Bassett (1997) Maximal - Oxygen - Uptake - Classical - Vs - Contemporary - Viewpoints

Ovid: BASSETT: Med Sci Sports Exerc, Volume 29(5).May 1997.
591-603 Page 1 of 27
© Williams & Wilkins 1997. All Rights Reserved. Volume 29(5), May 1997, pp 591-603
Maximal oxygen uptake: “classical”

versus“contemporary” viewpoints
[1996 J.B. Wolffe Memorial Lecture: Response to the Challenge]
BASSETT, DAVID R. JR.; HOWLEY, EDWARD T.
Exercise Science Unit, University of Tennesee, Knoxville, TN 37919

Submitted for publication January 1997.
Accepted for publication January 1997.
Support was provided by the Exhibit, Performance and Publication Expense
fund of the UTK office of Research Administration.
Address for correspondence: David R. Bassett, Exercise Science Unit, 1914
Andy Holt Ave., Knoxville, TN 37919. E-mail: DBassett@utk.edu.
ABSTRACT
The traditional view of ·VO2max owes a great deal to the work of A. V. Hill, who conducted
experiments on exercising man in Manchester, England, in the 1920's. Hill and colleagues proposed that
there is an upper limit to oxygen uptake (·VO2max), that there are inter-individual differences in this
variable, and that ·VO2max is limited by the circulatory and/or respiratory systems. They demonstrated
that oxygen uptake increases linearly with running speed, but in some subjects it eventually“reaches a
maximum beyond which no effort can drive it,” a phenomenon now referred to as the ·VO2 plateau. In
recent years, Timothy Noakes has strongly criticized Hill's concept of ·VO2max. He maintains that the
absence of a ·VO2 plateau in some subjects is proof that oxygen delivery is not a limiting factor for
·VO2max. This view fails to recognize that the plateau is not the principal evidence for a cardiorespiratory
limitation. Noakes rejects the ·VO2max paradigm of A.V. Hill in its entirety. The alternative paradigm he
proposes is that endurance performance is limited by “muscle factors.” Noakes suggests that the best
distance runners have muscle characteristics that allow them to achieve higher running speeds, and
since running speed is linearly related to oxygen uptake, an indirect consequence of this is that they will
have higher ·VO2max values. This is exactly the opposite of how the relationship between ·VO2max and
running speed at the end of a maximal exercise test should be viewed. Noakes offers little evidence to
support his views, and they conflict with a vast body of scientific evidence showing that oxygen
transport is a major determinant of endurance performance. After carefully reviewing the evidence on
both sides of the issue, we conclude that the older “classical” ·VO2max paradigm of A.V. Hill is the correct
one.
Over the past nine years, Dr. Tim Noakes has proposed some controversial new ideas concerning
the factors that limit maximal oxygen uptake (·VO2max), and the importance of ·VO2max in endurance
performance. The primary outlets for these ideas have been an article in Medicine and Science in Sports
and Exercise entitled“Implications of exercise testing for prediction of athletic performance: a
contemporary perspective” (52), his popular book Lore of Running (53), and the J. B. Wolffe Memorial
Lecture entitled “Challenging Beliefs: There is Always Something New from South Africa” presented at
the 1996 American College of Sports Medicine conference (54).
Dr. Noakes is a South African M.D., whose interest in athletics led him to take up the study of
exercise physiology. He has stated that being“self-taught” in the latter field may have freed him from
some of the constraints of conventional thinking, allowing him to challenge widely held beliefs (54). Over
the years, Noakes has developed radically different views of some of the “central tenets” in exercise
physiology. However, these new interpretations of older concepts appear to conflict with many of the
established studies.
http://gateway.uk.ovid.com/gw1/ovidweb.cgi 29/01/2007
Ovid: BASSETT: Med Sci Sports Exerc, Volume 29(5).May 1997.591-603 Page 2 of 27
We have read these sources carefully and weighed Noakes' arguments against the conventional
thinking. Four of his most controversial views are: 1) that A.V. Hill did not demonstrate a plateau in ·VO2
at higher running speeds, 2) that oxygen transport does not limit ·VO2max, 3) that maximal oxygen
uptake does not limit endurance performance, and 4) that various “muscle factors” (such as skeletal
muscle myosin-ATPase activity and calcium sensitivity) are the primary factors limiting endurance
performance. Noakes himself states that “obviously these ideas are quite heretical, and it will be some
time before they are either proven to be incorrect or are accepted by the international community.”(54,
p. 20).
In the following sections we will respond to some of Noakes' more controversial statements and
contrast them with evidence in support of the classical view. We will begin with a discussion of A.V. Hill's
concept of·VO2max because Noakes' objection to this concept is the foundation of his alternative
hypothesis.
1. A.V. HILL'S CONCEPT OF ·VO2MAX
“...the popular interpretation of the ·VO2max test results may be simplistic and is based on a
fundamental misinterpretation of historical studies.” From Noakes (52).
“Hill, Long, and Lupton...did not establish that the rate of oxygen consumption plateaus during
exercise of increasing intensity.” From Noakes (52).
“There has only been one experimental procedure in which someone has specifically looked for the
real plateau phenomenon, and that study was done by Jonathon Myers and his colleagues in Long
Beach, California.... This is a critically important study and it should be required reading for all exercise
scientists...I would ask you to look at that study because it is the only study in the literature which has
