2.3 Exercise, Lactate and Anaerobic Threshold

Transcription

Dangerous Curves : A Perspective on
Exercise, Lactate, and the Anaerobic
Threshold
Jonathan Myers and Euan Ashley
Chest 1997;111;787-795
DOI 10.1378/chest.111.3.787
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1997 by the American College of Chest Physicians
exercise and the heart
Dangerous Curves*
A Perspective on Exercise,
Anaerobic Threshold
Lactate, and the
Jonathan Myers, PhD; and Euan Ashley, MD
(CHEST 1997; 111:787-95)
Abbreviations: EMG.electromyogram; LDH=lactate dehy¬
drogenase; NADH=the reduced form of nicotinamide adenine
dinucleotide; RER=respiratory exchange ratio; Vco2=carbon
dioxide output; Vo2 oxygen consumption
=
"If then, life is an action of the soul and seems to be
aided by respiration, how long are we likely
greatly
to be ignorant of the way in which respiration is
useful?"
Galen of Pergamum
Circa 130-201 AD
TP hough it is
unlikely the Greek physician Galen
had the anaerobic threshold per se in mind, he
may have been the first to document something of
relevance to it. The increase in blood lactate level
that occurs in response to progressive exercise, and
changes in ventilation that are associated with it,
have engendered a great deal of interest from
coaches, athletes, clinicians, and educators for most
of this century. Few areas in the exercise sciences
have generated as many scientific reports, editorials,
or debate. Among the issues in dispute include the
mechanisms responsible for blood lactate increase,
the pattern of the lactate response to exercise, and
the ability to choose a "threshold" (including intraob¬
server and interobserver reliability and reproducibility, methods of choosing a threshold, and the relation
of lactate appearance to ventilatory changes during
exercise). Recent reports have even questioned the
existence of an "anaerobic" threshold, a concept that
some consider heretical. The anaerobic threshold
continues to be used widely in the clinical setting,
but many clinicians remain confused as to how to
-*-
*From the
Cardiology Division, Palo Alto Department of Veter¬
Affairs Medical Center, Stanford University, Palo Alto, Calif
(Dr, Myers); and the Institute of Physiology, University of
(Dr. Ashley).
Glasgow, Scotland
Manuscript received August 13, 1996; accepted August 14.
ans
interpret the lactate response to exercise. A wide gap
physiology
exists between the
and clinical literature
in
to this issue. The
summarizes
regard
following
studies related to the lactate response to
exercise and provides a perspective in the context of
clinical exercise testing.
recent
Historical Perspective
The concept that muscle contraction can occur for
extended periods of time without sufficient oxygen
supply may have been first suggested by Hermann1
in 1871. As early as 1909, Douglass and Haldane2
surmised that lactate stimulated respiration during
high-intensity exercise. Between 1910 and 1915,
Meyerhof34 and Hill57 suggested that lactate was
the "signal" that initiated muscle contraction, and the
role of oxygen was to remove lactate once it was
formed (it is now known, of course, that lactate is the
cause of, muscle contraction).
product of, not theseveral
other laboratories in the
Shortly thereafter,
United States and Europe independently reported
that exercise intensity, lactate production, metabolic
acidosis, and bicarbonate buffering appeared to be
linked.813 The accumulation of lactate in the blood
was thought to reflect a point during exercise in
which oxygen supply was inadequate to meet the
energy requirements of the working muscle. In the
and colleagues14 linked lac¬
early 1960s, Hollmann
tate production in the blood to endurance perfor¬
mance among German athletes. In 1964, Wasserman
and Mcllroy15 explicitly developed the concept that a
critical threshold exists in which (1) the metabolic
needs for oxygen in the muscle exceed the capacity
of the cardiopulmonary system to supply them, (2)
there is a sudden increase in anaerobic metabolism,
and (3) lactate is formed in the muscle.
