Limiting factors for maximum oxygen uptake and determinants of endurance performance

BASIC SCIENCES
Commentaries
Limiting factors for maximum oxygen
uptake and determinants of
endurance performance
DAVID R. BASSETT, JR. and EDWARD T. HOWLEY
Department of Exercise Science and Sport Management, University of Tennessee, Knoxville, TN
ABSTRACT
BASSETT, D. R., JR. and E. T. HOWLEY. Limiting factors for maximum oxygen uptake and determinants of endurance performance.
Med. Sci. Sports Exerc., Vol. 32, No. 1, pp. 70–84, 2000. In the exercising human, maximal oxygen uptake (V˙ O2max) is limited by
the ability of the cardiorespiratory system to deliver oxygen to the exercising muscles. This is shown by three major lines of evidence:
1) when oxygen delivery is altered (by blood doping, hypoxia, or beta-blockade), V˙ O2max changes accordingly; 2) the increase in
V˙ O2max with training results primarily from an increase in maximal cardiac output (not an increase in the a-v៮ O2 difference); and 3)
when a small muscle mass is overperfused during exercise, it has an extremely high capacity for consuming oxygen. Thus, O2 delivery,
not skeletal muscle O2 extraction, is viewed as the primary limiting factor for V˙ O2max in exercising humans. Metabolic adaptations in
skeletal muscle are, however, critical for improving submaximal endurance performance. Endurance training causes an increase in
mitochondrial enzyme activities, which improves performance by enhancing fat oxidation and decreasing lactic acid accumulation at
a given V˙ O2. V˙ O2max is an important variable that sets the upper limit for endurance performance (an athlete cannot operate above 100%
V˙ O2max. for extended periods). Running economy and fractional utilization of V˙ O2max also affect endurance performance. The speed
at lactate threshold (LT) integrates all three of these variables and is the best physiological predictor of distance running performance.
Key Words: CARDIORESPIRATORY, FITNESS, EXERCISE, OXYGEN TRANSPORT, MARATHON, RUNNING, RUNNING
ECONOMY, LACTATE THRESHOLD
M
aximum oxygen uptake (V˙ O2max ) is defined as
the highest rate at which oxygen can be taken up
and utilized by the body during severe exercise. It
is one of the main variables in the field of exercise physi-
ology, and is frequently used to indicate the cardiorespira-
tory fitness of an individual. In the scientific literature, an
increase in V˙ O2max is the most common method of demon-
strating a training effect. In addition, V˙ O2max is frequently
used in the development of an exercise prescription. Given
these applications of V˙ O2max, there has been great interest in
identifying the physiological factors that limit V˙ O2max and
determining the role of this variable in endurance
performance.
The current concept of V˙ O2max began with the work of
Hill et al. (41,42) in 1923–24. Their view of maximum
oxygen uptake has been validated, accepted, and extended
by many world-renowned exercise physiologists
(2,17,58,68,74,83). However, it has recently been argued
that Hill’s V˙ O2max paradigm is an outdated concept, based
upon critical flaws in logic (62). To consider these points of
view, we weighed the arguments on both sides and con-
cluded in 1997 (5) that the “classical” view of V˙ O2max was
correct. The present article is an attempt to clarify our views
on V˙ O2max and to present further evidence in support of
Hill’s theory.
Part I of this article reviews the history of the concept of
V˙ O2max. Part II describes the evidence for each of the four
potentially limiting factors for V˙ O2max. Part III discusses the
role of V˙ O2max and other factors in determining endurance
performance.
PART I: HISTORY OF MAXIMUM
OXYGEN UPTAKE
The term “maximal oxygen uptake” was coined and de-
fined by Hill et al. (41,42) and Herbst (39) in the 1920s (74).
The V˙ O2max paradigm of Hill and Lupton (42) postulates
that:
0195-9131/00/3201-0070/0
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Copyright © 2000 by the American College of Sports Medicine
Submitted for publication June 1999.
Accepted for publication September 1999.
70

1. there is an upper limit to oxygen uptake,
2. there are interindividual differences in V˙ O2max,
3. a high V˙ O2max is a prerequisite for success in middle-
and long-distance running,
4. V˙ O2max is limited by ability of the cardiorespiratory
system to transport O2 to the muscles.
In 1923, Hill and Lupton (42) made careful measurements
of oxygen consumption on a subject (A.V.H.) who ran
around an 85-m grass track. The graph shown in Figure 1
was drawn primarily for the purpose of illustrating the
change in V˙ O2 over time at three speeds (181, 203, and 267
m⅐minϪ1
). In a study published the following year, Hill et al.
(41) reported more V˙ O2 measurements on the same subject.
After 2.5 min of running at 282 m⅐minϪ1
, his V˙ O2 reached
a value of 4.080 L⅐minϪ1
(or 3.730 L⅐minϪ1
above that
measured at standing rest). Since the V˙ O2 at speeds of 259,
267, 271, and 282 m⅐minϪ1
did not increase beyond that
measured at 243 m⅐minϪ1
, this confirmed that at high speeds
the V˙ O2 reaches a maximum beyond which no effort can
drive it.
Today, it is universally accepted that there is a physio-
logical upper limit to the body’s ability to consume oxygen.
This is best illustrated in the classic graph of Åstrand and
Saltin (4) shown in Figure 2. In a discontinuous test proto-
col, repeated attempts to drive the oxygen uptake to higher
values by increasing the work rate are ineffective. The rate
of climb in V˙ O2 increases with each successive attempt, but
the “upper ceiling” reached in each case is about the same.
The subject merely reaches V˙ O2max sooner at high power
outputs. V˙ O2 does not continue to increase indefinitely with
increases in work rate (or running speed). This finding was
predicted by Hill and Lupton ((42), p. 156), who stated that
eventually, “. . . however much the speed [or work rate] be
increased beyond this limit, no further increase in oxygen
intake can occur”.
Not all subjects show a plateau in V˙ O2 at the end of a
graded exercise test (GXT), when graphed against work
intensity. It has repeatedly been shown that about 50% of
subjects do not demonstrate a plateau when stressed to
maximal effort (46). Failure to achieve a plateau does not
mean that these subjects have failed to attain their “true”
V˙ O2max (26). In the first place, with a continuous GXT
protocol a subject may fatigue just as V˙ O2max is reached.
Thus, the plateau may not be evident even though V˙ O2max
has been reached (69). Second, even with a discontinuous
GXT protocol most researchers require that a subject com-
plete 3–5 min at each stage (3,26,83). Thus, if a subject
reaches V˙ O2max in 2 min at a supramaximal intensity and
then becomes too fatigued to continue, this data point would
not be graphed. In this case, the V˙ O2 plateau will not be
apparent in the final graph of work rate versus oxygen
uptake, even though V˙ O2max has been attained (Fig. 3). For
these reasons, the plateau in V˙ O2 cannot be used as the sole
criterion for achievement of V˙ O2max. This is why it is
recommended that secondary criteria be applied to verify a
maximal effort. These include a respiratory exchange ra-
tioϾ1.15 (47) and blood lactic acid level Ͼ8–9 mM (2), an
approach that has been confirmed in our laboratory (26).
The V˙ O2 plateau represents a leveling off in cardiac
output and a-v៮ O2 difference that may be seen toward the
end of a GXT. Since the V˙ O2 fails to keep pace with the
increasing oxygen demand, there is an increased reliance on
oxygen-independent pathways (i.e., anaerobic glycolysis).
