Testing for maximum oxygen consumption has produced a brainless model of human exercise performance.

Br J Sports Med. 2008 Jul;42(7):551-5. Epub 2008 Apr 18. Review
Noakes TD.

Perhaps the hallmark study in human exercise physiology was performed by Nobel Laureate Professor AV Hill on himself in Manchester, England in the early 1920’s. Hill circled an 88m grass running track at three different speeds each for four minutes whilst he measured his average oxygen consumption every 30 seconds. He concluded that his oxygen consumption reached a maximum at 16km/hr “beyond which no bodily effort can drive it”. This experiment established the single most popular test in the exercise sciences – the progressive exercise test for the measurement of the maximum oxygen consumption (VO2max). The experimental protocol in this test forces the subject progressively to increase the work rate until voluntary exhaustion.

According to the modern interpretation, the outcome of this test defines the limits of the human cardio-respiratory system since it apparently terminates when the cardiac output reaches a maximum value. It also established a model to explain the biology of human exercise performance. For if the cardiovascular system determines maximal exercise performance, then it must also determine performance during many other forms of exercise as argued by Bassett and Howley and others. Thus, champion athletes able to run very fast for long distances do so because of the metabolic consequences in their skeletal muscles of their superior cardiovascular function even though they exercise at intensities below that at which the VO2max is reached and at which, according to that model, cardiovascular function is not maximal and cannot therefore, by definition, be the “limiting” factor.

This explanation seems paradoxical since, if correct, it predicts that athletes should be able to exercise more vigorously and for longer simply by increasing their (submaximal) cardiac outputs until maximal values are reached. Only then should exhaustion occur. Or that any athlete chasing the race leader should be able to increase the cardiac output to a maximal value and so pass the leading athlete who is exercising at a lower and submaximal cardiac output. But this does not happen; as is well known, prolonged exercise always terminates at submaximal levels of cardiac output.

It is my opinion that the manner in which the VO2max test is conducted has encouraged a reductionist mindset which teaches that the “limits” of exercise performance can be explained by one or two cardiovascular variables, such as the cardiac output and muscle blood flow. But the VO2max test includes three components that are foreign to all forms of freely chosen exercise.

First, the tested subject does not know the expected duration of the exercise bout when it begins. Accurate knowledge of the exercise duration optimizes the exercise performance.

Second the intensity of the exercise increases progressively, sometimes rapidly from low to “maximal” work rates. Humans do not usually exercise this way.

Third, the tested subject cannot regulate the exercise intensity except by choosing when to stop. This adds a subjective component to the test since the athlete’s conscious brain makes the final decision when to terminate the exercise. Thus psychological and not purely physiological factors can presumably influence that decision.

More to the point, a characteristic of freely-chosen exercise is the choice of different pacing strategies that change continuously from moment-to-moment. Unique, constantly-changing pacing strategies are most likely produced by a central motor command that continually modulates the number of motor units recruited in the exercising limbs. But during the VO2max test this critical brain function cannot be evaluated since the change in work rate is preset and immutable, thereby controlling the tested subject’s level of central motor output in an unnatural way (Figure 1).



Finally the VO2max test has produced an unusual definition of the intensity at which exercise is performed. For the intensity is expressed relative to that at which the VO2max occurs. Workloads beyond those reached during the VO2max test are defined as “supramaximal”. But this does not make sense. For a (lower) exercise intensity cannot be maximal if a higher exercise intensity can be achieved, even if under different circumstances.

Experimental models such as the VO2max test have their uses for they can define the maximal capacity of each human for oxygen use but their generalizability must be carefully scrutinized. Thus one must ask: Is it appropriate to explain the physiological factors determining human exercise performance according to an experimental model of exercise (i) in which
humans do not usually engage and (ii) in which the brain of the tested subject
does not set the pacing strategy as is usual in freely-chosen exercise? If we
base our interpretations exclusively on a testing model which is so unnatural
that it excludes the usual function of the brain during exercise, we may miss
the obvious.

Thus this traditional reductionist explanation of the factors limiting the VO2max
excludes any possible contribution of the brain and central motor
command.[3-9, 11-14] For the point is, as Kayser[18] reminds us, that
exercise begins and ends in the brain. Thus before any movement can occur
the appropriate number of motor units in the exercising skeletal muscles must
first be activated by the central nervous system. As a result the power output
of the exercising limbs increases, raising the whole body oxygen consumption
consequent to metabolite-induced arteriolar vasodilation which directs the
increase in blood flow to the exercising muscles. Thus, as is usually taught in
standard textbooks of human physiology[22] increases in blood flow and
cardiac output during exercise are the consequence and not the cause of the
increase in power output by the exercising muscles. Attempts to point this out
are usually dismissed out of hand.[23]

But the logical point is that this critical role of central motor command cannot
be identified if its most important function – the setting of the pacing strategy –
is the controlled variable in the experimental model – the VO2max test – used

Is the measurement of maximal oxygen intake passé?

Br J Sports Med. 2009 Feb;43(2):83-5.
Shephard RJ.

Limiting factors for maximum oxygen uptake and determinants of endurance performance.

Med Sci Sports Exerc. 2000 Jan;32(1):70-84. Review.
Bassett DR Jr, Howley ET.

Maximum oxygen uptake (VO2max) is defined as the highest rate at which oxygen can be taken up and utilized by the body during severe exercise. It is one of the main variables in the field of exercise physiology, and is frequently used to indicate the cardiorespiratory fitness of an individual. In the scientific literature, an increase in VO2max is the most common method of demonstrating a training effect. In addition, VO2max is frequently used in the development of an exercise prescription. Given these applications of VO2max, there has been great interest in identifying the physiological factors that limit VO2max and determining the role of this variable in endurance performance.

The current concept of VO2max began with the work of Hill et al. in 1923-24. Their view of maximum oxygen uptake has been validated, accepted, and extended by many world-renowned exercise physiologists. However, it has recently been argued that Hill’s VO2max paradigm is an outdated concept, based upon critical flaws in logic. To consider these points of view, we weighed the arguments on both sides and concluded in 1997 that the “classical” view of VO2max was correct. The present article is an attempt to clarify our views on VO2max and to present further evidence in support of Hill’s theory.

Part I of this article reviews the history of the concept of VO2max. Part II describes the evidence for each of the four potentially limiting factors for VO2max. Part III discusses the role of VO2max and other factors in determining endurance performance.

PART I: HISTORY OF MAXIMUM OXYGEN UPTAKE

The term “maximal oxygen uptake” was coined and defined by Hill et al. and Herbst in the 1920s. The VO2max paradigm of Hill and Lupton postulates that:

1. there is an upper limit to oxygen uptake,
   
2. there are interindividual differences in VO2max,
   
3. a high VO2max is a prerequisite for success in middle and long-distance running,
   
4. VO2max is limited by ability of the cardiorespiratory system to transport O2 to the muscles.

In 1923, Hill and Lupton made careful measurements of oxygen consumption on a subject (A.V.H.) who ran around an 85-m grass track. The graph shown in Figure 1 was drawn primarily for the purpose of illustrating the change in VO2 over time at three speeds (181, 203, and 267 m/min). In a study published the following year, Hill et al. reported more VO2 measurements on the same subject. After 2.5 min of running at 282 m/min, his VO2 reached a value of 4.080 L/min (or 3.730 L/min above that measured at standing rest). Since the VO2 at speeds of 259, 267, 271, and 282 m/min did not increase beyond that measured at 243 m/min, this confirmed that at high speeds the VO2 reaches a maximum beyond which no effort can drive it.



Today, it is universally accepted that there is a physiological upper limit to the body’s ability to consume oxygen. This is best illustrated in the classic graph of Åstrand and Saltin shown in Figure 2. In a discontinuous test protocol, repeated attempts to drive the oxygen uptake to higher values by increasing the work rate are ineffective. The rate of climb in VO2 increases with each successive attempt, but the “upper ceiling” reached in each case is about the same. The subject merely reaches VO2max sooner at high power outputs. VO2 does not continue to increase indefinitely with increases in work rate (or running speed). This finding was predicted by Hill and Lupton, who stated that eventually, “. . . however much the speed [or work rate] be
increased beyond this limit, no further increase in oxygen intake can occur”.

Not all subjects show a plateau in VO2 at the end of a graded exercise test (GXT), when graphed against work intensity. It has repeatedly been shown that about 50% of subjects do not demonstrate a plateau when stressed to maximal effort. Failure to achieve a plateau does not mean that these subjects have failed to attain their “true” VO2max. In the first place, with a continuous GXT protocol a subject may fatigue just as VO2max is reached. Thus, the plateau may not be evident even though VO2max has been reached. Second, even with a discontinuous GXT protocol most researchers require that a subject complete 3-5 min at each stage. Thus, if a subject reaches VO2max in 2 min at a supramaximal intensity and then becomes too fatigued to continue, this data point would not be graphed. In this case, the VO2 plateau will not be apparent in the final graph of work rate versus oxygen uptake, even though VO2max has been attained (Fig. 3). For these reasons, the plateau in VO2 cannot be used as the sole criterion for achievement of VO2max. This is why it is recommended that secondary criteria be applied to verify a maximal effort. These include a respiratory exchange ratio greater than 1.15 and blood lactic acid level greater than 8-9 mM, an approach that has been confirmed in our laboratory.

