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.     

Effect of exercise duration during incremental exercise on the determination of anaerobic threshold and the onset of blood lactate accumulation

To determine the effect of the duration of incremental exercise on the point at which arterial blood lactate concentration (HLa) increases above the resting value (anaerobic threshold: AT) and on the point at which HLa reaches a constant value of 4 mM (onset of blood lactate accumulation: OBLA), eight male students performed two different kinds of incremental exercise. A comparison of arterial HLa and venous HLa was made under both conditions of incremental exercise. The incremental bicycle exercise tests consisted of 25 W increase every minute (1-min test) and every 4 min (4-min test). At maximal exercise, there were no significant differences in either gas exchange parameters or HLa values for the two kinds of incremental exercise. However, the peak workloads attained during the two exercises were significantly different (P less than 0.01). At OBLA and AT, there were no significant differences in gas exchange parameters during the 1-min and 4-min tests except for the workload (at OBLA P less than 0.01; at AT P less than 0.05). When venous blood HLa was used instead of arterial HLa for a 4-min test, AT was not significantly different from that obtained by arterial HLa, but OBLA was significantly different from that obtained by arterial HLa (P less than 0.05). On the other hand, for the 1-min test, venous HLa values yielded significantly higher AT and OBLA compared with those obtained using arterial HLa (P less than 0.01). It was concluded that when arterial blood was used, there was no effect of duration of workload increase in an incremental exercise test on the determination of the AT and OBLA expressed in VO2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mediation of reduced ventilatory response to exercise after endurance training

To investigate the mechanism by which ventilatory (VE) demand is modulated by endurance training, 10 normal subjects performed cycle ergometer exercise of 15 min duration at each of four constant work rates. These work rates represented 90% of the anaerobic threshold (AT) work rate and 25, 50, and 75% of the difference between maximum O2 consumption and AT work rates for that subject (as determined from previous incremental exercise tests). Subjects then underwent 8 wk of strenuous cycle ergometer exercise for 45 min/day. They then repeated the four constant work rate tests at work rates identical to those used before training. During tests before and after training, VE and gas exchange were measured breath by breath and rectal temperature (Tre) was measured continuously. A venous blood sample was drawn at the end of each test and assayed for lactate (La), epinephrine (EPI), and norepinephrine (NE). We found that the VE for below AT work was reduced minimally by training (averaging 3 l/min). For the above AT tests, however, training reduced VE markedly, by an average of 7, 23, and 37 l/min for progressively higher work rates. End-exercise La, NE, EPI, and Tre were all lower for identical work rates after training. Importantly, the magnitude of the reduction in VE was well correlated with the reduction in end-exercise La (r = 0.69) with an average decrease of 5.8 l/min of VE per milliequivalent per liter decrease in La. Correlations of VE with NE, EPI, and Tre were much less strong (r = 0.49, 0.43, and 0.15, respectively).     

Lactate and ventilatory thresholds: disparity in time course of adaptations to training

We tested the hypothesis that the lactate threshold (Tlac) during incremental exercise could be increased significantly during the first 3 wk of endurance training without any concomitant change in the ventilatory threshold (Tvent). Tvent is defined as O2 uptake (VO2) at which ventilatory equivalent for O2 [expired ventilation per VO2 (VE/VO2)] increased without a simultaneous increase in the ventilatory equivalent for CO2 (VE/VCO2). Weekly measurements of ventilatory gas exchange and blood lactate responses during incremental and steady-rate exercise were performed on six subjects (4 male; 2 female) who exercised 6 days/wk, 30 min/session at 70-80% of pretraining VO2max for 3 wk. Pretraining Tlac and Tvent were not significantly different. After 3 wk of training, significant increases (P less than 0.05) occurred for mean (+/- SE) VO2max (392 +/- 103 ml/min) and Tlac (482 +/- 135 ml/min). Tvent did not change during the 3 wk of training, despite significant (P less than 0.05) reductions in VE responses to both incremental and steady-rate exercise. Thus ventilatory adaptations to exercise during the first 3 wk of exercise training were not accompanied by a detectable alteration in the ventilatory "threshold" during a 1-min incremental exercise protocol. The mean absolute difference between pairs of Tlac and Tvent posttraining was 499 ml/min. Despite the significant training-induced dissociation between Tlac and Tvent a high correlation between the two parameters was obtained posttraining (r = 0.86, P less than 0.05). These results indicate a coincidental rather than causal relationship.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of carotid body resection on ventilatory and acid-base control during exercise.