specifically tried to answer the question,`Is there a plateau, a real plateau in oxygen consumption?”'
From Noakes' Wolffe Memorial Lecture (54).
Maximal oxygen uptake (·VO2max) is traditionally defined as the maximal rate at which oxygen can be
taken up and used by the body during exercise (32). Much of our modern day conception of·VO2max can
be attributed to the early work from Hill's physiology laboratory in Manchester, England. Hill (see Fig. 1)
et al. were among the first to describe the concept of an upper limit to the body's ability to consume
oxygen in their 1923 paper on Muscular Exercise, Lactic Acid, and the Supply and Utilization of Oxygen.
Figure 1-Archibald Vivian Hill. Nobel Laureate, 1922. Photograph courtesy of the Nobel
Committee.
“In running the oxygen requirement increases continuously as the speed increases, attaining
enormous values at the highest speeds; the actual oxygen intake, however, reaches a maximum beyond
which no effort can drive it...The oxygen intake may attain its maximum and remain constant merely
because it cannot go any higher owing to the limitations of the circulatory and respiratory
system...” (32).
Another paper in which Hill and his colleagues dealt with the concept of·VO2max was in a 1924
monograph, of the same title. This latter paper is divided into two sections: (A) The relation
between oxygen intake and severity of exertion, and (B) Factors determining the maximum oxygen
intake. In both papers, they suggest that maximal oxygen intake is limited by the cardiovascular and
respiratory systems:
“However much the speed be increased beyond this limit, no further increase in oxygen intake can
occur: the heart, lungs, circulation and the diffusion of oxygen to the active muscle-fibers have attained
their maximum activity. At the higher speeds the requirement of the body for oxygen...cannot be
satisfied...lactic acid accumulates, a continuously increasing oxygen debt being incurred, fatigue and
exhaustion setting in”(31).
Noakes (52,54) criticizes Hill, contending that he lacked the data to show a plateau in ·VO2max with
increasing running speeds. However, Table 1 and Figure 2 show the original data from A.V. Hill's paper
(31). Clearly, A.V. Hill did demonstrate a plateau in himself and also in subject J (whose ·VO2 was nearly
identical at 4.25 and 4.98 m·s-1, despite a marked increase in oxygen requirement). In his 1988 article,
Noakes chose to re-fit Hill's velocity versus ·VO2 data using a linear equation (52). We are puzzled by this
re-interpretation of A.V. Hill's data, since it appears to be biased towards the view that a plateau does
not exist. Hill was not guilty of “circular reasoning” as Noakes suggests, but rather conducted
experiments that clearly demonstrated the ·VO2 plateau.
TABLE 1. Oxygen intake running at different speeds.
Figure 2-Relationship between speed of running and (a) oxygen intake, (b) lung ventilation,
and (c) respiratory quotient. Original graph from reference 31. Hill, A. V., C. N. H. Long, and H.
Lupton. Muscular exercise, lactic acid and the supply and utilisation of oxygen-parts VII-VIII.
Proc. Roy. Soc. B. 97:84-138, 1924.
What has become clear since the time of A. V. Hill is that even under carefully controlled laboratory
conditions a variable percentage (30% to 95%) of subjects will exhibit a plateau in ·VO2 at the end of a
graded exercise test. The percentage achieving a plateau varies with the protocol (27), age of subject
(4,21,66), and whether an absolute plateau criterion or some quantitative cut-off (e.g., 54 mL·min (45);
80 mL·min-1(2,3); and 150 mL·min-1(69)) is used. These latter studies attempted to set a limit around
which a plateau in ·VO2 could be said to have occurred. For the most part these cut-off values, especially
54 and 80 mL·min-1, are within the ability of investigators to measure·VO2 at very high metabolic rates,
especially using 30-s gas collections. An example of a very carefully done study in which the
investigators looked at the plateau issue and other ·VO2max criteria is that of I. Astrand et al. (3), shown
in Figure 3. It is clear that the plateau issue has been addressed by many scientists over the past 40
years.
Figure 3-Relationship of oxygen uptake to work rate during a discontinuous maximal exercise
test, showing that some subjects achieve a plateau whereas others do not. Original data
fromreference 3. Åstrand, I., P.-O.Åstrand, and K. Rodahl. Maximal heart rate during work in
older men. J. Appl. Physiol. 14:562-566, 1959.
Noakes has stated that only one study in the literature has attempted to answer the question of
whether a real plateau phenomenon exists. The study referred to was carried out by Myers et al. (47).
They had six subjects perform maximal treadmill tests using a continuous ramp protocol. Gas exchange
variables were measured by breath-by-breath analysis, and the following sample intervals were
evaluated: 60, 30, 20 15, 10, and 5 s, breath-by-breath, and 3 moving averages. The moving averages
included an eight-breath average, a seven-breath median, and a five-breath average. Their first
conclusion was that the variability in ·VO2 increases with shorter sampling intervals, which supports the
use of longer (i.e., 30-s) sampling intervals. Their second conclusion was that wide variability exists in
the slope of the change in ·VO2 for a given change in external work rate. This was a rather unique and
intricate approach to analyzing data, which had not previously been used. If the slope of the change
in·VO2 were equal to zero, it meant a perfectly linear increase in·VO2 over time. A positive value meant
the rate of increase in·VO2 was less than it had been previously, though·VO2 could still be climbing.
During submaximal exercise the slope of the change in ·VO2 varied about zero, suggesting a fairly linear
