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.     

Brainstem excitability is not influenced by blood lactate levels

The influence of blood lactate on brainstem excitability was tested by using the blink reflex (BR) recovery cycle on 18 sprinters. Blood lactate was measured before maximal cycling, at the end, as well as 5 and 10?min after the exhaustion. Blood lactate was associated with a decrement of R2 whereas only small changes were observed after an intravenous infusion of lactate. It seems, therefore, that lactate influences BR mainly by acting at the cortical level.     

Relationship between blood lactate and cortical excitability between taekwondo athletes and non-athletes after hand-grip exercise

Objectives: In taekwondo competitions, fatigue has a large influence on performance. Recent studies have reported that the excitability in the primary hand motor cortex, investigated with transcranial magnetic stimulation (TMS), is enhanced at the end of a maximal exercise and that this improvement correlates with blood lactate. The aim of the present study was to investigate the relationship between blood lactate and cortical excitability in taekwondo athletes and non-athletes.

Methods: The excitability of the primary motor cortex was measured before and after fatiguing hand-grip exercise by TMS. Capillary blood lactate was measured at rest (pre-test), at the end (0?min), and at 3 and 10?min after the exercise by using a “Lactate Pro” portable lactate analyzer.

Results: Significant differences in cortical excitability between the two groups were found after the exercise (p?p?Conclusion: The present findings showed changes in the excitability in the athletes group and also in the non-athletes group. However, blood lactate seems to have the greater effect in trained subjects compared to untrained subjects. In fact, it appears that, during extremely intensive exercise in taekwondo athletes, lactate may delay the onset of fatigue not only by maintaining the excitability of muscle, but also by increasing the excitability of the primary motor cortex more than in non-athletes.     

Gender differences in changes of motor cortex excitability during elevated blood lactate levels

Gender differences in cortical excitability have been detected by using transcranial magnetic stimulation (TMS). The present study was carried out to compare the effects of high blood lactate levels, induced by performing a maximal exhausting exercise, on the excitability of the primary motor cortex in young male and female athletes. The study was carried out on 21 young males and 20 females from the Middle Distance Track Team of our university. Before the exercise, at the end, as well as 5 and 10 min after the conclusion, venous blood lactate and glucose were measured and excitability of the motor cortex was evaluated by using TMS. We observed a similar enhancement of excitability of primary motor cortex, concomitantly with an increase of blood lactate, in both young male and female athletes. However, the improvement was significantly higher (p < 0.05) in women (37.4% ± 3.97) than in men (42.0% ± 6.43), suggesting a greater sensitiveness of female cerebral cortex to blood lactate.     

Exercise and recovery ventilatory and VO2 responses of patients with McArdle's disease

This study was designed to determine whether patients with McArdle's disease, who do not increase their blood lactate levels during and after maximal exercise, have a slow "lactacid" component to their recovery O2 consumption (VO2) response after high-intensity exercise. VO2 was measured breath by breath during 6 min of rest before exercise, a progressive maximal cycle ergometer test, and 15 min of recovery in five McArdle's patients, six age-matched control subjects, and six maximal O2 consumption- (VO2 max) matched control subjects. The McArdle's patients' ventilatory threshold occurred at the same relative exercise intensity [71 +/- 7% (SD) VO2max] as in the control groups (60 +/- 13 and 70 +/- 10% VO2max) despite no increase and a 20% decrease in the McArdle's patients' arterialized blood lactate and H+ levels, respectively. The recovery VO2 responses of all three groups were better fit by a two-, than a one-, component exponential model, and the parameters of the slow component of the recovery VO2 response were the same in the three groups. The presence of the same slow component of the recovery VO2 response in the McArdle's patients and the control subjects, despite the lack of an increase in blood lactate or H+ levels during maximal exercise and recovery in the patients, provides evidence that this portion of the recovery VO2 response is not the result of a lactacid mechanism. In addition, it appears that the hyperventilation that accompanies high-intensity exercise may be the result of some mechanism other than acidosis or lung CO2 flux.     