The significance of the V˙ O2 plateau has often been misin-
terpreted. In 1988, it was suggested that the absence of a
V˙ O2 plateau in some persons meant that V˙ O2max was not
limited by the cardiovascular system (61). This led to the
suggestion that “muscle factors” must be important in lim-
iting V˙ O2max. However, as we pointed out, the V˙ O2 plateau
is not the principal evidence for a cardiovascular limitation
Figure 1—The attainment of a “steady state” for oxygen uptake, at
several constant running speeds. The horizontal axis depicts time from
the start of each run; the vertical axis shows oxygen uptake (L⅐min؊1
)
in excess of standing. The speeds are 181, 203, 203, and 267 m⅐min؊1
(from bottom to top). The three lower curves represent a genuine
steady state, while in the top curve the oxygen requirement exceeds the
measured oxygen consumption. From reference 42. Hill, A. V. and H.
Lupton. Muscular exercise, lactic acid, and the supply and utilization
of oxygen. Q. J. Med. 16:135–171, 1923. Used with permission of
Oxford University Press.
Figure 2—Time course of the increase in oxygen uptake during heavy
exercise on a cycle ergometer. Arrows show the time when the subject
stopped exercise because of fatigue. The power output (W) for each
bout is also shown. Subject could continue exercising at a power output
of 275 W for more than 8 min. From reference 3. Åstrand, P.-O. and
K. Rodahl. Textbook of Work Physiology. New York: McGraw-Hill,
1970. Used with permission.
V˙ O2max AND ENDURANCE PERFORMANCE Medicine & Science in Sports & Exerciseா 71

(5). More recently, it has been suggested that the V˙ O2
plateau signifies a leveling off in cardiac output, caused by
progressive and irreversible myocardial ischemia (63).
However, there is no evidence to support this view. In fact,
a V˙ O2 plateau occurs in about half of all healthy adults
performing maximal exertion (46), without accompanying
signs or symptoms of myocardial ischemia. A more reason-
able explanation is that maximal cardiac output is limited by
the maximal rate of depolarization of the sino-atrial (SA)
node and the structural limits of the ventricle.
Regarding the variability in V˙ O2max, Hill and Lupton
((42), p. 158) stated, “A man may fail to be a good runner
by reason of a low oxygen uptake, a low maximal oxygen
debt, or a high oxygen requirement.” This clearly shows that
they recognized the presence of interindividual differences
in V˙ O2max. They did not believe in a universal V˙ O2max of
4.0 L⅐minϪ1
, as has been suggested (63). Furthermore, they
recognized the importance of a high V˙ O2max for elite per-
formers (42). They also stated that other physiological fac-
tors, such as running economy, would influence the race
outcome (42). Subsequent researchers have verified these
points (see discussion in Part III).
The fourth point in the V˙ O2max paradigm has been the
most controversial. Hill et al. (41) identified several deter-
minants of V˙ O2max. Based on the limited data available to
them, they speculated that in exercising man, V˙ O2max is
limited by the rate at which O2 can be supplied by the
cardiorespiratory system (heart, lungs, and blood). Over the
next 75 years, many distinguished exercise physiologists
studied this problem using a wide array of new experimental
techniques. They have arrived at a consensus that supports
the original V˙ O2max paradigm of Hill et al. (41). The pre-
vailing view is that in the exercising human V˙ O2max is
limited primarily by the rate of oxygen delivery, not the
ability of the muscles to take up oxygen from the blood (see
part II).
PART II: LIMITING FACTORS FOR
MAXIMUM OXYGEN UPTAKE
The pathway for O2 from the atmosphere to the mito-
chondria contains a series of steps, each of which could
represent a potential impediment to O2 flux. Figure 4 shows
the physiological factors that could limit V˙ O2max: 1) the
pulmonary diffusing capacity, 2) maximal cardiac output, 3)
oxygen carrying capacity of the blood, and 4) skeletal mus-
cle characteristics. The first three factors can be classified as
“central” factors; the fourth is termed a “peripheral” factor.
The evidence for each of these factors is discussed in the
following sections.
The Pulmonary System
In the average individual exercising at sea level, the lungs
perform their job of saturating the arterial blood with O2
extremely well. Even during maximal work, the arterial O2
saturation (%SaO2) remains around 95% (65). Hill et al.
((41) p. 161) predicted that a significant drop in arterial
saturation (SaO2 Ͻ 75%) does not occur, based on the
appearance of their subjects, “who have never, even in the
severest exercise, shown any signs of cyanosis.” However,
they cautioned against assuming that a complete alveolar-
arterial equilibrium is present because of the rapidity of the
passage of the red blood cells within the pulmonary capil-
lary at high work rates ((42) p. 155).
Modern researchers have verified that the pulmonary
system may indeed limit V˙ O2max under certain circumstances.
Figure 3—Oxygen uptake and blood lactate response to a discontin-
uous exercise test. Left side shows the increase in oxygen uptake
(L⅐min؊1
) over time, with different intensities performed for 5 min
each. Right side shows the oxygen uptake (L⅐min؊1
) graphed against
power output (W). Note that a power output of 250 W elicited this
subject’s V˙ O2max and that 300 W did not further increase the oxygen
uptake. This increase in power output was achieved through anaerobic
processes. From reference 3. Åstrand, P.-O. and K. Rodahl. Textbook
of Work Physiology. New York: McGraw-Hill, 1970. Used with per-
mission.
Figure 4—Physiological factors that potentially limit maximum oxy-
gen uptake (V˙ O2max) in the exercising human.
72 Official Journal of the American College of Sports Medicine http://www.msse.org

Dempsey et al. (25) showed that elite athletes are more
likely to undergo arterial O2 desaturation during maximal
work compared with normal individuals. Trained individu-
als have a much higher maximal cardiac output than un-
trained individuals (40 vs 25 L⅐minϪ1
). This leads to a
decreased transit time of the red blood cell in the pulmonary
capillary. Consequently, there may not be enough time to
saturate the blood with O2 before it exits the pulmonary
capillary.
This pulmonary limitation in highly trained athletes can
be overcome with O2-enriched air. Powers et al. (65) had
highly trained subjects and normal subjects perform two
V˙ O2max tests (Fig. 5). In one test the subjects breathed room
air and in the other they breathed a 26% O2 gas mixture. On
hyperoxic gas, the highly trained group had an increase in
V˙ O2max from 70.1 to 74.7 mL⅐kgϪ1
⅐minϪ1
and an increase
in arterial O2 saturation (SaO2) from 90.6% to 95.9% during
maximal work. None of these changes were observed in
normal subjects (V˙ O2max ϭ 56.5 mL⅐kgϪ1
⅐minϪ1
).
Pulmonary limitations are evident in people exercising at
moderately high altitudes (3,000–5,000 m) (22,31,53). In-
dividuals with asthma and other types of chronic obstructive
pulmonary disease (COPD) suffer from a similar problem (a
reduction in arterial PO2). Under these conditions, exercise
ability can be increased with supplemental O2, which in-
creases the “driving force” for O2 diffusion into the blood
(23,67). The ability to increase exercise capacity in this
manner shows the presence of a pulmonary limitation.
