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.     

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.     

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)     

Increase in atrial natriuretic peptide in response to physical exercise

Circulating atrial natriuretic peptide (ANP) level was determined during physical exercise to investigate the correlation between changes in ANP level and heart rate increases. Six subjects exercised at a work level of 75% VO2max for 30 min, two also performed two successive exercises at 75% VO2max while two more exercised for longer at 55% VO2max. Plasma ANP levels and heart rate increased in all the exercising subjects. At the end of the exercise, the ANP level fell immediately, suggesting an immediate reduction in ANP secretion by the heart. Pre-exercise values were reached after 30 min. Successive exercises gave the same heart rate related ANP patterns without previous secretory episodes having any effect. These results lead to the conclusion that ANP intervenes in the cardiovascular adjustments to exercise.     

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.     

Decreased exercise blood lactate concentrations after respiratory endurance training in humans

For many years, it was believed that ventilation does not limit performance in healthy humans. Recently, however, it has been shown that inspiratory muscles can become fatigued during intense endurance exercise and decrease their exercise performance. Therefore, it is not surprising that respiratory endurance training can prolong intense constant-intensity cycling exercise. To investigate the effects of respiratory endurance training on blood lactate concentration and oxygen consumption (VO2) during exercise and their relationship to performance, 20 healthy, active subjects underwent 30 min of voluntary, isocapnic hyperpnoea 5 days a week, for 4 weeks. Respiratory endurance tests, as well as incremental and constant-intensity exercise tests on a cycle ergometer, were performed before and after the 4-week period. Respiratory endurance increased from 4.6 (SD 2.5) to 29.1 (SD 4.0) min (P < 0.001) and cycling endurance time was prolonged from 20.9 (SD 5.5) to 26.6 (SD 11.8) min (P < 0.01) after respiratory training. The VO2 did not change at any exercise intensity whereas blood lactate concentration was lower at the end of the incremental [10.4 (SD 2.1) vs 8.8 (SD 1.9) mmol x l(-1), P < 0.001] as well as at the end of the endurance exercise [10.4 (SD 3.6) vs 9.6 (SD 2.7) mmol x l(-1), P < 0.01] test after respiratory training. We speculate that the reduction in blood lactate concentration was most likely caused by an improved lactate uptake by the trained respiratory muscles. However, reduced exercise blood lactate concentrations per se are unlikely to explain the improved cycling performance after respiratory endurance training.     

Comparison of incremental and steady state tests of endurance training

To compare the results obtained by incremental or constant work load exercises in the evaluation of endurance conditioning, a 20-week training programme was performed by 9 healthy human subjects on the bicycle ergometer for 1 h a day, 4 days a week, at 70-80% VO2max. Before and at the end of the training programme, (1) the blood lactate response to a progressive incremental exercise (18 W increments every 2nd min until exhaustion) was used to determine the aerobic and anaerobic thresholds (AeT and AnT respectively). On a different day, (2) blood lactate concentrations were measured during two sessions of constant work load exercises of 20 min duration corresponding to the relative intensities of AeT (1st session) and AnT (2nd session) levels obtained before training. A muscle biopsy was obtained from vastus lateralis at the end of these sessions to determine muscle lactate. AeT and AnT, when expressed as % VO2max, increased with training by 17% (p less than 0.01) and 9% (p less than 0.05) respectively. Constant workload exercise performed at AeT intensity was linked before training (60% VO2max) to a blood lactate steady state (4.8 +/- 1.4 mmol.l-1) whereas, after training, AeT intensity (73% VO2max) led to a blood lactate accumulation of up to 6.6 +/- 1.7 mmol.l-1 without significant modification of muscle lactate (7.6 +/- 3.1 and 8.2 +/- 2.8 mmol.kg-1 wet weight respectively). It is concluded that increase in AeT with training may reflect transient changes linked to lower early blood lactate accumulation during incremental exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Preconditioning with hydrogen peroxide (H2O2) or ischemia in H2O2-induced cardiac dysfunction

