Ingenious investigations in which athletes exercise one leg intensely while the other leg remains dormant suggest that, in this unique situation, the capacity of the leg muscles to use oxygen does not limit O2max. In this research, the O2max associated with one-leg exercise is more than half the O2max for a two-leg exertion, which means that the leg muscles can increase their rate of oxygen consumption if given the opportunity to do so. A greater supply of oxygenated blood from the cardiovascular system presents such an opportunity. This opportunity is possible in one-leg exercise because the cardiovascular system diverts blood from the nonworking to the working leg.
However, during a two-leg exertion such as running, the cardiovascular system is not able to supply both legs with enough blood and oxygen to reach each limb’s highest-possible level of oxygen usage. This is probably a protective mechanism. If the cardiovascular system opened the flood gates and permitted more blood to flow into the legs, cerebral blood pressure could drop significantly, leading to a potential collapse.
The ability of the leg muscles to raise the oxygen-consumption rate when supplied with a greater inflow of blood during one-leg exercise suggests that the cardiovascular system might limit O2max during demanding running. However, as Dr. Tim Noakes and colleagues at the University of Cape Town have pointed out, stroke volume (the amount of blood ejected from the heart per beat) and cardiac output (the amount of blood pushed out of the heart per minute) often do not reach plateaus (i.e., do not attain topmost values) during laboratory tests that are used to determine O2max values in runners.8 If stroke volume and the total outflow of blood from the heart have not peaked, yet O2max is reached, it is possible that the cardiovascular system is not capping O2max.
As T.D. Noakes and A. St. Clair Gibson have noted, overall muscular performance and thus the oxygen-consumption rate during running are determined by the nervous system’s recruitment of motor units (collections of muscle cells) inside the leg muscles.9, 10 If this seems confusing, remember that the muscles cannot act alone during running; they must wait for commands from the brain and spinal cord in order to engage themselves in the act of running.
A sustained, high level of muscle engagement by the nervous system would inevitably lead to a high O2max in an individual runner. In contrast, a more limited level of recruitment would produce a lower O2max, even in a case in which a runner had ample reserves for oxygen shipment and use in the heart and leg muscles. As Noakes has observed, runners with higher values of O2max appear to have nervous systems that not only recruit a greater number of muscle cells during intense running but also sustain this recruitment for greater than average time periods.8 This observation has important implications for training that will be discussed throughout this book.
Basically, the research on neural output means that in order to maximize O2max and performance, endurance runners must train their nervous systems in ways that optimize motor-unit recruitment. This can hardly be accomplished by high-volume, submaximal training, the traditional way to train for O2max enhancement, since motor recruitment during such work is modest. Rather, it can only result from highly intense, Kenyan-style training that relentlessly provokes greater neural outputs and motor-unit activations. For an individual runner, the key to developing the highest-possible O2max appears to involve optimizing motor-unit recruitment, with supporting roles played by expanded heart and leg muscles that can sate an intense thirst for oxygen by the neurally fired-up muscles.
Impact of Training on O2max
O2max usually responds readily to training, but the response depends on a variety of different factors and can be quite unpredictable. When a relatively untrained group of individuals embarks on a 3-month program of endurance-running training, the average increase in O2max after 12 weeks will be about 15 to 20 percent, but some subjects may boost O2max by just 2 to 3 percent—or not at all.11 A small number of individuals will increase O2max to a considerable degree, that is by as much as 30 to 50 percent.12-14 If the training program is uniform across all individuals, genetic factors will be responsible for some portion of this variation in response. (Refer to chapter 2 for a discussion of the interaction between genetics and endurance-running performance.)
Intrinsic O2max also plays a role: Individuals with naturally high values of O2max at the beginning of training will tend to increase maximal aerobic capacity less than individuals with lower values. Intrinsic O2max, or the maximal aerobic capacity present in a person who is not engaged in regular endurance training, may to some extent also be under genetic control.
