Inspiratory muscle training reduces blood lactate concentration during volitional hyperpnoea

Although reduced blood lactate concentrations ([lac(-)](B)) have been observed during whole-body exercise following inspiratory muscle training (IMT), it remains unknown whether the inspiratory muscles are the source of at least part of this reduction. To investigate this, we tested the hypothesis that IMT would attenuate the increase in [lac(-)](B) caused by mimicking, at rest, the breathing pattern observed during high-intensity exercise. Twenty-two physically active males were matched for 85% maximal exercise minute ventilation (.V(E) max) and divided equally into an IMT or a control group. Prior to and following a 6 week intervention, participants performed 10 min of volitional hyperpnoea at the breathing pattern commensurate with 85% .V(E) max. The IMT group performed 6 weeks of pressure-threshold IMT; the control group performed no IMT. Maximal inspiratory mouth pressure increased (mean +/- SD) 31 +/- 22% following IMT and was unchanged in the control group. Prior to the intervention in the control group, [lac(-)](B) increased from 0.76 +/- 0.24 mmol L(-1) at rest to 1.50 +/- 0.60 mmol L(-1) (P < 0.05) following 10 min volitional hyperpnoea. In the IMT group, [lac(-)](B) increased from 0.85 +/- 0.40 mmol L(-1) at rest to 2.02 +/- 0.85 mmol L(-1) following 10 min volitional hyperpnoea (P < 0.05). After 6 weeks, increases in [lac(-)](B) during volitional hyperpnoea were unchanged in the control group. Conversely, following IMT the increase in [lac(-)](B) during volitional hyperpnoea was reduced by 17 +/- 37% and 25 +/- 34% following 8 and 10 min, respectively (P < 0.05). In conclusion, increases in [lac(-)](B) during volitional hyperpnoea at 85% .V(E) max were attenuated following IMT. These findings suggest that the inspiratory muscles were the source of at least part of this reduction, and provide a possible explanation for some of the IMT-mediated reductions in [lac(-)](B), often observed during whole-body exercise.     

Gentle exercise with a previously inactive muscle group hastens the decline of blood lactate concentration after strenuous exercise

Summary The aim of this study was to elucidate the mechanism by which the disappearance of blood lactate following severe exercise is enhanced during active recovery in comparison with recovery at rest. Rates of decline of arterialised venous blood lactate concentrations in man after maximal one-leg exercise were compared during four different modes of recovery: passive (PR), exercise of the muscles involved in the initial exercise (SL), exercise of the corresponding muscles in the hitherto-inactive leg (OL), or exercise of one arm (RA). Recovery exercise workloads were each 40% of the onset of blood lactate accumulation (OBLA) for the limb used. In comparison with PR, SL and OL accelerated the fall in blood lactate to similar extents whereas RA was without effect. The first-order rate constant (min^–1) for decline of arterialised venous blood lactate concentration after the intense exercise was 0.027 (0.003) in PR, 0.058 (0.025) in SL, 0.034 (0.002) in OL, and in RA was 0.028 (0.002) [mean (SEM),n = 6 subjects]. Preliminary studies had shown that RA in isolation elevated blood lactate whereas SL and OL did not. Thus, with appropriate workloads, exercise of either hitherto active or passive muscles enhanced blood lactate decline during recovery from intense exercise. This suggests that the effect resulted principally from the uptake and utilisation of lactate in the circulation by those exercising muscles rather than from increased transport of lactate to other sites of clearance by sustained high blood flow through the previously active muscles.     

The effect of inspiratory muscle training upon maximum lactate steady-state and blood lactate concentration