Gluconeogenesis in humans with induced hyperlactatemia during low-intensity exercise

We studied the role of lactate in gluconeogenesis (GNG) during exercise in untrained fasting humans. During the final hour of a 4-h cycle exercise at 33-34% maximal O(2) uptake, seven subjects received, in random order, either a sodium lactate infusion (60 micromol x kg(-1) x min(-1)) or an isomolar sodium bicarbonate infusion. The contribution of lactate to gluconeogenic glucose was quantified by measuring (2)H incorporation into glucose after body water was labeled with deuterium oxide, and glucose rate of appearance (R(a)) was measured by [6,6-(2)H(2)]glucose dilution. Infusion of lactate increased lactate concentration to 4.4 +/- 0.6 mM (mean +/- SE). Exercise induced a decrease in blood glucose concentration from 5.0 +/- 0.2 to 4.2 +/- 0.3 mM (P < 0.05); lactate infusion abolished this decrease (5.0 +/- 0.3 mM; P < 0.001) and increased glucose R(a) compared with bicarbonate infusion (P < 0.05). Lactate infusion increased both GNG from lactate (29 +/- 4 to 46 +/- 4% of glucose R(a), P < 0.001) and total GNG. We conclude that lactate infusion during low-intensity exercise in fasting humans 1). increased GNG from lactate and 2). increased glucose production, thus increasing the blood glucose concentration. These results indicate that GNG capacity is available in humans after an overnight fast and can be used to sustain blood glucose levels during low-intensity exercise when lactate, a known precursor of GNG, is available at elevated plasma levels.     

Blood lactate disappearance at various intensities of recovery exercise

Numerous studies have reported that following intense exercise the rate of blood lactate (La) disappearance is greater during continuous aerobic work than during passive recovery. Recent work indicates that a combination of high- and low-intensity work may be optimal in reducing blood La. We tested this hypothesis by measuring the changes in blood La levels following maximal exercise during four different recovery patterns. Immediately following 50 S of maximal work, subjects (n = 7) performed one of the following recovery treatments for 40 min: 1) passive recovery (PR); 2) cycling at 35% maximal O2 uptake (VO2 max) (35% R); 3) cycling at 65% VO2 max (65% R); 4) cycling at 65% for 7 min followed by cycling at 35% for 33 min (CR). The treatment order was counterbalanced with each subject performing all treatments. Serial blood samples were obtained throughout recovery treatments and analyzed for La. The rate of blood La disappearance was significantly greater (P less than 0.05) in both the 35% R and CR when compared with either the 65% R or PR. No significant difference (P greater than 0.05) existed in the rate of blood La disappearance between the 35% R and CR. These data do not support the hypothesis that exercise recovery at a combination of intensities is superior to a recovery involving continuous submaximal exercise in lowering blood La following maximal work.     

Splanchnic and muscle fructose metabolism during and after exercise

Regional substrate exchange was studied in 12 healthy males during 90 min of bicycle exercise at 30% of maximal O2 consumption with a 20-min recovery. Six subjects received an intravenous fructose infusion (8.5 mmol/min) from 40 min of exercise to the end of recovery. Splanchnic glucose output, muscle glucose uptake, arterial glucose, and insulin were uninfluenced by the infusion. The respiratory exchange ratio rose to 0.93 +/- 0.04, and arterial free fatty acids fell by 50% (P less than 0.05). Fructose was taken up by splanchnic tissues (45% of administered load), leg muscle (28%), and resting muscle (28%). During infusion, arterial lactate and pyruvate rose two- to threefold, and these substrates were released from splanchnic tissues and taken up by exercising and resting muscle. Splanchnic release of lactate, pyruvate, and glucose accounted for 78% of fructose uptake at 90 min of exercise. Uptake of fructose, lactate, and pyruvate accounted for 55% and together with glucose for 103% of the total oxidative metabolism by exercising muscle. The regional fructose uptakes and lactate exchanges persisted throughout recovery. The present results indicate that fructose infusion during leg exercise 1) results in increased carbohydrate oxidation from fructose, lactate, and pyruvate in exercising muscle, 2) exerts a glycogenic effect in resting muscle and liver during exercise and in liver and muscle recovering from exercise, and 3) does not interfere with glucose metabolism, and that fructose transport into muscle differs from that of glucose.     

Motor cortex excitability does not increase during sustained cycling exercise to volitional exhaustion

The excitability of the motor cortex increases as fatigue develops during sustained single-joint contractions, but there are no previous reports on how corticospinal excitability is affected by sustained locomotor exercise. Here we addressed this issue by measuring spinal and cortical excitability changes during sustained cycling exercise. Vastus lateralis (VL) and rectus femoris (RF) muscle responses to transcranial magnetic stimulation of the motor cortex (motor evoked potentials, MEPs) and electrical stimulation of the descending tracts (cervicomedullary evoked potentials, CMEPs) were recorded every 3 min from nine subjects during 30 min of cycling at 75% of maximum workload (W(max)), and every minute during subsequent exercise at 105% of W(max) until subjective task failure. Responses were also measured during nonfatiguing control bouts at 80% and 110% of W(max) prior to sustained exercise. There were no significant changes in MEPs or CMEPs (P > 0.05) during the sustained cycling exercise. These results suggest that, in contrast to sustained single-joint contractions, sustained cycling exercise does not increase the excitability of motor cortical neurons. The contrasting corticospinal responses to the two modes of exercise may be due to differences in their associated systemic physiological consequences.     

