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Maximal oxygen uptake: “classical” versus“contemporary” viewpoints


Medicine & Science in Sports & Exercise: May 1997 - Volume 29 - Issue 5 - p 591-603
1996 J.B. Wolffe Memorial Lecture: Response to the Challenge

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.

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:

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.

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.

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“...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.

“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 andFigure 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.

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 inFigure 3. It is clear that the plateau issue has been addressed by many scientists over the past 40 years.

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).

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“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 inFigure 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.

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).

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.

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.

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.

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.

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“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.

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.

˙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.

%˙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.

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.

˙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.

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“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.

Figure 1-Archibald Vivian Hill. Nobel Laureate, 1922. Photograph courtesy of the Nobel Committee.

Figure 1-Archibald Vivian Hill. Nobel Laureate, 1922. Photograph courtesy of the Nobel Committee.

Figure 2-Relationship between speed of running and (a) oxygen intake, (b) lung ventilation, and (c) respiratory quotient. Original graph from

Figure 2-Relationship between speed of running and (a) oxygen intake, (b) lung ventilation, and (c) respiratory quotient. Original graph from

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 from

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 from

Figure 4-Potential physiological factors limiting˙VO2max. From

Figure 4-Potential physiological factors limiting˙VO2max. From

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 of

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 of

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. From

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. From

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

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

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

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

Figure 9-Linear relationship between running speed on the treadmill and oxygen uptake (mL·kg-1·min-1). Adapted from

Figure 9-Linear relationship between running speed on the treadmill and oxygen uptake (mL·kg-1·min-1). Adapted from

Figure 10-Relationship between maximal oxygen consumption(˙VO2max) and distance running performance. Regression line represents the running times in a 10-mile test race. From

Figure 10-Relationship between maximal oxygen consumption(˙VO2max) and distance running performance. Regression line represents the running times in a 10-mile test race. From

Figure 11-Variability in the steady state oxygen uptake at fixed running speeds in 12 highly-trained and experienced male distance runners. From

Figure 11-Variability in the steady state oxygen uptake at fixed running speeds in 12 highly-trained and experienced male distance runners. From

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

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

Figure 13-Summary of the major variables related to˙VO2max and the maximum velocity that can be maintained in distance races.

Figure 13-Summary of the major variables related to˙VO2max and the maximum velocity that can be maintained in distance races.

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