In recent years, however, evidence has accumu¬
lated that dissociates lactate production from anaerobiosis. Studies performed over the last 15 years
using isotopic tracer technology have suggested that
CHEST / 111 / 3 / MARCH, 1997
787
muscles can release lactate when their oxygen supply
more than adequate.16 Moreover, evidence that
muscles become anaerobic when exercise ap¬
an intensity in which blood lactate level
proaches
rises precipitously is in dispute.16"19 The formation of
lactate appears to depend on several factors, includ¬
ing but not limited to the availability of oxygen. In
the following, current perspectives on lactate con¬
trol, lactate as a substrate, and recent studies on the
pattern of the lactate response to exercise are re¬
viewed along with their clinical implications.
is
Control
of
Lactate Production
The relationship between the increase in blood
lactate and oxygen supply to the muscle has a long
Studies performed early in this century
history. linked
exercise intensity, lactate appearance,
closely
metabolic acidosis, and bicarbonate buffering.814
These associations provided a convenient and logical
for lactate production during exercise.
explanation
Numerous studies have supported the link between
oxygen supply and the magnitude of the increase in
blood lactate, albeit without direct evidence of cause
and effect. For example, the extent to which lactate
increases in the blood during exercise is reduced as
fitness increases or with training,2021 and is in¬
creased in the presence of reduced cardiac output
states2224 or disease of the electron transport
chain.25 When oxygen supply is experimentally al¬
tered, blood lactate is profoundly affected. With an
increase in inspired oxygen tension, either by in¬
creasing the oxygen content of the inspired air or by
increasing the barometric pressure, the exerciseinduced increase in lactate level is attenuated.2628
Decreasing the fraction of inspired oxygen either
experimentally or by exposure to altitude increases
blood lactate.26-27-29'30 In normal subjects, reducing
blood volume causes an increase in blood lactate
level during exercise.3132 In patients with chronic
heart failure, increasing cardiac output with inotro¬
pic therapy attenuates the increase in blood lactate
during exercise.33-34
Despite these compelling observations, manipula¬
tions in oxygen supply that affect the relationship
between oxygen availability and lactate do not prove
causation, and the concept that the availability of
oxygen is the sole determinant of lactate production
has been highly controversial. The idea that lactate
is dependent solely on oxygen supply to
production
the tissue is not consistently supported by the avail¬
able data. It is now appreciated that lactate can be
formed under conditions that are fully aerobic,16-35
findings which appear to negate the concept that
anaerobiosis per se causes lactate production. An
observation that has perplexed many in this debate is
that, between normoxic and hypoxic conditions, ox¬
ygen consumption (Vo2) remains unchanged (sug¬
gesting that 02-limited metabolism is not present)
but lactate level is increased.20 The picture is analo¬
gous to that before and after athletic training, in
which lactate level is generally lower for any given
submaximal work rate while Vo2 is unchanged (al¬
though Katz and Sahlin36 argue that this does not
take into account adaptive changes in the muscle).
Katz and Sahlin17 summarized experimental data
and theoretical reasons supporting the concept that
lactate production is Os dependent. In effect, they
argue that when oxygen supply is limited, mitochondrial respiration is stimulated by increases in aden¬
osine diphosphate, inorganic phosphate (Pi), and the
reduced form of nicotinamide adenine dinucleotide
(NADH). This favors the stimulation of glycolysis,
which will increase cytosolic NADH formation,
which will shift the lactate dehydrogenase (LDH)
toward increased lactate production.
equilibrium
While they acknowledge that lactate production is
also dependent on the glycolytic and mitochondrial
respiration rates as well as LDH, they propose that
oxygen supply has the most pivotal role in lactate
production. Connett and colleagues37 describe an
alternative scenario in which 02 "deficiency" (02limited cytochrome turnover) is characterized by the
(1) it can be defined only by specifying
following:
adenosine triphosphate demand; (2) it is dependent
on aerobic capacity relative to glycolytic capacity in a
tissue; and (3) a critical Po2 exists for a given
specificand
the specific Po2 depends on the supply of
tissue,
substrate to the mitochondrial and glycolytic sub¬
systems, along with the redox state. These metabolic
compensations depend on cell Po2, but the glycolytic
rate is not
directly coupled to 02 supply.
