Blood lactate production and recovery from anaerobic exercise in trained and untrained boys

Summary Blood lactate production and recovery from anaerobic exercise were investigated in 19 trained (AG) and 6 untrained (CG) prepubescent boys. The exercises comprised 3 maximal test performances; 2 bicycle ergometer tests of different durations (15 s and 60 s), and running on a treadmill for 23.20±2.61 min to measure maximal oxygen uptake. Blood samples were taken from the fingertip to determine lactate concentrations and from the antecubital vein to determine serum testosterone. Muscle biopsies were obtained from vastus lateralis. Recovery was passive (seated) following the 60 s test but that following the treadmill run was initially active (10 min), and then passive. Peak blood lactate was highest following the 60 s test (AG, 13.1±2.6 mmol·l^–1 and CG, 12.8±2.3 mmol·l^–1). Following the 15 s test and the treadmill run, peak lactate values were 68.7 and 60.6% of the 60 s value respectively. Blood lactate production was greater (p<0.001) during the 15s test (0.470±0.128 mmol·l^–1·s^–1) than during the 60s test (0.184±0.042 mmol·l^–1·s^–1). Although blood lactate production was only nonsignificantly greater in AG, the amount of anaerobic work in the short tests was markedly greater (p<0.05-0.01) in AG than CG. Muscle fibre area (type II%) and serum testosterone were positively correlated (p<0.05) with blood lactate production in both short tests. Blood lactate elimination was greater (p<0.001) at the end of the active recovery phase than in the next (passive) phase. It is concluded that blood lactate production in prepubescent boys is related to serum testosterone level and muscle type II fibre area, indicating the role of maturation and training. Submaximal exercise is likely to increase blood lactate removal during recovery.     

Lactate disposal in resting trained and untrained forearm skeletal muscle during high intensity leg exercise

Summary At a given oxygen uptake ( O₂) and exercise intensity blood lactate concentrations are lower following endurance training. While decreased production of lactate by trained skeletal muscle is the commonly accepted cause, the contribution from increased lactate removal, comprising both uptake and metabolic disposal, has been less frequently examined. In the present study the role of resting skeletal muscle in the removal of an arterial lactate load (approximately 11 mmol·-l^–1) generated during high intensity supine leg exercise (20 min at approximately 83% maximal oxygen uptake) was compared in the untrained (UT) and trained (T) forearms of five male squash players. Forearm blood flow and the venoarterial lactate concentration gradient were measured and a modified form of the Fick equation used to determine the relative contributions to lactate removal of passive uptake and metabolic disposal. Significant lactate uptake and disposal were observed in both forearms without any change in forearm O₂. Neither the quantity of lactate taken up [UT, 344.2 (SEM 118.8) mol·100 ml^–1; T, 330.3 (SEM 85.3) mol·100 ml^–1] nor the quantity disposed of [UT, 284.0 (SEM 123.3) mol·100 ml^–1, approximately 83% of lactate uptake; T, 300.8 (SEM 77.7) mol·100 ml^–1, approximately 91% of lactate uptake] differed between the two forearms. It is concluded that while significant lactate disposal occurs in resting skeletal muscle during high intensity exercise the lower blood lactate concentrations following endurance training are unlikely to result from an increase in lactate removal by resting trained skeletal muscle.     

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     

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.     

The effect of pedal rate on pulmonary O2 uptake kinetics during very heavy intensity exercise in trained and untrained teenage boys

This study tested the hypothesis that the VO2 kinetic response would be slowed in untrained (UT) but not trained (T) teenage participants whilst cycling at 115 rev min(-1) compared to 50 rev min(-1). Eight UT and seven T boys completed two square-wave transitions to very heavy-intensity exercise pedalling at 50 rev min(-1) and 115 rev min(-1). In UT at the higher pedal rate, the phase II VO2 was significantly (P < 0.01) slower (50 rev min(-1): 32 ± 5 vs. 115 rev min(-1): 42 ± 11 s) and the relative VO2 slow component was significantly (P < 0.01) elevated (50 rev min(-1): 10 ± 3 vs. 115 rev min(-1): 16 ± 5%). The phase II VO2 (50 rev min(-1): 26 ± 4 vs. 115 rev min(-1): 22 ± 6s) and relative VO2 slow component (50 rev min(-1): 14 ± 5 vs. 115 rev min(-1): 17 ± 3%) were unaltered by pedal rate in T (P > 0.05). These data are consistent with the notion that VO2 kinetics are influenced by muscle fibre recruitment in youth but this effect is attenuated in endurance trained teenage boys.     

Effects of 2-chloropropionate on venous plasma lactate concentration and anaerobic power during periods of incremental intensive exercise in humans

We investigated the effects of a stimulation of pyruvate dehydrogenase (PDH) activity induced by 2-chloropropionate (2-CP) on venous plasma lactate concentration and peak anaerobic power (W _{an, peak}) during periods (6 s) of incremental intense exercise, i.e. a force-velocity (F-) test known to induce a marked accumulation of lactate in the blood. TheF- test was performed twice by six subjects according to a double-blind randomized crossover protocol: once with placebo and once with 2-CP (43 mg · kg^–1 body mass). Blood samples were taken at ingestion of the drug, at 10, 20, and 40 Min into the pretest period, at the end of each period of intense exercise, at the end of each 5-min recovery period, and after completion of theF- test at 5, 10, 15, and 30 min. During theF- test, venous plasma lactate concentrations with both placebo and 2-CP increased significantly when measured at the end of each period of intense exercise (F = 33.5,P < 0.001), and each 5-min recovery period (F = 24.6,P < 0.001). Venous plasma lactate concentrations were significantly lower with 2-CP at the end of each recovery period (P < 0.01), especially for high braking forces, i.e. 8 kg (P < 0.05), 9 kg (P < 0.02), and maximal braking force (P < 0.05). After completion of theF- test, venous plasma lactate concentrations were also significantly lower with 2-CP (P < 0.001). The percentage of lactate decrease between 5- and 30-min recovery was significantly higher with 2-CP than with the placebo [59 (SEM 4)% vs 44.6 (SEM 5.5)%,P < 0.05]. Furthermore,W _{an, peak} was significantly higher with 2-CP than with the placebo [1016 (SEM 60) W vs 957 (SEM 55) W,P < 0.05]. In conclusion, PDH activation by 2-CP attenuated the increase in venous plasma lactate concentration during theF- test. Ingestion of 2-CP led to an increasedW _{an, peak}.     