To assess whether allantoin levels in serum and urine are influenced by exhaustive and moderate exercise and whether allantoin is a useful indicator of exercise-induced oxidative stress in humans, we made subjects perform exhaustive and moderate (100% and 40% VO₂max) cycling exercise and examined the levels of allantoin, thiobarbituric acid reactive substances (TBARS) and urate in serum and urine. Immediately after exercise at 100% VO₂max, the serum allantoin/urate ratio was significantly elevated compared with the resting levels while the serum urate levels was significantly elevated 30 min after exercise. The serum TBARS levels did not increase significantly compared with the resting levels. Urinary allantoin excretion significantly increased during 60 min of recovery after exercise, however, urinary urate excretion decreased significantly during the same period. The urinary allantoin/urate ratio also rapidly increased during 60 min of recovery after exercise. Urinary TBARS excretion decreased during the first 60 min of the recovery period and thereafter significantly increased during the latter half of the recovery period. On the contrary, after 40% VO₂max of exercise, no significant changes in the levels of urate, allantoin and TBARS in serum or urine were observed. These findings suggest that allantoin levels in serum and urine may reflect the extent of oxidative stress in vivo and that the allantoin which appeared following exercise may have originated not from urate formed as a result of exercise but from urate that previously existed in the body. Furthermore, these findings support the view that allantoin in serum and urine is a more sensitive and reliable indicator of in vivo oxidative stress than lipid peroxidation products measured as TBARS.     

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.     

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.     

Different times of day do not change heart rate variability recovery after light exercise in sedentary subjects: 24 hours Holter monitoring

Incidence of cardiovascular events follows a circadian rhythm with peak occurrence during morning. Disturbance of autonomic control caused by exercise had raised the question of the safety in morning exercise and its recovery. Furthermore, we sought to investigate whether light aerobic exercise performed at night would increase HR and decrease HRV during sleep. Therefore, the aim of this study was to test the hypothesis that morning exercise would delay HR and HRV recovery after light aerobic exercise, additionally, we tested the impact of late night light aerobic exercise on HR and HRV during sleep in sedentary subjects. Nine sedentary healthy men (age 24 ± 3 yr; height 180 ± 5 cm; weight 79 ± 8 kg; fat 12 ± 3%; mean±SD) performed 35 min of cycling exercise, at an intensity of first anaerobic threshold, at three times of day (7 a.m., 2 p.m. and 11 p.m.). R-R intervals were recorded during exercise and during short-time (60 min) and long-time recovery (24 hours) after cycling exercise. Exercise evoked increase in HR and decrease in HRV, and different times of day did not change the magnitude (p < 0.05 for time). Morning exercise did not delay exercise recovery, HR was similar to rest after 15 minutes recovery and HRV was similar to rest after 30 minutes recovery at morning, afternoon, and night. Low frequency power (LF) in normalized unites (n.u.) decreased during recovery when compared to exercise, but was still above resting values after 60 minutes of recovery. High frequency power (HF-n.u.) increased after exercise cessation (p < 0.05 for time) and was still below resting values after 60 minutes of recovery. The LF/HF ratio decreased after exercise cessation (p < 0.05 for time), but was still different to baseline levels after 60 minutes of recovery. In conclusion, morning exercise did not delay HR and HRV recovery after light aerobic cycling exercise in sedentary subjects. Additionally, exercise performed in the night did change autonomic control during the sleep. So, it seems that sedentary subjects can engage physical activity at any time of day without higher risk.     

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.     