Lactate
accumulation may occur both above and below a
critical Po2 since it depends not only on the glyco¬
across the cell mem¬
lytic rate but also on exchange
brane and consumption in neighboring cells. These
investigators have observed lactate formation at low
levels of exercise (<10% Vo2 max) in dog gracillis
muscle (a purely aerobic, red muscle fiber).35 They
argue that lactate formation cannot be due to an 02
limitation, and that the anaerobic threshold cannot
to red muscle.
apply
These two sources seem to directly contrast one
another. In effect, however, both Katz and Sah¬
lin17-36 and Connett et al37 suggest that with increas¬
ing work loads, a situation must arise whereby
metabolic change within the cell occurs in order for
the cell to maintain full aerobic (mitochondrial)
function. This change is an increase in the mitochon¬
drial NADH/NAD ratio (ie, the redox potential
increases), which in turn is transmitted to the cytosol
788
Exercise and the Heart
where it pushes the lactate/pyruvate ratio in the
direction of lactate. Whether this is labeled anaero¬
bic metabolism18 or metabolic change37 does not
alter its presence, which is agreed on by all.
twitch fibers, and different individuals have different
percentages of fiber types.
Lactate
Other Factors
Controlling
Brooks,16 Stainsby and Brooks,19 and others have
suggested that (3-adrenergic stimulation of muscle
glycogenolysis is an important factor controlling lac¬
tate production. This is evidenced by high correla¬
tions between catecholamine concentration and
blood lactate,38"40 by similar threshold responses for
lactate and catecholamines,4041 by studies demon¬
strating that infusion of epinephrine elicits an in¬
crease in blood lactate,4244 and by the observation
that (3-blockade causes a reduction in blood lactate
during exercise.19'45-46 Mazzeo and Marshall40 have
shown that the inflection point during incremental
exercise for plasma epinephrine shifts in an identical
manner and simultaneously with lactate from cycling
to treadmill running. Podolin and associates41 ex¬
tended these findings by observing simultaneous
inflections in lactate, epinephrine, and norepineph¬
rine in both normal muscle glycogen and glycogendepleted states. Weltman et al47 recently contrasted
these findings by observing similar norepinephrine
and epinephrine thresholds between running and
rowing, but the lactate threshold occurred at a lower
oxygen uptake (7 and 10% lower for running and
cycling, respectively). Weltman et al47 suggest that it
may not be an epinephrine threshold per se that
underlies the lactate threshold, but rather a critical
plasma
epinephrine level.
An
Lactate Production
additional persuasive argument put forth in¬
volves the association between the increase in lactate
level and the progressive recruitment of ever more
aerobically scarce motor units (culminating of course
in the recruitment of extreme lib fibers which, as a
result of their aerobic paucity, steadily release H+
ions and lactate irrespective of Po2).48 Some evi¬
dence also exists correlating the percentage of type I
fibers with the lactate threshold.4950 However, it
could equally be that the recruitment of lib fibers is
a consequence of the increase in H+ rather than a
cause. A decrease in intracellular pH interferes with
the contraction-coupling mechanism and its ability to
maintain force. To compensate, more lib fibers are
recruited resulting in greater glycogenolysis and
lactate production. Underlying the role of muscle
fiber types is the fact that the isozyme form of LDH,
which converts lactate to pyruvate and vice-versa,
differs between muscle fibers. Fast-twitch fibers
have an LDH isozyme form that favors the formation
of lactate, whereas the opposite is true for slow-
as a
Substrate
Long considered to have only toxic effects, an
appreciation for lactate as a metabolic substrate has
emerged in recent years. This is due in large part to
the application of isotopic tracer technology to the
study of metabolism during exercise.1651 It has be¬
clear from these studies that the skeletal
muscles actively produce and consume lactate dur¬
ing exercise. It is now recognized that a significant
portion of the lactate produced and released into the
blood during exercise is taken up by tissues other
than those from which it was formed.16-52 In fact,
these studies suggest that during exercise, lactate
may be the predominant fuel for the heart, and the
preferred fuel for slow-twitch fibers. Lactate also
appears to be an important intermediate in glycogen
formation by the liver, and a precursor for liver
gluconeogenesis. Lactate formation occurs even at
rest, and during exercise, lactate production and
removal are highly correlated to the metabolic
come
rate.35-51
Role
of
Lactate
in
Fatigue
misconception that remains pervasive is the
perception that lactate is the major cause of both
fatigue during exercise and postexercise muscle sore¬
ness. In fact, lactate has little direct effect on either.