The VO2 plateau represents a leveling off in cardiac output and a-v O2 difference that may be seen toward the end of a GXT. Since the VO2 fails to keep pace with the increasing oxygen demand, there is an increased reliance on oxygen-independent pathways (i.e., anaerobic glycolysis). The significance of the VO2 plateau has often been misinterpreted. In 1988, it was suggested that the absence of a VO2 plateau in some persons meant that VO2max was not limited by the cardiovascular system. This led to the suggestion that “muscle factors” must be important in limiting VO2max. However, as we pointed out, the VO2 plateau is not the principal evidence for a cardiovascular limitation. More recently, it has been suggested that the VO2 plateau signifies a leveling off in cardiac output, caused by progressive and irreversible myocardial ischemia. However, there is no evidence to support this view. In fact, a VO2 plateau occurs in about half of all healthy adults performing maximal exertion, without accompanying signs or symptoms of myocardial ischemia. A more reasonable explanation is that maximal cardiac output is limited by the maximal rate of depolarization of the sino-atrial (SA) node and the structural limits of the ventricle.

Regarding the variability in VO2max, Hill and Lupton stated, “A man may fail to be a good runner by reason of a low oxygen uptake, a low maximal oxygen debt, or a high oxygen requirement.” This clearly shows that they recognized the presence of interindividual differences in VO2max. They did not believe in a universal VO2max of 4.0 L/min, as has been suggested. Furthermore, they recognized the importance of a high VO2max for elite performers. They also stated that other physiological factors, such as running economy, would influence the race outcome. Subsequent researchers have verified these points (see discussion in Part III).

The fourth point in the VO2max paradigm has been the most controversial. Hill et al. identified several determinants of VO2max. Based on the limited data available to them, they speculated that in exercising man, VO2max is limited by the rate at which O2 can be supplied by the cardiorespiratory system (heart, lungs, and blood). Over the next 75 years, many distinguished exercise physiologists studied this problem using a wide array of new experimental techniques. They have arrived at a consensus that supports the original VO2max paradigm of Hill et al.. The prevailing view is that in the exercising human VO2max is limited primarily by the rate of oxygen delivery, not the ability of the muscles to take up oxygen from the blood (see part II).

PART II: LIMITING FACTORS FOR MAXIMUM OXYGEN UPTAKE

The pathway for O2 from the atmosphere to the mitochondria contains a series of steps, each of which could represent a potential impediment to O2 flux. Figure 4 shows the physiological factors that could limit VO2max: 1) the pulmonary diffusing capacity, 2) maximal cardiac output, 3) oxygen carrying capacity of the blood, and 4) skeletal muscle characteristics. The first three factors can be classified as “central” factors; the fourth is termed a “peripheral” factor. The evidence for each of these factors is discussed in the following sections.



The Pulmonary System

In the average individual exercising at sea level, the lungs perform their job of saturating the arterial blood with O2 extremely well. Even during maximal work, the arterial O2 saturation (%SaO2) remains around 95%. Hill et al. predicted that a significant drop in arterial saturation (SaO2 less than 75%) does not occur, based on the appearance of their subjects, “who have never, even in the severest exercise, shown any signs of cyanosis.” However, they cautioned against assuming that a complete alveolararterial equilibrium is present because of the rapidity of the passage of the red blood cells within the pulmonary capillary at high work rates.

Modern researchers have verified that the pulmonary system may indeed limit VO2max under certain circumstances. Dempsey et al. showed that elite athletes are more likely to undergo arterial O2 desaturation during maximal work compared with normal individuals. Trained individuals have a much higher maximal cardiac output than untrained individuals (40 vs 25 L/min). This leads to a decreased transit time of the red blood cell in the pulmonary capillary. Consequently, there may not be enough time to saturate the blood with O2 before it exits the pulmonary capillary.

This pulmonary limitation in highly trained athletes can be overcome with O2-enriched air. Powers et al. had highly trained subjects and normal subjects perform two VO2max tests (Fig. 5). In one test the subjects breathed room air and in the other they breathed a 26% O2 gas mixture. On hyperoxic gas, the highly trained group had an increase in VO2max from 70.1 to 74.7 mL/kg/min and an increase in arterial O2 saturation (SaO2) from 90.6% to 95.9% during maximal work. None of these changes were observed in normal subjects (VO2max 5 56.5 mL/kg/min).

Pulmonary limitations are evident in people exercising at moderately high altitudes (3,000-5,000 m). Individuals with asthma and other types of chronic obstructive pulmonary disease (COPD) suffer from a similar problem (a reduction in arterial PO2). Under these conditions, exercise ability can be increased with supplemental O2, which increases the “driving force” for O2 diffusion into the blood. The ability to increase exercise capacity in this manner shows the presence of a pulmonary limitation.

Maximum Cardiac Output

Hill et al. proposed that maximal cardiac output was the primary factor explaining individual differences in VO2max. This was a major insight given the state of knowledge in 1923. Einthoven had only discovered electrocardiography a decade earlier. Hill used this new technique to measure maximal heart rates of around 180 beats/min. However, it was not until around 1930 that trained subjects were shown to have a lower heart rate at a fixed, submaximal work rate, providing evidence of increased stroke volumes. Other methods of showing enlarged hearts in endurance athletes (x-ray and ultrasound) did not become available until 1940-1950. Given the level of technology in 1923, it is incredible that Hill et al. were able to deduce that endurance athletes have hearts with superior pumping capacities. How did they arrive at this remarkable conclusion? In 1915, Lindhard had measured cardiac outputs of 20 L/min in average subjects during exercise and demonstrated the strong, linear relationship between cardiac output and VO2. Hill and Lupton speculated that maximal cardiac output values of 30-40 L/min were possible in trained athletes. These speculations were based on knowledge of the Fick equation and assumed values for VO2max, arterial oxygen content, and mixed venous oxygen content.

Today, we know that the normal range of VO2max values (L/min) observed in sedentary and trained men and women of the same age is due principally to variation in maximal stroke volume, given that considerably less variation exists in maximal HR and systemic oxygen extraction. During maximum exercise, almost all of the available oxygen is extracted from blood perfusing the active muscles. The oxygen content of arterial blood is approximately 200 mL O2/L; in venous blood draining maximally working muscles it falls to about 20-30 mL O2/L. This shows that there is little oxygen left to be extracted out of the blood during heavy exercise. Hence, the dominant mechanism for the increase in VO2max with training must be an increase in blood flow (and O2 delivery). It is estimated that 70-85% of the limitation in VO2max is linked to maximal cardiac output.

Longitudinal studies have shown that the training-induced increase in VO2max results primarily from an increase in maximal cardiac output rather than a widening of the systemic a-v O2 difference (Fig. 6). Saltin et al. examined VO2max in sedentary individuals after 20 d of bed rest and 50 d of training. The difference in VO2max between the deconditioned and trained states resulted mostly from a difference in cardiac output. In a similar study, Ekblom et al. found that 16 wk of physical training increased VO2max from 3.15 to 3.68 L/min. This improvement in VO2max resulted from an 8.0% increase in cardiac output (from 22.4 to 24.2 L/min) and a 3.6% increase in a-v O2 difference (from 138 to 143 mL/L).

One way to acutely decrease the cardiac output is with beta-blockade. Tesch has written an authoritative review of 24 studies detailing the cardiovascular responses to beta blockade. Beta-blockers can decrease maximal heart rate (HR) by 25–30%. In these studies, maximal cardiac output decreases by 15–20%, while stroke volume increases slightly. Although the decreased cardiac output is partially compensated for by an increase in a-v O2 difference, VO2max declines by 5–15%. Tesch concludes that the decline in VO2max seen with cardio-selective beta-blockade is caused by diminished blood flow and oxygen delivery.

Oxygen Carrying Capacity

Another method of altering the O2 transport to working muscles is by changing the hemoglobin (Hb) content of the blood. Blood doping is the practice of artificially increasing a person’s volume of total red blood cells through removal, storage, and subsequent reinfusion. Gledhill completed comprehensive reviews of 15–20 studies that have examined the effects of blood doping. Reinfusion of 900–1,350 mL blood elevates the oxygen carrying capacity of the blood. This procedure has been shown to increase VO2max by 4–9% in well designed, double-blind studies (Fig. 7). No improvement is seen in sham-treated
individuals, infused with a small volume of saline. Once again, these studies provide evidence of a cause-and-effect link between O2 delivery and VO2max.

The evidence that VO2max is limited by the cardiac output, the oxygen carrying capacity, and in some cases the pulmonary system, is undeniable. This statement pertains to healthy subjects performing whole-body, dynamic exercise. Next we will consider whether skeletal muscle could also be a limiting factor for VO2max.

Skeletal Muscle Limitations

Peripheral diffusion gradients. In a symposium on limiting factors for VO2max, Honig et al. presented evidence for a peripheral O2 diffusion limitation in red canine muscle. According to their experiments and a mathematical model, the principal site of resistance to O2 diffusion occurs between the surface of the red blood cell and the sarcolemma. They report a large drop in PO2 over this short distance. Honig et al. conclude that O2 delivery per se is not the limiting factor. They found that a low cell PO2 relative to blood PO2 is needed to maintain the driving force for diffusion and thus enhance O2 conductance.

The experimental model of Honig et al. is quite different from that seen in an exercising human. They noted that simply increasing blood flow to isolated muscle is not sufficient to cause VO2 to increase. The isolated muscle must also undergo contractions so that the mitochondria consume O2 (drawing down the intracellular PO2). Without a peripheral diffusion gradient, oxygen uptake will not increase. Their overall conclusion is that VO2max is a distributed property, dependent on the interaction of O2 transport and mitochondrial O2 uptake. We agree with this conclusion. However, this model cannot determine which of these two factors limits VO2max in the intact human performing maximal exertion.