A reduction in the hyperventilation threshold by intravenous infusion of adrenaline in the treadmill exercise

Seven healthy male subjects underwent a treadmill incremental work test in control conditions and during an intravenous epinephrine infusion (10 micrograms/min). At all exercise intensities, epinephrine increased heart rate, ventilation, respiratory quotient and plasma lactate levels without significant changes in oxygen consumption. Under epinephrine infusion, the "anaerobic threshold", considered as the critical intensity at which ventilation began to increase non linearly with oxygen consumption, appeared at a lower intensity and for a higher plasma lactate level than in control conditions. We conclude that the hyperventilation threshold does not necessarily reflect a muscular hypoxia. It could be due to an effect of catecholamines on peripheral chemoreceptors, maybe by alpha-adrenergic vasoconstriction in the carotid bodies.     

Acute plasma volume expansion: effect on metabolism during submaximal exercise.

To examine the effect of acute plasma volume expansion (PVE) on substrate selection during exercise, seven untrained men cycled for 40 min at 72 +/- 2% peak oxygen uptake (VO(2 peak)) on two occasions. On one occasion, subjects had their plasma volume expanded by 12 +/- 2% via an intravenous infusion of the plasma substitute Haemaccel, whereas on the other occasion no such infusion took place. Muscle samples were obtained before and immediately after exercise. In addition, heart rate and pulmonary gas and venous blood samples were obtained throughout exercise. No differences in oxygen uptake or heart rate during exercise were observed between trials, whereas respiratory exchange ratio, blood glucose, and lactate were unaffected by PVE. Muscle glycogen and lactate concentrations were not different either before or after exercise. In addition, there was no difference in total carbohydrate oxidation between trials (control: 108 +/- 2 g; PVE group: 105 +/- 2 g). Plasma catecholamine levels were not affected by PVE. These data indicate that substrate metabolism during submaximal exercise in untrained men is unaltered by acute hypervolemia.     

Effect of dichloroacetate on lactate concentration in exercising humans

The precise mechanism responsible for the increase in plasma lactate concentration during exercise in humans is not known. We have used dichloroacetate to test the hypothesis that a limitation in pyruvate dehydrogenase activity is responsible for the rise in plasma lactate. Dichloroacetate stimulates the activity of pyruvate dehydrogenase, which is normally the regulatory enzyme in the oxidation of glucose when tissue oxygenation is adequate. Six subjects were studied twice according to a randomized, crossover protocol, involving one test with saline infusion and another with dichloroacetate infusion. Exercise load on a bicycle ergometer was increased progressively until exhaustion. Blood samples were drawn each minute throughout exercise and periodically throughout 120 min of recovery. Dichloroacetate significantly lowered the lactate concentration during exercise performed at less than 80% of the average maximal O2 consumption. The peak concentration of lactate at exhaustion was not affected by dichloroacetate treatment, but dichloroacetate did lower lactate concentration throughout recovery. These results suggest that a limitation in pyruvate dehydrogenase activity contributes to the increase in plasma lactate during submaximal exercise and recovery.     

Lactate acidosis and the increase in VE/VO2 during incremental exercise

The purpose of this investigation was to determine whether the onset of lactate acidosis is responsible for the increase in ventilatory equivalent (VE/VO2) during exercise of increasing intensity. Eight male subjects performed maximal incremental exercise tests on a cycle ergometer on two separate occasions. For the control (C) treatment, the initial work rates consisted of 4 min of unloaded pedaling (60 rpm) and 1 min of pedaling at a work rate of 30 W. Thereafter, the work rate was increased each minute by 22 W until volitional fatigue. Venous blood samples were taken before the onset of exercise and at the end of each work rate for determination of pH and lactate. Ventilatory parameters at each work rate were also monitored. Before the experimental treatment (E), the subjects performed two 3-min work bouts at high intensity (210-330 W) on the cycle ergometer in order to prematurely raise blood lactate levels and lower blood pH. The same incremental exercise test as C was then performed. The results indicated that the increase in VE/VO2 occurred at similar work rates and %VO2max although the venous H+ and lactate concentrations were significantly elevated during the E treatment. These results suggest that a decrease in the blood pH resulting from blood lactate accumulation is not responsible for the increase in VE/VO2 during incremental exercise.     

Does exercise-induced hypoxemia modify lactate influx into erythrocytes and hemorheological parameters in athletes?