Maximum Cardiac Output
Hill et al. (41,42) proposed that maximal cardiac output
was the primary factor explaining individual differences in
V˙ O2max. This was a major insight given the state of knowl-
edge in 1923. Einthoven had only discovered electrocardi-
ography a decade earlier. Hill used this new technique to
measure maximal heart rates of around 180 beats⅐minϪ1
((41) p. 165). However, it was not until around 1930 that
trained subjects were shown to have a lower heart rate at a
fixed, submaximal work rate (11), providing evidence of
increased stroke volumes. Other methods of showing en-
larged hearts in endurance athletes (x-ray and ultrasound)
did not become available until 1940–1950. Given the level
of technology in 1923, it is incredible that Hill et al. (41,42)
were able to deduce that endurance athletes have hearts with
superior pumping capacities. How did they arrive at this
remarkable conclusion? In 1915, Lindhard (55) had mea-
sured cardiac outputs of 20 L⅐minϪ1
in average subjects
during exercise and demonstrated the strong, linear relation-
ship between cardiac output and V˙ O2. Hill and Lupton
((42), p. 154) speculated that maximal cardiac output values
of 30–40 L⅐minϪ1
were possible in trained athletes. These
speculations were based on knowledge of the Fick equation
and assumed values for V˙ O2max, arterial oxygen content,
and mixed venous oxygen content.
Today, we know that the normal range of V˙ O2max values
(L⅐minϪ1
) observed in sedentary and trained men and
women of the same age is due principally to variation in
maximal stroke volume, given that considerably less varia-
tion exists in maximal HR and systemic oxygen extraction.
During maximum exercise, almost all of the available oxy-
gen is extracted from blood perfusing the active muscles
(76). The oxygen content of arterial blood is approximately
200 mL O2⅐LϪ1
; in venous blood draining maximally work-
ing muscles it falls to about 20–30 mL O2⅐LϪ1
. This shows
that there is little oxygen left to be extracted out of the blood
during heavy exercise. Hence, the dominant mechanism for
the increase in V˙ O2max with training must be an increase in
blood flow (and O2 delivery). It is estimated that 70–85%
of the limitation in V˙ O2max is linked to maximal cardiac
output (10).
Longitudinal studies have shown that the training-in-
duced increase in V˙ O2max results primarily from an increase
in maximal cardiac output rather than a widening of the
systemic a-v៮ O2 difference (Fig. 6). Saltin et al. (71) exam-
ined V˙ O2max in sedentary individuals after 20 d of bed rest
and 50 d of training. The difference in V˙ O2max between the
deconditioned and trained states resulted mostly from a
difference in cardiac output. In a similar study, Ekblom et al.
(27) found that 16 wk of physical training increased V˙ O2max
from 3.15 to 3.68 L⅐minϪ1
. This improvement in V˙ O2max
resulted from an 8.0% increase in cardiac output (from 22.4
to 24.2 L⅐minϪ1
) and a 3.6% increase in a-v៮ O2 difference
(from 138 to 143 mL⅐LϪ1
).
One way to acutely decrease the cardiac output is with
beta-blockade. Tesch (84) has written an authoritative re-
view of 24 studies detailing the cardiovascular responses to
beta blockade. Beta-blockers can decrease maximal heart
rate (HR) by 25–30%. In these studies, maximal cardiac
output decreases by 15–20%, while stroke volume increases
slightly. Although the decreased cardiac output is partially
Figure 5—Effects of hyperoxia on maximum oxygen uptake (V˙ O2max)
in normal and highly trained individuals. The highly trained subjects
had an increase in V˙ O2max when breathing oxygen-enriched air, show-
ing the presence of a pulmonary limitation in these subjects under
normoxic conditions. From reference 65. Powers, S. K., J. Lawler, J. A.
Dempsey, S. Dodd, and G. Landry. Effects of incomplete pulmonary
gas exchange on V˙ O2max. J. Appl. Physiol. 66:2491–2495, 1989. Used
with permission.

compensated for by an increase in a-v៮ O2 difference,
V˙ O2max declines by 5–15%. Tesch (84) concludes that the
decline in V˙ O2max seen with cardio-selective beta-blockade
is caused by diminished blood flow and oxygen delivery.
Oxygen Carrying Capacity
Another method of altering the O2 transport to working
muscles is by changing the hemoglobin (Hb) content of the
blood (28). Blood doping is the practice of artificially in-
creasing a person’s volume of total red blood cells through
removal, storage, and subsequent reinfusion. Gledhill
(35,36) completed comprehensive reviews of 15–20 studies
that have examined the effects of blood doping. Reinfusion
of 900–1,350 mL blood elevates the oxygen carrying ca-
pacity of the blood. This procedure has been shown to
increase V˙ O2max by 4–9% in well designed, double-blind
studies (35,36) (Fig. 7). No improvement is seen in sham-
treated individuals, infused with a small volume of saline
(8). Once again, these studies provide evidence of a cause-
and-effect link between O2 delivery and V˙ O2max.
The evidence that V˙ O2max is limited by the cardiac out-
put, the oxygen carrying capacity, and in some cases the
pulmonary system, is undeniable. This statement pertains to
healthy subjects performing whole-body, dynamic exercise.
Next we will consider whether skeletal muscle could also be
a limiting factor for V˙ O2max.
Skeletal Muscle Limitations
Peripheral diffusion gradients. In a symposium on
limiting factors for V˙ O2max, Honig et al. (45) presented
evidence for a peripheral O2 diffusion limitation in red
canine muscle. According to their experiments and a math-
ematical model, the principal site of resistance to O2 diffu-
sion occurs between the surface of the red blood cell and the
sarcolemma. They report a large drop in PO2 over this short
distance. Honig et al. (45) conclude that O2 delivery per se
is not the limiting factor. They found that a low cell PO2
relative to blood PO2 is needed to maintain the driving force
for diffusion and thus enhance O2 conductance.
The experimental model of Honig et al. (45) is quite
different from that seen in an exercising human. They noted
Figure 7—Changes in hemoglobin, hematocrit (Hct), and maximum
oxygen uptake (V˙ O2max ) following autologous blood transfusions of
either 1, 2, or 3 units of whole blood. An increase in the oxygen
carrying capacity of the blood results in an increase in V˙ O2max. From:
Spriet, L. L, N. Gledhill, A. B. Froese, and D. L. Wilkes. Effect of
graded erythrocythemia on cardiovascular and metabolic responses to
exercise. J. Appl. Physiol. 61:1942–1948, 1986. Used with permission.
Figure 6—Summary of changes that occur in maximum oxygen up-
take (V˙ O2max) following bed rest and physical training. The higher
V˙ O2max under sedentary conditions compared with that under bed rest
results from an increased maximal cardiac output. The further in-
crease after training results from an increase in cardiac output and, to
a lesser extent, an increase in the a-v៮ O2 difference. From reference 3.
Åstrand, P.-O. and K. Rodahl. Textbook of Work Physiology. New
York: McGraw-Hill, 1970. Used with permission. Data are from
rerference 71. Saltin, B., B. Blomquist, J. H. Mitchell, R. L. Johnson,
K. Wildenthal, and C. B. Chapman. Response to submaximal and
maximal exercise after bed rest and after training. Circulation
38(Suppl.7):1–78, 1968. Used with permission.