O2max can be expressed by the following equation:
O2max = HRmax × SVmax × (a-v O2 difference)max
HRmax is maximal heart rate, SVmax is maximal stroke volume (the greatest amount of blood the heart can pump out of its left side per beat), and (a-v O2 difference)max is maximal arteriovenous oxygen difference, which reflects the disparity in oxygen content of the arterial blood coming into the muscles from the oxygen content of the venous blood flowing away from the muscles. An increase in the (a-v O2 difference)max means that the muscles are extracting more oxygen from incoming blood.
Clearly, O2max can be increased in endurance runners only by working the right side of this equation, that is, by enhancing HR max, SVmax, or the arteriovenous difference. Scientific studies reveal little difference in maximal heart rate between sedentary individuals and well-trained endurance runners, so upgrades in stroke volume or the (a-v O2 difference)max or both must account for gains in O2max associated with training. Although considerable variation can exist among runners, research suggests that about 50 percent of the increase in O2max that results from endurance training is often produced by an upswing in maximal stroke volume with the other 50 percent coming from upticks in the arteriovenous difference.12-14
Increases in Stroke Volume
Endurance training enhances stroke volume in a variety of ways. First, the heart’s key pumping chamber, the left ventricle, expands in size in response to endurance work. In addition, plasma volume, or the volume of the liquid portion of blood without the red and white cells, also increases so that the left ventricle can fill with more blood between beats. This allows more blood to be ejected per beat, thus fostering a greater rate of movement of oxygen toward the muscles.
In intriguing research, exercise scientists have mimicked this endurance-training effect by infusing about 200 to 300 milliliters (7-10 oz) of fluid into runners’ bloodstreams; when this occurs, O2max automatically increases by about 4 percent. When runners don’t train for a couple of weeks, the resulting drop in O2max is caused primarily by a loss in plasma volume, which is a key aspect of detraining.15, 16 In effect, fitness is urinated out of the body.
Increases in Arteriovenous Difference
Advances in the arteriovenous difference occur for two key reasons. First, endurance-running training stimulates an increase in capillary density around muscle fibers in the legs. The capillaries are tiny blood vessels with thin walls across which oxygen can easily diffuse.17, 18 This upswing in capillary density increases blood flow to the muscles during running, decreases the distance across which oxygen must move to get to the mitochondria where the electron transport chain is located, and slows the velocity of blood flow through the sinews. While this latter effect might seem like a bad thing, it actually provides more time for oxygen in the capillaries to diffuse through capillary and muscle cell walls and travel into the mitochondria. An increase in capillary density enhances leg-muscle blood flow and whole-body O2max during endurance training.13
Secondly, the arteriovenous difference is advanced by the upswing in motor-unit recruitment described earlier as a key limiting factor for O2max. As more motor units are activated within a muscle during running, the muscle becomes a heavier consumer of oxygen and thus permits less oxygen to end up in the veins, draining the muscle.
O2max as an Indicator of Performance
An individual runner’s endurance performances will usually improve as O2max increases. A runne
r who trains diligently and pushes O2max from 50 to 60 ml • kg-1 • min-1 over a period of several months will often upgrade 5K time from 22 to about 18 minutes, for example.19 Research also tells us that O2max is generally a quite good predictor of endurance-performance capability when athletes of widely varying abilities are compared. The runners finishing in the top 20 percent of a 10K race will almost always have higher maximal aerobic capacities than individuals finishing in the last 20 percent.20-28
Paradoxically, there is little relationship between O2max and performance when runners with fairly similar training backgrounds and performance capacities are compared. For example, two famous U.S. runners, Frank Shorter and Steve Prefontaine, had personal records for 3-mile (4.8 km) races that differed by only .2 seconds and yet their O2max values varied by 16 percent. Prefontaine’s O2max registered 84 ml • kg-1 • min-1 while Shorter was able to push his oxygen meter up to a mere 71 ml • kg-1 • min-1.5
Steve Prefontaine (lead runner, top) and Frank Shorter (lead runner, bottom) had very similar three-mile performances even though Shorter’s O2max was about 16 percent below Prefontaine’s.