To investigate the role of the carotid bodies in exercise hyperpnea and acid-base control, normal and carotid body-resected subjects (CBR) were studied during constant-load and incremental exercise. There was no significant difference in the first-breath ventilatory responses to exercise between the groups; some subjects in each reproducibly exhibited abrupt responses. The subsequent change in Ve toward steady state was slower in the CBR group. The steady-state ventilatory responses were the same in both groups at work rates below the anaerobic threshold (AT). However, above the AT, the hyperpnea was less marked in the CBR group. Ve and acid-base measurements revealed that the CBR group failed to hyperventilate in response to the metabolic acidosis of either constant-load or incremental exercise. We conclude that the carotid bodies 1) are not responsible for the initial exercise hyperpnea, 2) do affect the time course of Ve to its steady state, and 3) are responsible for the respiratory compensation for the metabolic acidosis of exercise.     

Anaerobic threshold and maximal steady-state blood lactate in prepubertal boys

To elucidate further the special nature of anaerobic threshold in children, 11 boys, mean age 12.1 years (range 11.4-12.5 years), were investigated during treadmill running. Oxygen uptake, including maximal oxygen uptake (VO2max), ventilation and the "ventilatory anaerobic threshold" were determined during incremental exercise, with determination of maximal blood lactate following exercise. Within 2 weeks following this test four runs of 16-min duration were performed at a constant speed, starting with a speed corresponding to about 75% of VO2max and increasing it during the next run by 0.5 or 1.0 km.h-1 according to the blood lactate concentrations in the previous run, in order to determine maximal steady-state blood lactate concentration. Blood lactate was determined at the end of every 4-min period. "Anaerobic threshold" was calculated from the increase in concentration of blood lactate obtained at the end of the runs at constant speed. The mean maximal steady-state blood lactate concentration was 5.0 mmol.l-1 corresponding to 88% of the aerobic power, whereas the mean value of the conventional "anaerobic threshold" was only 2.6 mmol.l-1, which corresponded to 78% of the VO2max. The correlations between the parameters of "anaerobic threshold", "ventilatory anaerobic threshold" and maximal steady-state blood lactate were only poor. Our results demonstrated that, in the children tested, the point at which a steeper increase in lactate concentrations during progressive work occurred did not correspond to the true anaerobic threshold, i.e. the exercise intensity above which a continuous increase in lactate concentration occurs at a constant exercise intensity.     

Increased blood ammonia in hypoxia during exercise in humans

The effect of acute hypoxia on blood concentration of ammonia ([NH3]b) and lactate (la-]b) was studied during incremental exercise(IE), and two-step constant workload exercises (CE). Fourteen endurance-trained subjects performed incremental exercise on a cycle ergometer under normoxic (21% O2) and hypoxic (10.4% O2) conditions. Eight endurance-trained subjects performed two-step constant workload exercise at sea level and at a simulated altitude of 5000 m (hypobaric chamber, P(B)=405 Torr; P(O2)=85 Torr) in random order. In normoxia, the first step lasted 25 minutes at an intensity of 85 % of the individual ventilatory anaerobic threshold (AT(vent), ind) at sea level. This reduced workload was followed by a second step of 5 minutes at 115% of their AT(vent), ind. This test was repeated into a hypobaric chamber, at a simulated altitude of 5,000 m. The first step in hypoxia was at an intensity of 65 % of AT(vent), ind., whereas workload for the second step at simulated altitude was the same as that of the first workload in normoxia (85 % of AT(vent), ind). During IE, [NH3]b and [la-]b were significantly higher in hypoxia than in normoxia. Increases in these metabolites were highly correlated in each condition. The onset of [NH3]b and [la-]b accumulation occurred at different exercise intensity in normoxia (181W for lactate and 222W for ammonia) and hypoxia (100W for lactate and 140W for ammonia). In both conditions, during CE, [NH3]b showed a significant increase during each of the two steps, whereas [la-]b increased to a steady-state in the initial step, followed by a sharp increase above 4 mM x L(-1) during the second. Although exercise intensity was much lower in hypoxia than in normoxia, [NH3]b was always higher at simulated altitude. Thus, for the same workload, [NH3]b in hypoxia was significantly higher (p<0.05) than in normoxia. Our data suggest that there is a close relationship between [NH3]b and [la-]b in normoxia and hypoxia during graded intensity exercises. The accumulation of ammonia in blood is independent of that of lactate during constant intense exercise. Hypoxia increases the concentration of ammonia in blood during 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)     