increase in ·VO2.
However, in the final 1-2 min of the ramp test, some subjects had values that differed significantly
from zero, indicative of a leveling off in·VO2. Myers et al. (47) noted that only 33% of their subjects (2 of
6) met the criteria for a plateau in ·VO2 established by Taylor et al. (69). This failure to demonstrate a
plateau in all subjects is consistent with previous studies using more conventional open-circuit
spirometry techniques. The authors concluded that the plateau is not a reliable physiological marker for
maximal effort in all subjects. This is precisely the reason that investigators have spent considerable
effort in finding other objective physiological criteria for the determination of ·VO2max (33).
Regardless of whether a particular individual achieves a plateau or not, there is an upper “ceiling” on
the body's ability to take up and utilize oxygen. This measure (·VO2max) does not differ significantly for
continuous versus discontinuous treadmill protocols (38,41,64,67). It is highly repeatable for any given
individual and is accompanied by other variables indicating that failure is imminent. These include a
respiratory exchange ratio above 1.10 and a blood lactate concentration in excess of 8 to 9 mM (for a
review see (33)). Hence, it is clear that termination of a graded exercise test is determined by certain
physiological constraints.
The issue of what limits ·VO2max is where Noakes radically departs from traditional thinking. He
interprets the absence of a plateau in some individuals as a clear indication that oxygen delivery is not
the limiting factor for ·VO2max (52). It is argued that if a plateau does not exist in certain individuals, then
the cardiovascular system must not be limiting (52, p. 323). This leads to the deduction that “muscle
factors” must limit·VO2max. Unfortunately, the theory is flawed because there is a tremendous body of
evidence suggesting that oxygen transport is the limiting factor for ·VO2max (see Section I below).
Noakes fails to see that the evidence for a cardiorespiratory limitation to ·VO2max does not critically
depend on a plateau in ·VO2.
As we will show in the next section, A. V. Hill was correct when he speculated in 1923 that ·VO2max
was limited by the capacity of the cardiovascular and respiratory systems to transport oxygen (32). He
arrived at this viewpoint despite his lack of modern methods for measuring cardiac output (CO), stroke
volume (SV), a-v O2 difference, hemoglobin saturation, and muscle metabolites in the exercising human.
Not only did Hill correctly identify the potential limiting factors for ·VO2max, he even made quantitative
estimates about variables that were beyond his ability to measure in 1923, which later were shown to be
quite accurate. For example, he estimated that during maximal exercise in an athletic subject (·VO2max =
4.0 L·min-1, O2 carrying capacity = 18.5 cc·100 cc blood-1), the arterial blood would be 90% saturated,
the mixed venous blood would be 10-30% saturated, and maximal C.O. would be 27-36 L·min-1. In our
minds, this reaffirms the incredible insights that A. V. Hill had into the physiological functioning of the
human being during exercise. The careful and elegant experiments he performed on exercising man
closely paralleled the work he did in measuring work, heat production, and energy metabolism in
isolated amphibian muscle, for which was awarded the 1922 Nobel Prize for Physiology or Medicine (12).
Hill shared the award with German biochemist Otto Meyerhoff, who conducted experiments to elucidate
the Embden-Meyerhoff pathway(glycolysis).
2. FACTORS LIMITING ·VO2MAX
“It is crucially important to remember that Hill formulated his hypothesis on the basis of a handful of
measurements of expired respiratory gases. He included no measurements of cardiovascular or detailed
respiratory function, or indeed of skeletal muscle metabolism or contractile function, and an unfortunate
consequence of this is that generations of exercise scientists have grown up believing the same-that you
can use respiratory gas analysis to give you answers on the factors that limit human exercise
performance. It's an inherited wisdom that I think is incorrect.” (From Noakes, 1996 Wolffe Memorial
Lecture (54)).
“Another factor potentially limiting the ·VO2max is the maximum rate at which that oxygen can be
transported to the active tissues by the blood. This is measured as the maximum volume of blood that
the heart can pump each minute (the cardiac output) and is calculated in liters per minute. Whether or
not cardiac output limits the ·VO2max has not yet been determined.”
“Despite the close attention of some of the most eminent exercise physiologists in the world, the
question of what limits the ·VO2max is still open and is unlikely to be answered definitively in the near
future.” (From Noakes, Lore of Running(53), p. 21).
Physiologists have closely examined a number of factors that may limit·VO2max, including: 1)
pulmonary diffusion capacity for O2, 2) maximal cardiac output, 3) the peripheral circulation, and 4) the
metabolic capacity of skeletal muscle. Rowell (58) discusses these factors in his text Human Circulation:
Regulation during Physical Stress (see “What limits the Ability to Increase Oxygen Uptake?”). The
potential limiting factors are illustrated in Figure 4. Today, most physiologists believe that the capacity of
the central cardiovascular system to transport oxygen to the tissues is the principal determinant of
·VO2max(58). The evidence for this view is not based on a plateau in oxygen uptake, as Noakes asserts,
but on a large number of scientific experiments which will be discussed.
Figure 4-Potential physiological factors limiting·VO2max. From reference 58. Rowell, L. B.