Several studies have reported that improvements in endurance performance following respiratory muscle training (RMT) are associated with a decrease in blood lactate concentration ([Lac]_B). The present study examined whether pressure threshold inspiratory muscle training (IMT) elicits an increase in the cycling power output corresponding to the maximum lactate steady state (MLSS). Using a double-blind, placebo-controlled design, 12 healthy, non-endurance-trained male participants were assigned in equal numbers to an experimental (IMT) or sham training control (placebo) group. Cycling power output at MLSS was initially identified using a lactate minimum protocol followed by a series of constant power output rides (2.5% increments) of 29.5 min duration; MLSS was reassessed following six weeks of IMT or sham IMT. Maximum inspiratory mouth pressure increased significantly (26%) in the IMT group, but remained unchanged in the placebo group. The cycling power output corresponding to MLSS remained unchanged in both groups after the intervention. After IMT, [Lac]_B decreased significantly at MLSS power in the IMT group [–1.17 (1.01) mmol l^–1 after 29.5 min of cycling; mean (SD)], but remained unchanged in the placebo group [+0.37 (1.66) mmol l^–1]. These data support previous observations that IMT results in a decrease in [Lac]_B at a given intensity of exercise. That such a decrease in [Lac]_B was not associated with a substantial (>2.5%) increase in MLSS power is a new finding suggesting that RMT-induced increases in exercise tolerance and reductions in [Lac]_B are not ascribable to a substantial increase in the lactate threshold.     

The influence of blood sampling site on lactate concentration during submaximal exercise at 4 mmol · 1−1 lactate level

This study examined lactate concentration during incremental and submaximal treadmill exercise at work rates corresponding to 4 mmol· 1^–1 lactate concentration, determined by fingertip (OBLAI) and venous blood (OBLA2). Initially, eight subjects performed a 4-min incremental exercise test until exhaustion. On two other occasions, seven of the subjects undertook submaximal exercise tests (30 min) at work rates corresponding to OBLA1 and OBLA2. Blood was simultaneously obtained from both sites at rest and at the end of each exercise stage during the incremental exercise, and at 5, 10, 20 and 30 min during the submaximal exercise and 5 min into recovery. Fingertip blood lactate concentrations were significantly higher (P<0.05) than venous blood at rest, throughout the incremental exercise, consistently during exercise at OBLA1 and OBLA2, and into recovery. Data also revealed an exercise intensity-dependent lactate difference between the two sampling sites during both exercise protocols. Exercise at OBLA1 did not result in a progressive increase in lactate level nor exhaustion, and the lactate value at the end of 30 min corresponded to the predetermined value. However, exercise at OBLA2 resulted in a significantly higher (P<0.05) lactate level than OBLA1, the lactate concentration at the end of 30 min was substantially higher than the predetermined value (P<0.05) and exhaustion was evident. It is concluded that the lactate concentration value during incremental and submaximal exercise (at 4 mmol·l^–1 OBLA) is dependent on the blood sampling site. This finding should be considered in studies concerned with the determination of OBLA.     

Maximal lactate steady state determination with a single incremental test exercise

The aim of this study was to determine whether the power output associated with a maximal lactate steady state (MLSS) (Ẇ_MLSS) can be assessed using a single incremental cycling test. Eleven recreational sportsmen (age: 22±1 years, height: 175±6 cm, weight: 71±5 kg) volunteered to participate in the study. For each subject the first and second ventilatory thresholds (VT₁ and VT₂, respectively) and the power output corresponding to (respiratory exchange ratio) RER=1.00 were determined during an incremental test to exhaustion. Thereafter, each subject performed several 30-min constant load tests to determine MLSS. The workload used in the first constant test was set to the Ẇ_RER=1.00 determined during the incremental test. Ẇ_VT1 (175±24 W) and Ẇ_VT2 (265±31 W) were significantly different from Ẇ_MLSS (220±36 W). Whereas, Ẇ_RER=1.00 (224±33 W) was similar to Ẇ_MLSS. HR, RER and V̇E were significantly different between the 10th and the 30th minutes when exercising at Ẇ_RER=1.00 and at Ẇ_MLSS. In contrast, V̇O₂ and V̇CO₂ were stable over those 30-min constant tests. Power output at VT₁, RER=1.00 and VT₂ were all correlated to Ẇ_MLSS but the relationship was stronger between RER=1.00 and MLSS (R ²=0.95). The present study shows that the power output associated with a RER value equal to 1.00 during an incremental test does not differ from that determined for MLSS. Hence, the MLSS can be estimated with a single exercise test.     

