In a separate study, also carried out at the University of Cape Town, nine black runners and eight Caucasian distance runners with similar 10K race times, O2max values, and peak treadmill velocities were compared. Peak treadmill velocity is the maximal speed reached on the treadmill during a O2max test; it has actually been found to be a better predictor of performance than O2max.2 Despite the close similarities between the groups in O2max, 10K performance, and peak treadmill velocity, the black runners had superior resistance to fatigue: They could run for 21 percent longer at an intensity of 92 percent of peak treadmill velocity compared with the Caucasians.3
Such inquiries suggest that the physiological factors that determine O2max and the factors that determine resistance to fatigue—the percent of O2max that can be sustained over an extended period—might be quite different. After all, the runners in these two key studies had quite similar O2max values but very different characteristics with respect to resistance to fatigue. Exercise scientists have struggled to explain the mechanisms responsible for these kinds of variations.
Glycogen Concentrations
One theory that might explain differences in resistance to fatigue has to do with glycogen concentrations. Runners with superior resistance to fatigue might have a higher capacity to store glycogen in their muscles and liver. If this were the case, they would run low on essential fuel less quickly during endurance competitions and thus would be able to sustain faster paces for longer periods of time.
This glycogen hypothesis has a logical basis: Research shows that the appearance of fatigue during distance running often coincides with the development of low glycogen levels in the liver and muscles.4, 5 Ingesting easy-to-absorb carbohydrates to counteract glycogen depletion during prolonged runs of 60 minutes or more improves performance, most likely by giving muscles something to turn to for fuel when internal supplies of glycogen begin to run short.6 Carbohydrate availability is certainly important for performance.
Overall, the greater resistance to fatigue displayed by certain distance runners might be a consequence of their above-normal ability to store liver and muscle glycogen before competitions. It could also be the result of an enhanced capacity of their livers to produce glucose during long-distance running or a slowdown in the rate at which glycogen is used while running at a specific speed.
Scientific research has been unable to verify this glycogen-depletion model of resistance to fatigue, however. The energy-depletion hypothesis suggests that individuals with different degrees of resistance to fatigue would begin their races at similar percentages of O2max, with those who were less fatigue resistant gradually falling off the pace as glycogen depletion develops. There is no scientific or anecdotal evidence to suggest that this is the case. Rather, runners with greater resistance to fatigue seem to adopt faster paces at early stages in their races before glycogen depletion becomes a factor, compared with runners with diminished resistance to fatigue.
Heat Dissipation
A competing theory suggests that resistance to fatigue is closely related to an athlete’s ability to dissipate heat while running. A high rate of heat accumulation during running is directly related to fatigue: Race times during the marathon7 and also during 10K competitions and the 3K steeplechase worsen as the environmental heat load increases.8 Runners whose internal temperatures rise slowly during running tend to experience less fatigue compared with individuals who heat up quickly.9 Small runners tend to dissipate heat more quickly and experience slower increases in body temperature during running compared with larger runners. This is thanks in part to the larger surface-to-mass ratio in the smaller individuals.10
The black runners in the South African fatigue-resistance study discussed previously were considerably smaller than their Caucasian competitors. The black runners weighed an average of 56 kilograms (123 lbs) compared with 68 kilograms (150 lbs) for the white runners, and the blacks were only 169 centimeters (5.6 ft) in height compared with 181 centimeters (5.9 ft) for the Caucasians.1 Presumably, this would have allowed the black runners to get rid of heat more easily during longer-distance running and thus have cooler body temperatures. During shorter events of 1.5K to 3K, heat dissipation is not such an important factor because shorter duration of effort makes it more difficult to attain a critically high core body temperature. The performances of both groups of runners were equivalent for distances of 1.5K to 3K.
Fatigue tends to increase as the environmental temperature rises, and some research suggests that the ability to dissipate heat promotes fatigue resistance.