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 vitamin E supplementation on post-exercise plasma lipid peroxidation and blood antioxidant status in smokers: with special reference to haemoconcentration effect

The oxidative effects were investigated of exhausting exercise in smokers, and the possible protective role of 400 mg day(-1) vitamin E (Vit E) supplementation over a period of 28 days. The subjects exercised to exhaustion including concentric-eccentric contractions following maximal cycling. The haematocrit and haemoglobin, leucocyte (WBC), plasma lactic acid (La) and malondialdehyde (MDA), erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GPx), serum Vit E and ceruloplasmin (CER) concentrations were measured pre and post exercise. Supplementation increased Vit E concentrations 28% and 31% in the controls and the smokers, respectively. Cigarette smoking and/or Vit E supplementation did not influence plasma lipid peroxidation or the antioxidant status at rest. Exercise caused significant haemoconcentration in all groups. When the post-exercise concentrations were adjusted for haemoconcentration, a significant elevation in La concentrations due to exercise was observed in all groups. Similarly, there were significant elevations in the adjusted WBC counts in all groups except the Vit E supplemented controls. The MDA concentrations on the other hand, when adjusted for haemoconcentration, did not exhibit any difference due to exercise. Exercise did not affect the GPx and CER activities either, while causing a SOD activity loss in all groups except the Vit E supplemented non-smokers. Serum Vit E concentrations diminished significantly in all groups after exercise. Post-exercise plasma MDA and blood antioxidant concentrations were not altered by smoking. The results would suggest that plasma volume changes should always be taken into account when assessing post-exercise plasma concentrations and that smoking and exercise do not have an additional collective effect on plasma lipid peroxidation and the dose of Vit E administered was insufficient to maintain the serum concentrations after exercise.     

海洋矿物质对急性力竭诱发的肌肉耗氧量的影响

高强度运动造成肌肉损伤进而提高肌肉的耗氧量,而矿物质是细胞能量代谢的重要的物质。本研究为了探讨摄入海洋性矿物质对肌肉组织耗氧量的影响,选取了10名大学生采用交叉试验设计分别在单次高强度运动前后,测量体重来判定运动员的脱水量,并在高强度运动挑战后按照脱水量的1.5倍给予饮料摄入。饮料分成海洋性矿物质饮料及安慰剂两种,并在安静期与摄入海洋性矿物质饮料后2 h后使用近红外光谱仪检测肌肉组织氧含量及耗氧量。研究显示,高强度运动会降低肌肉组织的血液量((93.82±5.06)μmol/L>(80.35±3.71)μmol/L)及提高耗氧量((0.53±0.12) mL·min-1·100 g^-1<(0.79±0.12) mL·min^-1·100 g^-1),摄入海洋性矿物可以降低高强度运动后2 h肌肉组织的耗氧量((0.79±0.12) m L·min^-1·100 g^-1>(0.44±0.09) m L·min^-1·100 g^-1)。因此运动员在高强度运动挑战后,摄入海洋性矿物质饮料可抑制高强度运动所造成的肌肉耗氧量增加的现象。     

Effects of magnesium supplementation on blood parameters of athletes at rest and after exercise

The effects of magnesium supplementation on blood parameters were studied during a period of 4 wk in adult tae-kwon-do athletes at rest and exhaustion. Thirty healthy subjects of ages ranging in age from 18 to 22 yr were included in the study. The subjects were separated into three groups, as follows: Group 1 consisted of subjects who did not train receiving 10 mg/kg/d magnesium. Group 2 included subjects equally supplemented with magnesium and exercising 90–120 min/d for 5 d/wk. Group 3 were subject to the same exercise regime but did not receive magnesium supplements. The leukocyte count (WBC) was significantly higher in groups 1 and 2 than in the subjects who did not receive any supplements (p < 0.05). There were no significant differences in the WBC of the two groups under magnesium supplementation. The erythrocyte, hemoglobin, and trombocyte levels were significantly increased in all groups (p < 0.05), but the hematocrit levels did not show any differences between the groups although they were increased after supplementation and exercise. These results suggest that magnesium supplementation positively influences the performance of training athletes by increasing erythrocyte and hemoglobin levels.     

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.     

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.