Caffeine increases maximal anaerobic power and blood lactate concentration

Summary The aim of this study was to specify the effects of caffeine on maximal anaerobic power (W _max). A group of 14 subjects ingested caffeine (250 mg) or placebo in random double-blind order. TheW _max was determined using a force-velocity exercise test. In addition, we measured blood lactate concentration for each load at the end of pedalling and after 5 min of recovery. We observed that caffeine increasedW _max [964 (SEM 65.77) W with caffeine vs 903.7 (SEM 52.62) W with placebo;P<0.02] and blood lactate concentration both at the end of pedalling [8.36 (SEM 0.95) mmol · l^–1 with caffeine vs 7.17 (SEM 0.53) mmol · l^–1 with placebo;P<0.011 and after 5 min of recovery [10.23 (SEM 0.97) mmol · l^–1 with caffeine vs 8.35 (SEM 0.66) mmol · l^–1 with placebo;P<0.04]. The quotient lactate concentration/power (mmol · l^–1 · W^–1) also increased with caffeine at the end of pedalling [7.6 · 10^–3 (SEM 3.82 · 10^–5) vs 6.85 · 10^–3 (SEM 3.01 · 10^–5);P<0.01] and after 5 min of recovery [9.82·10^–3 (SEM 4.28 · 10^–5) vs 8.84 · 10^–3 (SEM 3.58 · 10^–5);P<0.02]. We concluded that caffeine increased bothW _max and blood lactate concentration.     

Prolonged stage duration during incremental cycle exercise: effects on the lactate threshold and onset of blood lactate accumulation

The aim of this study was to investigate whether increasing the duration of workloads from 3 min to 8 min during incremental exercise would influence workload (W), oxygen consumption ( ) and heart rate (HR) at the lactate threshold (LT) and the onset of blood lactate accumulation(OBLA). Two groups of six male cyclists were assigned to a well-trained (WT) and recreational (REC) group on the basis of their performance in a maximal incremental ramp test. Each subject then performed two incremental lactate tests (EXT) consisting of six workloads of either 3 min (EXT_3-min) or 8 min (EXT_8-min) duration. At the completion of each workload whole capillary blood samples were obtained for the determination of blood lactate (BLa) concentration (mM). Power output (Watts, W), HR and were averaged in the final minute of each workload as well as in the third minute of the EXT_8-min. The workload, HR and at the LT and OBLA were subsequently determined from the data of EXT_3-min and EXT_8-min. The results demonstrate that workload and , but not HR, at the LT and OBLA were higher in the WT cyclists. At the same time, the workload at the LT obtained from the results of the EXT_3-min was significantly (P<0.05) higher then the value obtained in the EXT_8-min in the WT subjects but not the REC subjects. However, the workload, and HR at the OBLA, together with the and HR at the LT were not significantly different when calculated from data obtained from EXT_3-min or EXT_8-min. The data obtained in this study suggest that incremental exercise protocols using workloads of duration longer than 3 min have the effect of increasing the workload at the LT in well-trained cyclists. However, the OBLA determined in exercise tests using stage increments of either 3 min or 8 min is similar in cyclists of different training status. Electronic Publication     

Threshold increases in plasma growth hormone in relation to plasma catecholamine and blood lactate concentrations during progressive exercise in endurance-trained athletes

Plasma human growth hormone ([HGH]), adrenaline ([A]), noradrenaline ([NA]) and blood lactate ([La^–]_b) concentrations were measured during progressive, multistage exercise on a cycle ergometer in 12 endurance-trained athletes [aged 32.0 (SEM 2.0) years]. Exercise intensities (3 min each) were increased by 50 W until the subjects felt exhausted. Venous blood samples were taken after each intensity. The [HGH] and catecholamine concentrations increased negligibly during exercise of low to moderate intensities revealing an abrupt rise at the load corresponding to the lactate threshold ([La^–]-T). Close correlations (P < 0.001) were found between [La^–]_b and plasma [HGH] (r = 0.64), [A] (r = 0.71) and [NA] (r = 0.81). The mean threshold exercise intensities for [HGH], [A] and [NA], detected by log-log transformation, [154 (SEM 19) W, 162 (SEM 15) W and 160 (SEM 17) W, respectively] were not significantly different from the [La^–]-T [161 (SEM 12) W]. The results indicated that the threshold rise in plasma [HGH] followed the patterns of plasma catecholamine and blood lactate accumulation during progressive exercise in the endurancetrained athletes.     

