MEASUREMENT OF ANAEROBIC CAPACITIES IN HUMANS - DEFINITIONS, LIMITATIONS AND UNSOLVED PROBLEMS

Anaerobic capacity is defined as the maximal amount of adenosine triphosphate resynthesised via anaerobic metabolism (by the whole organism) during a specific mode of short-duration maximal exercise. This review focuses on laboratory measures which attempt to quantify anaerobic capacity; it examines the evidence supporting or challenging the validity of these measures and provides research foci for future investigations. Discussion focuses on anaerobic capacity measured during running and cycling, since almost all data reviewed were collected using these exercise modes. The validity of the oxygen debts (alactic and total), maximal blood lactate and oxygen deficit as measures of anaerobic capacity was examined. The total oxygen debt, now termed the excess post-exercise consumption, was used in investigations in the 1920s and 1930s to quantify anaerobic energy production; it has since been shown to be an invalid measure of anaerobic capacity, since its magnitude is known to be influenced by factors (e.g. temperature, catecholamines, substrate cycling, lactate glycogenesis) other than those directly involved in anaerobic metabolism. Maximal blood lactate, a measure also used in some of those early investigations, is often used in exercise and sports physiology. Opinion on the utility of maximal blood lactate as an estimate of anaerobic (lactic) capacity is, however, divided. Despite problems interpreting the physiological meaning of maximal blood lactate levels (due primarily to acute changes in blood volume), this measure is still used in both research and athletic settings to describe anaerobic capacity. Its use is supported by (a) the high correlations observed between maximal blood lactate and short-duration exercise performance presumably dependent upon anaerobic capacity, and (b) the higher maximal blood lactate values observed in sprint and power athletes (who would demonstrate higher anaerobic capacities) compared with endurance athletes or untrained people. However, training-induced changes in other performance, physiological and biochemical markers of anaerobic capacity have not always been paralleled by changes in maximal blood lactate, its relatively high variability also diminishes its usefulness to athletic populations, since relatively small changes in anaerobic capacity may not be detected by a measure with such high variability. These latter findings may be partially related to the confounding influence of blood volume which often changes in response to short and long term exercise demands. Maximal blood lactate is known to be influenced by the intensity and duration of the preceding exercise bout; therefore, it is plausible that these factors may also influence the degree to which maximal blood lactate accurately reflects anaerobic capacity. The oxygen deficit was used in several Scandinavian investigations during the early years of this century; its potential to quantify anaerobic capacity regained momentum in the early 1970s, and at present it is claimed by some to be the only measure with the potential to quantify anaerobic capacity. The validity of the oxygen deficit is supported by: (a) a quantitative similarity with anaerobic capacity determined by the change in anaerobic metabolites in muscle and blood; (b) higher values in sprint athletes than in endurance athletes and untrained people; and (c) the fact that it is increased following high-intensity training expected to improve anaerobic capacity, and changes in parallel with in vitro determinants of anaerobic capacity. Its validity, however, is based on several assumptions. One of these, that the oxygen.demand at high exercise intensities can be estimated via the linear extrapolation of the submaximal VO2-workload relationship, is tenuous: it may be a major source of error in determining the oxygen deficit and thus quantifying anaerobic capacity. A universal method of determining the submaximal VO2-workload relationships has also not been established and warrants further investigation. Moreover, the majority of evidence which supports the validity of the oxygen deficit has been collected using untrained people. It is not known to what degree such evidence can be extrapolated to well-trained athletic populations. Therefore, future investigations should also focus on the use of the oxygen deficit in well-trained athletic populations. In conclusion, the oxygen debts should not be used to quantify anaerobic capacities. Maximal blood lactate can only, at best, reflect anaerobic capacity; applied sport scientists should also consider the time and cost involved in measuring this variable, given that the monitoring of short and long term changes in blood volume will also be required to increase the sensitivity of maximal blood lactate to changes in anaerobic capacity. The oxygen deficit is the only measure which can potentially quantify anaerobic capacity; it has been claimed to accurately quantify anaerobic capacity. Evidence presented in this review suggests, however, that its validity, especially in athletic populations, is not clearly established and requires further examination.