Baumann/Imago/Icon SMI
Karl-Heinz Stana/Imago/Icon SMI
Exercise scientists have also noted that elite athletes with nearly identical O2max values can have vastly different race times. Three elite marathon runners, Alberto Salazar, Cavin Woodward, and Grete Waitz, had O2max readings of about 74 to 75 ml • kg-1 • min-1, and yet their best performance times in the marathon were 2:08:13, 2:19:50, and 2:25:29, respectively.5
In a similar vein, Joan Benoit-Samuelson had the highest O2max ever recorded in a female runner, 78 ml • kg-1 • min-1, and her maximal aerobic capacity was 13 percent higher than the O2max of former world-record holder Derek Clayton (69 m ml • kg-1 • min-1); however, Benoit-Samuelson actually ran the marathon about 10 percent slower than Clayton (2:21 for Benoit-Samuelson versus 2:08:33 for Clayton).
In her prime, Joan Benoit-Samuelson had a O2max similar to an elite male endurance runner.
WEREK/Imago/Icon SMI
For the past 85 years, it has been assumed that differences in endurance-running capability result primarily from differences in the maximal ability to transport and use oxygen.5 For the past 50 years, the most popular laboratory test for assessing endurance-running ability has been the O2max exam,5 and many coaches and runners consider a high O2max to be the sine qua non of endurance performance. However, the O2max performance comparisons mentioned above reveal that these basic assumptions are incorrect.
The truth is that there is a very poor association between O2max and race times among competitive distance runners. A startling paradox is that a single individual who improves O2max from 60 to 66 can usually be assured of an approximate 10 percent improvement in performance, but a runner with a O2max of 66 has no assurance that he or she is 10 percent better than a competitor with a O2max of 60. Such observations make it certain that physiological and biomechanical factors other than O2max are required to explain observed differences among runners in their endurance-running performances. These key elements will be discussed in upcoming chapters. The traditional view that O2max is the primary predictor of performance has been destroyed.
O2max and the Faulty Muscle Fatigue Theory
O2max is also at the very core of a key theory that attempts to explain why performance-thwarting muscular fatigue occurs during endurance running. Careful scientific research has led to the rejection of this theory, but it continues to be used as the linchpin of many popular endurance-running training programs.
According to the theory, fatigue during intense endurance running occurs in the following way: A runner moving along at a high-quality pace reaches a plateau in oxygen consumption, that is, the runner’s O2max. Further increases in speed cause the leg muscles to begin working anaerobically, which leads to the release of high amounts of lactic acid. The lactic acid then interferes with muscle contraction, producing fatigue and necessitating a slower pace or leading to complete exhaustion.
This model of fatigue has reinforced the idea that increasing O2max should be the key goal of endurance training. In theory, such an increase would keep endurance athletes away from the dangerous realm of anaerobic muscle contractions and consequent fatigue by permitting increasingly higher training and race speeds to be handled aerobically, without the need for anaerobic energy production.
For example, the traditional Lydiard system of training endurance runners, created by legendary New Zealand coach Arthur Lydiard, has as its primary goal the aggrandizement of maximal aerobic capacity accomplished via the completion of huge amounts of running and the relative minimization of high-speed, anaerobic training. As Noakes has pointed out, this represents “brainless” training and exercise physiology since it ignores the need for an endurance-athlete’s nervous system to develop the capacity to sustain high levels of motor-unit recruitment.29
The traditional theory of fatigue has not held up well under close scrutiny. As Noakes and other exercise scientists have determined, some endurance runners become exhausted and are unable to continue during their laboratory O2max tests without ever hitting a plateau in oxygen consumption (i.e., without ever reaching an actual O2max).29 Thus, they are never falling into anaerobic peril, and still they are becoming completely fatigued.
The explanation based on reaching an oxygen plateau followed by anaerobiosis cannot adequately account for fatigue during endurance running. The research has also revealed that among runners who do reach a plateau, and thus exhibit a O2max, the top speed attained during the test is a far better predictor of performance than O2max itself.30, 31 Additional research has demonstrated that lactic acid does not hamper muscle contractility; in fact, it is a key fuel for leg muscles and can advance rather than retard endurance.32, 33
Nonetheless, the traditional conception of the origin of fatigue continues to be used to justify the creation of high-mileage training programs to increase O2max.
