At rest and during easy exercise (50% of the maximal oxygen uptake, VO2max), lactic acid is produced and removed at equal rates. This balance of production and removal is called turnover (Rt) (Brooks, 1985). In the lactate steady state the processes of lactate production are balanced by the processes of removal, there is an equilibrium in turnover (Rt), appearance (Ra) and disappearance (Rd) so Rt = Ra = Rd. The blood lactate at MLSS represents the highest point in this equilibrium. Therefore, the "maximal lactate steady state" is defined as the highest blood lactate concentration (MLSSc) and work load (MLSSw) that can be maintained over time without a continual blood lactate accumulation (Beneke & Von Duvillard, 1996; Beneke et al., 2000; Farrel et al., 1979; Billat et al., 1994; Billat, 1996; Billat et al., 1995; Farrell et al., 1979; Lafontaine et al., 1981). MLSSw is used in the assessment of subject's endurance capacity (Billat, 1996; Baldarini & Guidetti, 2000). MLSSw elicits a blood lactate concentration around 4.0 mM and for that reason has long been estimated by the onset of blood lactate accumulation which is the load corresponding to blood lactate levels of 4.0 mM determined in an incremental test (Billat, 1996). However, MLSSc has been reported to have a great variability between subjects (from 2 to 8 mM in capillary blood) and not to be related with performance (Beneke et al., 2000). For an individual, MLSSw delineates the mild to- to hard- intensity exercises at which no VO2 steady-state is observed and at which the fuel mix switches (crosses over) from fat to carbohydrate and this velocity is close to the average marathon velocity (Billat et al., 2001). The determining of the lactate steady state maximal speed (MLSSv) requires work grades lasting 10 to 30 minutes. In effect, the accumulation of lactate is only evident after 10 minutes if the running speed is only slightly greater than at MLSSv (Lajoie et al., 2000). This explains why the measurement of the lactate steady state maximal speed requires the repetition of several independent speed grades carried out around the speed where the onset of lactate accumulation takes place. The determination of MLSSw is associated with those of the blood lactate concentration at MLSS (MLSSc) that shows great inter-individual difference. If many studies have focused on the impact of glycogen depletion on the anaerobic and ventilatory threshold determination (Glass et al., 1997) and performance (endurance time at the anaerobic threshold) (Genovely and Stamford, 1982), no studies have attempted to measure the endurance time at MLSS. Therefore, the intensity involving the maximal lactate steady-state (MLSS) has often been overestimated, especially in highly trained endurance athletes using the anaerobic threshold as part of their training (Stegmann & Kindermann, 1982; Mognoni et al., 1990; Oyono-Enguelle et al., 1990). If MLSS is accurately determined, whatever the training state or glycogen reserves (also influenced by training state), endurance time at MLSS is about one hour as this duration is used to assess the MLSS determination validity (Billat, 1996), and unpublished data recently performed by our team confirmed this estimation. Indeed, MLSS is below the world hour record and above the marathon pace as the use of glycogen is the most important substrate utilised at this speed (the rate of expiratory ratio, RER = 1) (Beneke, 2000). It has been recently reported that lactate transport was mediated by carrier proteins: the monocarboxylate transporters (MCT) (Garcia et al., 1994). These carriers are also sensitive to endurance and intensive training and are modified after exhaustive exercise. Several data suggest that among the family of MCTs, MCT1 and MCT4 are primarily responsible for lactate uptake from the circulation and lactate extrusion out of muscle, respectively. Few studies have still focused on the relationship between MLSS and lactate transporters. Nine weeks of endurance training at 75% of VO2max increase the expression of MCT1 with intervariable effects on MCT4 (Dubouchaud et al., 2000). This training led to a huge increase in VO2max (+23%) and in VO2 at the lactate threshold (+ 22%). Moreover, citrate synthase activity was increased by 75% and co-varied with those of MCT1. In a recent study, Evertsen et al. (2001) reported that already highly-trained cross-country skiers following 5 months of either " moderate " (60-70% of VO2max) or " high-intensity " (80-90% of VO2max for 16% of the training i.e. 1.6 hours over 10 hours per week) decreased or maintained respectively the number of their MCT1. The concentration of MCT4 did not change during the training period. However, as noted by the authors themselves, the " pre-training " values of MCT's were in fact measured just after the competitive period and were already high due to the fact that the first biopsies were taken immediately after an intensive racing season. Intensive training carried out during the racing season might explain that the concentration of MCT1 decreased after moderate intensity training, probably because less high intensity training was carried out during the training period compared with the racing season (Evertsen et al., 2001). Moreover, these authors noticed a lack of correlation between the MCTs and the other enzymes among elite skiers, probably because they represented a relatively homogeneous group, with quite similar muscle patterns. Interestingly, they demonstrated that these data were not affected by the gender. This is the only study having focused on the relationship between MCTs and enzyme in elite athletes and despite the bias of the so called " pretraining " biopsies, this opens the research field to the effects of intensive training on lactate transport in elite athletes. No studies have focused on the effects of training at MLSS on MCTs and we have to underline that probably more than 16% of training volume at least at MLSS is needed to obtain some modification of MCTs in already well-trained subjects. Evertsen (2001) reported an enhancement of 3.2 ± 0.9% of the speed at the lactate threshold for the group who trained at the highest intensity. However, it is not specified whether this enhancement is due to the decreased energy cost of running or rather to an enhanced oxygen uptake expressed as a fraction of VO2max (to eliminate the running economy and VO2max factors). The relationship between the enhancement of lactate transporters and the MLSSw has not been yet demonstrated. In a same way the effects of training on the value of blood lactate concentration at MLSS has not been yet clearly established since only two studies have reported contradictory data in swimming rats (Gobatto et al., 2001) and in human (Bergman et al., 1999). The training adaptations brought by training at a speed associated with the lactate steady state for which the rate of lactate freed into the blood is similar to the rate of lactate recovered by the tissues (liver, heart, oxidative skeletal muscle) are not yet known. Evertsen et al. (2001) reported that the blood lactate concentration after exhaustive 20-min treadmill running was correlated with the concentration of muscle MCT1 in each subjects. However, no studies have as yet focused on the relationship between the MCTs and the value of the blood lactate concentration at the maximal steady state level. The factors behind such a wide inter-individual difference in MLSSc remain unknown and have not yet been debated especially with different types of training performed below, at or above MLSS speed. In conclusion the problematic of the maximal lactate steady state is typical of the need to conciliate systemic and molecular approach for solve the mechanisms of performance improvement by training.
© Copyright 2002 Expertise in Elite sport. 2nd International Days of Sport Sciences, 12.-15. November 2002, INSEP, Paris (France). Veröffentlicht von INSEP. Alle Rechte vorbehalten.