A
Accumulation of lactate in the muscle occurs only
bouts of exercise of relatively high
during short
Even
after endurance events lasting several
intensity.
hours, lactate levels in the blood are near their levels
at rest. Moreover, when lactate is infused into the
blood, it has minimal noticeable effects. Rather than
lactate causing fatigue per se, it is the accumulation
of H+ ions during glycolysis that contributes to
fatigue.
High concentrations of H+ lower the blood's
which
pH
adversely influences energy production
and muscle contraction. Energy production is af¬
fected by the inhibition of phosphofructokinase, a
key glycolytic
enzyme. In fact, at a pH of 6.4,
can
cease
glycolysis
completely. Excessive H+ ions
affect muscle contraction by displacing calcium
within the muscle fiber, interfering with actin-myosin cross-bridge formation and reducing contractile
force. During short-term maximal exercise, this is
the major factor limiting performance. During
longer endurance-type exercise, fatigue is primarily
related to energy supply, the most important factor
being the depletion of muscle glycogen.53
CHEST/ 111 73/MARCH, 1997
789
Because lactate is so rapidly removed from the
muscle and blood after exercise,54 the assumption
that lactic acid causes muscle soreness is also incor¬
rect. Even extremely high blood lactate levels return
to normal within an hour after intense exercise.54
most muscle soreness occurs after
Interestingly,
endurance exercise performed below an intensity
required to illicit the accumulation of lactate in the
blood.55 Electron microscopy and other studies have
demonstrated that muscle soreness is almost cer¬
due to muscle cell microdamage and inflam¬
tainly
mation.56'57
Ventilation
The idea that ventilatory variables may be linked
these metabolic processes also has a long history.
Recent studies have made the long-held cause and
effect relationship between lactate accumulation and
ventilatory changes another source of debate. In
1975, Wasserman and associates58 appeared to con¬
firm what had been widely held for many years by
observing an absence of a ventilatory threshold
among subjects whose carotid bodies had been
resected. In the absence of peripheral arterial che¬
moreceptors to detect changes in pH caused by
lactic acid production, no ventilatory changes during
exercise were observed. In the 1980s, however, a
wide variety of experimental manipulations have
raised questions about how closely ventilatory pro¬
cesses mirror metabolic ones. For example, numer¬
ous studies have demonstrated that the ventilatory
threshold can be detected prior to the lactate thresh¬
old during progressive exercise.59"61 In addition,
nonlinear increases in ventilation have been ob¬
served among subjects who do not produce lactate
(McArdles syndrome).62-63 Others have demon¬
strated that relative to control conditions, ventilation
either increases or remains constant among normal
subjects in a glycogen-depleted state, in which both
lactate and carbon dioxide partial pressure are re¬
duced.64-65 Together, these studies suggest that stim¬
ulation of peripheral chemoreceptors by lactic acid
cannot be solely responsible for the ventilatory
threshold.