Mitochondrial enzyme levels. Physiologists have done extensive work to examine whether mitochondrial enzyme levels are a limiting factor for VO2max. Within the muscle fibers, the mitochondria are the sites where O2 is consumed in the final step of the electron transport chain. In theory, doubling the number of mitochondria should double the number of sites for O2 uptake in muscle. However, human studies show that there is only a modest increase in VO2max (20–40%) despite a 2.2-fold increase in mitochondrial enzymes. This is consistent with the view that VO2max, measured during whole-body dynamic exercise, is limited by oxygen delivery (not muscle mitochondria).

Shephard has asked, “If we reject the view that there is a significant limitation of oxygen transport at the tissue level, what alternative explanation can be offered to the teleologists to account for the doubling of tissue enzyme activity during endurance training?” In their landmark 1984 review paper, Holloszy and Coyle propose an answer to this question. They argue that as a consequence of the increase in mitochondria, exercise at the same work rate elicits smaller disturbances in homeostasis in the trained muscles. Two metabolic effects of an increase in mitochondrial enzymes are that 1) muscles adapted to endurance exercise will oxidize fat at a higher rate (thus sparing muscle glycogen and blood glucose) and 2) there is decreased lactate production during exercise. These muscle adaptations are important in explaining the improvement in endurance performance that occurs with training. (This will be discussed further in Part III.)

The main effect of increasing mitochondrial enzymes is to improve endurance performance rather than to increase VO2max. Holloszy and Coyle note that even in individuals with nearly identical VO2max values there can be a two-fold range in mitochondrial enzymes (1976). Furthermore, low-intensity training may elicit small changes in mitochondrial enzymes without any change in VO2max, and vice versa. On the other hand, there is some evidence that the increase in mitochondria play a permissive role in allowing VO2max to increase. Holloszy and Coyle note that the lowest value for SDH activity in the elite
runners studied by Costill was still 2.5-fold greater than that found for untrained individuals in the same study. The increase in muscle mitochondria may allow a slightly greater extraction of O2 from the blood by the working muscles, thus contributing in a minor way to an increased VO2max.

Capillary density. In 1977 Andersen and Henriksson showed that capillary density increases with training. Other studies noted a strong relationship between the number of capillaries per fiber in the vastus lateralis and VO2max (mL/kg/min) measured during cycle ergometery. The main significance of the training-induced increase in capillary density is not to accommodate blood flow but rather to maintain or elongate mean transit time. This enhances oxygen delivery by maintaining oxygen extraction (a-v O2 difference) even at high rates of muscle blood flow. The ability of skeletal muscle to adapt to training in this way is far greater than what is observed in the lung.

Central or Peripheral Limitation?

The issue of central versus peripheral factors limiting VO2max has been a long-standing debate. Work conducted in the early 1970s supported the idea of central factors being limiting for VO2max. Clausen et al. showed that two-legged bicycle training resulted in an increase in arm VO2max. They correctly interpreted this as evidence of a central cardiovascular training effect.

In 1976 Saltin et al. examined the effects of one-legged cycle training on the increase in VO2max in a trained leg, a control leg, and 2-legged bicycling. The trained leg had a 23% increase compared with a 7% increase in VO2max in the control leg (Fig. 8). The disparity between legs was attributed to peripheral adaptations occurring within the trained skeletal muscle. The authors concluded that peripheral factors were dominant in limiting VO2max. This study was conducted during the 1970s as new discoveries about fiber type, capillary density, and oxidative enzyme activities in athletes were being made. At that time, the investigators thought that these changes were essential for increasing VO2max.

However, in 1985 Saltin et al. performed the definitive experiment showing that VO2max is limited by blood flow. They observed what happens when a subject does maximal exercise using only a small muscle mass (i.e., knee extensions with only one leg). This allowed a greater proportion of cardiac output to be directed to an isolated area. Under these conditions, the highest O2 uptake in an isolated quadriceps muscle group was 2-3 times higher than that measured in the same muscle group during a whole-body maximum effort. They concluded that skeletal muscle has a tremendous capacity for increasing blood flow and VO2, which far exceeds the pumping capacity of the heart during maximal whole-body exercise. This experiment proved that VO2max is constrained by oxygen delivery and not by the mitochondria’s ability to consume oxygen.

How can we reconcile the results of the two experiments by Saltin et al.? In the earlier study, they measured VO2max during one-legged cycling. However, it must be remembered that maximal cardiac output is not the dominant factor limiting VO2max in exercise with an isolated muscle group (i.e., one-legged cycling). Whole-body VO2max is primarily limited by cardiac output, while for exercise with small muscle groups the role of cardiac output is considerably less important. Since the 1976 conclusion about peripheral limitations does not apply to VO2max measured in severe whole-body exercise, the later conclusion does not conflict with their earlier work. The current belief is that maximal cardiac output is the principal limiting
factor for VO2max during bicycling or running tests.

Comparative Physiology and Maximum Oxygen Uptake

Taylor et al. and Weibel have studied the physiological factors limiting VO2max from a different perspective. They examined different animal species to see what physiological factors explain the superior VO2max of the more athletic ones. These studies in comparative physiology provide a way to test the concept of “symmorphosis” which hypothesizes that animals are built in a reasonable manner. Their underlying assumption is that all parts of the pathway for O2 (from atmosphere to mitochondria) are matched to the functional capacity of the organism. If any one system involved in the O2 pathway were overbuilt, then there would be a redundancy that would be wasteful, from an energetic standpoint.

The first series of experiments compared mammalian species of similar size, but with a 2.5-fold difference in VO2max (dog vs goat, racehorse vs steer). This is referred to as “adaptive variation” (adaptation was defined in the evolutionary sense, as the end-result of natural selection). The high VO2max values in the more athletic species were accompanied by a 2.2-fold increase in stroke volume, nearly identical maximal heart rate, and a large increase in mitochondria. In general, these adaptive pairs show similar physiological differences as observed when trained and untrained humans are compared (Table 1).

A second series of experiments examined a variety of animal species ranging in size from a few grams to 250 kg. The difference in VO2max seen in animals of varying body mass (Mb) is termed “allometric variation.” VO2max values (L/min) increase with body mass to the power of 0.81. However, when adjusted for body mass, small animals have VO2max/Mb values that are 8–10 times higher than large animals (Fig. 9). Across a wide range of animal species, there is a very close match between mitochondrial density and VO2max/Mb. The smaller species have an abundance of mitochondria, so that the capacity of the muscles to consume oxygen is enhanced. It would be impossible for the smaller species to achieve such incredibly high metabolic rates (200 to 260 mL/kg/min) without an increase in mitochondrial density. Thus, it can be said that the muscles “set the demand for O2 ”.

The more athletic animals also have an increase in the size of the structures involved in supplying O2 to the working muscles. Lung size and function are scaled in proportion to VO2max. In addition, the heart’s pumping capacity is tightly coupled to VO2max. In adaptive variation (animals of same size), the more athletic animals achieve this by an increase in heart size. In allometric variation, small animals achieve an increase in O2 transport with a higher maximal heart rate (1300 beats/min in the shrew). The general conclusion of these studies is that the principle of symmorphosis is upheld. The structures involved in the O2 pathway are scaled in proportion to VO2max, meaning that animals are built in a reasonable manner.

However, there are exceptions where one sees redundancies at various levels in the pathway for O2. For example, the mitochondria’s ability to consume O2 exceeds the ability of the cardiorespiratory system to supply it. To illustrate this point, in maximally exercising animals the mitochondria have a fixed respiratory capacity, with an invariant value of 4-5 mL O2/mL of mitochondria per minute across species. However, the respiratory capacity of isolated mitochondria has been measured at 5.8 mL O2/mL of mitochondria per minute. Using these values, Taylor and Weibel conclude that animals are able to exploit 60-80% of the in vitro oxidative capacity when they exercise at VO2max. The reason that mitochondria cannot fully exploit their oxidative ability is a result of the limitation on O2 delivery imposed by the central cardiovascular system.

Reaching Consensus on Limiting Factors for Maximum Oxygen Uptake

Physiologists have often asked, “What is the limiting factor for VO2max?” The answer depends on the definition of a limiting factor and the experimental model used to address the problem (R.B. Armstrong, personal communication, February, 1999). If one talks about the intact human being performing maximal, whole-body exercise, then the cardiorespiratory system is the limiting factor. If one discusses the factors that limit the increase in VO2 in an isolated dog hindlimb, then the peripheral diffusion gradient is limiting. If one talks about the factors that explain the difference in VO2max across species, mitochondrial content and O2 transport capacity are both important.

Wagner, Hoppeler, and Saltin have succeeded in reconciling the different viewpoints on factors limiting VO2max. They conclude that while VO2max is broadly related to mitochondrial volume across a range of species, in any individual case VO2max is determined by the O2 supply to muscle. They state that in humans “...the catabolic capacity of the myosin ATPase is such that it outstrips by far the capacity of the respiratory system to deliver energy aerobically. Thus, VO2max must be determined by the capability to deliver O2 to muscle mitochondria via the O2 transport system, rather than by the properties of the muscle’s contractile machinery.”

Wagner, Hoppeler, and Saltin maintain that there is no single limiting factor to VO2max. They conclude that “... each and every step in the O2 pathway contributes in an integrated way to determining VO2max , and a reduction in the transport capacity of any of the steps will predictably reduce VO2max.” For instance, a reduction in the inspired PO2 at altitude will result in a decreased VO2max. A reduced hemoglobin level in anemia will result in a decreased VO2max. A reduction in cardiac output with cardioselective beta-blockade will result in a decreased VO2max. There are also instances where substrate supply (not O2) is the limiting factor. For example, metabolic defects in skeletal muscle, such as McArdle’s disease (phosphorylase deficiency) or phospho-fructokinase deficiency, will result in a decreased VO2max.