Perceived exertion related to heart rate and blood lactate during arm and leg exercise

Summary To compare some psychophysiological responses to arm exercise with those to leg exercise, an experiment was carried out on electronically braked bicycle ergometers, one being adapted for arm exercise. Eight healthy males took part in the experiment with stepwise increases in exercise intensity every 4 min: 40—70—100—150—200 W in cycling and 20—35—50—70—100 W in arm cranking. Towards the end of each 4 min period, ratings of perceived exertion were obtained on the RPE scale and on a new category ratio (CR) scale: heart rate (HR) and blood lactate accumulation (BL) were also measured. The responses obtained were about twice as high or more for arm cranking than for cycling. The biggest difference was found for BL and the smallest for HR and RPE. The incremental functions were similar in both activities, with approximately linear increases in HR and RPE and positively accelerating functions for CR (exponents about 1.9) and BL (exponents 2.5 and 3.3 respectively). When perceived exertion (according to the CR scale) was set as the dependent variable and a simple combination of HR and BL was used as the independent variable, a linear relationship was obtained for both kinds of exercise, as has previously been found in cycling, running, and walking. The results thus give support for the following generalization: For exercise of a steady state type with increasing loads the incremental curve for perceived exertion can be predicted from a simple combination of HR and BL. This study was supported by a research grant from The Bank of Sweden Tercentenary Foundation No. 85/291     

Effect of hypoxia on arterial and venous blood levels of oxygen,carbon dioxide,hydrogen ions and lactate during incremental forearm exercise

Summary The purpose of the present study was to investigate whether, in humans, hypoxia results in an elevated lactate production from exercising skeletal muscle. Under conditions of both hypoxia [inspired oxygen fraction (F_IO₂): 11.10%] and normoxia (F_IO₂: 20.94%), incremental exercise of a forearm was performed. The exercise intensity was increased every minute by 1.6 kg·m·min^–1 until exhaustion. During the incremental exercise the partial pressure of oxygen (PO₂) and carbon dioxide (PCO₂), oxygen saturation (SO₂), pH and lactate concentration [HLa] of five subjects, were measured repeatedly in blood from the brachial artery and deep veins from muscles in the forearm of both the active and inactive sides. The hypoxia (arterial SO₂ approximately 70%) resulted in (1) the difference in [HLa] in venous blood from active muscle (values during exercise — resting value) often being more than twice that for normoxia, (2) a significantly greater difference in venous-arterial (v-a) [HLa] for the exercising muscle compared to normoxia, and (3) a difference in v-a [HLa] for non-exercising muscle that was slightly negative during normoxia and more so with hypoxia. These studies suggest that lower O₂ availability to the exercising muscle results in increased lactate production.     

Validity of criteria for establishing maximal O<Subscript>2</Subscript> uptake during ramp exercise tests

The incremental or ramp exercise test to the limit of tolerance has become a popular test for determination of maximal O₂ uptake However, many subjects do not evidence a definitive plateau of the -work rate relationship on this test and secondary criteria based upon respiratory exchange ratio (RER), maximal heart rate (HR_max) or blood [lactate] have been adopted to provide confidence in the measured We hypothesized that verification of using these variables is fundamentally flawed in that their use could either allow underestimation of (if, for any reason, a test were ended at a sub-maximal ), or alternatively preclude subjects from recording a valid Eight healthy male subjects completed a ramp exercise test (at 20 W/min) to the limit of tolerance on an electrically braked cycle ergometer during which pulmonary gas exchange was measured breath-by-breath and blood [lactate] was determined every 90 s. Using the most widely used criterion values of RER (1.10 and 1.15), as determined during the ramp test (4.03 ± 0.10 l/min) could be undermeasured by 27% (2.97 ± 0.24 l/min) and 16% (3.41 ± 0.15 l/min), respectively (both P < 0.05). The criteria of HR_max (age predicted HR_max ± 10 b/min) and blood [lactate] (≥8 mM) were untenable because they resulted in rejection of 3/8 and 6/8 of the subjects, most of whom (5/8) had demonstrated a plateau of at These findings provide a clear mandate for rejecting these secondary criteria as a means of validating on ramp exercise tests.     