Human Circulation: Regulation During Physical Stress. New York: Oxford University Press,
1986 with permission.
The first line of evidence supporting this belief comes from studies examining the effects of active
muscle mass on ·VO2max. In general, researches have found that ·VO2max for combined arm-and-leg work
is similar to that measured during leg work alone (Table 2). Arm work alone typically elicits 65-75% of
·VO2max values measured during maximal leg work (56). One might, therefore, expect combined arm-
and-leg work to elicit ·VO2max values far exceeding those seen in maximal leg work, but this is not the
case. Combined arm-and-leg work results in little, if any, increase in ·VO2max, owing to the limitations of
the central cardiovascular system (6,8,28,48,56,61,65,68).
TABLE 2. Summary of previous studies examining maximal oxygen uptake in leg versus combined arm-
and-leg exercise. Adapted from Shipe (65).
More direct evidence implicating the cardiovascular system as a limiting factor for ·VO2max comes
from studies in which direct measurements of cardiac output, leg blood flow, and ·VO2 were made.
Secher et al. (62) had seven subjects cycle for 20 min (Fig. 5). During the first 10 min subjects pedaled at
approximately 68% of leg ·VO2max. They then added arm-cranking while continuing to maintain the same
power output with the legs. Superimposing arm work of sufficient intensity on leg work caused a
reduction in leg blood flow and leg oxygen uptake, with no change in mean arterial pressure. They
concluded that the blood flow to the exercising legs is limited by vasoconstriction when another large
muscle group is simultaneously active. In other words, the cardiac output was unable to supply the
demands of the combined muscle mass (arms + legs) and still maintain blood pressure. Vasoconstriction
of some arterioles in the active muscle was thus needed to maintain mean arterial blood pressure.
Figure 5-Evidence that the heart's capacity to supply blood flow to active muscle is limited.
When heavy exercise is performed with the legs, the addition of arm work causes a reduction
in both leg blood flow and leg oxygen uptake (not shown). During combined arm-and-leg
work, the muscle's capacity to vasodilate exceeds the ability of the heart to supply blood
flow. Data ofreference 62. Secher, N. H., J. P. Clausen, K. Klausen, I. Noer, and J. J. T. Central and
regional circulatory effects of adding arm exercise to leg exercise. Acta. Physiol. Scand. 100:
1979 as shown in reference 58. Rowell, L. B. Human Circulation: Regulation During Physical
Stress. New York: Oxford University Press, 1986.
The muscle's incredible capacity for blood flow can be shown when a small muscle mass is used and
the cardiac output can easily meet its needs (1,57,59). If isolated knee extensions are performed with
one leg, the amount of active muscle mass is only 2-3 kg (Fig. 6). Under these conditions, the blood flow
reaches 240 mL·100 g tissue-1·min-1 and oxygen uptake can attain values 300-400 mL·kg-1·min-1! So
clearly the limitation to increasing ·VO2max does not reside in the peripheral skeletal muscles. These data
show that the tremendous capacity of small muscle groups to vasodilate and to increase their ·VO2 far
exceeds the heart's pumping capacity. However, when exercise is performed with large muscle groups
whose capacity for blood flow exceeds maximal cardiac output, the heart becomes the limiting factor
that determines how much blood(and oxygen) are supplied to the muscles.
Figure 6-Illustration showing experimental set-up for performing isolated muscle

