(-1), n = 8, 4 female) subjects after cycling exercise for 6 min at 50 and 90% of the subjects' individually determined VO(2 max). There was no significant difference between groups in the T(2) increase measured in quadriceps muscles within 3 min after the exercises, despite the fact that the absolute work rates were 60% higher in the trained group (253 +/- 15 vs. 159 +/- 21 W for the 90% exercise). In both groups, the increase in T(2) of vastus muscles was twofold greater after the 90% exercise than after the 50% exercise. The recovery of T(2) after the 90% exercise was significantly faster in vastus muscles of the trained compared with the sedentary group (mean recovery half-time 11.9 +/- 1.2 vs. 23.3 +/- 3.7 min). The results show that the increase in muscle T(2) varies with work rate relative to muscle maximum aerobic power, not with absolute work rate.     

Circulating plasma VEGF response to exercise in sedentary and endurance-trained men.

The skeletal muscle capillary supply is an important determinant of maximum exercise capacity, and it is well known that endurance exercise training increases the muscle capillary supply. The muscle capillary supply and exercise-induced angiogenesis are regulated in part by vascular endothelial growth factor (VEGF). VEGF is produced by skeletal muscle cells and can be secreted into the circulation. We investigated whether there are differences in circulating plasma VEGF between sedentary individuals (Sed) and well-trained endurance athletes (ET) at rest or in response to acute exercise. Eight ET men (maximal oxygen consumption: 63.8 +/- 2.3 ml x kg(-1) x min(-1); maximum power output: 409.4 +/- 13.3 W) and eight Sed men (maximal oxygen consumption: 36.3 +/- 2.1 ml x kg(-1) x min(-1); maximum power output: 234.4 +/- 13.3 W) exercised for 1 h at 50% of maximum power output. Antecubital vein plasma was collected at rest and at 0, 2, and 4 h postexercise. Plasma VEGF was measured by ELISA analysis. Acute exercise significantly increased VEGF at 0 and 2 h postexercise in ET subjects but did not increase VEGF at any time point in Sed individuals. There was no difference in VEGF between ET and Sed subjects at any time point. When individual peak postexercise VEGF was analyzed, exercise did increase VEGF independent of training status. In conclusion, exercise can increase plasma VEGF in both ET athletes and Sed men; however, there is considerable variation in the individual time of the peak VEGF response.     

Controlled trial of supervised exercise training in chronic bronchitis.

In a controlled trial of exercise retraining in patients with severe chronic bronchitis, 33 subjects were followed for a mean period of 10.3 months. The exercise programme was supervised once a week, and daily training comprised a 12-minute walk and simple stair climbing exercises. The subjects in the exercise group showed a highly significant improvement in their walking distance, attaining a maximum increase of 24% after eight to 12 months. There was also considerable subjective improvement. The control group did not improve. No significant changes in cardiorespiratory function or muscle strength were seen. Simple exercise rehabilitation is of benefit to patients with disabling obstructive lung disease.     

Effect of prior exercise and insulin on potential thermogenic systems in rat skeletal muscle.

We previously reported that insulin stimulates oxygen consumption by the perfused rat hindquarter after high-intensity exercise. The purpose of the present study was to examine whether fructose 6-phosphate-fructose 1,6-bisphosphate cycling or an uncoupling of mitochondrial respiration contributes to this phenomenon. Hindquarter skeletal muscle was analyzed after perfusion in the absence or presence of insulin (150-200 microU/ml) for high-energy phosphate content, fructose 6-phosphate-fructose 1,6-bisphosphate cycling of glucose before incorporation into glycogen, and mitochondrial respiratory control. Muscle from exercised rats perfused with insulin did not display greater rates of glucose cycling or mitochondrial uncoupling; in fact, insulin decreased the rate of fructose 6-phosphate cycling and tended to increase respiratory control in skeletal muscle mitochondria. In addition, the concentrations of ATP and creatine phosphate and the calculated free ADP level in muscle of previously exercised rats perfused with insulin were similar to those of control rats. The results do not exclude the possibility that localized subcellular changes in ADP occurred, however. In conclusion, the results suggest that insulin-induced increases in other substrate cycles, ion transport systems, and/or as yet unidentified energy-requiring processes account for the 25-30% increase in hindquarter oxygen consumption after intense exercise.     