Blood lactate during submaximal exercises

Summary Values of oxygen consumption, carbon dioxide production, ventilation and blood lactate concentration were determined in eight active male subjects during the minute following submaximal square-wave exercise on a treadmill under two sets of conditions. Square-wave exercise was (1) integrated in a series of intermittent incremental exercises of 4-min duration separated by 1-min rest periods; (2) isolated, of 4- and 12-min duration, and of intensity corresponding to each of the intermittent incremental periods of exercise. For square-wave exercise of the same duration (4 min) and intensity, no significant differences in the above-mentioned parameters were noted between intermittent incremental exercise and isolated exercise. Only at high work rate (>92% maximal oxygen uptake), were blood lactate levels in three subjects slightly higher after 12-min of isolated exercise than after the 4-min periods of isolated exercise. Examination of these results suggests that (1) 80–90% of the blood lactate concentration observed under our experimental conditions results from the accumulation of lactate in the blood during the period of oxygen deficit; (2) therefore the blood lactate concentration/exercise intensity relationship, for the most part, appears to represent the lactate accumulated early in the periods of intermittent incremental exercise.     

Peak blood lactate after short periods of maximal treadmill running

Summary Blood lactate was determined in 19 untrained subjects after maximal treadmill exercise lasting for about 1 min. It was found that blood lactate increases after exercise, reaching a maximum level 6–9 min after the cessation of exercise, and the average time for the appearance of the peak blood lactate concentration was 7.65 min. Peak blood lactate concentration at 7.65 min (CLA_7.65), which was calculated by substituting t (7.65) into the equation for the lactate recovery curve for each subject, agreed well with the observed peak blood lactate concentration (r=0.98, p<0.001). In addition, correlations of r=–0.65, r=–0.78, r=–0.79 were found between CLA_7.65 and the running times of 100 m, 200 m, and 400 m sprints, respectively. These results suggest that CLA_7.65 may be used as a valid indicator of anaerobic work capacity in man.     

Independence of ventilation and blood lactate responses during graded exercise

The effect of power output increment, based on an increase in pedal rate, on blood lactate accumulation during graded exercise is unknown. Therefore, in the present study, we examined the effect of two different rates of power output increments employing two pedal rates on pulmonary ventilation and blood lactate responses during graded cycle ergometry in young men. Males (n=8) with an mean (SD) peak oxygen uptake of 4.2 (0.1) 1·min^–1 served as subjects. Each subject performed two graded cycle ergometer tests. The first test, conducted at 60 rev· min^–1, employed 4 min of unloaded pedaling followed by a standard power output step increment (SI) of 60 W every 3rd min. The second test, conducted at 90 rev·min^–1, employed 4 min of unloaded pedaling followed by a high power output step increment (HI) of 90 W every 3rd min. Venous blood was sampled from a forearm vein after 5 min of seated rest, 4 min of unloaded pedaling, and every 3rd min of graded exercise. Peak exercise values for heart rate, oxygen uptake ( O₂), and ventilation ( _E) were similar (P > 0.05) for SI and HI exercise, as was the relationship between _E and O₂, and between _E and carbon dioxide production ( CO₂). However, the relationship between blood lactate concentration and O₂ was dissimilar between SI and HI exercise with blood lactate accumulation beyond the lowest ventilatory equivalent of oxygen, and peak exercise blood lactate concentration values significantly higher (P < 0.05) for SI [12.8 (2.6) mmol·l^–1] compared to HI [8.0(1.9) mmol·l^–1] exercise. Our findings demonstrate that blood lactate accumulation and _E during graded exercise are dissociated. Blood lactate accumulation is influenced by the rate of external power output increment, while _E is related to O₂ and CO₂.     