that simply increasing blood flow to isolated muscle is not
sufficient to cause V˙ O2 to increase. The isolated muscle
must also undergo contractions so that the mitochondria
consume O2 (drawing down the intracellular PO2). Without
a peripheral diffusion gradient, oxygen uptake will not in-
crease. Their overall conclusion is that V˙ O2max is a distrib-
uted property, dependent on the interaction of O2 transport
and mitochondrial O2 uptake (45). We agree with this con-
clusion. However, this model cannot determine which of
these two factors limits V˙ O2max in the intact human per-
forming maximal exertion.
Mitochondrial enzyme levels. Physiologists have
done extensive work to examine whether mitochondrial
enzyme levels are a limiting factor for V˙ O2max. Within the
muscle fibers, the mitochondria are the sites where O2 is
consumed in the final step of the electron transport chain. In
theory, doubling the number of mitochondria should double
the number of sites for O2 uptake in muscle. However,
human studies show that there is only a modest increase
V˙ O2max in (20–40%) despite a 2.2-fold increase in mito-
chondrial enzymes (72). This is consistent with the view that
V˙ O2max, measured during whole-body dynamic exercise, is
limited by oxygen delivery (not muscle mitochondria).
Shephard (76) has asked, “If we reject the view that there
is a significant limitation of oxygen transport at the tissue
level, what alternative explanation can be offered to the
teleologists to account for the doubling of tissue enzyme
activity during endurance training?” In their landmark 1984
review paper, Holloszy and Coyle (44) propose an answer to
this question. They argue that as a consequence of the
increase in mitochondria, exercise at the same work rate
elicits smaller disturbances in homeostasis in the trained
muscles. Two metabolic effects of an increase in mitochon-
drial enzymes are that 1) muscles adapted to endurance
exercise will oxidize fat at a higher rate (thus sparing muscle
glycogen and blood glucose) and 2) there is decreased
lactate production during exercise. These muscle adapta-
tions are important in explaining the improvement in en-
durance performance that occurs with training. (This will be
discussed further in Part III.)
The main effect of increasing mitochondrial enzymes is
to improve endurance performance rather than to increase
V˙ O2max. Holloszy and Coyle (43,44) note that even in
individuals with nearly identical V˙ O2max values there can be
a two-fold range in mitochondrial enzymes (1976). Further-
more, low-intensity training may elicit small changes in
mitochondrial enzymes without any change in V˙ O2max, and
vice versa (38,52,64). On the other hand, there is some
evidence that the increase in mitochondria play a permissive
role in allowing V˙ O2max to increase. Holloszy and Coyle
(44) note that the lowest value for SDH activity in the elite
runners studied by Costill (16) was still 2.5-fold greater than
that found for untrained individuals in the same study. The
increase in muscle mitochondria may allow a slightly
greater extraction of O2 from the blood by the working
muscles, thus contributing in a minor way to an increased
V˙ O2max (44).
Capillary density. In 1977 Andersen and Henriksson
(1) showed that capillary density increases with training.
Other studies noted a strong relationship between the num-
ber of capillaries per fiber in the vastus lateralis and V˙ O2max
(mL⅐kgϪ1
⅐minϪ1
) measured during cycle ergometery (72).
The main significance of the training-induced increase in
capillary density is not to accommodate blood flow but
rather to maintain or elongate mean transit time (70). This
enhances oxygen delivery by maintaining oxygen extraction
(a-v៮ O2 difference) even at high rates of muscle blood flow.
The ability of skeletal muscle to adapt to training in this way
is far greater than what is observed in the lung (24).
Central or Peripheral Limitation?
The issue of central versus peripheral factors limiting
V˙ O2max has been a long-standing debate. Work conducted in
the early 1970s supported the idea of central factors being
limiting for V˙ O2max. Clausen et al. (12) showed that two-
legged bicycle training resulted in an increase in arm
V˙ O2max. They correctly interpreted this as evidence of a
central cardiovascular training effect.
In 1976 Saltin et al. (73) examined the effects of one-
legged cycle training on the increase in V˙ O2max in a trained
leg, a control leg, and 2-legged bicycling. The trained leg
had a 23% increase compared with a 7% increase in V˙ O2max
in the control leg (Fig. 8). The disparity between legs was
attributed to peripheral adaptations occurring within the
trained skeletal muscle. The authors concluded that periph-
eral factors were dominant in limiting V˙ O2max. This study
was conducted during the 1970s as new discoveries about
fiber type, capillary density, and oxidative enzyme activities
in athletes were being made. At that time, the investigators
thought that these changes were essential for increasing
V˙ O2max (73).
However, in 1985 Saltin et al. (70) performed the defin-
itive experiment showing that V˙ O2max is limited by blood
flow. They observed what happens when a subject does
maximal exercise using only a small muscle mass (i.e., knee
extensions with only one leg). This allowed a greater pro-
portion of cardiac output to be directed to an isolated area.
Under these conditions, the highest O2 uptake in an isolated
quadriceps muscle group was 2–3 times higher than that
measured in the same muscle group during a whole-body
maximum effort. They concluded that skeletal muscle has a
tremendous capacity for increasing blood flow and V˙ O2
(70), which far exceeds the pumping capacity of the heart
during maximal whole-body exercise. This experiment
proved that V˙ O2max is constrained by oxygen delivery and
not by the mitochondria’s ability to consume oxygen.
How can we reconcile the results of the two experiments
by Saltin et al. (70,73)? In the earlier study, they measured
V˙ O2max during one-legged cycling. However, it must be
remembered that maximal cardiac output is not the domi-
nant factor limiting V˙ O2max in exercise with an isolated
muscle group (i.e., one-legged cycling) (66). Whole-body
V˙ O2max is primarily limited by cardiac output, while for
exercise with small muscle groups the role of cardiac output

is considerably less important (10). Since the 1976 conclu-
sion about peripheral limitations does not apply to V˙ O2max
measured in severe whole-body exercise, the later conclu-
sion does not conflict with their earlier work. The current
belief is that maximal cardiac output is the principal limiting
factor for V˙ O2max during bicycling or running tests (66).
Comparative Physiology and Maximum
Oxygen Uptake
Taylor et al. (79,80,82) and Weibel (87) have studied the
physiological factors limiting V˙ O2max from a different per-
spective. They examined different animal species to see
what physiological factors explain the superior V˙ O2max of
the more athletic ones. These studies in comparative phys-
iology provide a way to test the concept of “symmorphosis”
which hypothesizes that animals are built in a reasonable
manner. Their underlying assumption is that all parts of the
pathway for O2 (from atmosphere to mitochondria) are
matched to the functional capacity of the organism. If any
one system involved in the O2 pathway were overbuilt, then
there would be a redundancy that would be wasteful, from
an energetic standpoint.
The first series of experiments compared mammalian
species of similar size, but with a 2.5-fold difference in
V˙ O2max (dog vs goat, racehorse vs steer) (49,81). This is
referred to as “adaptive variation” (adaptation was defined
in the evolutionary sense, as the end-result of natural selec-
tion). The high V˙ O2max values in the more athletic species
were accompanied by a 2.2-fold increase in stroke volume,
nearly identical maximal heart rate, and a large increase in
mitochondria (49,81). In general, these adaptive pairs show
similar physiological differences as observed when trained
and untrained humans are compared (Table 1).
