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On the basis of the “O2 depth” theory developed by Hill & Meyerhof, Wasserman and co-workers introduced the concept of the anaerobic threshold in the mid 1960s, to assess the cardio–respiratory fitness in patients and athletes. Directed towards identification of reliable performance biomarkers and precise lactate measurement devices, subsequent research, which was essentially influenced by the group around George Brooks, greatly facilitated our understanding and interpretation of lactate metabolism. Moreover, the time course of blood lactate during an incremental exercise has become one of the most widely used methods to assess endurance capacity. However, the variety and the lack of sufficiently validated threshold concepts led to considerable confusion and misinterpretation.

We started our first experiments on that topic in 1996, by using minor workload increments near the so called maximal lactate steady state and found a sharp lactate increase at some point, which could be stopped by a slight workload (WL) reduction. In order to better understand these observations, we developed an automated setup for running and cycling, which allows an optimization of former test algorithms and re-evaluation of data sets.

Here, we used slight WL variations at the maximal steady state workload (MLSS_w) to study the effects on lactate kinetics in 426 treadmill and bicycle ergometer tests. At the lactate threshold (LT), increments of 0.1 - 0.15 m/s on the treadmill or 7 - 10W on the bicycle ergometer caused a steep increase of arterial lactate concentration between 0.5 and 2.4 mM. A subsequent WL reduction resulted in the stabilization of lactate levels which was used for MLSS_w determination. The LT was detected by means of 2 threshold criteria. 

We found a high reproducibility of the running velocity at the MLSS_w on a day-to-day basis and a high correlation between running velocities during ILT-Tests, 10 km constant velocity tests and a half marathon race field test. Thus, the ILT-Test allows a reliable and valid determination of the MLSS_W.

A common explanation for the rapid lactate accumulation at the LT, is the imbalance between production and removal within the complex shuttle network of lactate metabolism. During the ILT-Test, the arterial lactate accumulation did not occur in a curvilinear manner as described for graded test protocols. The lactate accumulation occurred at a specific WL with no relation to the absolute lactate concentration and the number of previous steps. These data suggest that enhanced activity in motor units (e. g. close to the MLSS_w) within muscles with high lactate efflux caused an accelerated arterial lactate accumulation in relation to power output, when activity in lactate consuming motor units was unchanged. The change in neuronal activity at exercise intensities near MLSS_w can occur intramuscularly or might be mediated between muscles with different fiber distributions. The latter scenario is supported by data showing specific mitochondrial adaptations to different training intensities in rats, and may also contribute to the rapid arterial lactate accumulation at the LT. The cellular mechanisms of lactate transportation and metabolism are located in muscle fibers and may be neuronally tuned in relation to mechanical demands. We conclude that arterial lactate kinetics might reflect force control and fatigue, without being causally involved.

Link to the publication:  https://doi.org/10.3389/fphys.2018.00310