A method for determining the maximal steady state of blood lactate concentration from two levels of submaximal exercise

The aim of this study was to estimate the characteristic exercise intensity _CL which produces the maximal steady state of blood lactate concentration (MLSS) from submaximal intensities of 20 min carried out on the same day and separated by 40 min. Ten fit male adults [maximal oxygen uptake _max 62 (SD 7) ml · min^–1 · kg^–1] exercisOed for two 30-min periods on a cycle ergometer at 67% (test 1.1) and 82% of _max (test 1.2) separated by 40 min. They exercised 4 days later for 30 min at 82% of _max without prior exercise (test 2). Blood lactate was collected for determination of lactic acid concentration every 5 min and heart rate and O₂ uptake were measured every 30 s. There were no significant differences at the 5th, 10th, 15th, 20th, 25th, or 30th min between , lactacidaemia, and heart rate during tests 1.2 and 2. Moreover, we compared the exercise intensities _CL which produced the MLSS obtained during tests 1.1 and 1.2 or during tests 1.1 and 2 calculated from differential values of lactic acid blood concentration ([1a^–]_b) between the 30th and the 5th min or between the 20th and the 5th min. There was no significant difference between the different values of _CL [68 (SD 9), 71 (SD 7), 73 (SD 6),71 (SD 11) % of _max (ANOVA test,P<0.05). Four subjects ran for 60 min at their _CL determined from periods performed on the same day (test 1.1 and 1.2) and the difference between the [la^–]_b at 5 min and at 20 min ( ([la^–]_b)) was computed. The [la^–]_b remained constant during exercise and ranged from 2.2 to 6.7 mmol · l^–1 [mean value equal to 3.9 (SD 1) mmol · l^–1]. These data suggest that the _CL protocol did not overestimate the exercise intensity corresponding to the maximal fractional utilization of _max at MLSS. For half of the subjects the _CL was very close to the higher stage (82% of _max where an accumulation of lactate in the blood with time was observed. It can be hypothesized that _CL was very close to the real MLSS considering the level of accuracy of [la^–]_b measurement. This study showed that exercise at only two intensities, performed at 65% and 80% of _max and separated by 40 min of complete rest, can be used to determine the intensity yielding a steady state of [la^–1]_b near the real MLSS workload value.     

Influence of cold exposure on blood lactate response during incremental exercise

Summary This study examined the effect of acute exposure of the whole body to cold on blood lactate response during incremental exercise. Eight subjects were tested with a cycle ergometer in a climatic chamber, room temperature being controlled either at 24° C (MT) or at –2° C (CT). The protocol consisted of a step increment in exercise intensity of 30 W every 2 min until exhaustion. Oxygen consumption ( ) was measured at rest and during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for estimations of plasma norepinephrine (NE), epinephrine (E), free fatty acid (FFA) and glucose concentrations, during the last 15 s of each exercise step and also during the 1^st, 4^th, 7^th, and the 10^th min following exercise for the determination of blood lactate (LA) concentration. The , was higher during CT than during MT at rest and during nearly every exercise intensity. At CT, lactate anaerobic threshold (LAT), determined from a marked increase of LA above resting level, increased significantly by 49% expressed as absolute , and 27% expressed as exercise intensity as compared with MT. The LA tended to be higher for light exercise intensities and lower for heavy exercise intensities during CT than during MT. The E and NE concentrations increased during exercise, regardless of ambient temperature. Furthermore, at rest and at exhaustion E concentrations did not differ between both conditions, while NE concentrations were greater during CT than during MT. Moreover, an increase of FFA was found only during CT. The difference in FFA level suggests that alterations in fat metabolism, possibly initiated by an enhanced secretion of NE, may have contributed to a decrease in lactate production.     

Critical power test for ramp exercise

The critical power test for cycle ergometry has been criticised as providing an overestimate of the real value of the critical power. Part of the blame may rest in the practical problem associated with getting reliable measurements of longer endurance times when power settings are not much above the critical power. However, by adjusting the incremental slope of ramp exercises, exhaustion brought about by high power and in a reasonably short time can be ensured, so avoiding this practical problem. This communication presents the theory and methods required to obtain estimates of both anaerobic work capacity and critical power from several ramp tests conducted to exhaustion. The method is illustrated with published laboratory data collected from exercising subjects.     

