Unlike most LTTEs, this letter is primarily meant to commend and less to critique Batterson, Kirby, Hasselmann, and Feldmann on their recent article: “Muscle oxygen saturation rates coincide with lactate‑based exercise thresholds” (Batterson et al. 2023).

The authors’ main finding of close negative relationships between blood lactate concentrations ([La]b) and muscle oxygen saturation (SmO2) in various muscles, may not be deemed surprising. However, the study’s remarkable, and indeed surprising finding, is the strength of these relationships (r = 0.907‒0.974 in four discrete muscles). The 82.2‒94.8% of explained variance is particularly notable because [La]b is a whole-body measure, while SmO2 is a local, muscle-specific variable.

Although the authors rightly recognize the curvilinear nature of the relationships between running velocity and both [La]b and SmO2 and calculate their correlations as such, it is unclear why the curvilinearity of the ‘flagship’ [La]b‒SmO2 relationship (Batterson et al. 2023, Fig. 3) is not recognized and similarly dealt with. That curvilinearity is likely due to the fact that while SmO2 only reflects the decreasing O2 availability (increasing O2 deficit), the concomitantly increasing [La]b reflects the continuing lactate accumulation on top of the prevailing, intensity-dependent lactate production (O2 deficit rise). Had the authors employed a curvilinear (e.g., 2nd-order polynomial) rather than linear regression analysis, the correlation coefficients would have been markedly stronger and the findings even more remarkable.

A final note regarding the observed thresholds. It could be anticipated that SmO2’s first breakpoint (BP1) would not precisely match LT1, as the latter is merely a concentration equilibrium that can fluctuate within and particularly between individuals at any given lactate production rate. On the other hand, the reported BP2‒LT2 identity is reassuring because LT2, typically akin to the maximal lactate steady state, reflects the highest lactate production rate that can be sustained without further O2 deficit increase. Since SmO2 changes also reflect changing O2 deficits, it can be expected that BP2 would at least approximate LT2, which the study nicely showed.

The authors have demonstrated the potential practicality of using the non-invasive NIRS-based SmO2 determinations as a valid alternative to the invasive lactate sampling, or to the more involved and cumbersome ventilatory threshold protocols. With the suggested improved analysis, this message could be even more convincing.