A second series of experiments examined a variety of
animal species ranging in size from a few grams to 250 kg
(79). The difference in V˙ O2max seen in animals of varying
body mass (Mb) is termed “allometric variation.” V˙ O2max
values (L⅐minϪ1
) increase with body mass to the power of
0.81. However, when adjusted for body mass, small animals
have V˙ O2max/Mb values that are 8–10 times higher than
large animals (Fig. 9). Across a wide range of animal
species, there is a very close match between mitochondrial
density and V˙ O2max/Mb (80). The smaller species have an
abundance of mitochondria, so that the capacity of the
muscles to consume oxygen is enhanced. It would be im-
possible for the smaller species to achieve such incredibly
high metabolic rates (200 to 260 mL⅐kgϪ1
⅐minϪ1
) without
an increase in mitochondrial density. Thus, it can be said
that the muscles “set the demand for O2 ” (80).
The more athletic animals also have an increase in the
size of the structures involved in supplying O2 to the work-
ing muscles. Lung size and function are scaled in proportion
to V˙ O2max. In addition, the heart’s pumping capacity is
tightly coupled to V˙ O2max. In adaptive variation (animals of
same size), the more athletic animals achieve this by an
increase in heart size (80). In allometric variation, small
animals achieve an increase in O2 transport with a higher
maximal heart rate (1300 beats⅐minϪ1
in the shrew) ((87), p.
400). The general conclusion of these studies is that the
principle of symmorphosis is upheld (80). The structures
involved in the O2 pathway are scaled in proportion to
V˙ O2max, meaning that animals are built in a reasonable
manner (88).
However, there are exceptions where one sees redundan-
cies at various levels in the pathway for O2. For example,
the mitochondria’s ability to consume O2 exceeds the ability
of the cardiorespiratory system to supply it (80). To illus-
trate this point, in maximally exercising animals the mito-
chondria have a fixed respiratory capacity, with an invariant
value of 4–5 mL O2⅐mLϪ1
of mitochondria per minute
across species (80). However, the respiratory capacity of
isolated mitochondria has been measured at 5.8 mL
O2⅐mLϪ1
of mitochondria per minute (75). Using these
values, Taylor and Weibel (80) conclude that animals are
able to exploit 60–80% of the in vitro oxidative capacity
when they exercise at V˙ O2max. The reason that mitochondria
cannot fully exploit their oxidative ability is a result of the
limitation on O2 delivery imposed by the central cardiovas-
cular system.
Reaching Consensus on Limiting Factors for
Maximum Oxygen Uptake
Physiologists have often asked, “What is the limiting
factor for V˙ O2max?” The answer depends on the definition of
Figure 8—Effects of one-legged cycle training on V˙ O2max in the
trained leg, untrained control leg, and both legs. Training consisted of
four to five sessions of endurance training at 75% V˙ O2max (1 leg),
35–45 min per session, for 4 wk. This study provided support for the
role of peripheral adaptations. From reference 73. Saltin, B., K. K.
Nazar, D. L. Costill, et al. The nature of the training response: periph-
eral and central adaptations to one-legged exercise. Acta Physiol.
Scand. 96:289–305, 1976. Used with permission.

a limiting factor and the experimental model used to address
the problem (R.B. Armstrong, personal communication,
February, 1999). If one talks about the intact human being
performing maximal, whole-body exercise, then the cardio-
respiratory system is the limiting factor (36,74,84). If one
discusses the factors that limit the increase in V˙ O2 in an
isolated dog hindlimb, then the peripheral diffusion gradient
is limiting (45). If one talks about the factors that explain the
difference in V˙ O2max across species, mitochondrial content
and O2 transport capacity are both important (80).
Wagner, Hoppeler, and Saltin (86) have succeeded in
reconciling the different viewpoints on factors limiting
V˙ O2max. They conclude that while V˙ O2max is broadly related
to mitochondrial volume across a range of species, in any
individual case V˙ O2max is determined by the O2 supply to
muscle. They state that in humans “. . . the catabolic capac-
ity of the myosin ATPase is such that it outstrips by far the
capacity of the respiratory system to deliver energy aerobi-
cally. Thus, V˙ O2max must be determined by the capability to
deliver O2 to muscle mitochondria via the O2 transport
system, rather than by the properties of the muscle’s con-
tractile machinery (86).”
Wagner, Hoppeler, and Saltin (86) maintain that there is
no single limiting factor to V˙ O2max. They conclude that “. . .
each and every step in the O2 pathway contributes in an
integrated way to determining V˙ O2max , and a reduction in
the transport capacity of any of the steps will predictably
reduce V˙ O2max (85,86).” For instance, a reduction in the
inspired PO2 at altitude will result in a decreased V˙ O2max
(22,31,53). A reduced hemoglobin level in anemia will
result in a decreased V˙ O2max (36,78). A reduction in cardiac
output with cardioselective beta-blockade will result in a
decreased V˙ O2max (84). There are also instances where
substrate supply (not O2) is the limiting factor. For example,
metabolic defects in skeletal muscle, such as McArdle’s
disease (phosphorylase deficiency) or phospho-fructokinase
deficiency, will result in a decreased V˙ O2max (54).
In the field of exercise physiology, when limiting factors
for V˙ O2max are discussed, it is usually with reference to
human subjects, without metabolic disease, undergoing
maximal whole-body exercise, at sea level. Under these
conditions, the evidence clearly shows that it is mainly the
ability of the cardiorespiratory system (i.e., heart, lungs, and
blood) to transport O2 to the muscles, not the ability of
muscle mitochondria to consume O2, that limits V˙ O2max .
We conclude that there is widespread agreement with regard
to the factors limiting V˙ O2max, and that this agreement is
based on sound scientific evidence. In general, the 75 years
of subsequent research have provided strong support for the
brilliant insights of Hill et al. (41,42).
PART III: DETERMINANTS OF
ENDURANCE PERFORMANCE
A first principle in exercise physiology is that work
requires energy, and to maintain a specific work rate or
running velocity over a long distance, ATP must be supplied
to the cross bridges as fast as it is used. As the duration of
an all-out performance increases there is greater reliance on
ATP production via oxidative phosphorylation to maintain
cross bridge cycling. Consequently, the rate at which oxy-
gen is used during prolonged submaximal exercise is a
measure of the rate at which ATP is generated. In our
previous paper (5) we summarized the conventional under-
standing of how oxygen uptake is linked to endurance
running performance. A variety of criticisms were directed
at our attempt, ranging from suggestions that correlation
data were being used to establish “cause and effect,” to
concerns that our model was not adequately explained (63).
In the following paragraphs we will summarize the physi-
ological model linking oxygen uptake with performance in
distance running.
Figure 10 shows that the V˙ O2 maintained during an
endurance run (called the “performance V˙ O2 ” by Coyle
(19)) is equal to the product of the runner’s V˙ O2max and
the percent of V˙ O2max that can be maintained during the
Figure 9—Maximum oxygen uptake (V˙ O2max/Mb in mL⅐kg؊1
⅐min؊1
)
of various animal species in relation to body mass (Mb). The smaller
animals have incredibly high V˙ O2max/Mb values, which are made
possible by an increased mitochondrial density (which enables their
muscles to consume more oxygen) as well as an increased capacity for
oxygen transport.
