Hagberg, J. M. (1984). Physiological implications of the lactate threshold. International Journal of Sports Medicine, 5, 106-109.

" . . lactic acid, while still important from the exercise physiologist's viewpoint, now is known to contribute much less than originally believed to the regulation of man's physiological responses to exercise." (p. 106)

On the relationship between blood lactate and ventilation using standard protocols:

"Thus, the potential risk inherent with this protocol is that while the ventilatory and blood lactate changes generally occur at roughly the same point, this is not the case in all situations; therefore, the relationship between blood lactate and ventilation may not be cause-and-effect." (p. 106)

There have been attempts to predict the lactate threshold from non-invasive techniques: "However, a number of theoretical limitations exist which may make such extrapolations misleading." (p. 106)

The question of the validity of lactate threshold measures is important.

• A variation in range for an individual exists on a day-to-day basis.
• The sensitivity of assays is not great and consequently much error is involved.
• The way lactate is formed depends upon how the exercise bout is performed.
• In most individuals the lactate threshold is lower than the level of VO2max that needs to be sustained for competitive endurance performances.

In 1961 Hollmann described the aerobic-anaerobic threshold as a concept for predicting performance capacity in events lasting from 30 seconds to 6 minutes where "lactic acid production is the true limiting factor in performance." [cited by Mader, A., Heck, M., & Hollmann, W. (1978). Evaluation of lactic acid anaerobic energy contribution by determination of post exercise lactic acid concentration of ear capillary blood in middle-distance runners and swimmers. In F. Landry & W. A. Orban, (Eds.). Exercise physiology, Volume 14. Miami: Symposia Specialists, pp. 187-200.]

Since then there have been many different protocols, purposes, and labels developed which imply that erroneous uses and conceptual structures exist in the literature. Different names have emerged:

• lactate threshold (the original);
• maximal steady state (MSS);
• onset of plasma lactate accumulation (OPLA);
• onset of blood lactate accumulation (OBLA); and
• individual anaerobic threshold (IAT).

Depending upon the lactate kinetics of the individual, lactate thresholds occur within a range of blood lactate levels from 1.4 to 7.5 mM. An individual's threshold will also differ between activities.

The production of lactate at work rates that are clearly below the muscle's maximum capacity to use O2 is thought to be due to an imbalance between glycolysis and oxidative metabolism.

VO2max and Lactate Threshold

VO2max and submaximal exercise capacity are limited by different mechanisms. VO2max appears to be related more to cardiovascular factors such as maximal cardiac output, whereas skeletal muscle metabolic factors including respiratory enzyme activity play more of a role in determining submaximal exercise capacity. This interpretation is supported by the fact that after training individuals work closer to their VO2max before attaining their lactate threshold. That means that cellular adaptations occurred more than changes in cardiovascular capacity. Oxidative enzymes increase as much as 100% through training while cardiac output increases to a much smaller extent.

Muscle respiratory enzyme activity is closely related to a person's LT when expressed in terms of absolute work rate. The correlations between mitochondrial respiratory enzyme activity and LT are generally better than those between enzyme activity and VO2max. "VO2max and LT are, within limits, determined by different physiological mechanisms, . . . LT is better related to the metabolic status of the peripheral musculature (i.e., skeletal muscle respiratory enzyme activity levels) while VO2max is more dependent upon cardiovascular factors relating to maximal cardiac output." (p. 108)

Lactate Threshold and Endurance Performance

Metabolic acidosis accompanying excessive muscle lactate production is generally believed to limit performance in short-term events lasting less than six minutes. On the other hand, lactate, or the accompanying decrease in muscle pH, is not believed to be a limiting factor for events lasting 10 to 120 minutes since blood lactate does not attain maximum levels.

"It is more likely that blood lactate level may provide an index of some other physiological signal which is actually the mechanism for limiting performance in prolonged steady-state competitive events." (p. 108)

While VO2max plays a role in determining the upper limit for aerobic expenditure in prolonged endurance events, LT measures provide a more precise prediction of endurance performance capacity. The preferred measures of LT come from long-duration continuous activity protocols rather than shorter, incremental protocols. The shorter protocols may be beneficial for studying ventilatory responses, but are tenuous when used to predict endurance performance capacities.

Thus, tests for LT, or whatever label is used, are better if they are of relatively longer rather than shorter duration, despite the greater time required for testing.

It is likely that "time available for testing" has entered into testing protocol formulations. The quicker, cheaper, and easier test is always appealing on efficiency grounds. The plethora of testing procedures for both LT and VO2max has led to the implicit inclusion of error into physiological measures. It is better to do something correctly, than more expediently. LT is best measured under extensive testing protocols and is the better index for predicting endurance performance.

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