contractions of an isolated muscle mass. Only 2 to 3 kg of muscle are active, and blood flow
and oxygen uptake values in the region are incredibly high. This demonstrates that if blood
flow is not limiting, extremely high values of oxygen uptake can be obtained. Fromreference 59.
Saltin, B. Hemodynamic adaptations to exercise. Am. J. Cardiol. 55:42D-47D, 1985 with
permission.
Table 3 shows values for each variable in the cardiovascular Fick equation linking CO to ·VO2max for
athletic and nonathletic subjects. The nearly two-fold difference in ·VO2max between these groups is a
result of variations in maximal cardiac output(specifically, stroke volume). Whole-body arteriovenous
oxygen difference is the same so improved oxygen extraction is not responsible for the higher·VO2max
values in athletes. Another point is that during maximal exercise the O2 content of femoral vein blood
draining active leg muscles falls to incredibly low values of about 2 mL·100 mL-1(58), meaning that
nearly all of the oxygen delivered to the working skeletal muscles is removed. These observations are
consistent with the notion that oxygen delivery is a limiting factor for·VO2max.
TABLE 3. Physiological mechanisms behind the elevated ·VO2max seen in elite endurance athletes,
compared to normally active control subjects. Adapted from Rowell (58), p. 218.
Taken together, these studies demonstrate that the central cardiovascular system is the primary
determinant of ·VO2max in the average individual performing large muscle group activities. However,
there are certain instances where other factors can become the “weak link” in the transport and
utilization of oxygen. For instance, at high altitudes the decreased PO2 gradient between the alveolus
and the pulmonary capillary can result in a pulmonary diffusion limitation (9,70,74). In elite athletes with
extremely high maximal cardiac outputs, the decreased transit time of red blood cells in the pulmonary
capillary can also lead to a pulmonary diffusion limitation. In 1965, Peter Snell (the former mile
world record holder from New Zealand) had a hemoglobin saturation of 80% at the end of a maximal
treadmill test (11). Dempsey et al. (22,55) later confirmed that arterial desaturation occurs in elite
athletes, and they showed that if these subjects breathe hyperoxic gas mixtures (26%), their
hemoglobin saturation and ·VO2max increases. This proved that the athletes' ·VO2max was constrained by a
pulmonary diffusion limitation.
A number of muscle metabolic diseases can limit ·VO2max in patient populations. Lewis and Haller
(29,37) have researched several of these diseases, including myophosphosphorylase deficiency (i.e.,
McArdle's disease), phosphofructokinase (PFK) deficiency, and defects in mitochondrial electron
transport. Under these conditions,·VO2max and a-v O2 difference are markedly subnormal, indicating that
skeletal muscle can limit ·VO2max if disorders of muscle metabolism are present. However, in the vast
majority of healthy subjects the evidence points to the pumping capacity of the heart (cardiac output)
as being the major limiting factor for ·VO2max.
In 1924, Hill et al. (31) wrote that there are four principal determinants of ·VO2max: 1) arterial
saturation(%SaO2), 2) mixed venous saturation (%Sv-O2), 3) the oxygen capacity of the blood, and 4)
the circulation rate. Hill lamented his inability to make direct measurements of arterial and mixed
venous blood gases during exercise. Nevertheless, he correctly concluded that it would be unwise to
“assume an equilibrium to exist between the arterial blood and the gases in the lung alveoli” during
severe exercise (31). Not only did Hill predict the occurance of a pulmonary limitation, but he also
envisioned that it was of lesser importance than maximal cardiac output in limiting ·VO2max. He wrote:
“Some individuals can naturally run, or walk up hill for long periods without distress... This may be
partly a matter of the diffusion constant of the lungs for oxygen; largely, however, it is probably one of
the capacity of the heart itself.” (31).
This agrees with our current understanding of the factors limiting·VO2max.
3. ROLE OF OXYGEN DELIVERY IN DETERMINING ENDURANCE PERFORMANCE
“The belief that oxygen delivery alone limits maximal exercise performance has straightjacketed
exercise physiology for the past 30 years. Thus, performance, particularly during maximal but also
during submaximal exercise, has been explained exclusively in terms of oxygen transport and fuel
utilization, and other factors determining muscle contractile function have largely been ignored.” (From
Noakes (52, p. 329).
“My personal bias is that the rate of oxygen transport is not the critical factor determining exercise
performance. Rather, I suggest that the best athletes have muscles with superior contractility either on
the basis of superior myosin ATPase activity or enhanced sensitivity to calcium. Thus, they are able to
achieve higher work loads and therefore higher rates of oxygen consumption during maximal exercise.
The result is that their·VO2max values will tend to be high, leading to the erroneous conclusions that
·VO2max is a good predictor of athletic potential and that oxygen availability must therefore be the most
important factor limiting exercise performance.” (From Noakes, Lore of Running,(53), p. 21).
In the 30 years prior to the publication of Noakes' 1988 paper, researchers in exercise physiology
made great progress unraveling the factors limiting submaximal endurance performance. These studies
recognized that the ability to sustain repetitive muscle contractions was dependent on oxidative
phosphorylation and the rate of oxygen delivery needed to meet the ATP demands of muscle. If this is
the straightjacket referred to in the above quote, then exercise physiologists can be said to have worn it
well. The underlying theories related to oxidative energy production and oxygen transport to muscle
during exercise in humans have been supported by numerous experiments. In contrast to Noakes'
assertion, the research literature provides considerable support for the hypothesis that performance in
endurance events is limited by oxygen delivery (mL·kg-1·min-1), which is set by the subject's ·VO2max
and the percent of ·VO2max that can be maintained. The individual's running economy determines the
actual speed that results from that rate of oxygen consumption. In the following paragraphs we will
expand on each of these points.
Aerobic versus anaerobic energy production.Figure 7 describes how the ATP demand during
exercise is met by aerobic and anaerobic sources of energy in all-out performances of difference
durations. For this figure Åstrand and Rodahl (5) used a maximal aerobic power of 5 L·min-1 (25
kcal·min-1) and a maximal anaerobic capacity of 45 kcal. Further, they set the percent of ·VO2max that
could be maintained during the performances to 100% for 10 min, 95% for 30 min, 85% for 60 min,
and 80% during 120 min. It is clear that as the distance(duration) of a performance increases, the
proportion of energy for overall ATP production from aerobic metabolism also increases, accounting for
99% of ATP production for 2-h all-out performances. Figure 8 supports these calculations, showing that
the blood lactate concentration(measured at the end of a variety of races) decreases as the distance of
the race increases (14). In summary, the contribution of aerobic metabolism (and consequently, oxygen
delivery) to performance increases with race distance.
Figure 7-Relative contribution in percent of energy yield from aerobic and anaerobic
processes, respectively, during maximal work of different durations. Drawn from data of
reference 5. Åstrand, P.-O. and K. Rodahl. Textbook of Work Physiology. New York: McGrawHill,
1970, pp. 303-304.
Figure 8-Blood lactate values of men after distance races of 1.5-42.2 km. Broken line
represents average resting value observed among runners in the laboratory. From reference 14.
Costill, D. L. Metabolic responses during distance running. J. Appl. Physiol. 28:251-255, 1970
with permission.
Oxygen requirement for running. Hill and Lupton (32) recognized and elaborated on the notion of
an oxygen requirement needed to meet the energy demand of muscle during submaximal work. Oxygen
uptake (·VO2) increases during the first minutes of submaximal work to a level consistent with the ATP
requirement. By measuring steady-state ·VO2 values at different speeds, they were able to demonstrate
a linear relationship between running speed and ·VO2. This was subsequently confirmed by a number of
the early pioneers in exercise physiology (4,7,23,39).Figure 9 shows such a relationship for trained men
(10). One can see from this figure that, on average, a runner wishing to run a 2:15 marathon (312
m·min-1) would have to consume oxygen at a rate 59.8 mL·kg-1·min-1 throughout the entire race. If the
rate of oxygen consumption is an important variable limiting the speed that can be maintained over a
long run, then one might expect to see a strong relationship between ·VO2max and performance in
distance runs.
Figure 9-Linear relationship between running speed on the treadmill and oxygen uptake
(mL·kg-1·min-1). Adapted fromreference 10. Bransford, D. R. and E. T. Howley. Oxygen cost of
running in trained and untrained men and women.Med. Sci. Sports Exerc. 9:41-44, 1977.
·VO2max. Maximal oxygen uptake, a measure of oxygen transport to muscle, sets the upper limit
for performance in endurance events (20,34). Figure 10 shows the relationship (r = -0.91) between ·VO2max
and time for a 10-mile run in runners with ·VO2max values ranging from 54.8 to 81.6 mL·kg-1·min-1 (18).
This is to be expected based on the earlier figure showing the relationship between running speed and
·VO2. However, when the population of runners being studied has similar ·VO2max values, other variables
have been shown to be linked to endurance performance, notably, the percent of maximal oxygen
uptake that can be used during the run, and running economy.
Figure 10-Relationship between maximal oxygen consumption(·VO2max) and distance