TABLE 1. Body mass and oxygen transport parameters of the cardiovascular system in horses and steers, during maximal exercise (mean Ϯ SD). Adapted from Jones et al.
(J. Appl. Physiol. 67:862–870, 1989).
Body mass
(kg)
V˙O2max
(mL ⅐ kg؊1
⅐ min؊1
)
HRmax
(beats ⅐ min؊1
)
COmax
(L ⅐ min؊1
)
Ca-v O2
(ml O2 ⅐ L blood؊1
) Hct (%)
Horses (N ϭ 4) 453 Ϯ 34 134 Ϯ 2 202 Ϯ 7 288 Ϯ 22 213 Ϯ 13 55 Ϯ 2
Steers (N ϭ 3) 449 Ϯ 9 51 Ϯ 1 216 Ϯ 5 143 Ϯ 1 161 Ϯ 3 40 Ϯ 2
V˙O2max, maximum oxygen uptake; HRmax, maximal heart rate; COmax, maximal cardiac output; Ca-v O2
, maximum arterio-venous oxygen difference; Hct, hematocrit.

performance. The percent of V˙ O2max is related to the V˙ O2
measured at the lactate threshold (LT), so that for endur-
ance events the performance V˙ O2 is closely linked to the
V˙ O2 at the LT. The V˙ O2max is limited primarily by central
cardiovascular factors (see Part II above), while the per-
cent of V˙ O2max that can be maintained is linked primarily
to adaptations in muscles resulting from prolonged train-
ing (44). The actual running velocity realized by this rate
of oxidative ATP generation (the performance V˙ O2) is
determined by the individual’s ability to translate energy
(e.g., running economy) into performance (19,20). We
will again summarize the role of each of these variables
in distance running performance.
Role of Maximum Oxygen Uptake in
Running Performance
Previously we stated that “V˙ O2max sets the upper limit for
performance in endurance events” (5), not that it is “the best
predictor of athletic ability” ((63), p. 1381). Data of Costill
et al. (17) were presented to show an inverse correlation (r ϭ
Ϫ0.91) between V˙ O2max and time in a 10-mile run. These
investigators used subjects with a wide range of V˙ O2max
values (54.8 to 81.6 mL⅐kgϪ1
⅐minϪ1
) to examine this rela-
tionship. This was an appropriate research design to see
whether a correlation existed between these two variables in
that such a relationship must be evaluated over an appro-
priate range of values. If one were to narrow the range of
values over which this relationship was examined, the cor-
relation coefficient would approach zero as the range of
values approaches zero. Consequently, we acknowledged
the fact that V˙ O2max was not a good predictor of perfor-
mance in runners with similar V˙ O2max values ((5) p. 598). If
Costill et al. (17) had found the correlation between V˙ O2max
and time in a 10-mile run in this diverse group of runners to
be r ϭ Ϫ0.09 rather than r ϭ Ϫ0.91, there would have been
little debate. We are in agreement that a high correlation
does not imply “cause and effect;” however, to simply
dismiss a high correlation between two variables having
high construct validity might result in an investigator miss-
ing an important point.
V˙ O2max is directly linked to the rate of ATP generation
that can be maintained during a distance race, even though
distance races are not run at 100% V˙ O2max. The rate of ATP
generation is dependent on the V˙ O2 (mL⅐kgϪ1
⅐minϪ1
) that
can be maintained during the run, which is determined by
the subject’s V˙ O2max and the percent of V˙ O2max at which the
subject can perform (Fig. 10). For example to complete a
2:15 marathon, a V˙ O2 of about 60 mL⅐kgϪ1
⅐minϪ1
must be
maintained throughout the run. Consequently, even if a
marathon could be run at 100% V˙ O2max, the runner would
need a V˙ O2max of 60 mL⅐kgϪ1
⅐minϪ1
for the above perfor-
mance. However, since the marathon is typically run at
about 80–85% of V˙ O2max, the V˙ O2max values needed for
that performance would be 70.5–75 mL⅐kgϪ1
⅐minϪ1
. In this
way V˙ O2max sets the upper limit for energy production in
endurance events but does not determine the final perfor-
mance. As we stated in the previous article (5) there is no
question that runners vary in running economy as well as in
the percent of V˙ O2max that can be maintained in a run; both
have a dramatic impact on the speed that can be maintained
in an endurance race. These will be discussed in the fol-
lowing paragraphs.
Running Economy
Mechanical efficiency is the ratio of work done to energy
expended. The term “running economy” is used to express
the oxygen uptake needed to run at a given velocity. This
can be shown by plotting oxygen uptake (mL⅐kgϪ1
⅐minϪ1
)
versus running velocity (m⅐minϪ1
) or by simply expressing
economy as the energy required per unit mass to cover a
horizontal distance (mL O2⅐kgϪ1
⅐kmϪ1
). In our previous
paper we showed that running economy explains some of
the variability in distance running performance in subjects
with similar V˙ O2max values (5). Data from Conley and
Krahenbuhl (14) were used to show a relatively strong
correlation (r ϭ 0.82) between running economy and per-
formance in a 10-km run in a group of runners with similar
V˙ O2max values but with a range of 10-km times of 30.5–33.5
min. As was pointed out in the rebuttal (63), when one
examines the fastest four runners (10 km in 30.5–31 min)
there was considerable variability in the economy of run-
ning (45–49 mL⅐kgϪ1
⅐minϪ1
at 268 m⅐minϪ1
), suggesting a
lack of association between the variables. As mentioned
above, this is to be expected. A correlation coefficient will
approach zero as the range of values for one of the variables
(in this case, performance times ranging from 30.5 to 31
min) approaches zero. There is little point in looking at a
correlation unless the range of values is sufficient to deter-
mine whether a relationship exists.
There is a linear relationship between submaximal run-
ning velocity and V˙ O2 (mL⅐kgϪ1
⅐minϪ1
) for each individ-
ual. However, there is considerable variation among indi-
viduals in how much oxygen it costs to run at a given speed,
Figure 10—Simplified diagram of linkages between maximal aerobic
power (V˙ O2max ), the percent of maximal aerobic power (% V˙ O2max)
and running economy as they relate to distance running performance.

that is, running economy (6,59). Figure 11 shows a bar
graph of the variation in running economy (expressed in
mL⅐kgϪ1
⅐kmϪ1
) among groups that differ in running ability
(59). The group of elite runners had a better running econ-
omy than the other groups of runners, and all running groups
were better than the group of untrained subjects. However,
one of the most revealing aspects of this study was the
within-group variation; there was a 20% difference between
the least and most economical runner in any group (59).
One of the best descriptions of how V˙ O2max and run-
ning economy interact to affect running velocity was
provided by Daniels (20) in his description of “velocity at
V˙ O2max” (vV˙ O2max). Figure 12 shows a plot of male and
female runners equal in terms of V˙ O2max, but differing in
running economy (21). A line was drawn through the
series of points used to construct an economy-of-running
line, and was extrapolated to the subject’s V˙ O2max. A
perpendicular line was then drawn from the V˙ O2max value
to the x-axis to estimate the velocity that subject would
have achieved at V˙ O2max. This is an estimate of the
maximal speed that can be maintained by oxidative phos-
phorylation. In this example, the difference in running
economy resulted in a clear difference in the speed that
could be achieved if that race were run at V˙ O2max. In like
manner, Figure 13 shows the impact that a difference in
V˙ O2max has on the vV˙ O2max in groups with similar run-
ning economy values. The 14% difference in V˙ O2max
resulted in a 14% difference in the vV˙ O2max. Conse-
quently, it is clear that both V˙ O2max and running economy
interact to set the upper limit of running velocity that can
be maintained by oxidative phosphorylation. However,
since distance races are not run at V˙ O2max, the ability of
the athlete to run at a high percentage of V˙ O2max has a
significant impact on running performance (17).