Blood lactate during constant-load exercise at aerobic and anaerobic thresholds

Venous blood lactate concentrations [1ab] were measured every 30 s in five athletes performing prolonged exercise at three constant intensities: the aerobic threshold (Thaer), the anaerobic threshold (Than) and at a work rate (IWR) intermediate between Thaer and Than. Measurements of oxygen consumption (VO2) and heart rate (HR) were made every min. Most of the subjects maintained constant intensity exercise for 45 min at Thaer and IWR, but at Than none could exercise for more than 30 min. Relationships between variations in [1ab] and concomitant changes in VO2 or HR were not statistically significant. Depending on the exercise intensity (Thaer, IWR, or Than) several different patterns of change in [1ab] have been identified. Subjects did not necessarily show the same pattern at comparable exercise intensities. Averaging [1ab] as a function of relative exercise intensity masked spatial and temporal characteristics of individual curves so that a common pattern could not be discerned at any of the three exercise levels studied. The differences among the subjects are better described on individual [1ab] curves when sampling has been made at time intervals sufficiently small to resolve individual characteristics.     

Exercise hyperventilation in patients with McArdle's disease

This study was undertaken to determine if patients who lack muscle phosphorylase (i.e., McArdle's disease), and therefore the ability to produce lactic acid during exercise, demonstrate a normal hyperventilatory response during progressive incremental exercise. As expected these patients did not increase their blood lactate above resting levels, whereas the blood lactate levels of normal subjects increased 8- to 10-fold during maximal exercise. The venous pH of the normal subjects decreased markedly during exercise that resulted in hyperventilation. The patients demonstrated a distinct increase in ventilation with respect to O2 consumption similar to that seen in normal individuals during submaximal exercise. However their hyperventilation resulted in an increase in pH because there was no underlying metabolic acidosis. End-tidal partial pressures of O2 and CO2 also reflected a distinct hyperventilation in both groups at approximately 70-85% maximal O2 consumption. These data show that hyperventilation occurs during intense exercise, even when there is no increase in plasma [H+]. Since arterial CO2 levels were decreasing and O2 levels were increasing during the hyperventilation, it is possible that nonhumoral stimuli originating in the active muscles or in the brain elicit the hyperventilation observed during intense exercise.     

Prolactin responses to chronic exercise in males

Chronic, as well as acute, exercise increases circulating PRL in females. The response of males to repeated exercise, however, is unknown. The purpose of the present study was to examine the effects of acute and chronic exercise on plasma PRL levels in untrained males. Eight male subjects performed cycle ergometer exercise at 50% of their maximal oxygen uptake on 10 consecutive days. The subjects exercised in an environmental chamber maintained at 39 degrees C and 30% relative humidity. PRL levels were measured on days 1, 5, and 10 before exercise, and after 20 and 45 minutes of exercise. Acute exercise increased PRL levels. However, plasma levels did not significantly increase during exercise on days 5 and 10. This suggests a similarity in the PRL response to acute exercise in males and females, but a sex difference in the response to chronic exercise.     

Feedforward sympathetic coronary vasodilation in exercising dogs.

The hypothesis that exercise-induced coronary vasodilation is a result of sympathetic activation of coronary smooth muscle beta-adrenoceptors was tested. Ten dogs were chronically instrumented with a flow transducer on the circumflex coronary artery and catheters in the aorta and coronary sinus. During treadmill exercise, coronary venous oxygen tension decreased with increasing myocardial oxygen consumption, indicating an imperfect match between myocardial blood flow and oxygen consumption. This match was improved after alpha-adrenoceptor blockade with phentolamine but was significantly worse than control after alpha + beta-adrenoceptor blockade with phentolamine plus propranolol. The response after alpha-adrenoceptor blockade included local metabolic vasodilation plus a beta-adrenoceptor vasodilator component, whereas the response after alpha + beta-adrenoceptor blockade contained only the local metabolic vasodilator component. The large difference in coronary venous oxygen tensions during exercise between alpha-adrenoceptor blockade and alpha + beta-adrenoceptor blockade indicates that there is significant feedforward beta-adrenoceptor coronary vasodilation in exercising dogs. Coronary venous and estimated myocardial interstitial adenosine concentrations did not increase during exercise before or after alpha + beta-adrenoceptor blockade, indicating that adenosine levels did not increase to compensate for the loss of feedforward beta-adrenoceptor-mediated coronary vasodilation. These results indicate a meaningful role for feedforward beta-receptor-mediated sympathetic coronary vasodilation during exercise.     

Spinal cord excitability is not influenced by elevated blood lactate levels

The aim of the present study was to examine the association of high blood lactate levels, induced with a maximal cycling or with an intravenous infusion, with spinal cord excitability. The study was carried out on 17 male athletes; all the subjects performed a maximal cycling test on a mechanically braked cycloergometer, while 6 of them were submitted to the intravenous infusion of a lactate solution (3?mg/kg in 1?min). Before the exercise or the injection, also at the end as well as 5 and 10?min after the conclusion, venous blood lactate was measured and excitability of the spinal α-motoneurons was evaluated by using the H reflex technique. In both experimental conditions, it has been observed that an exhaustive exercise is associated with a strong increase of blood lactate (but not of blood glucose) and with a significant reduction of spinal excitability. Since a similar augment of blood lactate induced by an intravenous infusion, in subjects not performing any exercise, is not associated with significant changes of spinal excitability, it can be concluded that the increase of blood lactate levels during a maximal exercise is not per se capable of modifying the excitability of spinal α-motoneurons.     