running performance. Regression line represents the running times in a 10-mile test race.
Fromreference 18. Costill, D. L., H. Thomason, and E. Roberts. Fractional utilization of the aerobic
capacity during distance running. Med. Sci. Sports Exerc. 5:248-252, 1973 with permission.
%·VO2max (fractional utilization of·VO2max). Although ·VO2max sets the upper limit for
oxidative energy production in endurance events, most distance races are not run at 100% of maximal
oxygen uptake. Instead, a runner is able to operate at a certain fraction of maximal oxygen uptake that
decreases as the distance of the race increases. Consequently, the actual oxygen uptake(mL·kg-1·min-1)
available for energy production during an endurance run is a function of the ·VO2max and the percent of
·VO2max that can be sustained for the run (25). If two distance runners have the same·VO2max, the one
performing at a higher percentage of·VO2max during the run will have a better chance of maintaining a
faster pace and winning the race (18). Measurement of the lactate threshold (LT) has been shown to be
closely linked to the%·VO2max that can be maintained in endurance races (18,25) (see later discussion).
Alternatively, a runner with a ·VO2max lower than other runners could compensate by running at a higher
percentage of ·VO2max to achieve the same·VO2 (mL·kg-1·min-1) during the race. However, even though
both runners may be able to function at the same rate of oxygen consumption, variations in running
economy have to be considered in determining the outcome of a race.
Running economy. Hill and Lupton ((32), p. 158) recognized running economy as a factor affecting
running performance:
“A man may fail to be a good runner by reason of a low oxygen uptake, a low maximum oxygen
debt, or a high oxygen requirement; clumsy and uneconomical movements may lead to exhaustion just
as well as may an imperfect supply of oxygen.”
Figure 11 shows that there is considerable variability in the oxygen requirement of running at any
given speed, even for highly trained runners (13). This observation has been confirmed over the years
(46). What this means in practical terms is that if two runners have the same ·VO2max and the ability to
sustain the same percent of that ·VO2max during a run (they are running at exactly the same ·VO2[mL·kg-
1
·min-1]), the more economical runner will run faster (49). To study this question, Conley and Krahenbuhl
(13) recruited elite 10-km runners who had a narrow range of ·VO2max values (67.7-77.7 mL·kg-1·min-1).
They measured running economy at different speeds and examined the relationship between the oxygen
cost of running at these speeds and 10-km race time. Figure 12 shows the results for the running speed
of 268 m·min-1. This figure shows that there is a strong relationship between running economy and
endurance performance in populations of runners with little variation in·VO2max.
Figure 11-Variability in the steady state oxygen uptake at fixed running speeds in 12 highly-
trained and experienced male distance runners. From reference 13. Conley, D. L. and G.
Krahenbuhl. Running economy and distance running performance of highly trained athletes.
Med. Sci. Sports Exerc. 12:357-360, 1980.
Figure 12-Relationship between 10 km race time (y-axis) and steady-state oxygen uptake at
268 m·min-1 in 12 highly-trained and experienced male distance runners. From reference 13.
Conley, D. L. and G. Krahenbuhl. Running economy and distance running performance of