Improving O2max
Although O2max is a weak predictor of endurance performance unless runners of widely varying ability levels are compared, it is nonetheless true that individual endurance runners who increase their personal O2max will often improve their individual performances. As a result, exercise scientists have attempted to identify training strategies that have the greatest possible positive impact on O2max. Many runners believe that the best way to optimize O2max is to conduct high-mileage training. However, the scientific study that detected one of the largest improvements ever recorded in O2max in well-trained runners actually linked an upswing in intense training and a decrease in mileage with the big jump in O2max.34
In this investigation, experienced runners were using a variety of different training techniques prior to the onset of the research, including long, slow distance work; speed sessions; tempo training; overspeed efforts; and weight training. Over a 4-week period, the athletes conducted two high-intensity interval sessions per week. Each workout consisted of six intervals performed at the intense pace of vO2max, or the minimal running velocity that elicits O2max. (Chapter 9 provides a method for estimating vO2max.) These work intervals lasted from 3 to 4.5 minutes. The rest of the weekly training was composed of light recovery runs.
After just 4 weeks, the runners upgraded their 3K performance times by about 3 percent, and O2max jumped by 5 percent from 61 to 64 ml • kg-1 • min-1. This kind of aggressive increase in aerobic capacity is totally unexpected and almost unprecedented in highly trained distance runners, who often have a difficult time getting O2max to budge at all. As mentioned, this is one of the largest increases in aerobic capacity ever recorded in a published scientific study carried out with experienced runners.35
Separate research also supports the idea that intense training has the strongest impact on O2max By definition, intense training means work carried out at a high percentage of O2max—that is, at high speed. It is far different from high-volume training, which means heavy mileage running carried ou
t at moderate intensity. In a study completed with relatively inexperienced athletes, 12 individuals exercised at an intensity of 100 percent of O2max over a 7-week period, while 12 other subjects worked at an intensity of 60 percent of O2max. For a 20-minute 5K runner, 100 percent of O2max would be a pace of about 90 seconds per 400 meters (~6 minutes per mi), while 60 percent would correspond with 150 seconds per 400 meters (10 minutes per mi).
The latter group actually trained for longer periods of time so that the total amount of work per training session was equivalent between groups. After 7 weeks, the group working at 100 percent of O2max achieved a 38 percent greater increase in O2max compared with the lower-intensity, greater duration of training group, prompting the researchers to conclude that high-intensity exercise at around 100 percent of O2max is the key factor for the promotion of optimal O2max improvements.36, 37
A follow-up review that looked at 78 published scientific studies exploring the relationship between intensity, training volume, workout duration, and O2max found that optimal gains in O2max could be achieved by training as often as possible at an intensity of 90 to 100 percent of O2max.38 Ninety percent of O2max roughly corresponds with 10K race speed, while 100 percent of O2max is often close to competitive speed for a mile.
Traditionally, high-volume training carried out at moderate intensities has been categorized as aerobic running, while low-volume training conducted at high intensities has been termed anaerobic running (and has been presumed to have a smaller impact on maximal aerobic capacity), but research indicates that these concepts are misleading. In an inquiry carried out at the August Krogh Institute at the University of Copenhagen, one group of experienced endurance runners ran about 100 kilometers (62 mi) per week at an average intensity of 60 to 80 percent of O2max (so-called aerobic running), while a second group of experienced runners ran just 50 kilometers (31 mi) per week while emphasizing fast-paced interval sessions (so-called anaerobic running); work-interval length varied from 60 to 1,000 meters (.03-.6 mi). After 14 weeks, the lower-mileage, higher-intensity runners had improved the main marker of aerobic metabolism, O2max, by 7 percent, while the higher-mileage, lower-intensity runners had failed to upgrade O2max at all. The 1K performance times also improved for the lower-mileage, higher-intensity group (from 2:41 to 2:37) but failed to increase for the higher-mileage, lower-intensity runners.39, 40
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