This study investigated 1) red blood cells (RBC) rigidity and 2) lactate influxes into RBCs in endurance-trained athletes with and without exercise-induced hypoxemia (EIH). Nine EIH and six non-EIH subjects performed a submaximal steady-state exercise on a cyclo-ergometer at 60% of maximal aerobic power for 10 min, followed by 15 min at 85% of maximal aerobic power. At rest and at the end of exercise, arterialized blood was sampled for analysis of arterialized pressure in oxygen, and venous blood was drawn for analysis of plasma lactate concentrations and hemorheological parameters. Lactate influxes into RBCs were measured at three labeled [U-14C]lactate concentrations (1.6, 8.1, and 41 mM) on venous blood sampled at rest. The EIH subjects had higher maximal oxygen uptake than non-EIH (P < 0.05). Total lactate influx was significantly higher in RBCs from EIH compared with non-EIH subjects at 8.1 mM (1,498.1 +/- 87.8 vs. 1,035.9 +/- 114.8 nmol.ml(-1).min(-1); P < 0.05) and 41 mM (2,562.0 +/- 145.0 vs. 1,618.1 +/- 149.4 nmol.ml(-1).min(-1); P < 0.01). Monocarboxylate transporter-1-mediated lactate influx was also higher in EIH at 8.1 mM (P < 0.05) and 41 mM (P < 0.01). The drop in arterial oxygen partial pressure was negatively correlated with total lactate influx measured at 8.1 mM (r = -0.82, P < 0.05) and 41 mM (r = -0.84, P < 0.05) in the two groups together. Plasma lactate concentrations and hemorheological data were similar in the two groups at rest and at the end of exercise. The results showed higher monocarboxylate transporter-1-mediated lactate influx in the EIH subjects and suggested that EIH could modify lactate influx into erythrocyte. However, higher lactate influx in EIH subjects was not accompanied by an increase in RBC rigidity.     

Delayed appearance of blood lactate with reduced frequency breathing during exercise

The purpose of the present study was to investigate the blood lactate (LA-) responses to hypoventilation induced by reduced frequency breathing (RFB) during recovery from exercise. Five male subject performed 16 4 min cycling bouts alternating with 16 min rest periods. Exercise intensities were chosen at power outputs corresponding to 30% VO2max at 2 mMLA-, VO2 at 4 mMLA-, and 90% VO2max in each subject. Breathing frequency was voluntarily controlled starting 10 s before each 3rd min of exercise and maintained throughout the rest of the exercise period. Four different breathing patterns at each exercise intensity were used: normal breathing (NB), breathing every 4 s, breathing every 8 s, and maximal RFB. Except for the NB trials, subjects held their breath at functional residual capacity during each breathing interval. The concentration difference of LA- between the 3rd min sample and the 4th min sample was defined as the lactate change during exercise (delta LA-ex), and that between the 4th min sample and the sample at the 3rd min after the end of the exercise as the lactate change during recovery (delta LA-rec). An ANOVA showed significant (p less than 0.05) differences in breathing procedures only in delta LA-rec. delta LA-rec seemed to increase as compared to NB only at VO2 at 4 mMLA- and 90% VO2max, while delta LA-ex remained unchanged as compared to NB in spite of reduced VA. These results might indicate that RFB inhibited lactate removal from working muscles during exercise.     

Disposal of blood [1-13C]lactate in humans during rest and exercise

Lactate irreversible disposal (RiLa) and oxidation (RoxLa) rates were studied in six male subjects during rest (Re), easy exercise [EE, 140 min of cycling at 50% of maximum O2 consumption (VO2max)] and hard exercise (HE, 65 min at 75% VO2max). Twenty minutes into each condition, subjects received a Na+-L(+)-[1-13C]lactate intravenous bolus injection. Blood was sampled intermittently from the contralateral arm for metabolite levels, acid-base status, and enrichment of 13C in lactate. Expired air was monitored continuously for determination of respiratory parameters, and aliquots were collected for determination of 13C enrichment in CO2. Steady-rate values for O2 consumption (VO2) were 0.33 +/- 0.01, 2.11 +/- 0.03, and 3.10 +/- 0.03 l/min for Re, EE, and HE, respectively. Corresponding values of blood lactate levels were 0.84 +/- 0.01, 1.33 +/- 0.05, and 4.75 +/- 0.28 mM in the three conditions. Blood lactate disposal rates were significantly correlated to VO2 (r = 0.78), averaging 123.4 +/- 20.7, 245.5 +/- 40.3, and 316.2 +/- 53.7 mg X kg-1 X h-1 during Re, EE, and HE, respectively. Lactate oxidation rate was also linearly related to VO2 (r = 0.81), and the percentage of RiLa oxidized increased from 49.3% at rest to 87.0% during exercise. A curvilinear relationship was found between RiLa and blood lactate concentration. It was concluded that, in humans, 1) lactate disposal (turnover) rate is directly related to the metabolic rate, 2) oxidation is the major fate of lactate removal during exercise, and 3) blood lactate concentration is not an accurate indicator of lactate disposal and oxidation.     

