ANAEROBIC THRESHOLD - A RELATIVELY USELESS CONCEPT FOR COACHING
Billat, L. V. (1996). Use of blood lactate measurements for prediction of exercise
performance and for control of training: Recommendations for long-distance running.
Sports Medicine, 22, 157-175.
This article contains a very concise summary of the concept of anaerobic threshold
and how it is depicted in the literature. The implications of each individual
statement are particularly important given the pre-occupation of many coaches with
this concept. The major points of the article are discussed below. Further features
are introduced in the "Implications" section.
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The concept of anaerobic threshold itself is not universally consistent. Long
dynamic exercise that is predominantly aerobic ranges between two extremes of
physiological dynamics resulting in very different blood lactate levels.
* At the lowest level, an exercise can be sustained for a very long time. After
2-5 min a state of overall oxidative energy supply is established where lactate
production is balanced by lactate elimination at a low level. Fat (lipid)
metabolism is the primary source of fuel. Exercise limits are mainly associated
with eventual increases in internal temperature. Potential dehydration can be
prevented by supplementation of water and substrate (carbohydrate and
electrolytes) during performance. (p. 158)
* At the highest extreme, the workload requires an additional formation and
accumulation of lactate to maintain power output. Exhaustion results through
the disturbance of the internal biochemical environment of the working muscles
and whole body caused by a high or maximal acidosis. Generally, accumulation of
lactate limits performance to periods from 30 sec to 15 min. For example, the
average time to exhaustion at the minimal velocity that elicits VO2max is 6:30
and is not correlated with the blood lactate level developed during the task.
(p. 159)
Between these two extremes are transition stages, several of which are labeled
similarly as "anaerobic threshold" or "lactate threshold." Thus, the same label is
used for different concepts and their assessment protocols which lead to different
values and training implications. Billat displays the various implications of this
confusing situation. According to a variety of "authorities," changes in blood
lactate accumulation are termed and defined differently as well as being associated
with different levels and characteristics of accumulated lactate. They are also
differentiated by the protocols used to measure them. Some examples are listed
below.
* "Onset of plasma lactate accumulation" is established as being exercise induced
levels which are 1 mM/l above baseline lactate values. [Farrel, P. E., Wilmore,
J. H., Coyle, E. F., et al. (1979). Plasma lactate accumulation and distance
running performance. Medicine and Science in Sports and Exercise, 11, 338-344.]
* "Maximal steady-state" is displayed when oxygen, heart rate, and/or treadmill
velocity produce a lactate level that is 2.2 mM/l. [Londeree, B. R., & Ames, A.
(1975). Maximal steady state versus state of conditioning. European Journal of
Applied Physiology, 34, 269-278.]
* "Onset of blood lactate accumulation" (OBLA) occurs when continuous incremental
exercise produces a lactate level of 4 mM/l. [Sjodin, B., & Jacobs, I. (1981).
Onset of blood lactate accumulation and marathon running performance.
International Journal of Sports Medicine, 2, 23-26.]
* "Individual anaerobic threshold" is the state where the increase of blood
lactate is maximal and equal to the rate of diffusion of lactate from the
exercising muscle. Values range from 2-7 mM/l. [Stegemann. H., & Kindermann, W.
(1982). Comparison of prolonged exercise tests at the individual anaerobic
threshold and the fixed anaerobic threshold of 4 mM/l. International Journal of
Sports Medicine, 3, 105-110.]
* "Lactate threshold" is the starting point of an accelerated lactate
accumulation and is usually around 4 mM/l and is expressed as %VO2max. [Aunola,
S., & Rusko, H. (1984). Reproducibility of aerobic and anaerobic thresholds in
20-25 year old men. European Journal of Applied Physiology, 69, 196-202.
* "Maximal steady-state of blood lactate level" is the exercise intensity that
produces the maximal steady-state of blood lactate level and ranges from
2.2-6.8 mM/l. [Billat, V., Dalmay, F., Antonini, M. T., et al. (1994). A method
for determining the maximal steady state of blood lactate concentration from
two levels of submaximal exercise. European Journal of Applied Physiology, 69,
196-202.
Many scientists and coaches use the label "anaerobic threshold" interchangeably
with these concepts confusing what is supposed to be a scientific coaching
principle. Just because the same label is used does not mean analogous concepts are
being discussed. Since there would be different coaching and performance
implications from each of the above concepts, the blanket use of this term will
foster many erroneous coaching prescriptions and procedures.