Effects of hypnosis on plasma proenkephalin peptide F and perceptual and cardiovascular responses during submaximal exercise

Little information is available concerning the influence of subconscious mechanisms on neuroendocrine function, more specifically, proenkephalin peptide F release. Ten men [5 middle distance runners (21.6 (SD 0.54 years) and 5 untrained men (24.0 (SD 4.3 years)] consented to be volunteers in this investigation. Submaximal exercise intensities of 25% and 50% of peak oxygen consumption (VO2) (8 min stages) were used for both the control and hypnosis treatments. A traditional hypnotic induction was used, with the suggestion of two higher intensities of exercise stress (50% and 75% peak VO2) previously experienced in familiarization and testing by each subject. Each minute oxygen consumption was measured using open circuit spirometry, heart rate via an ECG, and ratings of perceived exertion (RPE) using the Borg scale. Plasma peptide F immunoreactivity (ir) [preproenkephalin-(107-140)] in blood sampled from an indwelling cannula was measured by radioimmunoassay at 7-8 min of each stage of the exercise test. Expected significant increases were observed for all cardiorespiratory and perceptual variables over the increasing exercise intensities and there were no significant differences between trained and untrained groups for peptide F if response patterns. Hypnosis did not significantly affect peptide F ir concentrations (P > 0.05) and did not significantly alter exercise heart rate, RPE or minute ventilation (P > 0.05). However, hypnosis did significantly increase oxygen consumption during exercise (P = 0.0095) but not of the magnitude needed for the metabolic demands of the higher exercise intensities. Thus, traditional hypnosis was unable to make functionally significant changes in the cardiorespiratory variables.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cytokine immunoreactivity in plasma does not change after moderate endurance exercise.

We investigated whether increased concentrations of circulating cytokines may be responsible for exercise-induced priming of blood neutrophils (J. A. Smith et al. Int. J. Sports Med. 11: 179-187, 1990). The plasma concentrations of tumor necrosis factor-alpha, interleukin- (IL) 1 beta, IL-6, granulocyte-macrophage colony-stimulating factor, and neopterin in trained and untrained human subjects were measured by immunoassay before and after 1 h of cycling at 60% of maximal oxygen uptake. C-reactive protein and creatine kinase (CK) were also measured before and 24 h after exercise as markers of the "acute-phase response" and muscle damage (C. Taylor et al. J. Appl. Physiol. 62: 464-469, 1987), respectively. The small changes in the plasma concentrations of cytokines or neopterin observed after exercise in both trained and untrained subjects were not significantly different to those found in a control group of nonexercised subjects. However, untrained subjects did exhibit an acute-phase response (P = 0.04) 24 h after exercise without additional release of CK into plasma. Baseline training differences were confined to a twofold elevation in CK activity (P = 0.04). The results show that circulating cytokines are unlikely to be responsible for the priming of neutrophil microbicidal activity observed after moderate endurance exercise (J. A. Smith et al. Int. J. Sports Med. 11: 179-187, 1990).     

Plasma agouti-related protein (AGRP), growth hormone, insulin responses to a single circuit-resistance exercise in male college students

The ability of acute exercise to stimulate appetite and food intake depends on intensity, duration, and agouti-related protein (AGRP) levels. Fasting, as well as any negative energy balance, has been reported to increase AGRP expression in the arcuate nucleus (ARC) of the hypothalamus and other extra-hypothalamic tissues in human and rats. The purpose of the present study was to investigate the response of plasma AGRP, GH and insulin to a single circuit-resistance exercise. Twenty volunteer male college students completed a single bout of circuit-resistance training (10 exercises at 35% of 1RM). Blood samples were collected before, immediately and 30 min following the exercise protocol. Plasma AGRP and GH levels showed a significant increase immediately after exercise and returned to pre exercise values during the recovery period. The data indicate that exercise protocol was able to increase plasma AGRP and GH levels. A higher plasma AGRP level might result in an acute exercise-induced hyperphagia and help to fuel post-exercise restoration processes.     

Effects of short-term oral salbutamol administration on exercise endurance and metabolism.