Percent of Maximum Oxygen Uptake
Figure 14, from the classic Textbook of Work Physiology
by Åstrand and Rodahl (3) characterizes the impact that
training has on one’s ability to maintain a certain percentage
of V˙ O2max during prolonged exercise. Trained individuals
functioned at 87% and 83% of V˙ O2max for 1 and 2 h,
respectively, compared with only 50% and 35% of V˙ O2max
for the untrained subjects. This figure shows clearly the
impact that the % V˙ O2max has on the actual (performance)
V˙ O2 that a person can maintain during an endurance per-
formance. In addition, Figure 15, taken from the same text,
shows how V˙ O2max and the % V˙ O2max change over months
of training. V˙ O2max increases during the first 2 months and
levels off, while the % V˙ O2max continues to change over
time. Consequently, while changes in both V˙ O2max and the
% V˙ O2max impact changes in the performance of a subject
early in a training program, subsequent changes in the
performance V˙ O2 are caused by changes in the % V˙ O2max
alone. This classic figure is supported by later work showing
that the V˙ O2 at the LT (%V˙ O2max at the LT) increases much
Figure 11—Minimum, mean, and maximum aerobic demand running
economy values for elite runners (Category 1), subelite runners (Cat-
egory 2), good runners (Category 3), and untrained subjects (Category
4). From reference 59. Morgan, D. W., D. R. Bransford, D. L. Costill,
et al. Variation in the aerobic demand of running among trained and
untrained subjects. Med. Sci. Sports Exerc. 27:404–409, 1995. Used
with permission.
Figure 12—Comparison of male and female runners of equal V˙ O2max.
The males are significantly favored in economy and in v V˙ O2max (P <
0.05). From reference 21. Daniels, J. and N. Daniels. Running economy
of elite male and elite female runners. Med. Sci. Sports Exerc. 24:483–
489, 1992. Used with permission.
Figure 13—Comparison of male and female runners of equal running
economy, over common test velocities. Males are favored in V˙ O2max
and in v V˙ O2max (P < 0.05). From reference 21. Daniels, J. and N.
Daniels. Running economy of elite male and elite female runners. Med.
Sci. Sports Exerc. 24:483–489, 1992. Used with permission.

more as a result of training than does V˙ O2max (see review in
(89) p. 59).
The Lactate Threshold and
Endurance Performance
The model presented earlier in Figure 10 showed how
V˙ O2max and % V˙ O2max interact to determine the perfor-
mance V˙ O2 and how running economy shapes the final
performance. In this model the V˙ O2 at the LT integrates
both V˙ O2max and the % V˙ O2max. In our previous paper (5)
we used a more detailed model to show that running velocity
at the LT integrates all three variables mentioned earlier (the
V˙ O2max, the %V˙ O2max, and running economy) to predict
distance running performance. We will now use that same
model (Fig. 16) to expand our discussion with a focus on the
lactate threshold.
To determine a lactate threshold, a subject completes a
series of tests at increasing running speeds, and after each
test a blood sample is taken for lactate analysis. The speed
at which the lactate concentration changes in some way
(e.g., to an absolute concentration, a break in the curve, a
delta amount) is taken as the speed at the LT and is used as
the predictor of performance. Numerous studies have shown
the various indicators of the LT to be good predictors of
performance in a variety of endurance activities (e.g., run-
ning, cycling, race walking) and for both trained and un-
trained populations ((89) p. 49). In most of these studies the
association between the LT and endurance performance was
evaluated in groups of athletes that were heterogeneous
relative to performance. As discussed earlier, this is an
appropriate design to see whether a relationship (correla-
tion) exists between the variables. On the other hand, if one
were to narrow the range of performances (or the LT) over
which this relationship were examined, one would expect
the correlation to be markedly reduced. This means that
even though the speed at the LT explains the vast majority
of the variance in performance in distance races (30) other
factors can still influence the final performance. If any
model could explain all of the variance in performance, gold
medals would be handed out in the lab!
The classical model that has been passed down to us
revolves around the proposition that the ability to maintain
a high running speed is linked to the ability to maintain a
high rate of oxidative ATP production. Both logic and
empirical data provide support for that proposition; to argue
otherwise would suggest that “oxygen independent” (anaer-
obic) sources of ATP are important in such perfor-
mances—a clear impossibility given the small amount of
potential energy available via those processes.
It has been known for some time (43,44) that lactate
production is related to a number of variables, including the
mitochondrial content of muscle, as measured by mitochon-
drial enzyme activity. Variations in the LT across diverse
groups of endurance athletes and improvements in the LT
resulting from training are linked to differences and in-
creases in mitochondrial enzyme activity, respectively ((19),
(89), p. 49–59). An explanation for this connection was
provided by Holloszy and Coyle in 1984 (44). When mus-
cles contract to meet a specific submaximal power output,
ATP is converted to ADP and Pi to power the cross bridges,
and the latter two, in turn, drive metabolic reactions in the
cell to meet the ATP demand associated with that work rate.
In a muscle cell with relatively few mitochondria the ADP
concentration must rise to a high level to drive the limited
number of mitochondria to meet the ATP demand via oxi-
dative phosphorylation. This high concentration of ADP
also drives other metabolic pathways, including glycolysis,
because of the stimulatory effect of ADP on phosphofruc-
tose kinase (PFK). This results in a greater rate of carbo-
hydrate turnover, an accumulation of pyruvate and NADH
in the cytoplasm of the muscle fiber, and an increase in
lactate production (44,50). Following training there is a
large (50–100%) increase in the number of mitochondria in
Figure 14—A graphic illustration based on a few observations show-
ing approximately the percentage of a subject’s maximal aerobic
power he/she can tax during work of different duration and how this
is affected by training state. From reference 3. Åstrand, P.-O. and K.
Rodahl. Textbook of Work Physiology. New York: McGraw-Hill, 1970,
pp. 279–430. Used with permission.
Figure 15—Training causes an increase in maximal oxygen uptake.
With training a subject is also able to tax a greater percentage of
his/her maximal oxygen uptake during prolonged work. From refer-
ence 3. Åstrand, P.-O. and K. Rodahl. Textbook of Work Physiology.
New York: McGraw-Hill, 1970, pp. 279–430. Used with permission.

the muscles involved in the activity. Consequently, at the
same work rate the oxygen uptake is shared by a greater
number of mitochondria, and the ADP concentration does
not have to rise to the same level as before training to
achieve the same rate of oxidative phosphorylation (V˙ O2)
after training. The lower level of ADP after training results
in less stimulation of PFK and a reduction in carbohydrate
turnover, and the greater number of mitochondria increases
the capacity to use fat as a fuel. The result is less lactate
formation (44).