Threshold for muscle lactate accumulation during progressive exercise

The purpose of this study was to investigate the relationship between muscle and blood lactate concentrations during progressive exercise. Seven endurance-trained male college students performed three incremental bicycle ergometer exercise tests. The first two tests (tests I and II) were identical and consisted of 3-min stage durations with 2-min rest intervals and increased by 50-W increments until exhaustion. During these tests, blood was sampled from a hyperemized earlobe for lactate and pH measurement (and from an antecubital vein during test I), and the exercise intensities corresponding to the lactate threshold (LT), individual anaerobic threshold (IAT), and onset of blood lactate accumulation (OBLA) were determined. The test III was performed at predetermined work loads (50 W below OBLA, at OBLA, and 50 W above OBLA), with the same stage and rest interval durations of tests I and II. Muscle biopsies for lactate and pH determination were taken at rest and immediately after the completion of the three exercise intensities. Blood samples were drawn simultaneously with each biopsy. Muscle lactate concentrations increased abruptly at exercise intensities greater than the "below-OBLA" stage [50.5% maximal O2 uptake (VO2 max)] and resembled a threshold. An increase in blood lactate and [H+] also occurred at the below-OBLA stage; however, no significant change in muscle [H+] was observed. Muscle lactate concentrations were highly correlated to blood lactate (r = 0.91), and muscle-to-blood lactate ratios at below-OBLA, at-OBLA, and above-OBLA stages were 0.74, 0.63, 0.96, and 0.95, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Use of arterialized venous blood sampling during incremental exercise tests.

Close agreement between arterialized venous and arterial pH, PCO2, and lactate has previously been demonstrated during steady-state exercise. The purpose of the present study was to compare arterialized venous and arterial pH, PCO2, K+, lactate, pyruvate, and epinephrine during the constantly changing circumstances of an incremental exercise test. Eight normal subjects undertook an incremental exercise test (increasing by 20 W/min) to exhaustion on a cycle ergometer during which simultaneous arterial and arterialized venous samples were drawn over the last 20 s of each work load. Linear regression of arterialized venous on arterial values showed that r varied from 0.97 to 0.99 for the variables examined and, therefore, showed that accurate estimates of arterial values could be made from the arterialized venous results during incremental testing. For many purposes it could be assumed that arterialized venous values equaled arterial values without serious error.     

Lactate, pyruvate, and lactate-to-pyruvate ratio during exercise and recovery

The pattern of lactate increase and its relation to pyruvate and lactate-to-pyruvate (L/P) ratio were studied during exercise and early recovery in 10 normal subjects for incremental exercise on a cycle ergometer. Gas exchange was measured breath by breath. Lactate and pyruvate were measured by enzymatic techniques. Lactate and log lactate changed only slightly at low levels of O2 uptake (VO2) but both began to abruptly increase at approximately 40-55% of the maximal VO2. However, the point of abrupt increase in pyruvate occurred at higher work rates and the rate of increase was not as great as that for lactate. Thus L/P ratio increased at the same VO2 as the log lactate increase. Following the exercise, pyruvate continued to increase steeply for at least the first 5 recovery min, whereas at 2 min lactate increased only slightly or decreased. Thus arterial L/P ratio reversed its direction of change and decreased toward the resting value by 2 min of recovery. Lactate, as well as L/P ratios, decreased in all subjects by 5 min. This study demonstrates that lactate and pyruvate concentrations increase slightly at low levels of exercise without a change in L/P ratio until a threshold work rate at which lactate abruptly increases without pyruvate. The resulting increase in L/P ratio is progressive as work rate is incremented and abruptly reverses when exercise stops.     