The present study examined whether oral short-term administration of salbutamol (Sal) modifies performance and selected hormonal and metabolic variables during submaximal exercise. Eight recreational male athletes completed two cycling trials at 80-85% peak O(2) consumption until exhaustion after either gelatin placebo (Pla) or oral Sal (12 mg/day for 3 wk) treatment, according to a double-blind and randomized protocol. Blood samples were collected at rest, after 5, 10, and 15 min, and at exhaustion to determine growth hormone (GH), cortisol, testosterone, triiodothyronine (T(3)), C peptide, free fatty acid (FFA), blood glucose, lactate, and blood urea values. Time of cycling was significantly increased after chronic Sal intake (Sal: 30.5 +/- 3.1 vs. Pla: 23.7 +/- 1.6 min, P < 0.05). No change in any variable was found before cycling except a decrease in blood urea concentration and an increase in T(3) after Sal that remained significant throughout the exercise test (P < 0.05). Compared with rest, exercise resulted in a significant increase in GH, cortisol, testosterone, T(3), FFAs, and lactate and a decrease in C peptide after both treatments with higher exercise FFA levels and exhaustion GH concentrations after Sal (P < 0.05). Sal but not Pla significantly decreased exercise blood glucose levels. From these data, short-term Sal intake did appear to improve performance during intense submaximal exercise with concomitant increase in substrate availability and utilization, but the exact mechanisms involved need further investigation.     

Effect of head-out water immersion on response to exercise training

During spaceflight and head-out water immersion (WI) there is a cephalad shift in blood volume. We have recently shown that left ventricular end-diastolic dimension is significantly greater during moderate cycling exercise with WI compared with on land. The purpose of this study was to determine whether the cephalad shift in blood volume and accompanying increase in cardiac preload with WI alters the normal cardiovascular adaptations to aerobic exercise training. Nine middle-aged healthy men trained on cycle ergometers in water, nine trained on land, and four served as controls for 12 wk. Following training, both training groups showed similar increase (P less than 0.05) in stroke volume and similar decreases in heart rate (P less than 0.01) and blood pressure (P less than 0.05) at a given submaximal exercise O2 consumption (VO2). Maximal VO2 increased (P less than 0.01) similarly for both training groups. The control group did not demonstrate any significant changes in submaximal or maximal exercise responses. We conclude that the cephalad shift in blood volume with WI does not alter the normal cardiovascular adaptation to aerobic exercise training.     

Independent coding of movement duration in a repetitive non-visually guided movement

The aim of the present study was to examine the association of high blood lactate levels, induced with a maximal cycling or with an intravenous infusion, with spinal cord excitability. The study was carried out on 17 male athletes; all the subjects performed a maximal cycling test on a mechanically braked cycloergometer, while 6 of them were submitted to the intravenous infusion of a lactate solution (3?mg/kg in 1?min). Before the exercise or the injection, also at the end as well as 5 and 10?min after the conclusion, venous blood lactate was measured and excitability of the spinal α-motoneurons was evaluated by using the H reflex technique. In both experimental conditions, it has been observed that an exhaustive exercise is associated with a strong increase of blood lactate (but not of blood glucose) and with a significant reduction of spinal excitability. Since a similar augment of blood lactate induced by an intravenous infusion, in subjects not performing any exercise, is not associated with significant changes of spinal excitability, it can be concluded that the increase of blood lactate levels during a maximal exercise is not per se capable of modifying the excitability of spinal α-motoneurons.     

Hypoxia augments muscle sympathetic neural response to leg cycling

It was demonstrated that acute hypoxia increased muscle sympathetic nerve activity (MSNA) by using a microneurographic method at rest, but its effects on dynamic leg exercise are unclear. The purpose of this study was to clarify changes in MSNA during dynamic leg exercise in hypoxia. To estimate peak oxygen uptake (Vo(2 peak)), two maximal exercise tests were conducted using a cycle ergometer in a semirecumbent position in normoxia [inspired oxygen fraction (Fi(O(2)) = 0.209] and hypoxia (Fi(O(2)) = 0.127). The subjects performed four submaximal exercise tests; two were MSNA trials in normoxia and hypoxia, and two were hematological trials under each condition. In the submaximal exercise test, the subjects completed two 15-min exercises at 40% and 60% of their individual Vo(2 peak) in normoxia and hypoxia. During the MSNA trials, MSNA was recorded via microneurography of the right median nerve at the elbow. During the hematological trials, the subjects performed the same exercise protocol as during the MSNA trials, but venous blood samples were obtained from the antecubital vein to assess plasma norepinephrine (NE) concentrations. MSNA increased at 40% Vo(2 peak) exercise in hypoxia, but not in normoxia. Plasma NE concentrations did not increase at 40% Vo(2 peak) exercise in hypoxia. MSNA at 40% and 60% Vo(2 peak) exercise were higher in hypoxia than in normoxia. These results suggest that acute hypoxia augments muscle sympathetic neural activation during dynamic leg exercise at mild and moderate intensities. They also suggest that the MSNA response during dynamic exercise in hypoxia could be different from the change in plasma NE concentrations.