Lactate in blood,mixed skeletal muscle,and FT or ST fibres during cycle exercise in man

The relationship between muscle and blood lactate levels during progressively step-wise incrementing cycle exercise has been investigated in 10 male subjects. Steps between power outputs during exercise were 50 W and each stage, from loadless pedalling until voluntary exhaustion, lasted 4 min. Blood samples and biopsies (m. vastus lateralis) were taken for lactate determination at each power output beginning with the exercise intensity perceived by the subject as being “rather moderate”. The ratio muscle: blood lactate was greater than one at all power outputs and increased most markedly at the power output closest to that eliciting 4 mmol × I^-1 blood lactate (W_OBLA). At W_OBLA. blood lactate was positively correlated to muscle lactate concentrations which covaried widely among subjects (mean 8.3. range 4.5–14.4 mmol × kg^-l wet weight). Muscle fibres from the W_OBLA biopsy in 6 subjects were dissected out and identified as fast twitch (FT) or slow twitch (ST). No significant difference in lactate concentration was observed between pools of FT or ST fibres.     

Age and training effects on the lactate kinetics of master athletes during maximal exercise

Summary To study the effects of age and training on lactate production in older trained subjects, the lactate kinetics of highly trained cyclists [HT,n = 7; 65 (SEM 1.2) years] and control subjects with low training (LT,n = 7) and of similar age were compared to those of young athletes [YA,n = 7; 26 (SEM 0.7) years], during an incremental exercise test to maximum power. The results showed that the lactacidaemia at maximal oxygen uptake ( ) was lower for HT than for LT (P<0.05) and, in both cases, lower than that of YA (P<0.001). The respective values were HT: 3.9 (SEM 0.51), LT: 5.36 (SEM 1.12), and YA: 10.3 (SEM 0.63) mmol·1^–1. At submaximal powers, however, the difference in lactacidaemia was not significant between HT and YA, although the values for lactacidaemia at calculated per watt and per watt normalized by body mass were significantly lower for HT (P<0.001) and LT (P< 0.02). These results would indicate that the decline in power with age induced a decline in lactacidaemia. Yet this loss in power was not the only causative factor; indeed, our results indicated a complementary metabolic influence. In the older subjects training decreased significantly the lactacidaemia for the same submaximal power (P<0.01) and from 60% of onwards (P<0.05); as for YA it postponed the increase and accumulation of lactates. The lactate increase threshold (Th_1a–,1) was found at 46% for LT and at 56% for HT. The lactate accumulation threshold (Th_1a–,₂) was observed at approximately 80% for all three groups but at a value significantly different in each group. At Th_1a–,2 the lactate value of HT was 2 (SEM 0.19) mmol · 1^–1 thus closer to the value normally associated with the increase threshold instead of the accumulation threshold. In conclusion, the reduction in lactacidaemia was enhanced by training. Furthermore, the modification in the lactate kinetics with aging indicated that training at an intensity corresponding to a lactacidaemia of 2 and 4 mmol·1^–1 was inadequate for master endurance athletes.     

Endurance training increases skeletal muscle lactate transport

Lactate accumulation in skeletal muscle is reduced after a period of endurance training. Explanations for this phenomena include the increased oxidative capacity of the muscle, a reduction in lactate production, and increased lactate clearance. Muscle membrane transport of lactate can be seen to be a fundamental aspect of such clearance, and transmembrane lactate flux may well be an important aspect of the training response in skeletal muscle. Therefore, the lactate transport capacity in skeletal muscle sarcolemmal membranes in endurance-trained and sedentary rats was investigated. Training consisted of 6 weeks of progressively increased treadmill exercise. Twenty-four hours before being killed, both the trained and sedentary animals completed a brief exercise bout. Studies of lactate transport (zero-trans) were conducted using highly purified sarcolemmal vesicles. When low concentrations of L-lactate (1 mm) were used a 59.4% increase in lactate transport was observed (P < 0.05). However, when a high concentration of lactate (50 mm) was used no change in lactate transport was found (P > 0.05). Several interpretations are possible for these observations: (1) that there is an alteration in the K_m but not the V_max of the lactate transport system in skeletal muscle membranes; and (2) that specific changes occur in selected isoforms of the lactate transport protein which may co-exist in muscle.