highly trained athletes. Med. Sci. Sports Exerc. 12:357-360, 1980.
To summarize, any attempt to predict endurance performance would have to consider the subject's
·VO2max, running economy (RE), and the%·VO2max that could be sustained during the run. An example is
Joyner's model (34) to predict marathon running speed:
Marathon Running Speed = ·VO2max(mL·kg-1·min-1) ×%·VO2max at LT× RE [km·h-1··VO2-1(mL·kg-1·min-

1 )]
However, what was needed was single measurement that would incorporate all three variables and
simplify the prediction of performance. The answer was provided in the classic study by Farrell et al. (25)
dealing with the link between lactate accumulation and performance in endurance races.
Lactate threshold. It had been known for some time (40) that the blood lactate concentration does
not change much during the early stages of a graded exercise test, but once it does, it increases in an
exponential manner. Farrell et al. (25) built on these observations and on earlier work by Costill (14)
suggesting a link between the lactate concentration in submaximal work and endurance performance.
Farrell et al.(25) studied 18 male distance runners to determine the relationship of ·VO2max, running
economy, and the onset of plasma lactate accumulation (OPLA) to performance in distance runs of 3.2,
9.7, 15, 19.3, and 42.2 km. Each subject completed eight 10-min submaximal running tests to measure
running economy and the speed at which the plasma lactate concentration suddenly increased. In
addition, the subject's·VO2max was measured. Multiple regression, used to determine the variables that
were the best predictors of performance in the distance runs, showed that running speed at OPLA was
the best predictor of running performance for all distances. OPLA accounted for between 82.8% (3.2 km
race) and 96% (42.2 km) of the variance in performance. The actual marathon pace was 8 ± 5 m·min-1
faster than the velocity measured at OPLA. The ·VO2 at the lactate threshold (LT) is related to the
oxidative enzyme activity and capillary density of the muscles involved in the activity, as well as the
mass of muscle sharing the power output (20). In summary, running speed at the lactate threshold
integrates the variables of ·VO2max, the%·VO2max that can be sustained, and automatically considers the
individual's running economy. Figure 13 summarizes the connections between cardiovascular function and
·VO2max and the role of oxygen transport in determining running velocity in long distance races.
Figure 13-Summary of the major variables related to·VO2max and the maximum velocity that
can be maintained in distance races.
·VO2max and maximal running velocity: cause or effect? We now refer the reader to the
second quote of Noakes (53) that started this section. The classical view held by most exercise
physiologists is that elite distance runners are able to run fast in large part because they have a high
maximal cardiac output and·VO2max. However, Noakes argues that it is the other way around; he claims
they have a high ·VO2max because they possess the ability to run fast and because running speed is
linearly related to ·VO2.
Noakes' line of reasoning gets him into trouble because it suggests that world-class sprinters should
have some of the highest ·VO2max values. Even Noakes recognizes this dilemma, and he attempts to
rationalize it as follows. “This does not mean that the best sprinters will also be the best long-distance
runners. Although they may have the best quality muscles for explosive exercise, factors such as
temperament and body build prevent many top sprinters from achieving excellence at the longer
running distances. Alternatively, muscles able to achieve high rates of energy production for short
duration may fatigue more rapidly...” (53, p. 38).
From a physiological perspective, the factors that limit performance in the sprints are entirely
different from those limiting performance in distance running events. The reason that elite sprinters can
reach peak speeds in excess of 25 mph (42) is that they have a high percentage of Type II fibers with
faster cross-bridge cycling rates, enabling them to contract their skeletal muscles very rapidly (60). Elite
marathon runners who compete at slightly over 12 mph do not require a predominance of Type II
muscle fibers (60). The limiting factor in distance running is not myosin ATPase activity, but the ability to
regenerate ATP via aerobic metabolism. This in turn is determined largely by the maximal capabilities of
the heart and lungs to transport oxygen to the working muscles.
4. ROLE OF MUSCLE FACTORS IN DETERMINING ENDURANCE PERFORMANCE
“I have suggested that factors related to muscle, not the cardiovascular system (and thus not
oxygen transport), limit the maximal exercise performance of these persons (test subjects). I suggest
that whatever factors determine peak muscle-power production in short-duration, highintensity exercise
like running 800 to 1500 m also determine performance in more prolonged exercise, including marathon
and ultramarathon running.” (From Noakes, Lore of Running((53), p. 19).
“A muscle factor determines running performance at any distance. This muscle factor involves the
maximum power that the muscles can produce and is not likely related to factors determining oxygen
transport to or oxygen utilization by the muscles.” (From Lore of Running (53, p. 38).
“Sprinting speed in events lasting 2-4 min can predict running potential in endurance events.” (From
Lore of Running(53, p. 56).
We accept Noakes' finding (53) that running velocity in events lasting 2 to 4 min can predict
performance in longer races. However, we disagree that this shows the importance of maximum muscle
power in these events. Rather, we feel that it underscores the importance of·VO2max in events from the
800 m to the marathon. It is potentially misleading to refer to middle distance running events as sprints
because at least one-half of the energy required by these events is supplied by aerobic metabolism. A 2-
min race derives 50% of the energy requirement from oxidative pathways, and in a 4-min race the
percentage is even greater (67%). In the marathon, more than 99% of the energy is supplied by
aerobic metabolism (Fig. 6). In our view, ·VO2max is an important determinant of performance in both
middle and long distance running events since the higher an athlete's ·VO2max the more energy can be
supplied by aerobic metabolism. This factor, and inter-individual differences in running economy, would
explain why there is a correlation between running performance in middle and longer distance races.
Despite the fact that middle and long distance races both rely heavily on aerobic metabolism, most
exercise physiologists believe that the causes of fatigue in these events are different. Muscle fatigue
in the middle distance events is at least partially due to accumulation of H+ associated with lactic acid.
In this type of event, muscle lactate may reach values of approximately 20 mM·kg-1 wet weight (26,35),
resulting in severe acidosis (63). The increase in H+ within the muscles has been shown to cause fatigue
by two important mechanisms. First, it inhibits phospho-fructokinase (PFK), the rate limiting enzyme in
glycolysis, and decreases flux through the glycolytic pathway (71,72). Secondly, H+ has direct effects on
the contractile apparatus. With isolated muscle fiber preparations, decreasing the pH of the incubation
medium causes a pronounced decrease in force-generating capability (24,43,44,50). Further evidence that
an accumulation of H+ ion limits performance in middle distance events is provided by studies showing
that sodium bicarbonate ingestion increases blood buffer capacity (19), causing a significant
improvement in 800-m race performance (75).
Peak blood lactate values measured at the end of a marathon race, however, are barely above
resting levels (Fig. 7). Costill and Fox (17) reported blood lactate concentrations of 2 mM following a
marathon. Hence it is unlikely that the same factors causing fatigue in the 800 m are operating in the
marathon. Exhaustion in the marathon is usually attributed to factors such as muscle glycogen depletion
and hypoglycemia (15,16), which force the muscles to rely more on fatty acids for a fuel source.
Newsholme (51) has estimated that the maximal intensity that can be sustained by fat utilization alone is
about 50% ·VO2max. This suggests that if carbohydrate stores become depleted, the percentage of·VO2max
that a marathoner can sustain will decrease markedly.
Noakes proposes that performance in marathon running is determined by anaerobic performance