In the field of exercise physiology, when limiting factors for VO2max are discussed, it is usually with reference to human subjects, without metabolic disease, undergoing maximal whole-body exercise, at sea level. Under these conditions, the evidence clearly shows that it is mainly the ability of the cardiorespiratory system (i.e., heart, lungs, and blood) to transport O2 to the muscles, not the ability of muscle mitochondria to consume O2, that limits VO2max. We conclude that there is widespread agreement with regard to the factors limiting VO2max, and that this agreement is based on sound scientific evidence. In general, the 75 years of subsequent research have provided strong support for the brilliant insights of Hill et al..

PART III: DETERMINANTS OF ENDURANCE PERFORMANCE

A first principle in exercise physiology is that work requires energy, and to maintain a specific work rate or running velocity over a long distance, ATP must be supplied to the cross bridges as fast as it is used. As the duration of an all-out performance increases there is greater reliance on ATP production via oxidative phosphorylation to maintain cross bridge cycling. Consequently, the rate at which oxygen is used during prolonged submaximal exercise is a measure of the rate at which ATP is generated. In our previous paper we summarized the conventional understanding of how oxygen uptake is linked to endurance running performance. A variety of criticisms were directed at our attempt, ranging from suggestions that correlation data were being used to establish “cause and effect,” to concerns that our model was not adequately explained. In the following paragraphs we will summarize the physiological model linking oxygen uptake with performance in distance running.

Figure 10 shows that the VO2 maintained during an endurance run (called the “performance VO2 ” by Coyle) is equal to the product of the runner’s VO2max and the percent of VO2max that can be maintained during the performance. The percent of VO2max is related to the VO2 measured at the lactate threshold (LT), so that for endurance events the performance VO2 is closely linked to the VO2 at the LT. The VO2max is limited primarily by central cardiovascular factors (see Part II above), while the percent of VO2max that can be maintained is linked primarily to adaptations in muscles resulting from prolonged training. The actual running velocity realized by this rate of oxidative ATP generation (the performance VO2) is determined by the individual’s ability to translate energy (e.g., running economy) into performance. We
will again summarize the role of each of these variables in distance running performance.



Role of Maximum Oxygen Uptake in Running Performance

Previously we stated that “VO2max sets the upper limit for performance in endurance events”, not that it is “the best predictor of athletic ability”. Data of Costill et al. were presented to show an inverse correlation between VO2max and time in a 10-mile run. These investigators used subjects with a wide range of VO2max values (54.8 to 81.6 mL/kg/min) to examine this relationship. This was an appropriate research design to see whether a correlation existed between these two variables in that such a relationship must be evaluated over an appropriate range of values. If one were to narrow the range of values over which this relationship was examined, the correlation coefficient would approach zero as the range of values approaches zero. Consequently, we acknowledged the fact that VO2max was not a good predictor of performance in runners with similar VO2max values. If Costill et al. had found the correlation between VO2max and time in a 10-mile run in this diverse group of runners to be r = -0.09 rather than r = -0.91, there would have been little debate. We are in agreement that a high correlation does not imply “cause and effect;” however, to simply dismiss a high correlation between two variables having high construct validity might result in an investigator missing an important point.

VO2max is directly linked to the rate of ATP generation that can be maintained during a distance race, even though distance races are not run at 100% VO2max. The rate of ATP generation is dependent on the VO2 (mL/kg/min) that can be maintained during the run, which is determined by the subject’s VO2max and the percent of VO2max at which the subject can perform (Fig. 10). For example to complete a 2:15 marathon, a VO2 of about 60 mL/kg/min must be maintained throughout the run. Consequently, even if a marathon could be run at 100% VO2max, the runner would need a VO2max of 60 mL/kg/min for the above performance. However, since the marathon is typically run at about 80-85% of VO2max, the VO2max values needed for that performance would be 70.5-75 mL/kg/min. In this way VO2max sets the upper limit for energy production in endurance events but does not determine the final performance. As we stated in the previous article there is no question that runners vary in running economy as well as in the percent of VO2max that can be maintained in a run; both have a dramatic impact on the speed that can be maintained in an endurance race. These will be discussed in the following paragraphs.

Running Economy

Mechanical efficiency is the ratio of work done to energy expended. The term “running economy” is used to express the oxygen uptake needed to run at a given velocity. This can be shown by plotting oxygen uptake (mL/kg/min) versus running velocity (m/min) or by simply expressing economy as the energy required per unit mass to cover a horizontal distance (mL O2/kg/km). In our previous paper we showed that running economy explains some of the variability in distance running performance in subjects with similar VO2max values. Data from Conley and Krahenbuhl were used to show a relatively strong correlation (r = 0.82) between running economy and performance in a 10-km run in a group of runners with similar VO2max values but with a range of 10-km times of 30.5-33.5 min. As was pointed out in the rebuttal, when one examines the fastest four runners (10 km in 30.5-31 min) there was considerable variability in the economy of running (45-49 mL/kg/min at 268 m/min), suggesting a lack of association between the variables. As mentioned above, this is to be expected. A correlation coefficient will approach zero as the range of values for one of the variables (in this case, performance times ranging from 30.5 to 31 min) approaches zero. There is little point in looking at a correlation unless the range of values is sufficient to determine whether a relationship exists.

There is a linear relationship between submaximal running velocity and VO2 (mL/kg/min) for each individual. However, there is considerable variation among individuals in how much oxygen it costs to run at a given speed, that is, running economy. Figure 11 shows a bar graph of the variation in running economy (expressed in mL/kg/km) among groups that differ in running ability. The group of elite runners had a better running economy than the other groups of runners, and all running groups were better than the group of untrained subjects. However, one of the most revealing aspects of this study was the within-group variation; there was a 20% difference between the least and most economical runner in any group.

One of the best descriptions of how VO2max and running economy interact to affect running velocity was provided by Daniels in his description of “velocity at VO2max” (vVO2max). Figure 12 shows a plot of male and female runners equal in terms of VO2max, but differing in running economy. A line was drawn through the series of points used to construct an economy-of-running line, and was extrapolated to the subject’s VO2max. A perpendicular line was then drawn from the VO2max value to the x-axis to estimate the velocity that subject would have achieved at VO2max. This is an estimate of the maximal speed that can be maintained by oxidative phosphorylation. In this example, the difference in running economy resulted in a clear difference in the speed that could be achieved if that race were run at VO2max. In like manner, Figure 13 shows the impact that a difference in VO2max has on the vVO2max in groups with similar running economy values. The 14% difference in VO2max resulted in a 14% difference in the vVO2max. Consequently, it is clear that both VO2max and running economy interact to set the upper limit of running velocity that can be maintained by oxidative phosphorylation. However, since distance races are not run at VO2max, the ability of the athlete to run at a high percentage of VO2max has a significant impact on running performance.

Percent of Maximum Oxygen Uptake

Figure 14, from the classic Textbook of Work Physiology by Åstrand and Rodahl characterizes the impact that training has on one’s ability to maintain a certain percentage of VO2max during prolonged exercise. Trained individuals functioned at 87% and 83% of VO2max for 1 and 2 h, respectively, compared with only 50% and 35% of VO2max for the untrained subjects. This figure shows clearly the impact that the %VO2max has on the actual (performance) VO2 that a person can maintain during an endurance performance. In addition, Figure 15, taken from the same text, shows how VO2max and the %VO2max change over months of training. VO2max increases during the first 2 months and levels off, while the %VO2max continues to change over time. Consequently, while changes in both VO2max and the %VO2max impact changes in the performance of a subject early in a training program, subsequent changes in the performance VO2 are caused by changes in the %VO2max alone. This classic figure is supported by later work showing that the VO2 at the LT (%VO2max at the LT) increases much more as a result of training than does VO2max.





The Lactate Threshold and Endurance Performance

The model presented earlier in Figure 10 showed how VO2max and %VO2max interact to determine the performance VO2 and how running economy shapes the final performance. In this model the VO2 at the LT integrates both VO2max and the % VO2max. In our previous paper we used a more detailed model to show that running velocity at the LT integrates all three variables mentioned earlier (the VO2max, the %VO2max, and running economy) to predict distance running performance. We will now use that same model (Fig. 16) to expand our discussion with a focus on the lactate threshold.



To determine a lactate threshold, a subject completes a series of tests at increasing running speeds, and after each test a blood sample is taken for lactate analysis. The speed at which the lactate concentration changes in some way (e.g., to an absolute concentration, a break in the curve, a delta amount) is taken as the speed at the LT and is used as the predictor of performance. Numerous studies have shown the various indicators of the LT to be good predictors of performance in a variety of endurance activities (e.g., running, cycling, race walking) and for both trained and untrained populations. In most of these studies the association between the LT and endurance performance was evaluated in groups of athletes that were heterogeneous relative to performance. As discussed earlier, this is an appropriate design to see whether a relationship (correlation) exists between the variables. On the other hand, if one were to narrow the range of performances (or the LT) over which this relationship were examined, one would expect the correlation to be markedly reduced. This means that
even though the speed at the LT explains the vast majority of the variance in performance in distance races other factors can still influence the final performance. If any model could explain all of the variance in performance, gold medals would be handed out in the lab!

The classical model that has been passed down to us revolves around the proposition that the ability to maintain a high running speed is linked to the ability to maintain a high rate of oxidative ATP production. Both logic and empirical data provide support for that proposition; to argue otherwise would suggest that “oxygen independent” (anaerobic) sources of ATP are important in such performances - a clear impossibility given the small amount of potential energy available via those processes.

