The present study investigated whether muscular monocarboxylate transporter (MCT) 1 and 4 contents are related to the blood lactate removal after supramaximal exercise, fatigue indexes measured during different supramaximal exercises, and muscle oxidative parameters in 15 humans with different training status. Lactate recovery curves were obtained after a 1-min all-out exercise. A biexponential time function was then used to determine the velocity constant of the slow phase (gamma(2)), which denoted the blood lactate removal ability. Fatigue indexes were calculated during 1-min all-out (FI(AO)) and repeated 10-s (FI(Sprint)) cycling sprints. Biopsies were taken from the vastus lateralis muscle. MCT1 and MCT4 contents were quantified by Western blots, and maximal muscle oxidative capacity (V(max)) was evaluated with pyruvate + malate and glutamate + malate as substrates. The results showed that the blood lactate removal ability (i.e., gamma(2)) after a 1-min all-out test was significantly related to MCT1 content (r = 0.70, P < 0.01) but not to MCT4 (r = 0.50, P > 0.05). However, greater MCT1 and MCT4 contents were negatively related with a reduction of blood lactate concentration at the end of 1-min all-out exercise (r = -0.56, and r = -0.61, P < 0.05, respectively). Among skeletal muscle oxidative indexes, we only found a relationship between MCT1 and glutamate + malate V(max) (r = 0.63, P < 0.05). Furthermore, MCT1 content, but not MCT4, was inversely related to FI(AO) (r = -0.54, P < 0.05) and FI(Sprint) (r = -0.58, P < 0.05). We concluded that skeletal muscle MCT1 expression was associated with the velocity constant of net blood lactate removal after a 1-min all-out test and with the fatigue indexes. It is proposed that MCT1 expression may be important for blood lactate removal after supramaximal exercise based on the existence of lactate shuttles and, in turn, in favor of a better tolerance to muscle fatigue.

The present study investigated whether blood lactate removal after supramaximal exercise and fatigue indexes measured during continuous and intermittent supramaximal exercises are related to the maximal muscle oxidative capacity in humans with different training status. Lactate recovery curves were obtained after a 1-min all-out exercise. A biexponential time function was then used to determine the velocity constant of the slow phase (gamma(2)), which denoted the blood lactate removal ability. Fatigue indexes were calculated during all-out (FI(AO)) and repeated 10-s cycling sprints (FI(Sprint)). Biopsies were taken from the vastus lateralis muscle, and maximal ADP-stimulated mitochondrial respiration (V(max)) was evaluated in an oxygraph cell on saponin-permeabilized muscle fibers with pyruvate + malate and glutamate + malate as substrates. Significant relationships were found between gamma(2) and pyruvate + malate V(max) (r = 0.60, P < 0.05), gamma(2) and glutamate + malate V(max) (r = 0.66, P < 0.01), and gamma(2) and citrate synthase activity (r = 0.76, P < 0.01). In addition, gamma(2), glutamate + malate V(max), and pyruvate + malate V(max) were related to FI(AO) (gamma(2) - FI(AO): r = 0.85; P < 0.01; glutamate + malate V(max) - FI(AO): r = 0.70, P < 0.01; and pyruvate + malate V(max) - FI(AO): r = 0.63, P < 0.01) and FI(Sprint) (gamma(2) - FI(Sprint): r = 0.74, P < 0.01; glutamate + malate V(max) - FI(Sprint): r = 0.64, P < 0.01; and pyruvate + malate V(max) - FI(Sprint): r = 0.46, P < 0.01). In conclusion, these results suggested that the maximal muscle oxidative capacity was related to blood lactate removal ability after a 1-min all-out test. Moreover, maximal muscle oxidative capacity and blood lactate removal ability were associated with the delay in the fatigue observed during continuous and intermittent supramaximal exercises in well-trained subjects.

Two lactate/proton cotransporter isoforms (monocarboxylate transporters, MCT1 and MCT4) are present in the plasma (sarcolemmal) membranes of skeletal muscle. Both isoforms are symports and are involved in both muscle pH and lactate regulation. Accordingly, sarcolemmal MCT isoform expression may play an important role in exercise performance. Acute exercise alters human MCT content, within the first 24 h from the onset of exercise. The regulation of MCT protein expression is complex after acute exercise, since there is not a simple concordance between changes in mRNA abundance and protein levels. In general, exercise produces greater increases in MCT1 than in MCT4 content. Chronic exercise also affects MCT1 and MCT4 content, regardless of the initial fitness of subjects. On the basis of cross-sectional studies, intensity would appear to be the most important factor regulating exercise-induced changes in MCT content. Regulation of skeletal muscle MCT1 and MCT4 content by a variety of stimuli inducing an elevation of lactate level (exercise, hypoxia, nutrition, metabolic perturbations) has been demonstrated. Dissociation between the regulation of MCT content and lactate transport activity has been reported in a number of studies, and changes in MCT content are more common in response to contractile activity, whereas changes in lactate transport capacity typically occur in response to changes in metabolic pathways. Muscle MCT expression is involved in, but is not the sole determinant of, muscle H(+) and lactate anion exchange during physical activity.