Some compelling evidence has come from recent
studies on potassium. Paterson66 has made a strong
case for potassium as an important humoral factor in
the regulation of exercise ventilation. It is known, for
cat, hyperkalemia
example, that in the anesthetized
stimulates ventilation by excitation of the carotid
that denervation of these
body chemoreceptorsthisandeffect.6670
It appears also
abolishes
receptors
that for McArdle's subjects63 and in conditions of
glycogen loading,60 the plasma potassium level tracks
to
better than lactate.not only
ventilatory
changes
exercise
also
in the recovery period (when
but
during
lactate levels continue to rise). Despite indications
that the picture is not entirely clear cut (eg, the effect
of |3-adrenergic blockade, which should, by enhanc¬
ing exercise-induced hyperkalemia,71 increase venti¬
lation but fails to do so72 and the contradictory
findings of McLoughlin et al73), it is clear that to
ignore the role of humoral factors other than lactate
and H+ is to seriously misrepresent the true picture.
For
the safest
course for those who choose to
threshold model is to refer to two separate but
associated thresholds, one for ventilation and one for
lactate.
Evidence also exists that the lactate threshold
correlates well with an electromyogram (EMG)
"threshold" (abrupt increases in the frequency band
width at 70% of the peak frequency) and the inte¬
EMG, and that a gas exchange threshold
grated
correlates well with an EMG "fatigue threshold."74 ~77
These findings have raised the possibility that an
increase in neural activity, originating from higher
motor centers or the exercising muscle, may contrib¬
ute to the stimulation of ventilation. Mateika and
Duffin77 attenuated peripheral chemoreceptor activ¬
ity with hyperoxic breathing, and observed coinci¬
dent ventilatory and EMG thresholds during exer¬
cise. These investigators have also shown that, during
normoxic breathing, EMG and ventilatory thresholds
occur at similar exercise intensities, whereas the
lactate and ventilatory thresholds are uncoupled.78
These data suggest that changes in lactate concen¬
tration and thus peripheral chemoreceptor drive are
not strictly responsible for the ventilatory threshold,
but rather, the ventilatory threshold is mediated by
alterations in neural activity that occur in conjunc¬
tion with motor unit recruitment.
There has also been an evolution in recommended
for measuring the ventilatory threshold.
techniques
Over the years, there have been at least a dozen
criteria recommended for detecting a breakpoint in
ventilation, including the following: (1) an increase in
the respiratory exchange ratio (RER); (2) an abrupt
increase in the fraction of expired oxygen; (3) a
nonlinear increase in ventilation; (4) a nonlinear
some,
use a
increase in
C02 production; (5)
an
increase in
end-tidal 02 partial pressure; (6) a nonlinear increase
in the integrated EMG activity; (7) the point at
which the relationship between running speed and
heart rate departs from linearity; and (8) the begin¬
ning of a systemic increase in the ventilatory equiv¬
alent for oxygen (Ve/Vo2) without an increase in the
C02 (Ve/Vco2).15-18-79"91
ventilatory equivalent for that
the RER was use¬
Early reports suggested
ful,15-79"81 since, as an expression of the slope of
carbon dioxide output (Vco2) to Vo2, a value greater
790
than 1.0 should reflect a nonlinear increase in C02
studies suggested the RER was
production. Later
to changes in blood lactate
insensitive
comparatively
levels.8081 There have been numerous efforts to
address the subjective nature of determining an
have been raised re¬
"abrupt increase." Problems
and intraobserver
interobserver
peatedly concerning
and
reliability reproducibility,87-91'92 and there have
been many computerized efforts to improve the
detection of a ventilatory break point with mixed
success.87-90-93-96
Caiozzo and associates91
compared various venti¬
latory indexes with lactate changes and recom¬in
mended an "increase in Ve/Vo2 with no change
Ve/Vco2." This removed some of the subjectivity
because the ventilatory equivalent for 02 would
typically decrease initially in an incremental test
before beginning a systematic increase. The "no
change in the ventilatory equivalent for C02" was
included to guard against the somewhat erratic
nature of exercise hyperventilation. It was apparent,
however, that while this method removed much of
the subjectivity, it was not discernible in all subjects
and could still be affected by the multitude of other
factors influencing exercise ventilation. Thus, in
1986, Beaver et al97 came full circle in defining a new
criterion named the "V-slope." This was essentially
the point where the slope of the Vco2 and Vo2 curve
became >1.0. In theory, such a point would be more
reliable since it depends only on the bicarbonate
of
buffering response to lactate, and is independent
thus
the
and
respiratory chemoreceptor sensitivity
ventilatory removed
response to exercise. In a stroke, they
observer bias from the measure¬
effectively
ment. Even more important, however, the choice of
an inflection point was not affected by the choice of
model used to fit the data. Despite the assertion that
the choice of the model is "fundamental to the
understanding of exercise energetics,"98 whether one
takes a tangent to a continuous curve or a set square
to a threshold curve, the result will be the same
(more on this below). The measurement is reproduc¬
ible in a way that none of the others are and, not
surprisingly, it is discernible in most subjects. Fur¬
ther, although this is not absolutely the case, the fact
that ventilation generally cancels out on both axes
means that the measure is relatively independent of
the vicissitudes of exercise ventilation.