(see quote above). He also states that his laboratory has found “that the peak running speed that an
athlete could achieve during a maximal treadmill test was the best predictor of performance in marathon
and ultramarathon events, indicating a possible relationship between sprinting speed, which is a
measure of the ability to produce energy by oxygen-independent pathways, and endurance capacity,
which is believed to be a measure of the capacity for energy production by oxygen-dependent pathways.
At present we have no easy scientific explanation for this paradox.”(53, p. 56). This is not just a
paradox; it is an case ofreductio ad adsurdum (disproof of a hypothesis by showing the absurdity of its
inevitable conclusion).
Noakes (52) further suggests that two muscle factors limit performance in all running events: 1)
myosin ATPase activity and 2) calcium sensitivity of skeletal muscle. He states that an increased
percentage of Type II muscle fibers (up to 50% of the total) is a desireable trait for marathon runners.
This view assumes that the myosin cross-bridge cycling rate is the limiting factor in distance running.
However, cross-bridge cycling cannot occur without adequate quantities of ATP supplied via aerobic
metabolism. The majority of the evidence points to the cardiorespiratory system as being the limiting
factor for oxygen uptake (which is the quantitative measure of aerobic metabolism). Additionally,
Noakes provides no evidence that calcium sensitivity of skeletal muscle is a limiting factor for endurance
performance.
The ·VO2max paradigms of Hill versus Noakes. InThe Structure of Scientific Revolutions, Kuhn
(36) defines a paradigm as “one or more past scientific achievements... that some particular scientific
community acknowledges for a time as supplying the foundation for its further practice.” Two basic
characteristics of paradigms are that they are novel enough to attract a group of researchers who are
committed to the same fundamental beliefs and that they are open-ended enough to leave numerous
problems to be resolved. Thus, a paradigm serves as the foundation for future scientific research
questions and is a sign of maturity in the development of any given scientific field (36, p. 11).
A. V. Hill's concept of ·VO2max certainly meets this definition of a paradigm. Among the “central
tenets” of his paradigm are 1) the concept of an upper limit to oxygen uptake (·VO2max), 2) the
demonstration of inter-individual differences in ·VO2max, 3) a plateau in ·VO2 with increasing speed, 4)
speculation regarding the role of oxygen transport as a limiting factor for ·VO2max. Other contributions of
A. V. Hill include his discovery that isolated frog muscle produces heat in two separate phases, one
that takes place during contraction and does not require oxygen and a second that occurs during
recovery and requires oxygen (30). He attributed the first phase to the formation of lactic acid from a
precursor and the second phase to the oxidative removal of lactic acid (73). Hill and Lupton (32) also
made the critical distinction between the oxygen requirement, oxygen debt, and oxygen repayment. In
the last 70 years there have been several refinements to these theories. However, there is no question
that Hill's research and writing were instrumental in shaping the field of exercise physiology and will
continue to do so for generations to come.
Noakes is an iconoclast who argues that A.V. Hill's ·VO2max paradigm is wrong and must be
discarded. The dispute over whether a·VO2 plateau occurs has caused Noakes to dismiss the entire
concept of ·VO2max. In part, this relates to his view of science, which is that refutations are critically
important and it takes very little to refute a hypothesis (54). Thus, Noakes argues with the concept of an
“upper limit” to oxygen uptake, with the scientific evidence that oxygen transport limits ·VO2max and with
the well-documented importance of ·VO2max in endurance performance. The alternative paradigm he
proposes is that endurance performance is limited by muscle factors, a viewpoint that is incompatible
with a large body of literature supporting the ·VO2max paradigm of Hill.
Kuhn has studied the process by which scientific revolutions occur (36, p. 77). He states that “...
once it has achieved the status of a paradigm, a scientific theory is declared invalid only if an alternative
candidate is available to take its place.” Kuhn advises that we must ask which of the two actual and
competing theories fits the facts better (36, p. 77). When we weigh the scientific evidence on both sides
of the issue, it appears that Hill's views were amazingly accurate. Scientific investigations in the 70
years since Hill have served mainly to reinforce his paradigm and confirm that his scientific“hunches”
were correct. Only relatively minor refinements to his theories have been needed. In contrast, Noakes'
views are not supported by strong scientific evidence, and they raise numerous paradoxes and
unresolved dilemmas.
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OXYGEN REQUIREMENT; PLATEAU; CARDIAC OUTPUT; LACTATE THRESHOLD; RUNNING ECONOMY;

ENDURANCE; AEROBIC METABOLISM
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Ovid: BASSETT: Med Sci Sports Exerc, Volume 29(5).May 1997.

Maximal oxygen uptake: “classical”

BASSETT, DAVID R. JR.; HOWLEY, EDWARD T.

Exercise Science Unit, University of Tennesee, Knoxville, TN 37919

1. A.V. HILL'S CONCEPT OF ·VO2MAX

TABLE 1. Oxygen intake running at different speeds.

2. FACTORS LIMITING ·VO2MAX

Figure 4-Potential physiological factors limiting·VO2max. From reference 58. Rowell, L. B.

Figure 6-Illustration showing experimental set-up for performing isolated muscle

This agrees with our current understanding of the factors limiting·VO2max.

3. ROLE OF OXYGEN DELIVERY IN DETERMINING ENDURANCE PERFORMANCE

Figure 10-Relationship between maximal oxygen consumption(·VO2max) and distance

Conley, D. L. and G. Krahenbuhl. Running economy and distance running performance of

Marathon Running Speed = ·VO2max(mL·kg-1·min-1) ×%·VO2max at LT× RE [km·h-1··VO2-1(mL·kg-1·min-

4. ROLE OF MUSCLE FACTORS IN DETERMINING ENDURANCE PERFORMANCE

Noakes proposes that performance in marathon running is determined by anaerobic performance

OXYGEN REQUIREMENT; PLATEAU; CARDIAC OUTPUT; LACTATE THRESHOLD; RUNNING ECONOMY;

Accession Number: 00005768-199705000-00002

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