It has been known for some time that lactate production is related to a number of variables, including the mitochondrial content of muscle, as measured by mitochondrial enzyme activity. Variations in the LT across diverse groups of endurance athletes and improvements in the LT resulting from training are linked to differences and increases in mitochondrial enzyme activity, respectively. An explanation for this connection was provided by Holloszy and Coyle in 1984. When muscles contract to meet a specific submaximal power output, ATP is converted to ADP and Pi to power the cross bridges, and the latter two, in turn, drive metabolic reactions in the cell to meet the ATP demand associated with that work rate. In a muscle cell with relatively few mitochondria the ADP concentration must rise to a high level to drive the limited number of mitochondria to meet the ATP demand via oxidative phosphorylation. This high concentration of ADP also drives other metabolic pathways, including glycolysis, because of the stimulatory effect of ADP on phosphofructose kinase (PFK). This results in a greater rate of carbohydrate turnover, an accumulation of pyruvate and NADH in the cytoplasm of the muscle fiber, and an increase in lactate production. Following training there is a large (50-100%) increase in the number of mitochondria in the muscles involved in the activity. Consequently, at the same work rate the oxygen uptake is shared by a greater number of mitochondria, and the ADP concentration does not have to rise to the same level as before training to achieve the same rate of oxidative phosphorylation (VO2) after training. The lower level of ADP after training results in less stimulation of PFK and a reduction in carbohydrate turnover, and the greater number of mitochondria increases the capacity to use fat as a fuel. The result is less lactate formation.

As we mentioned throughout this section, the relationships between VO2max and performance, running economy and performance, and %VO2max and performance used groups with large variations in the independent variables. As one reduces the range of each of these variables, the correlations are reduced in magnitude or eliminated, suggesting that other variables also influence performance. Instead of dismissing the relationships as having little worth, investigators have used these observations as motivation to examine other factors that might be related to endurance performance. An excellent example of taking the next step is found in an experiment by Coyle et al..

Coyle et al. studied 14 trained cyclists (3–12 yr of training) who were similar in terms of VO2max (thus eliminating that as a variable) to examine the relationship between the LT and time to fatigue at 88% VO2max. Subjects were divided into high-LT (mean = 81.5% VO2max ) and low-LT (mean = 65.8% VO2max) groups. The performance test at 88% VO2max resulted in large differences in performance (60.8 vs 29.1 min), and the postexercise lactate concentration (7.4 vs 14.7 mM) for the high-LT and low-LT groups, respectively. The difference in performance between these groups that had the same VO2max, but differed in the %VO2max at the LT, was consistent with the model described above. On the other hand, the fact that the vastus lateralis of both groups had the same mitochondrial enzyme activities suggested a break in the chain of evidence linking the %VO2max at the LT and mitochondrial activity. This created a rare opportunity for the investigators to study two groups with the same VO2max and the same mitochondrial enzyme activity but with substantial differences in performance. The investigators examined the metabolic response of the cyclists to a 30-min test at 79% VO2max. They found that while the low-LT group used 69% more carbohydrate during this exercise bout than the high-LT group, the low-LT group reduced its vastus lateralis muscle glycogen concentration 134% more than the high-LT group. This difference in muscle glycogen depletion (relative to total carbohydrate oxidation) suggested that the high-LT group was able to distribute the same work rate (and VO2) over a larger muscle mass, resulting in less loading on the muscle fibers recruited to do the work. Use of a larger muscle mass also increased the mass of mitochondria sharing in the production of ATP by oxidative phosphorylation. Consequently, the study of Coyle et al. indicates that the mass of muscle involved in the activity (in addition to mitochondrial density) contributes to the %VO2max at the LT (as well as performance), in a manner consistent with the above model.

LT, THE CLASSICAL MODEL, AND ENVIRONMENTAL FACTORS

Noakes has asked, “...why should prolonged endurance exercise in which the oxygen consumption is not maximal and therefore not limiting be determined by the oxygen delivery to the active muscle?”. This is a good question because a marathon runner can certainly run at faster speeds and higher VO2 values over shorter distances - but not without some metabolic consequences. During submaximal exercise, oxygen delivery to muscle is closely tied to the mitochondrial oxygen demand which is driven by the cellular charge (i.e., [ADP + Pi]) provided by the exercise. As mentioned earlier, this same cellular charge also drives other metabolic pathways, notably, glycolysis. If a marathoner chose to run at a speed above the LT, the increased cellular charge needed to drive the VO2 to the higher level would also speed up glycolysis. This would deplete the limited carbohydrate store at a faster rate; the resulting increase in blood lactate accumulation would be caused by both an increase in lactate formation and a decrease in lactate removal. Given the obligatory need for carbohydrate at high exercise intensities and the negative impact of hydrogen ion accumulation on muscle function, neither of these changes are consistent with being able to maintain the faster pace over a marathon distance.

In this and our previous paper we attempted to explain how the variables of VO2max, the percentage of VO2max, and running economy can account for the vast majority of the variance in distance running performances. In addition, the model also accounts for the impact of certain environmental factors on endurance performance. Acute exposure to moderate altitude results in a decrease in arterial oxygen saturation and VO2max. Consequently, the “performance VO2” is decreased even though runners can still perform at a similar percentage of VO2max, and performance in endurance events is adversely affected. Historically, this effect of a lower PO2 causing a shift in the LT was interpreted as an “oxygen lack” at the muscle. However, it is now recognized that the lower PO2 results in a higher cellular charge to achieve the same steady state VO2 at a fixed submaximal work rate. These circumstances will result in a higher rate of glycolysis, an accumulation of NADH1, and an increase in lactate production.

Performance times in the marathon are adversely affected by high environmental temperatures, with race times being optimal at a temperature of 12-13°C, and a decrement of 40 s expected for every 1°C rise in temperature. Exercise in the heat increases the rate of carbohydrate oxidation, leading to a faster rate of muscle glycogen depletion and higher blood lactate concentrations during prolonged work. Consequently, changes in metabolism resulting from acute exposure to heat or altitude are associated with a decrease in endurance performance, consistent with the model.

Postscript

In summary, the “classical” model of VO2max passed down by Hill et al. has been modified and expanded upon by numerous investigators. We now have a much more complete understanding of the determinants of endurance performance than did exercise scientists from the 1920s. In hindsight, Hill et al. were wrong about some of the details, such as the notion of a strict 1:1 ratio of O2 deficit:O2 debt. However, Hill deserves recognition for his major role in the discovery of nonoxidative pathways in isolated frog muscle and the application of this discovery to the exercising human. Hill’s work shaped the emerging discipline of Exercise Physiology, and his ideas continue to be influential even to this day.

Hill welcomed challenges to his theories and urged others to critically analyze scientific beliefs. It is clear that he viewed errors in interpretation and scientific debate over the merits of competing theories to be a necessary part of progress. In Trails and Trials in Physiology, Hill stated that, “Knowledge advances by continual action and reaction between hypothesis on the one hand and observation, calculation, and experiment on the other.” In contrast to the view that the classical theory represents an “ugly and creaking edifice”, we have arrived at a very different point of view. Our conclusion is that Hill’s theories have served as an ideal theoretical framework. The work that has built upon this framework has allowed exercise scientists to learn much about the physiological factors governing athletic performance.

Effect of intensity of aerobic training on VO2max.

Gormley SE, Swain DP, High R, Spina RJ, Dowling EA, Kotipalli US, Gandrakota R.
Med Sci Sports Exerc. 2008 Jul;40(7):1336-43.

PURPOSE: To determine whether various intensities of aerobic training differentially affect aerobic capacity as well as resting HR and resting blood pressure (BP). METHODS: Sixty-one health young adult subjects were matched for sex and VO2max and were randomly assigned to a moderate- (50% VO2 reserve (VO2R), vigorous (75% VO2R), near-maximal-intensity (95% VO2R), or a nonexercising control group. Intensity during exercise was controlled by having the subjects maintain target HR based on HR reserve. Exercise volume (and thus energy expenditure) was controlled across the three training groups by varying duration and frequency. Fifty-five subjects completed a 6-wk training protocol on a stationary bicycle ergometer and pre- and posttesting. During the final 4 wk, the moderate-intensity group exercised for 60 min, 4 d.wk the vigorous-intensity group exercised for 40 min, 4 d.wk and the near-maximal-intensity group exercised 3 d.wk performing 5 min at 75% VO2R followed by five intervals of 5 min at 95% VO2R and 5 min at 50% VO2R. RESULTS: VO2max significantly increased in all exercising groups by 7.2, 4.8, and 3.4 mL.min.kg in the near-maximal-, the vigorous-, and the moderate-intensity groups, respectively. Percent increases in the near-maximal- (20.6%), the vigorous- (14.3%), and the moderate-intensity (10.0%) groups were all significantly different from each other. There were no significant changes in resting HR and BP in any group. CONCLUSION: When volume of exercise is controlled, higher intensities of exercise are more effective for improving VO2max than lower intensities of exercise in healthy, young adults.

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Only two studies have compared near-maximal intervals with lower-intensity continuous training in healthy adults, and both studies included only highly fit males as subjects (11, 16).

... groups: 1) moderate intensity (50% VO2R), 2) vigorous intensity (75% VO2R), 3) near-maximal intensity (intervals at 95% VO2R), and 4) nonexercising control.

DISCUSSION

The main finding of the study was that higher intensities of exercise elicit greater improvements in VO2max than lower intensities of exercise over a 4- to 6-wk training period in healthy, young adults. This finding is consistent with the original hypothesis. Unlike VO2max, there were no changes observed in resting HR and resting BP after training.