Acute altitude exposure and altered acid-base states. I. Effects on the exercise ventilation and blood lactate responses

This study examined the influence of acute altitude (AL) exposure alone or in combination with metabolic acid-base manipulations on the exercise ventilatory and blood lactate responses. Four subjects performed a 4 min, 30 W incremental test to exhaustion at ground level (GL) and a 4 min, 20 W incremental test during three acute exposures to a simulated altitude of 4200 m; (i) normal (NAL), (ii) following 0.2 g.kg-1 ingestion of sodium bicarbonate (BAL), and (iii) following 0.5 g.day-1 ingestion of acetazolamide for 2 days prior to exposure (AAL). VE.VO2-1 increased progressively throughout the incremental tests at AL and the minimum value was not related to a change in the blood lactate response. In contrast, the VE.VCO2-1 decreased initially to reach a minimum value at the same power output for each altitude trial and was related to a lactate threshold defined by a log-log transformation (r = 0.78). This transformation of the blood lactate data was not influenced by the altered acid-base states. The relative exercise intensity corresponding to both a delta lactate of 1 mM and an absolute lactate of 4 mM was significantly increased during the AAL (79.9 +/- 12.9 and 93.9 +/- 13.7% VO2max, respectively) compared with NAL (59.1 +/- 5.5 and 78.0 +/- 5.8% VO2max, respectively). These data suggest that strong relationships exist between the ventilatory and blood lactate response during AL exposure and altered acid-base states. Further, it is concluded that, unless the acid-base status is known, the use of an absolute or delta lactate value to compare submaximal exercise should be interpreted with caution.     

Response of left ventricular diastolic filling to graded exercise relative to the lactate threshold

During incremental exercise, the left ventricular ejection fraction increases up to the intensity of the anaerobic threshold and tends to level off at higher exercise intensities. Since there is a correlation between the response of peak filling rate and ejection fraction to exercise, this study was conducted to determine whether the response of left ventricular diastolic function is similar to the response of systolic function relative to lactate threshold. Twelve healthy men performed two exercise tests on a cycle ergometer. In the first test, lactate threshold and maximal power output were determined. In the second exercise test, gated radionuclide ventriculography was performed at rest, at the lactate threshold intensity, and at peak exercise to measure ejection fraction and peak filling rate. Ejection fraction increased significantly from rest [mean (SD): 62 (5)%] to lactate threshold [76 (7) %] and did not change significantly from lactate threshold to peak exercise [77 (7)%]. Likewise, peak filling rate (normalized for stroke counts) increased from resting [6.1 (0.9)V _s · s^–1] to lactate threshold [9.4 (1.8)V _s · s^–1] and did not change significantly from lactate threshold to peak exercise [9.6 (2.9)V _s · s^–1]. There was no correlation between the change in peak filling rate and the change in ejection fraction from rest to lactate threshold. Thus, during incremental exercise, left ventricular diastolic function responds qualitatively similar to systolic function.     

Blood lactate responses in incremental exercise as predictors of constant load performance

Seven trained male cyclists (VO2max = 4.42 +/- 0.23 l.min-1; weight 71.7 +/- 2.7 kg, mean +/- SE) completed two incremental cycling tests on the cycle ergometer for the estimation of the "individual anaerobic threshold" (IAT). The cyclists completed three more exercises in which the work rate incremented by the same protocol, but upon reaching selected work rates of approximately 40, 60 and 80% VO2max, the subjects cycled for 60 min or until exhaustion. In these constant load studies, blood lactate concentration was determined on arterialized venous ([La-]av) and deep venous blood ([La-]v) of the resting forearm. The av-v lactate gradient across the inactive forearm muscle was -0.08 mmol.l-1 at rest. After 3 min at each of the constant load work rates, the gradients were +0.05, +0.65* and +1.60* mmol.l-1 (*P less than 0.05). The gradients after 10 min at these same work rates were -0.09, +0.24 and +1.03* mmol.l-1. For the two highest work rates taken together, the lactate gradient was less at 10 min than 3 min constant load exercise (P less than 0.05). The [La-]av was consistently higher during prolonged exercise at both 60 and 80% VO2max than that observed at the same work rate during progressive exercise. At the highest work rate (at or above the IAT), time to exhaustion ranged from 3 to 36 min in the different subjects. These data showed that [La-] uptake across resting muscle continued to increase to work rates above the IAT. Further, the greater av-v lactate gradient at 3 min than 10 min constant load exercise supports the concept that inactive muscle might act as a passive sink for lactate in addition to a metabolic site.     