Lactate accumulation indicates a shift from solely oxidative to an additional
glycolytic energy supply. Lactic acid production is due to the activation of
glycolysis that is more rapid than activation of oxidative phosphorylation. This is
indicated by a steep non-linear increase of blood lactate in relation to power
output and time. That accumulation can be attributed to disparities in the rate of
lactate production and removal, even for work intensities under those which elicit
VO2max. Lactate production is not related to oxygen deficit but rather to the
increase of the glycolysis flux. (p. 159)
Lactate is produced constantly, not just during hard exercise. It may be the most
dynamic metabolite produced during exercise since its appearance exceeds that of
any other metabolite studied. The constancy of the blood lactate level means that
entry into and removal of lactate from the blood are in balance.
The turnover of lactic acid during exercise is several times greater for a given
blood lactate level than at rest. For a given blood lactate level, lactate removal
is several times greater in trained than in untrained persons.
Several factors are responsible for the lactate inflection point during graded
exercise.
* Contraction stimulates glycogenolysis and lactate production.
* Hormone recruitment affects both glycogenolysis and glycolysis.
* Recruitment of glycolytic fast-twitch fibers increases lactate production.
* Blood-flow redistribution from lactate-removing gluconeogenic tissues to
lactate-producing glycolytic tissues causes lactate levels to rise as exercise
requires continually increasing power output.
Lactate values differ according to several variables: the activity being performed,
the site from where the blood sample is taken, the environment itself (both
physical and its effect on the athlete's psychology), and the state of glycogen
stores prior to testing. Unless these variables and others, such as day-to-day
cycles in general physiology, as well as variations in test administration and
athlete performance of each test segment, can be controlled and made consistent
between test administrations it is likely that score differences will be
unreliable. The practice of attributing any observed lactate-test differences, no
matter how small, to training effects or as revealing the trained state is
extremely dubious at best.
Practical Implications
When scientists cannot agree upon a concept's definition, let alone the appropriate
label to use, as well as the appropriate method/protocol of assessment, then the
practical use of the "general implications" of the concept is foundationally
prohibited. Until this situation is clarified and discrepancies removed, field
testing for "lactate-threshold" should be avoided. There are more profitable and
useful activities for athletes and coaches to be engaged in.
Of significance to coaching is the concept itself. The common misunderstanding that
the anaerobic threshold is the state where aerobic activity is dominant and maximal
and anaerobic activity constant but "insignificant" is very prevalent. There are
few competitive activities or events where such a circumstance is desirable.
Most activities do not require all body parts to be involved in an activity at the
same intensity level. A cyclist will work the legs extremely hard but, by
comparison, the rest of the body will function comfortably in an aerobic zone of
metabolic activity. A swimmer pounding out stroke after stroke in a 1500 m race
works the arms at an intensity that employs a high level of anaerobic energy supply
but the rest of the body is "relaxed" and functioning at quite a basic aerobic
level. Even in running, in a marathon the legs work hard while the arms and upper
body "save energy." In these activities, lactate is produced by the primary working
muscles and resynthesized by the muscles engaged in mild supportive activity. Those
muscles cleanse or "sponge" out lactate so that the blood supply to the hard
working muscles is quite low in acidity when returned to those muscles. Thus, any
lactate measure is a measure of the "general functioning" of the body, not the
actual work performed by the primary sporting muscles. Differences in technique
most probably would account for a significant portion of many inter-individual
differences in lactate assessments than work levels or movement economy.
In many "aerobic" sports the actual prime mover muscle groups work at an anaerobic
level rather than aerobically as is inferred from anaerobic threshold testing. The
common perception of anaerobic threshold does not give any information or
understanding of what actually is happening in important aspects of a performance.
Even the slightest improvement in movement economy (technique) in the "anaerobic
prime movers" could make a significant difference to performance.
Of all the concepts of anaerobic-type thresholds or measures that are proposed
perhaps the maximum lactate steady-state (MLSS) is the one that is most applicable
to the field of sports. In cycling events of one hour, athletes have been measured
to "tolerate" and demonstrate sustained lactate levels in the region of 7 mM/l. In
most events where "effort" is required as part of the competitive strategy, lactate
levels will be sustained in a competitive performance in excess of the anaerobic
threshold (if one can be demonstrated). There is a much greater proportion of many
competitive performances that is more anaerobic than is generally acknowledged. If
appropriate and sane anaerobic training is ignored then an athlete will not be
trained optimally and a theoretically "best" performance will not be possible.
How can one test for maximum lactate steady state? Simply ask trained, experienced
athletes to perform a task equal to the duration of their competitive event and
they are likely to produce a performance that is close to demonstrating the MLSS.