Hepatic lactate uptake versus leg lactate output during exercise in humans.

The exponential rise in blood lactate with exercise intensity may be influenced by hepatic lactate uptake. We compared muscle-derived lactate to the hepatic elimination during 2 h prolonged cycling (62 +/- 4% of maximal O(2) uptake, (.)Vo(2max)) followed by incremental exercise in seven healthy men. Hepatic blood flow was assessed by indocyanine green dye elimination and leg blood flow by thermodilution. During prolonged exercise, the hepatic glucose output was lower than the leg glucose uptake (3.8 +/- 0.5 vs. 6.5 +/- 0.6 mmol/min; mean +/- SE) and at an arterial lactate of 2.0 +/- 0.2 mM, the leg lactate output of 3.0 +/- 1.8 mmol/min was about fourfold higher than the hepatic lactate uptake (0.7 +/- 0.3 mmol/min). During incremental exercise, the hepatic glucose output was about one-third of the leg glucose uptake (2.0 +/- 0.4 vs. 6.2 +/- 1.3 mmol/min) and the arterial lactate reached 6.0 +/- 1.1 mM because the leg lactate output of 8.9 +/- 2.7 mmol/min was markedly higher than the lactate taken up by the liver (1.1 +/- 0.6 mmol/min). Compared with prolonged exercise, the hepatic lactate uptake increased during incremental exercise, but the relative hepatic lactate uptake decreased to about one-tenth of the lactate released by the legs. This drop in relative hepatic lactate extraction may contribute to the increase in arterial lactate during intense exercise.     

Dexamethasone in resting and exercising men. I. Effects on bioenergetics, minerals, and related hormones.

A placebo and a low and a high dose of dexamethasone (Dex) were administered for 4.5 days, at 3-wk intervals, to 24 healthy men, following a double-blind, random-order, crossover procedure. After the last dose the subjects performed a maximal cycling exercise, during which respiratory exchanges, electrocardiogram, and blood pressures were monitored. Blood was sampled just before and after each exercise bout. Dex showed no significant effect on fitness, sleep, exhaustion during exercise, maximal O(2) consumption, ventilatory threshold, maximal blood lactate, or rest and exercise blood pressures. On the contrary, both doses of Dex significantly decreased heart rate at rest and during maximal exercise. Blood glucose at rest was higher after both doses of Dex than after placebo; the opposite was found during exercise. Blood levels of ACTH, beta-endorphin, cortisol, and cortisol-binding globulin were lowered by Dex at rest and after exercise. Dex stimulated the increase in atrial natriuretic factor during exercise and lowered rest and postexercise aldosterone. Finally, no difference between "fit or trained" and "less fit or untrained" subjects could be found with respect to Dex effects.     

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.     

The influence of dietary manipulation on plasma ammonia accumulation during incremental exercise in man

The influence of a pattern of exercise and dietary manipulation, intended to alter carbohydrate (CHO) availability, on pre-exercise acid-base status and plasma ammonia and blood lactate accumulation during incremental exercise was investigated. On three separate occasions, five healthy male subjects underwent a pre-determined incremental exercise test (IET) on an electrically braked cycle ergometer. Each IET involved subjects exercising for 5 min at 30%, 50%, 70% and 95% of their maximal oxygen uptake (VO2max) and workloads were separated by 5 min rest. The first IET took place after 3 days of normal dietary CHO intake. The second and third tests followed 3 days of low or high CHO intake, which was preceded by prolonged exercise to exhaustion in an attempt to deplete muscle and liver glycogen stores. Acid-base status and plasma ammonia and blood lactate levels were measured on arterialised venous blood samples immediately prior to and during the final 15 s of exercise at each workload and for 40 min following the completion of each IET. Three days of low CHO intake resulted in the development of a mild metabolic acidosis in all subjects. Plasma ammonia (NH3) accumulation on the low-CHO diet tended to be greater than normal at each exercise workload. Values returned towards resting levels during each recovery period. After the normal and high-CHO diets plasma NH3 levels did not markedly increase above resting values until after exercise at 95% VO2max. Plasma NH3 levels after the high-CHO diet were similar to those after the normal CHO diet.(ABSTRACT TRUNCATED AT 250 WORDS)