A study recently published by Helgerud et al. (16) examined the effects of 8 wk of aerobic endurance training at various exercise intensities in healthy, young-adult males. Groups performed running at a moderate-intensity (70% HRmax for 45 min each session), vigorous-intensity (85% HRmax for ~24 min per session), and two maximal-intensity interval training regimens that both alternated 90-95% HRmax with 70% HRmax, one using multiple 15-s intervals and one using four 4-min intervals. Both interval training groups significantly increased VO2max, whereas neither continuous training group did. Using a previously published formula, the moderate- and vigorous-intensity groups of Helgerudet al. were exercising at ~47% and ~72% HRR, respectively, which are comparable to the current study. The failure of the continuous training groups of Helgerud et al. to increase VO2max was probably due to their high baseline fitness, which averaged 58 mL/min/kg. Esfarjani and Laursen (11) recently compared interval training at VO2max with continuous training at 75% HRR in male runners. As in the study of Helgerud et al., the subjects’ baseline VO2max was greater than 50 mL/min/kg, and only the interval group increased VO2max. Both of these studies differed from the current study in the population (only males vs both males and females; high vs average fitness) and the mode of exercise (running vs cycling).

It should be noted that although interval training groups spend some of their training time at a very high intensity, a similar amount of time is spent at a lower intensity, and therefore the mean intensity of training may not be any higher than that of a continuous training program. In the current study, the interval training group used 5 min each for the work and the recovery phases of the intervals and had an average intensity of 72% HRR, which is slightly less than the 75% HRR of the vigorous group. The work–recovery periods of Helgerud et al. were 4 min at ~93% HRmax and 3 min at 70% HRmax, for a mean intensity of 83% HRmax in the interval group, whereas one of the continuous groups used 85% HRmax. Warburton et al. used 2 min at 90% HRR and 2 min at 40% HRR for the work and the recovery phases, yielding a mean intensity of 65% HRR in the interval group, and had the continuous training group use 65% HRR. Wisloff et al. used 4-min work phases at ~93% HRmax and 3-min recovery phases at 60% HRmax, for a mean intensity of 79% HRmax in the interval group, and used ~73% HRmax in the continuous training group. Despite the similarity of mean intensity between the interval and the continuous training groups, the interval groups in all of these studies experienced greater improvements in aerobic fitness after training. Therefore, although intensity is a key variable in cardiorespiratory training (as shown by comparing the two continuous training groups in this study), the mean intensity may not be as important as the highest intensity that is used for a significant portion of the training. A topic for future research is to determine what portion of training should be done at high intensities and using what work–recovery periods to obtain the greatest results.

The effect of endurance training on parameters of aerobic fitness.

Sports Med. 2000 Jun;29(6):373-86. Review.
Jones AM, Carter H.

The performance of repeated bouts of exercise over a period of time causes numerous physiological changes that result in improved performance in that exercise activity. The magnitude of the training response depends on the duration of the exercise bouts, their intensity and the frequency with which they are performed, along with the initial training status, genetic potential, age and gender of the individual. The specificity of the training stimulus is also important in terms of the type of training practised (endurance, strength or speed) and the exercise modality used. Appropriate recovery periods are required to allow adaptation to the training load: an insufficient training stimulus and/or too much recovery can lead to lack of progress or detraining while too great a training overload with insufficient recovery can lead to overtraining.

Endurance can be defined as the capacity to sustain a given velocity or power output for the longest possible time. Performance in endurance events is therefore heavily dependant upon the aerobic resynthesis of ATP; this requires an adequate delivery of oxygen from the atmosphere to cytochrome oxidase in the mitochondrial electron transport chain and the supply of fuels in the form of carbohydrates and lipids. Endurance can be crudely described through the generation of individual ‘velocity-time curves’ which relate a series of velocities (or power outputs) to the time for which these velocities or power outputs can be sustained. Endurance training causes adaptations in the pulmonary, cardiovascular and neuromuscular systems that improve the delivery of oxygen from the atmospheric air to the mitochondria and enhance the control of metabolism within the muscle cells. These adaptations shift the velocity-time curve to the right and therefore result in improved endurance exercise performance. This review will focus on the effect of endurance training on the 4 key parameters of aerobic (endurance) fitness identified by Whipp et al.: the maximal oxygen uptake (VO2max), exercise economy, the lactate/ventilatory threshold and oxygen uptake kinetics. For the purposes of this review, endurance exercise will be considered to be continuous events of approximately 5 to 240 minutes duration completed at around 65 to 100% of the VO2max. Events of shorter duration require a significant contribution from anaerobic metabolic pathways, while events of longer duration may be limited by psychological, nutritional, thermoregulatory or musculoskeletal factors rather than by ‘endurance fitness’, per se.

1. Maximal Oxygen Uptake (VO2max)

VO2max, which reflects an individual’s maximal rate of aerobic energy expenditure, has long been associated with success in endurance sports. In whole-body exercise such as running, cycling and rowing, it is widely accepted that VO2max is limited by the rate at which oxygen can be supplied to the muscles and not by the muscle’s ability to extract oxygen from the blood it receives. The VO2max appears to be strongly related to the maximal cardiac output (Qmax). The high Qmax and VO2max values commonly found in elite athletes are, in turn, related to very high maximal stroke volumes since maximal heart rates tend to be similar to those of sedentary individuals. Following training, exercising muscle may require less blood flow for the same submaximal exercise intensity because of an increase in the arterio-venous oxygen difference. The increased stroke volume resulting from increases in left ventricular size, myocardial contractility and end-diastolic volume with training, along with a decreased sensitivity to catecholamines, leads to a reduced heart rate during submaximal exercise. During maximal exercise, the greater cardiac output, along with an increased extraction of oxygen by the exercising muscle, results in a greater VO2max. In addition, the oxygen carrying capacity of the blood is increased following endurance training owing to an increased total blood haemoglobin content. There is also an increase in red cell 2,3-diphosphoglycerate which offsets the reduced haemoglobin concentration consequent to the relatively larger increase in plasma volume compared to red cell mass. The lower [Hb] following training may be advantageous in that the reduced blood viscosity may reduce the resistance of the vasculature to blood flow.

The magnitude of the increase in VO2max resulting from endurance training depends on a number of factors, notably the initial fitness status of the individual, the duration of the training programme and the intensity, duration and frequency of the individual training sessions. Since most studies of endurance training have shown some increase in VO2max with time, the optimal exercise volume and intensity for developing this parameter is not known. However, there is some evidence from the literature to suggest that a high intensity of training (approximately 80 to 100% of VO2max) may be of crucial importance provided that the minimal training volume for a particular event is covered. In a recent study, we examined the influence of 6 weeks of endurance training on parameters of aerobic fitness in 16 physical education students. Despite the relatively modest training programme (3 to 5 sessions per week of 20 to 30 minutes duration at a running speed close to the lactate threshold), we found that VO2max increased by approximately 10% (from 47.9 ± 8.4 to 52.2 ± 2.7 mg/kg/min). Other groups have also shown a 5 to 10% improvement in VO2max with short term endurance training programmes. Hickson et al. reported that VO2max increased by 23% over 9 weeks of endurance training, but the majority of this increase (14%) occurred after only 3 weeks. This rapid increase in VO2max and the similarly rapid reduction in submaximal exercise heart rate have been partly attributed to an early hypervolaemia which will increase stroke volume during exercise and also afford an increased tolerance to heat stress. There is some evidence that during longer term training programmes, VO2max will eventually stabilise, with subsequent improvements in performance resulting from continued improvements in submaximal factors such as exercise economy and lactate threshold.

2. Exercise Economy

Exercise economy has been defined as the oxygen uptake required at a given absolute exercise intensity. There is considerable interindividual variability in the oxygen cost of submaximal exercise, even in individuals of similar aerobic fitness (defined as VO2max) or similar performance capability. For example, Horowitz et al. demonstrated that elite cyclists exercising at the same power output required different rates of oxygen uptake. Interestingly, the more efficient cyclists had a greater percentage of type I fibres in the vastus lateralis, suggesting that the pattern of motor unit recruitment during exercise may be important in the determination of economy. In a classic study, Conley and Krahenbuhl reported that 10km race performance was closely related to running economy in a group of well-trained volunteers who had similarly high VO2max values. Better exercise economy (i.e. lower VO2 for a given absolute running speed or power output) can be considered to be advantageous to endurance performance because it will result in the utilisation of a lower percentage of the VO2max for any particular exercise intensity. It has been suggested that the relatively low VO2max scores that have been reported in some elite endurance athletes can be compensated for by exceptional exercise economy. Indeed, an inverse relationship between VO2max and running economy has been reported in samples of well-trained runners.

Although trained athletes are known to have better exercise economy than untrained individuals, studies that have examined the effect of endurance training on exercise economy have produced equivocal results. This may be because such training studies (typically of 6 to 12 weeks duration) are too short to produce a measurable improvement in economy, especially in individuals who are already trained. It may be speculated that good exercise economy is somehow related to the total volume of endurance training performed, since the best economy values are often found in older or more experienced athletes, or those who complete a large weekly training mileage. Furthermore, athletes’ most economical velocities or power outputs tend to be those at which they habitually train (unpublished data). This may indicate that athletes should train over a wide variety of speeds if they wish to lower the slope of the VO2-exercise intensity relationship. Only a few studies have tracked changes in exercise economy over a prolonged period of training. In one such study that measured changes in a number of physiological variables over a 5-year period in an elite female distance runner, it was reported that running economy improved appreciably with each year of training. For example, the VO2 at a running speed of 16.0 km/h decreased from 53.0 ml/kg/min in 1992 to 47.6 ml/kg/min in 1995. However, improvements in running economy can sometimes be observed even with short term training programmes. In a recent study, we found that 6 weeks of endurance running training caused a significant improvement in running economy in 16 recreationally active individuals (fig.1), with the VO2 at a representative running speed of 12.0 km/h decreasing from approximately 39 ml/kg/min to approximately 36 ml/kg/min. Franch et al. also reported that the running economy of trained volunteers could be reduced significantly following 6 weeks of high intensity distance running or long-interval training, and found that the reduction in submaximal VO2 was significantly correlated with the reduction in minute ventilation (VE).