Optimizing the exercise protocol for cardiopulmonary assessment

Twelve normal men performed 1-min incremental exercise tests to exhaustion in approximately 10 min on both treadmill and cycle ergometer. The maximal O2 uptake (VO2 max) and anaerobic threshold (AT) were higher (6 and 13%, respectively) on the treadmill than the cycle; the AT was reached at about 50% of VO2 max on both ergometers. Maximal CO2 output, heart rate, and O2 pulse were also slightly, but significantly higher on the treadmill. Maximal ventilation, gas exchange ratio, and ventilatory equivalents for O2 and CO2 for both forms of exercise were not significantly different. To determine the optimum exercise test for both treadmill and cycle, we exercised five of the subjects at various work rate increments on both ergometers in a randomized design. The treadmill increments were 0.8, 1.7, 2.5, and 4.2%/min at a constant speed of 3.4 mph, and 1.7 and 4.2%/min at 4.5 mph. Cycle increments were 15, 30, and 60 W/min. The VO2 max was significantly higher on tests where the increment magnitude was large enough to induce test durations of 8-17 min, but the AT was independent of test duration. Thus, for evaluating cardiopulmonary function with incremental exercise testing by either treadmill or cycle, we suggest selecting a work rate increment to bring the subject to the limit of his tolerance in about 10 min.     

Ventilatory response to incremental and constant-workload exercise in the presence of a thoracic restriction.

In the presence of an externally applied thoracic restriction, conflicting ventilatory responses to exercise have been reported, which could be accounted for by differences in exercise protocol. Seven male subjects performed two incremental and two constant-workload ergometer tests either unrestricted or in the presence of an inelastic corset. Ventilatory variables and arterial estimates of PCO(2) were obtained breath by breath. Subjects hyperventilated in the presence of restriction during the constant-workload test (38.4 +/- 3.0 vs. 32.8 +/- 3.0 l/min for the average of the last 3 min of exercise, P < 0.05), whereas, at an equivalent workload during the incremental test, ventilation was similar to unrestricted values (unrestricted = 26.3 +/- 1.6 vs. restricted = 27.9 +/- 2.3 l/min, P = 0.36). We used a first-order linear model to describe the effects of change in workload on minute ventilation (24). When the time constants and minute ventilation values measured during unrestricted and restricted constant-workload exercise were used to predict the ventilatory response to the respective incremental exercise tests, no significant difference was observed. This suggests that hyperventilation is not seen in the restricted incremental test because the temporal dynamics of the ventilatory response are altered.     

Relation between the change of slope of heart rate and second lactic and ventilatory thresholds in muscular exercise with large load]

The time-course of heart rate, blood lactate, and ventilatory gas exchange was studied during an incremental exercise test on cycloergometer in order to ascertain whether heart rate deflection occurred at the same load as the second lactate S[La]2) and ventilatory (SV2) thresholds. Twelve moderately trained subjects, 22 to 30 years old, participated in the study. The initial power setting was 30 W for 3 min with successive increases of 30 W every min except at the end of the test where the increase was reduced to 20 and 10 W.min-1. Ventilatory flow (VE), oxygen uptake (VO2), carbon dioxide production (VCO2, ventilatory equivalents of O2 (EO2 = VE/VO2) and CO2 (ECO2 = VE/VCO2), and heart rate (HR) were determined during the last 20 s of every min. Venous blood samples were drawn at the end of each stage of effort and analyzed enzymatically for lactate concentration ([La]). The HR deflection, S[La]2, and SV2 were represented graphically by two investigators using a double blind procedure. Following the method proposed by Conconi et al. 1982, the deflection in HR was considered to begin at the point beyond which the increase in work intensity exceeded the increase in HR and the linearity of the work rate/HR relationship was lost. S[La]2 corresponded to the second breaking point of the lactate time-course curve (onset of blood lactate accumulation) and SV2 was identified at the second breaking point in the increase in VE and ventilatory equivalent for O2 uptake accompanied by a concomitant increase in ventilatory equivalent for CO2 output. We observed that the deflection point in HR was present only in 7 subjects. The work load, VO2, HR, and [La] levels at which heart rate departed from linearity did not differ significantly from those determined with S[La]2 ans SV2. The VO2 and HR values at HR deflection point were significantly correlated with those measured at S[La]2 and SV2. It is concluded that deflection in heart rate does not always occur, and when it does, it coincides with the second lactate and ventilatory gas exchange thresholds. It can thus be used for the determination of optimal intensity for individualized aerobic training.     