Pattern
of the
Lactate Response
The concept that a "threshold" exists, in which
there is a sudden onset of anaerobic metabolism
in the blood,
resulting in theHillaccumulation of lactate
in
and
coworkers9
the
1920s and
proposed by
been
popularized by Wasserman et al,151879 has also some
this
issue
has
generated
challenged. Recently,
rather lively debate. Studies by Gladden et al93 and
Yeh and associates92 raised questions about the
subjective intraobserver and interobserver reliability
and reproducibility of ventilatory and lactate thresh¬
or
of a
olds. Concerns over the presence absence
discrete threshold point led Beaver et al95 to suggest
the use of a log-log transformation (ie, plotting
oxygen uptake, lactate, or C02 production on loga¬
rithmic axes). These investigators reported that lac¬
tate exhibited an abrupt transition from a slowly
increasing phase
to
a
rapidly accelerating phase,
findings consistent with the historic interpretation of
the anaerobic threshold. Despite its wide adoption,
unacceptable to
things, a log trans¬
many9498102
formation could "create" a visually apparent break¬
point where none existed before, by spreading out
the early data points over the X-axis relative to the
however, such
an
idea
was
since among other
later ones.
Five recent studies have used mathematical mod¬
eling to describe the relationship between oxygen
uptake and lactate during exercise, and addressed
whether the increase in lactate level was better
as a continuous (smooth) function or the
represented
data depicted a true threshold. Yeh et al92 used
semilog plots of arterial lactate vs time, and reported
that an exponential increase in lactate level occurred
during exercise without a threshold. Hughson and
coworkers99 compared the log-log transformation
model of Beaver et al95 with an exponential plus
constant model. These investigators observed that
in blood lactate levels during progressive
changes
exercise were more appropriately described mathe¬
matically as a continuous function, implying the
absence of a threshold. This was suggested by a
mean squared error term for the continuous model
that was 3.5 times lower than that for the threshold
model described by Beaver and associates.95 Similar
observations were made by this group over a variety
of ramp rates.101 Dennis et al102 corroborated the
findings of Hughson and coworkers,99101 reporting
that plots of ventilation, C02 production, and blood
lactate vs oxygen uptake were more appropriately
described by continuous rate laws rather than
threshold linear equations. We considered some of
the subsequent adversarial criticisms of these studies
(ie, insufficient number of subjects, inconsistent or
overly
demanding ramp rates, subjectivity, frequency
of data sampling),94 and found that a computerized
threshold model fit the data slightly better than a
continuous model. However, the differences were
quite small, leading to the conclusion that (1) a
meaningful difference did not exist between the
CHEST 7111/3/ MARCH, 1997
791
models, or (2) these models may not be capable of
a difference, if one exits.
detecting
Morton98 has added significantly to this debate,
arguing among other things, that (1) researchers
have sought to model the data and not the process
that produces the data, and (2) these studies have
ignored the importance of the distinction between
the lactate response and its first derivative. Other
arguments concerning modeling of lactate no doubt
serve only to confuse the average clinician not at ease
with the idiosyncrasies of these mathematics.100103"105
In retrospect, however, many of the points made in
regard to modeling the response may be academic. It
matters little, for example, that when investigators
used the term "threshold system" they actually meant
"a system which produces data possessing a discon¬
tinuous first derivative," when in fact a "threshold
system" mathematically defined can result in data
with either a continuous or discontinuous first deriv¬
ative. What Wasserman and associates originally
intended (and others undoubtedly understood) was
that these variables showed a continuous, kinked
response.a clear point of abrupt increase in slope.
and it was this interpretation which was disputed.