Running economy has been associated with anthropometric (including segmental mass distribution), physiological and metabolic, and biomechanical and technical factors. Improvements in exercise economy with endurance training may result from improved muscle oxidative capacity and associated changes in motor unit recruitment patterns, reductions in exercise ventilation and heart rate for the same exercise intensity, and improved technique. These improvements may be partly offset by an increased utilisation of fat as exercise substrate following training due to the greater amount of oxygen that is required for the resynthesis of ATP from fat metabolism compared to carbohydrate metabolism. Of interest is the possibility that exercise economy is related to muscle elasticity. It has been speculated that running economy might be related to ‘fluency’ of movement and that it might therefore be improved by flexibility training. However, recent observations from our laboratory suggest that the oxygen cost of running at 16.0 km/h is negatively related to lower limb flexibility (estimated with the sit-and-reach test) in 26 international-standard male distance runners, i.e. ‘stiffer ’ runners were more economical. Similar results can be found in the literature. One explanation for these results is that stiffer muscles and tendons are better able to store elastic energy during the eccentric phase of stretch-shortening activities and that this stored energy can be released during the concentric phase of the action, thus lowering the oxygen cost of the exercise. Alternatively, inflexibility in the trunk and hip may stabilise the pelvis during the stance phase and limit the requirement for stabilising muscular activity.

It has been suggested that increasing maximal leg strength through resistance training may improve economy and endurance performance by reducing the proportion of the maximal force required for each contraction (e.g. pedal thrust) and hence delaying the recruitment of type II motor units. However, traditional resistance training programmes which involve lifting moderate to high loads at relatively slow movement speeds have, with some exceptions, been shown to be ineffective in improving endurance performance. However, of great interest is a recent study which demonstrated that ‘explosive strength training’, involving sprinting and jumping exercises and weight training using high to maximal movement speeds and low loads (0 to 40% of the 1-repetition maximum), can improve both running economy and 5km race performance. The authors suggested that the improved neuromuscular control resulting from the training could have improved running economy by allowing a tighter regulation of muscle stiffness and better utilisation of muscle elasticity. It is also possible that strength training using maximal velocity contractions may improve economy by allowing for a better recruitment of motor units or a reduced cocontraction of antagonistic muscle groups. One other study has demonstrated a similar effect of explosive strength training on the economy of cross-country skiers. Clearly, additional research is required to confirm and extend these findings.

3. Interaction Between VO2max and Economy

The locomotory velocity associated with VO2max (V-VO2max), which is a function of individual VO2max and exercise economy characteristics and which can be calculated by solving the regression equation describing the relationship between VO2 and submaximal exercise intensity for VO2max, has been shown to be an important determinant of endurance exercise performance. Morgan et al. reported that the running speed at VO2max strongly predicted 10km running performance in a group of well trained male runners with homogeneous VO2max values (approximately 65 ml/kg/min). Jones and Doust presented a comprehensive battery of physiological tests to 13 trained runners with a wide range of VO2max values (53 to 67 ml/kg/min), and reported that V-VO2max correlated more strongly with 8km running performance (r = 0.93) than any of the other measures, including VO2max (r = 0.69) and running economy (r = –0.16). Although they are closely related, the V-VO2max should not be confused with the maximal velocity reached in a fast incremental treadmill test (Vmax). Although some studies have shown that the Vmax correlates highly with endurance exercise performance, Vmax is influenced not just by VO2max and exercise economy factors but also by anaerobic capability, muscle power and neuromuscular skill in exercising at high speeds.

Several studies have shown an increased V-VO2max following endurance training. Jones reported that V-VO2max increased from 19.0 to 20.4 km/h over a 5-year period in an elite female distance runner. This improvement in V-VO2max was the result of an improved running economy because VO2max fell slightly over the same period of time. The V-VO2max is similar to the velocity that can be sustained during distance running races of 3000m (approximately 8 minutes in the elite athlete), and so this parameter may be especially important for success in middle-distance events. Billat et al. reported that only 4 weeks of normal training caused a significant improvement in running economy and V-VO2max (from 20.5 to 21.1 km/h), with no significant change in VO2max (from 71.2 to 72.7 ml/kg/min), in 8 trained males. Berthoin et al. reported that V-VO2max was significantly improved only with high intensity training in adolescent volunteers. In another study, Jones et al. found that 6 weeks of endurance training increased V-VO2max from 15.3 to 16.6 km/h in 16 volunteers, with the increased V-VO2max resulting from significant improvements in both VO2max and running economy. The V-VO2max appears to be an important and sensitive measure of endurance fitness and can be usefully measured during longitudinal work with endurance athletes. An improvement in the V-VO2max with training will mean that certain percentages of the VO2max will be associated with higher speeds after training. This may be important in the improvement of endurance race performance because athletes tend to operate at quite similar percentages of VO2max for a given duration of exercise. However, while the V-VO2max construct is practically useful, great care should be taken in its measurement. This is because VO2max may be achieved during constant-load exercise over a wide range of submaximal exercise intensities above the ‘critical power ’ because of the upward drift in oxygen uptake with time (see section 5). Therefore, for the accurate determination of V-VO2max there is a requirement both for a valid measure of VO2max and for exercise economy to be measured at several moderate intensities below the lactate threshold.

It has been suggested that the V-VO2max might represent an optimal training stimulus for improvements in endurance fitness. Hill and Rowell contend that training at V-VO2max is important because V-VO2max is the lowest speed that will elicit VO2max and it is necessary to train at VO2max to improve it. A concept that is closely related to the V-VO2max is the time for which exercise at V-VO2max can be sustained (Tmax). It has been shown that training at 100% V-VO2max allows exercise at VO2max to be sustained for the longest possible time (approximately 4 to 8 minutes). Hill and Rowell demonstrated that if interval or repetition sessions are constructed with the goal of allowing the longest possible training time at V-VO2max, then each repetition needed to be longer than 60% of Tmax. Recently, it was shown that a 4-week training programme which included 2 interval training sessions per week (6 repetitions at V-VO2max intensity for an exercise duration of 60 to 75% of the pre-training Tmax) resulted in significant improvements in VO2max, V-VO2max, Tmax and 3000m performance in trained runners. Unfortunately, this study did not have a control group, and additional studies are needed to confirm the value of using V-VO2max to set training intensity and Tmax to set training duration when the goal is to improve the V-VO2max.

4. Lactate/Ventilatory Threshold

The exercise intensity corresponding to the increase in blood lactate above resting levels (lactate threshold; LT) and the associated changes in gas exchange (ventilatory threshold; VT) are powerful predictors of endurance performance. Numerous studies also testify to the sensitivity of the LT and VT to endurance training. A rightward shift of the LT/VT to a higher power output or running speed is characteristic of successful endurance training programmes. This adaptation allows a higher absolute (running speed or power output) and relative (%VO2max) exercise intensity to be sustained without the accumulation of blood lactate after training. Endurance training is also associated with a reduction in the degree of lactacidaemia for any given absolute or relative exercise intensity. This causes the power output or running speed corresponding to arbitrary ‘blood lactate reference values’ such as 4mmol/L blood lactate to increase following a period of endurance training. Exercise above the LT is associated with a nonlinear increase in metabolic, respiratory and perceptual stress. Furthermore, exercise above the LT is associated with more rapid fatigue, either through the effects of metabolic acidosis on contractile function or through an accelerated depletion of muscle glycogen. Therefore, an improvement in the LT/VT with training is a clear marker of an enhanced endurance capacity. However, it should be noted that the LT/VT is typically found at 50 to 80% VO2max even in highly trained individuals, and it therefore occurs at a lower exercise intensity than is maintained by endurance athletes during most forms of endurance competition. The maximal lactate steady state (MLSS), which is the highest exercise intensity at which blood lactate does not accumulate over time (see section 5), may be of more importance to success in these events.

Mader proposed that the precision with which training loads can be applied may be improved through individual consideration of the LT. Several authors have hypothesised that the LT represents the optimal intensity for improvement of endurance fitness. Training at the LT should provide a high quality aerobic training stimulus without the accumulation of lactate that would compromise training duration. Anecdotally, endurance athletes and coaches feel that training at LT through the inclusion of a regular ‘threshold’ or ‘tempo’ training session is a critical component of a balanced training programme. The effect of training intensity on improvements in the LT/VT has recently been reviewed. In general, it appears that training at intensities close to or slightly above the existing LT/VT is important in eliciting significant improvements in this parameter. For example, it was reported that increasing training intensity through the use of fartlek training on 3 days per week, or adding a 20 minute run at LT speed to the weekly training programme, caused an improvement in the LT with no change in VO2max in runners. Henritze et al. reported that training at intensities above the LT may be even more effective for improving the LT, while Keith et al. have shown that continuous training at the LT or intermittent training above and below the LT are equally effective in improving LT. Collectively, these studies indicate that exercise training at an appropriately high intensity might be most effective in stimulating improvements in LT and performance.