Effects of prior heavy exercise,prior sprint exercise and passive warming on oxygen uptake kinetics during heavy exercise in humans

Prior heavy exercise (above the lactate threshold, Th_la) increases the amplitude of the primary oxygen uptake (VO₂) response and reduces the amplitude of the VO₂ slow component during subsequent heavy exercise. The purpose of this study was to determine whether these effects required the prior performance of an identical bout of heavy exercise, or if prior short-duration sprint exercise could cause similar effects. A secondary purpose of this study was to determine the effect of elevating muscle temperature (through passive warming) on VO₂ kinetics during heavy exercise. Nine male subjects performed a 6-min bout of heavy exercise on a cycle ergometer 6 min after: (1) an identical bout of heavy exercise; (2) a 30-s bout of maximal sprint cycling; (3) a 40-min period of leg warming in a hot water bath at 42°C. Prior sprint exercise elevated blood [lactate] prior to the onset of heavy exercise (by ≅5.6 mM) with only a minor increase in muscle temperature (of ≅0.7°C). In contrast, prior warming had no effect on baseline blood lactate concentration, but elevated muscle temperature by ≅2.6°C. Both prior heavy exercise and prior sprint exercise significantly increased the absolute primary VO₂ amplitude (by ≅230 ml·min^–1 and 260 ml·min^–1, respectively) and reduced the amplitude of the VO₂ slow component (by ≅280 ml·min^–1 and 200 ml·min^–1, respectively) during heavy exercise, whereas prior warming had no significant effect on the VO₂ response. We conclude that the VO₂ response to heavy exercise can be markedly altered by both sustained heavy-intensity submaximal exercise and by short-duration sprint exercise that induces a residual acidosis. In contrast, passive warming elevated muscle temperature but had no effect on the VO₂ response. Electronic Publication     

Detection of the change point in oxygen uptake during an incremental exercise test using recursive residuals: relationship to the plasma lactate accumulation and blood acid base balance

The purpose of this study was to develop a method to determine the power output at which oxygen uptake (V˙O₂) during an incremental exercise test begins to rise non-linearly. A group of 26 healthy non-smoking men [mean age 22.1?(SD 1.4)?years, body mass 73.6?(SD 7.4)?kg, height 179.4?(SD 7.5)?cm, maximal oxygen uptake (V˙O_2max) 3.726?(SD 0.363)?l?·?min^?1], experienced in laboratory tests, were the subjects in this study. They performed an incremental exercise test on a cycle ergometer at a pedalling rate of 70?rev?·?min^?1. The test started at a power output of 30?W, followed by increases amounting to 30?W every 3?min. At 5?min prior to the first exercise intensity, at the end of each stage of exercise protocol, blood samples (1?ml each) were taken from an antecubital vein. The samples were analysed for plasma lactate concentration [La]_pl, partial pressure of O₂ and CO₂ and hydrogen ion concentration [H⁺]_b. The lactate threshold (LT) in this study was defined as the highest power output above which [La^?]_pl showed a sustained increase of more than 0.5?mmol?·?l^?1?·?step^?1. The V˙O₂ was measured breath-by-breath. In the analysis of the change point (CP) of V˙O₂ during the incremental exercise test, a two-phase model was assumed for the 3rd-min-data of each step of the test: X _i =at _i +b+? _i for i=1,2,…,T, and E(X _i )>at _i +b for i =T+1,…,n, where X ₁, … , X _n are independent and ? _i ～N(0,σ²). In the first phase, a linear relationship between V˙O₂ and power output was assumed, whereas in the second phase an additional increase in V˙O₂ above the values expected from the linear model was allowed. The power output at which the first phase ended was called the change point in oxygen uptake (CP-V˙O₂). The identification of the model consisted of two steps: testing for the existence of CP and estimating its location. Both procedures were based on suitably normalised recursive residuals. We showed that in 25 out of 26 subjects it was possible to determine the CP- O₂ as described in our model. The power output at CP-V˙O₂ amounted to 136.8?(SD 31.3)?W. It was only 11?W – non significantly – higher than the power output corresponding to LT. The V˙O₂ at CP-V˙O₂ amounted to 1.828?(SD 0.356)?l?·?min^?1 was [48.9?(SD 7.9)% V˙O_{2 max} ]. The [La^?]_pl at CP-V˙O₂, amounting to 2.57?(SD 0.69)?mmol?·?l^?1 was significantly elevated (P<0.01) above the resting level [1.85?(SD 0.46)?mmol?·?l^?1], however the [H⁺]_b at CP-V˙O₂ amounting to 45.1 (SD 3.0)?nmol?·?l^?1, was not significantly different from the values at rest which amounted to 44.14?(SD 2.79)?nmol?·?l^?1. An increase of power output of 30?W above CP-V˙O₂ was accompanied by a significant increase in [H⁺]_b above the resting level (P=0.03).