As we mentioned throughout this section, the relation-
ships between V˙ O2max and performance (15), running econ-
omy and performance (14), and % V˙ O2max and performance
(30) used groups with large variations in the independent
variables. As one reduces the range of each of these vari-
ables, the correlations are reduced in magnitude or elimi-
nated, suggesting that other variables also influence perfor-
mance. Instead of dismissing the relationships as having
little worth, investigators have used these observations as
motivation to examine other factors that might be related to
endurance performance. An excellent example of taking the
next step is found in an experiment by Coyle et al. (18).
Coyle et al. (18) studied 14 trained cyclists (3–12 yr of
training) who were similar in terms of V˙ O2max (thus elim-
inating that as a variable) to examine the relationship be-
tween the LT and time to fatigue at 88% V˙ O2max. Subjects
were divided into high-LT (mean ϭ 81.5% V˙ O2max ) and
low-LT (mean ϭ 65.8% V˙ O2max) groups. The performance
test at 88% V˙ O2max resulted in large differences in perfor-
mance (60.8 vs 29.1 min), and the postexercise lactate
concentration (7.4 vs 14.7 mM) for the high-LT and low-LT
groups, respectively. The difference in performance be-
tween these groups that had the same V˙ O2max, but differed
in the % V˙ O2max at the LT, was consistent with the model
described above. On the other hand, the fact that the vastus
lateralis of both groups had the same mitochondrial enzyme
activities suggested a break in the chain of evidence linking
the % V˙ O2max at the LT and mitochondrial activity. This
created a rare opportunity for the investigators to study two
groups with the same V˙ O2max and the same mitochondrial
enzyme activity but with substantial differences in perfor-
mance. The investigators examined the metabolic response
of the cyclists to a 30-min test at 79% V˙ O2max. They found
that while the low-LT group used 69% more carbohydrate
during this exercise bout than the high-LT group, the
low-LT group reduced its vastus lateralis muscle glycogen
concentration 134% more than the high-LT group. This
difference in muscle glycogen depletion (relative to total
carbohydrate oxidation) suggested that the high-LT group
was able to distribute the same work rate (and V˙ O2) over a
larger muscle mass, resulting in less loading on the muscle
fibers recruited to do the work. Use of a larger muscle mass
also increased the mass of mitochondria sharing in the
production of ATP by oxidative phosphorylation ((18,19)
and (87) p. 131). Consequently, the study of Coyle et al. (18)
indicates that the mass of muscle involved in the activity (in
addition to mitochondrial density) contributes to the %
V˙ O2max at the LT (as well as performance), in a manner
consistent with the above model.
LT, THE CLASSICAL MODEL, AND
ENVIRONMENTAL FACTORS
Noakes has asked, “. . . why should prolonged endurance
exercise in which the oxygen consumption is not maximal
and therefore not limiting be determined by the oxygen
delivery to the active muscle?” ((63) p. 1393). This is a good
question because a marathon runner can certainly run at
faster speeds and higher V˙ O2 values over shorter distanc-
es—but not without some metabolic consequences. During
submaximal exercise, oxygen delivery to muscle is closely
tied to the mitochondrial oxygen demand which is driven by
the cellular charge (i.e., [ADP ϩ Pi]) provided by the
exercise. As mentioned earlier, this same cellular charge
also drives other metabolic pathways, notably, glycolysis. If
a marathoner chose to run at a speed above the LT, the
increased cellular charge needed to drive the V˙ O2 to the
higher level would also speed up glycolysis. This would
deplete the limited carbohydrate store at a faster rate; the
resulting increase in blood lactate accumulation would be
caused by both an increase in lactate formation and a de-
crease in lactate removal (7,50). Given the obligatory need
for carbohydrate at high exercise intensities (13) and the
negative impact of hydrogen ion accumulation on muscle
function (29,56,57,60), neither of these changes are consis-
tent with being able to maintain the faster pace over a
marathon distance.
In this and our previous paper (5) we attempted to explain
how the variables of V˙ O2max, the percentage of V˙ O2max, and
running economy can account for the vast majority of the
variance in distance running performances (30,89). In addi-
tion, the model also accounts for the impact of certain
environmental factors on endurance performance. Acute
exposure to moderate altitude results in a decrease in arterial
oxygen saturation and V˙ O2max (22,53). Consequently, the
“performance V˙ O2” is decreased even though runners can
still perform at a similar percentage of V˙ O2max, and perfor-
mance in endurance events is adversely affected (22,31).
Figure 16—Summary of the major variables related to V˙ O2max and
the maximal velocity that can be maintained in distance races. From:
Bassett, D. R., Jr. and E. T. Howley. Maximal oxygen uptake: “clas-
sical” versus “contemporary” viewpoints. Med. Sci. Sports Exerc. 29:
591–603, 1997. Used with permission.

Historically, this effect of a lower PO2 causing a shift in the
LT was interpreted as an “oxygen lack” at the muscle.
However, it is now recognized that the lower PO2 results in
a higher cellular charge to achieve the same steady state
V˙ O2 at a fixed submaximal work rate (50). These circum-
stances will result in a higher rate of glycolysis, an accu-
mulation of NADHϩ
, and an increase in lactate production.
Performance times in the marathon are adversely affected
by high environmental temperatures, with race times being
optimal at a temperature of 12–13°C (34), and a decrement
of 40 s expected for every 1°C rise in temperature (33).
Exercise in the heat increases the rate of carbohydrate ox-
idation, leading to a faster rate of muscle glycogen depletion
and higher blood lactate concentrations during prolonged work
(32). Consequently, changes in metabolism resulting from
acute exposure to heat or altitude are associated with a decrease
in endurance performance, consistent with the model.
Postscript
In summary, the “classical” model of V˙ O2max passed
down by Hill et al. (41,42) has been modified and expanded
upon by numerous investigators. We now have a much more
complete understanding of the determinants of endurance
performance than did exercise scientists from the 1920s. In
hindsight, Hill et al. (41,42) were wrong about some of the
details, such as the notion of a strict 1:1 ratio of O2 defi-
cit:O2 debt. However, Hill deserves recognition for his
major role in the discovery of nonoxidative pathways in
isolated frog muscle and the application of this discovery to
the exercising human (9,51). Hill’s work shaped the emerg-
ing discipline of Exercise Physiology (37,48), and his ideas
continue to be influential even to this day.
Hill welcomed challenges to his theories and urged others
to critically analyze scientific beliefs ((40) p. 363). It is clear
that he viewed errors in interpretation and scientific debate
over the merits of competing theories to be a necessary part
of progress ((51) p. 82). In Trails and Trials in Physiology,
Hill stated that, “Knowledge advances by continual action
and reaction between hypothesis on the one hand and ob-
servation, calculation, and experiment on the other ((40), p.
361).” In contrast to the view that the classical theory
represents an “ugly and creaking edifice” (62), we have
arrived at a very different point of view. Our conclusion is
that Hill’s theories have served as an ideal theoretical frame-
work. The work that has built upon this framework has
allowed exercise scientists to learn much about the physio-
logical factors governing athletic performance.
Support was provided by the University of Tennessee, Knoxville,
Exhibit, Performance, and Publication Expense (EPPE) Fund.
Address for correspondence: David R. Bassett, Jr., Department
of Exercise Science and Sport Management, University of Tennes-
see, 1914 Andy Holt Ave., Knoxville, TN 37996. E-mail:
DBassett@utk.edu
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