The reduction in blood lactate for the same absolute and relative exercise intensities following endurance training may result from a reduction in the rate of lactate production (possibly consequent to a lower rate of muscle glycogen utilisation or to speeded oxygen uptake kinetics that may increase initial O2 availability/utilisation), or from an increase in the ability to exchange and remove lactate from the blood. Elite endurance athletes have a predominance of type I (‘slow-twitch’) muscle fibres in the trained musculature when compared to their sedentary peers. This is of interest because of the strong relationship that is known to exist between the percentage of type I muscle fibres and the LT. Endurance training causes a selective hypertrophy of the type I fibres and it is possible that a transformation of muscle fibre types from type IIb to type IIa, and even from type IIa to type I can eventually occur. There is also evidence that endurance training can cause an increased expression of slow myosin in type II fibres which reduces the maximal shortening speed in these fibres. Conversely, detraining and micro-gravity lead to a reduction in the expression of slow myosin in muscle fibres. The increased capillarity of skeletal muscle with endurance training has the effect of increasing both the maximal muscle blood flow capacity and the surface area available for exchange of gases, substrates and metabolites between blood and muscle. The longer mean transit time for red blood cells to pass through the muscle capillary bed will increase the time available for diffusion of oxygen from the red blood cell and increase the potential for widening the arterial-venous oxygen difference during exercise.

Endurance training results in numerous adaptations within skeletal muscle that may be significant for exercise performance, including increases in sodium-potassium pump concentration, lactate transport capacity and possibly myoglobin concentration. Endurance training also results in a marked increase in the oxidative capacity of skeletal muscle. This is due to an increase in the size and the number of mitochondria per unit area and an increase in the concentration of the enzymes of the Krebs cycle, electron transport chain and malate-aspartate shuttle. These adaptations help maintain cellular phosphorylation potential, improve the sensitivity of respiratory control and increase the capacity for aerobic ATP resynthesis during exercise in both type I and type II muscle. Muscle respiratory capacity is highly correlated with LT and these enzymatic adaptations may be important in allowing an athlete to exercise at a high percentage of VO2max for prolonged periods. It is possible that a greater oxidative enzyme complement in type I muscle fibres might delay the point at which the type II muscle fibres are recruited during exercise. Furthermore, an increase in the oxidative potential of the type II fibres might reduce their reliance on anaerobic glycolysis for ATP production. Animal studies suggest that low intensity training (approximately 50% VO2max) may be sufficient to maximise the increase in mitochondria in type I muscle, but that much higher intensities are needed to cause significant increases in mitochondrial volume in type II muscle.

The greater capacity of the Krebs cycle to accept pyruvate following training may be important in reducing the production of lactate by mass action at the onset of exercise and during high intensity exercise. However, the greater capillarity of trained muscle also allows for a greater uptake of free fatty acids from the blood and the increased activity of the enzymes involved in lipid metabolism increase the capacity for mitochondrial B-oxidation. It has been shown that there is a reduction in the rate of glycogen depletion, a decreased production and oxidation of blood-borne glucose and an increased storage and rate of utilisation of intramuscular triacylglycerol following training. The greater use of lipid during submaximal exercise, which can be documented in the lower respiratory exchange ratios found for the same absolute and relative exercise intensity following training, reduces the contribution of carbohydrate to ATP resynthesis and is therefore important in sparing muscle glycogen. This adaptation, along with evidence that endurance training increases the storage of muscle glycogen, is an important adaptation to endurance training because a depletion of muscle glycogen stores have been linked to fatigue during endurance exercise.

The hormonal response to exercise appears to change rather quickly following the onset of endurance training. For example, the catecholamine response appears to be substantially blunted for the same exercise intensity after only a few days of training. Since adrenaline is a major effector of lactate production through its modulation of muscle glycogenolysis, this may partly account for the reduction in muscle glycogen utilisation seen with endurance training. The reduced sympathetic nervous system activity may also contribute to the reduction in heart rate observed for the same exercise intensity following training.

5. Oxygen Uptake Kinetics

At the onset of ‘moderate’ exercise (that is, exercise that is below the LT) pulmonary oxygen uptake increases mono-exponentially to achieve a new steady state within 2 to 3 minutes. For constant-intensity exercise in this domain, the oxygen deficit that is incurred at the onset of exercise may cause blood lactate to rise transiently before it returns to resting levels as exercise proceeds. On the other hand, the imposition of an exercise challenge that is just above the LT causes blood lactate to rise until it attains a steady state level that is higher than the resting concentration. In this exercise domain, pulmonary VO2 will also attain a delayed steady state but the VO2 that is achieved may be higher than would be predicted based upon the relationship between VO2 and exercise intensity for moderate exercise. The MLSS can be defined as the highest running speed or power output at which blood lactate remains stable or increases only minimally (less than 1.0 mmol/L) between 10 and 30 minutes of exercise. The MLSS therefore demarcates the highest exercise intensity at which a balance exists between the appearance of lactate in the blood and the removal of lactate from the blood during long-term exercise, and is perhaps the ‘gold standard’ measure of endurance exercise capacity. In theory, the MLSS is the same as the concept of ‘critical power’ (CP) or ‘critical velocity’ that is represented by the asymptote of the hyperbolic relationship between exercise intensity and time to exhaustion. Submaximal exercise above the CP/MLSS is associated with an inexorable increase in blood lactate, pulmonary ventilation, and VO2 with time, and depending on the exercise intensity, VO2 may even rise to attain VO2max. This ‘drift’ in VO2 during constant-load exercise to values that are greater than might be expected has been termed the VO2 slow component. While the mechanisms responsible for this apparent metabolic inefficiency during high intensity submaximal exercise are not fully understood, exercise that elicits a VO2 slow component is poorly tolerated by volunteers. Therefore, training programmes that attenuate the VO2 slow component or that extend the range of exercise intensities over which the slow component does not develop will improve endurance exercise performance.

Several studies have evaluated the effects of endurance training on VO2 kinetics during cycle exercise. In general, the steady state VO2 for the same moderate intensity exercise has not been found to change following a period of endurance training, although the primary exponential increase in VO2 at the onset of exercise may be speeded. In cross-sectional studies, the VO2 on-kinetic adjustment to the same absolute or relative exercise intensity has been reported to be faster in individuals with higher VO2max values. Faster VO2 kinetics at exercise onset, resulting in a more rapid attainment of the requisite steady state oxygen uptake, might be important in reducing the initial oxygen deficit and limiting the early increase in blood lactate. A speeded VO2 on-kinetic response may facilitate the rapid establishment of an intracellular environment that allows tighter metabolic control later in exercise. Whether the primary mechanism for any speeding of the initial VO2 response to exercise is related to increased O2 delivery to muscle or to a reduced inertia of the intracellular oxidative machinery consequent to an increased muscle mitochondrial density is debated. Endurance training increases the CP, and reduces the magnitude of the VO2 slow component (defined as the increase in VO2 between 3 and 6 minutes of exercise) for the same absolute power output. Recent work in our laboratory has shown that 6 weeks of endurance running training results in a significant increase in the running speed at the MLSS, and a significant reduction in the amplitude of the VO2 slow component (from 321 to 217 ml/min on average) for the same absolute treadmill running speed (unpublished observations; fig. 3). Although the reductions in blood lactate levels, ventilation, heart rate and plasma catecholamine levels that accompany endurance training (see section 4) might partly explain the reduced O2 cost of heavy submaximal exercise after training, it appears that intramuscular changes and possibly alterations in motor unit recruitment patterns might be more important. Of interest in this respect is the suggestion that the relative contribution of the VO2 slow component to the total VO2 response to heavy exercise is negatively related to aerobic fitness (as VO2max) and/or the proportion of type I fibres in the working muscles.

6. Conclusion

Endurance exercise training results in numerous adaptations to the neuromuscular, metabolic, cardiovascular, respiratory and endocrine systems. These adaptations are reflected in improvements in the key parameters of aerobic fitness, namely the VO2max, exercise economy, the lactate/ventilatory threshold and the CP which will influence the oxygen uptake kinetics. An improvement in one or more of these parameters will result in an improvement in endurance exercise performance consequent to a rightward shift at various points on the velocity-time curve. The latter will allow an athlete to exercise for longer at the same exercise intensity or to sustain a higher speed for a given exercise duration. Although the aerobic parameters reviewed above are important determinants of endurance exercise performance, it should be borne in mind that competitive performance also depends upon psychological factors, race tactics and the prevailing environmental conditions. In addition, an athlete’s ability to generate ATP anaerobically can be important in sprint finishes between athletes whose aerobic capabilities are similar. Fukuba and Whipp have recently suggested that an athlete’s anaerobic work capacity (a derivative of the concept and computation of critical power) can determine his or her ability to initiate or respond to sections of a race that are faster than the athlete’s best average velocity for the distance.

While the parameters of aerobic fitness are interrelated, the specific emphasis placed on the training of each of these will depend upon an individual’s personal physiological ‘strengths’ and ‘weaknesses’ (which may be assessed in the sports physiology laboratory), and the duration of the event being trained for. For example, a 3000m runner may place special importance on the development of the V-VO2max and anaerobic capacity, while a marathon runner may focus on training to improve running economy and the running speed at lactate threshold. Presently, little is known about the most effective training practices for specifically improving the key parameters of aerobic fitness, or for altering different points on the velocity-time curve in order to effect a shift to the right of the velocity-time relationship. Exploration of the effect of various combinations of training volume, intensity and frequency on these determinants of endurance performance remains a fruitful area for future research.