Anaerobiosis, lactate, and gas exchange during exercise: the issues

The lactate increase during exercise is a critically important biochemical and physiological event that leads to decreasing cell pH, an accelerated rate of glycogen depletion in the muscle, and important changes in ventilatory and gas exchange dynamics. Lactate increases only slightly at low work rates, and this increase is proportional to pyruvate increase (i.e. compatible with accelerated glycolysis without a change in redox state). At high work rates lactate increases disproportionately to pyruvate, the increased rate of lactate accumulation and lactate/pyruvate ratio appearing to occur at a threshold O2 consumption for a given individual. This symposium addresses the biochemical origin and physiological consequences of the increased lactate production during exercise.     

Effects of training on glucose metabolism of gluconeogenesis-inhibited short-term-fasted rats

To evaluate the effects of endurance training on gluconeogenesis and blood glucose homeostasis, trained as well as untrained short-term-fasted rats were injected with mercaptopicolinic acid (MPA), a gluconeogenic inhibitor, or the injection vehicle. Glucose kinetics were assessed by primed-continuous venous infusion of [U-14C]- and [6-3H]glucose at rest and during submaximal exercise at 13.4 m/min on level grade. Arterial blood was sampled for the determination of blood glucose and lactate concentrations and specific activities. In resting untrained sham-injected rats, blood glucose and lactate were 7.6 +/- 0.2 and 1.3 +/- 0.1 mM, respectively; glucose rate of appearance (Ra) was 71.1 +/- 12.1 mumol.kg-1.min-1. MPA treatment lowered blood glucose, raised lactate, and decreased glucose Ra. Trained animals had significantly higher glucose Ra at rest and during exercise. At rest, trained MPA-treated rats had lower blood glucose, higher blood lactate, and similar glucose Ra and disappearance rates (Rd) than trained sham-injected animals. Exercising sham-injected untrained animals had increased blood glucose and glucose Ra compared with rest. Exercising trained sham-injected rats had increased blood glucose and glucose Ra and Rd but no change in blood lactate compared with untrained sham-injected animals. In the trained animals during exercise, MPA treatment increased blood lactate and decreased blood glucose and glucose Ra and Rd. There was no measurable glucose recycling in trained or untrained MPA-treated animals either at rest or during submaximal exercise. There was no difference in running time to exhaustion between trained and untrained MPA-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

The ventilation, lactate and electromyographic thresholds during incremental exercise tests in normoxia, hypoxia and hyperoxia

These experiments examined the effect of hypoxia and hyperoxia on ventilation, lactate concentration and electromyographic activity during an incremental exercise test in order to determine if coincident chances in ventilation and electromyographic activity occur during an incremental exercise test, despite an enhancement or reduction of peripheral chemoreceptor activity. In addition, these experiments were completed to determine if electromyographic activity and ventilation are enhanced or reduced in response to the inspiration of oxygen-depleted and oxygen-enriched air, respectively. Seven subjects performed three incremental exercise tests, until volitional exhaustion was achieved, while inspiring air with a fractional concentration of oxygen of either 66%, 21% or 17%. In addition, another single subject completed two tests while inspiring air with a fractional concentration of either 17% or 21%. During the tests, ventilation, mixed expired oxygen and carbon dioxide, arterialized venous blood and the electromyographic activity from the vastus lateralis were sampled. From these values ventilation, electromyographic and lactate thresholds were detected during normoxia, hypoxia and hyperoxia. The results showed that although ventilation and lactate concentration were significantly less during hyperoxia as compared to normoxia or hypoxia, the carbon dioxide production values were not significantly different between the normoxic, hypoxic and hyperoxic conditions. For a particular condition, the time, carbon dioxide production and oxygen consumption values that corresponded to the ventilation and electromyographic thresholds were not significantly different, but the values corresponding to the lactate threshold were significantly less than those for the electromyographic and ventilation thresholds. Comparisons between the three conditions showed that the time, carbon dioxide production and oxyen consumption values corresponding to each of these thresholds were not significantly different. These findings have led us to conclude that the changes in lactate concentration observed during exercise may not be directly related to the fractional concentration of inspired oxygen, and that the peripheral chemoreceptors may not be the sole mediators of the first ventilatory threshold. It is suggested that this threshold may be mediated by an increase in neural activity originating from higher motor centers or the exercising limbs, induced in response to the need to progressively recruit fast twitch muscle fibers as exercise power output is increased and as individual muscle fibers begin to fatigue.