To be sure of this, if performance intensities, usually velocities, are performed
at an increment above and below the first trial, verification should be
forthcoming. Repeating many trials usually is not necessary. Is this too simple of
a concept for complicated science? In practical circumstances it works. But since
this could be a procedure that is implemented by coaches would it be endorsed by
scientists which would seemingly remove a coach's dependence on them?
But a central perplexing question still remains: what does one get from measures of
lactate and performance? What do they tell more than is already known? If lactate
values are specific to the task/testing-protocol/event there can be no inference
beyond the observations themselves.
When two athletes with the same physiological capacities perform the same activity,
one using arms only the other using arms and legs, the performance results are
often different, particularly when energy supply is an important aspect of the task
demands. In this case, it is not the "anaerobic threshold" that differentiates the
two but the movement economies, one using more muscle mass to produce a performance
outcome. An attempt to shift the anaerobic threshold by further training of a
particular type in an hypothesized metabolic zone with appropriate heart rates is
clearly the wrong approach to solving the less-efficient athlete's problem. A skill
element change to reduce unnecessary movements would result in greater movement
economy and would shift the velocity that supports the MLSS to the right.
It is dubious to attribute shifts in anaerobic threshold values to physical
training. Given that so many variables render field tests of this phenomenon
practically unreliable, what is attributed to score differences obtained between
two tests is more of a guess than an informed judgment.
Sport scientists can produce graphs of swimmers, runners, rowers, etc. showing an
"inflection point" that occurs in a region of performance velocity. Equally, other
athletes tested with the same protocol do not show any inflection or exhibit
measures which cannot be interpreted in terms of a traditional anaerobic threshold.
A few selected demonstrations do not prove the existence of a phenomenon that can
be applied universally. The trend in field testing is rather one of more people not
demonstrating a clear "anaerobic threshold" than doing so. Complicate that further
with deciding upon which threshold protocol fits the sport from the existing array
of definitions and confusion results rather than a clearly usable training tool.
Anaerobic threshold results must be reliable, that is, capable of replication. When
a particular protocol is used for a series of periodic assessments, as is commonly
followed in "sport science testing" programs, if that protocol is altered, the
previous results cannot be used for comparison purposes. A protocol change will
produce unrelated results, often different response phenomena, and above all
different implications and interpretations. The definitions and discrepancies
listed above all originate from different testing protocols. Thus, results from one
protocol to the next, no matter how small the change is explained to be, should not
be compared. Essentially, a new database is developed.
An unavoidable dilemma. Sport scientists are ethically bound to represent the worth
of lactate testing and the inferences that are commonly proposed. This is what is
known.
1. Lactate concepts and measures are limited/specific to each testing protocol.
1. Results from one protocol cannot be used to generalize or infer values to other
testing protocols.
2. If one cannot infer from one lactate testing protocol to another then it is
illogical to generalize lactate testing results to a competitive performance.
3. It is a greater stretch of the imagination to leap conceptually from an
inferentially-limited measure under controlled conditions to the dynamic
circumstances of a competitive or practice setting.
4. At most, lactate and lactate threshold measurements reveal changes but have
limited to possibly non-existent inferential capacities about future
performances (even training performances let alone competitive performances).
5. Lactate and lactate threshold measurements can reveal that they have changed as
a result of training, but if those changes are unrelated to competitive
performances what is their value?
6. There are no national or international competitive events that reward medals
for lactate threshold changes, levels, or testing protocols.
A story. During the spring of 1996, this writer attended the ARCO Training Center
in Chula Vista, California. One day a USOC testing group had completed lactate
threshold and aerobic parameter testing sessions on the US men's heavyweight rowing
eight that was to compete later that year at the Atlanta Olympic Games.
The eight had just completed a European tour and performed worse than at any time
in the previous three years. Based on comparative racing performances, it was a
boat in trouble.
The head USOC scientist related that the members of the eight were still improving
in fitness as the measures that were taken were better than previous test results.
Despite improved "fitness measures" the eight recorded a performance that was worse
than any in the previous four Olympic Games, and compared to the boats that it had
raced during the recent European tour, it had also degraded in racing capability.
The fitness measures indicated that training was progressing satisfactorily.
Unfortunately, racing performances were declining. Training improvements in
physiological indices were negatively correlated with racing achievements. In 1994,
the eight were world champions, in 1995 world bronze medalists, and in 1996, when
they had the best testing results, were fifth out of six at the Olympic Games.
Just what is the value of lactate and lactate threshold/MLSS testing for making
coaching decisions that relate to competitive performances?
Xeno Muller, Olympic gold and silver medalist, indoor rowing, rowing technique.