The aim of this study was to compare the evolution of oxygen uptake (VO2) in specifically trained runners during running tests based on the 400-, 800-, and 1500-m pacing strategies adopted by elite runners to optimize performance. Final velocity decreased significantly for all three distances, with the slowest velocity in the last 100 m expressed relative to the peak velocity observed in the 400 m (77%), 800 m (88%), and 1500 m (96%). Relative to the previously determined VO2max values, the respective VO 2peak corresponded to 94% (400 m) and 100% (800 and 1500 m). In the last 100 m, a decrease in VO2 was observed in all participants for the 400-m (15.6 ± 6.5%) and 800-m races (9.9 ± 6.3%), whereas a non-systematic decrease (3.6 ± 7.6%) was noted for the 1500 m. The amplitude of this decrease was correlated with the reduction in tidal volume recorded during the last 100 m of each distance (r = 0.85, P < 0.0001) and with maximal blood lactate concentrations after the three races (r = 0.55, P < 0.005). The present data demonstrate that the 800 m is similar to the 400 m in terms of decreases in velocity and VO2.

We tested the hypothesis that reducing hydrogen ion accumulation during training would result in greater improvements in muscle oxidative capacity and time to exhaustion (TTE). Male Wistar rats were randomly assigned to one of three groups (CON, PLA, and BIC). CON served as a sedentary control, whereas PLA ingested water and BIC ingested sodium bicarbonate 30 min prior to every training session. Training consisted of seven to twelve 2-min intervals performed five times/wk for 5 wk. Following training, TTE was significantly greater in BIC (81.2 ± 24.7 min) compared with PLA (53.5 ± 30.4 min), and TTE for both groups was greater than CON (6.5 ± 2.5 min). Fiber respiration was determined in the soleus (SOL) and extensor digitorum longus (EDL), with either pyruvate (Pyr) or palmitoyl carnitine (PC) as substrates. Compared with CON (14.3 ± 2.6 nmol O2·min−1·mg dry wt−1), there was a significantly greater SOL-Pyr state 3 respiration in both PLA (19.6 ± 3.0 nmol O2·min−1·mg dry wt−1) and BIC (24.4 ± 2.8 nmol O2·min−1·mg dry wt−1), with a significantly greater value in BIC. However, state 3 respiration was significantly lower in the EDL from both trained groups compared with CON. These differences remained significant in the SOL, but not the EDL, when respiration was corrected for citrate synthase activity (an indicator of mitochondrial mass). These novel findings suggest that reducing muscle hydrogen ion accumulation during running training is associated with greater improvements in both mitochondrial mass and mitochondrial respiration in the soleus.

Bishop D, Edge J, Thomas C, Mercier J. Effects of high-intensity training on muscle lactate transporters and postexercise recovery of muscle lactate and hydrogen ions in women. Am J Physiol Regul Integr Comp Physiol 295: R1991-R1998, 2008. First published October 1, 2008 doi:10.1152/ajpregu.00863.2007.-The purpose of this study was to investigate the effects of high-intensity interval training (3 days/wk for 5 wk), provoking large changes in muscle lactate and pH, on changes in intracellular buffer capacity (␤min vitro), monocarboxylate transporters (MCTs), and the decrease in muscle lactate and hydrogen ions (H ϩ ) after exercise in women. Before and after training, biopsies of the vastus lateralis were obtained at rest and immediately after and 60 s after 45 s of exercise at 190% of maximal O2 uptake. Muscle samples were analyzed for ATP, phosphocreatine (PCr), lactate, and H ϩ ; MCT1 and MCT4 relative abundance and ␤min vitro were also determined in resting muscle only. Training provoked a large decrease in postexercise muscle pH (pH 6.81). After training, there was a significant decrease in ␤min vitro (Ϫ11%) and no significant change in relative abundance of MCT1 (96 Ϯ 12%) or MCT4 (120 Ϯ 21%). During the 60-s recovery after exercise, training was associated with no change in the decrease in muscle lactate, a significantly smaller decrease in muscle H ϩ , and increased PCr resynthesis. These results suggest that increases in ␤m in vitro and MCT relative abundance are not linked to the degree of muscle lactate and H ϩ accumulation during training. Furthermore, training that is very intense may actually lead to decreases in ␤m in vitro. The smaller postexercise decrease in muscle H ϩ after training is a further novel finding and suggests that training that results in a decrease in H ϩ accumulation and an increase in PCr resynthesis can actually reduce the decrease in muscle H ϩ during the recovery from supramaximal exercise.

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We tested the hypothesis that time course of O (2) uptake (VO (2)) measured during a supramaximal exercise performed in the field is driven to maximal oxygen uptake (VO (2max)). On an outdoor track, five middle-distance male runners first performed a test to determine VO (2max) and a supramaximal 800-m running test at least two days apart. VO (2) response was measured from the start to the end of exercise with the use of a miniaturised telemetric gas exchange system (Cosmed K4). VO (2max) was reached by all subjects 45 +/- 11 s (mean +/- SD) after the onset of the 800-m race (i.e., 316 +/- 75 m), and was maintained during the next 33 +/- 6 s (i.e., 219 +/- 41 m). The mean relative exercise intensity of the 800 m was 120 % VO (2max). An unexpected significant decrease in VO (2) (24.1 +/- 7.0 %; p < 0.05) was observed in all subjects during the final 38 +/- 17 s (i.e., the last 265 +/- 104 m). We concluded that, at onset of a simulated 800 m running event, VO (2) is quickly projected towards the VO (2max), and then becomes limited by the achievable VO (2max). This race profile shown by all athletes is in some contrast to what can be expected from earlier findings in a laboratory setting.