It is important that cross-disciplinary terminology
be both consistent and appropriate, but this does not
change the substance of the physiologic debate.
Phenomenologic modeling (modeling the data rather
than the system) is appealing to physiologists be¬
cause its meaning is readily understood. The practi¬
cal constraints of clinical exercise testing call for fast
and meaningful answers for physician and patient.
This is not to discount the substantial contribution
that mathematical modeling has made to the scien¬
tific debate, but merely to emphasize that a good
of others' fields of interest is a pre¬
understanding
for
requisite good cross-disciplinary research. What
is clear is that all functions fit the data well, as would
be expected for monotonic, smooth data, and one
must question the physiologic significance of small
differences in the fit of statistical models.
Summary
A number of general observations can be made
from these recent studies. Lactate is a ubiquitous
substance that is produced and removed from the
at all times, even at rest, both with and without
body
the availability of oxygen. It is now recognized that
lactate accumulates in the blood for several reasons,
not just the fact that oxygen supply to the muscle is
inadequate. Lactate production and removal is a
continuous process; it is a change in the rate of one
or the other that determines the blood lactate level.
Rather than a specific threshold, there is most likely
period of time during which lactate production
to remove it
begins to exceed theor body's capacity
in
oxidation
other
fibers). It
(through buffering
be
to
the
term
"anaerobic
may appropriate replace
threshold" to a more functional description, since the
muscles are never entirely anaerobic nor is there
always a distinct threshold ("oxygen independent
glycolysis" among others has been suggested) Lac¬
tate plays a major role as a metabolic substrate
during exercise, is the preferred fuel for slow-twitch
muscle fibers, and is a precursor for liver gluconeo^enesis.
The point at which lactate begins to accumulate in
the blood, causing an increase in ventilation, is
important to document clinically. Irrespective of the
mechanism or specific model that de¬
underlying
scribes the process, the physiologic changes associ¬
ated with lactate accumulation have significant im¬
port for cardiopulmonary performance. These
include metabolic acidosis, impaired muscle contrac¬
tion, hyperventilation, and altered oxygen kinetics,
all of which contribute to an impaired capacity to
work. Thus, any delay in the accumulation
perform
of blood lactate which can be attributed to an
intervention (drug, exercise training, surgical, etc)
may add important information concerning the effi¬
cacy of the intervention. A substantial body of evi¬
dence is available demonstrating that lactate accu¬
mulation occurs later (shifting to a higher percentage
of Vo2max) after a period of endurance training. In
athletes, the level of work that can be sustained prior
to lactate accumulation, visually determined, is an
accurate predictor of endurance performance. Pre¬
sumably, these concepts have implications related to
vocation/disability
among patients with cardiovascu¬
lar and pulmonary disease, but few such applied
studies have been performed outside the laboratory.
Blood lactate during exercise and its associated
maintain useful and interesting
ventilatory changes
in
the clinical exercise laboratory
both
applications
and the sport sciences. However, the mechanism,
interpretation, and application of these changes con¬
tinue to rely more on tradition and convenience than
science.
a
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CHEST / 111 / 3 / MARCH, 1997
795
Dangerous Curves : A Perspective on Exercise, Lactate, and the
Anaerobic Threshold
Jonathan Myers and Euan Ashley
Chest 1997;111; 787-795
DOI 10.1378/chest.111.3.787
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2.3 Exercise, Lactate and Anaerobic Threshold

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