Sarah Hoskins/Zuma Press/Icon SMI
It is unlikely that heat-dissipation capacity can completely account for differences in resistance to fatigue, however. For one thing, black runners from Kenya with similar degrees of resistance to fatigue can vary tremendously in height and weight.11 Their wide variations in body size should produce great differences in heat-loss capacity and thus broad disparities in resistance to fatigue, but they don’t.
Stretch-Shortening Cycle
A stronger theory may be that resistance to fatigue is related to the way in which runners’ leg muscles function as reverse springs during running. The leg muscles are often referred to as springs but in reality function quite differently. To understand how the leg muscles work, consider what happens when an automobile hits a bump in the road: its springs first compress to soak up the energy of impact and then expand, releasing that energy. The spring-like activity of the leg muscles is quite different: When a runner’s foot hits the ground, key leg muscles actually lengthen at impact instead of compressing and then shorten, the reverse of what happens with a mechanical spring. The quads, for example, are stretched out as the knee flexes after ground impact and only then shorten and straighten the leg to drive the body forward (see figure 12.1). The leg muscles are thus reverse springs during running, and the process they undergo, in which they stretch and then shorten, is often referred to as the stretch-shortening cycle.
Figure 12.1 The quadriceps undergo the stretch–shortening cycle during each stance phase of the gait cycle. They are at (a) midlength when the foot hits the ground, (b) stretched as the knee flexes, and (c) shortened as the leg straightens and drives the body forward.
This stretch-shortening cycle in the leg muscles is essential for economical running. The rubber-band-like snapback of the muscles after they have been lengthened provides much of the propulsive force required to move forward. Furthermore, the process is extremely sparing of energy and thus oxygen use: Once the muscles have been stretched during impact with the ground, the resulting shortening occurs without the need to expend additional energy. In effect, the energy stored in the leg muscles at impact is simply released to provide propulsive force. This is an extremely economical process, especially when compared with the alternative, which would require active, energy-consuming muscle contractions to move the body forward.
This stretch-shortening cycle, as economical as it is, is not without its problems and perils. Research suggests that muscles become more resistant to being stretched and less willing to transfer energy in the stretched-to-shortened phase of the cycle during an extended running effort. This breakdown in muscle functioning during running has been called stretch-shortening muscle fatigue.12
The resistance to stretching may decrease subsequent force production because less energy is stored in the reverse spring with each impact with the ground; the result will be to diminish stride length. The slowdown in energy transfer may create a situation in which the push-off phase of stance is elongated, leading to a decrease in stride rate and thus running speed. Such changes do not occur to different degrees in various runners because of differences in oxygen use or disparities in heat accumulation; rather, these variations are probably related to the quality of the muscles, the ability of the nervous system to optimally control the muscles to facilitate stretching and energy transfer, and the overall capacity of the neuromuscular system to stand up to the stresses of the stretch-shortening process. Runne
rs with a more effective neuromuscular system should sustain optimal stretch-shortening function longer during competitions and thus should have greater resistance to fatigue.
Why might some runners experience less loss of stretch-shortening function during running? Stretch-shortening expert Paavo Komi of Finland has determined that the stretch-shortening cycle creates real damage to muscle cells during prolonged running.12 Much of the breakdown probably occurs when muscles are stretched out at impact, and the damage has a significant effect on muscle mechanics, including the ability to “snap back” after stretching, and muscle and joint stiffness. Runners with the greatest resistance to fatigue might then be the ones with the least stretch-shortening muscle damage during running.
Optimizing running form and using running-specific strength training may limit stretch-shortening damage. From a form standpoint, research suggests that the use of a midfoot landing pattern reduces impact forces experienced by the legs compared with the more typical heel-strike technique.13 The result may be less wear and tear on the muscles during running. (See chapter 5 for a discussion of appropriate running form.) Strength training for running decreases the risk of running injury, probably in part by fortifying the muscles to such an extent that stretch-shortening damage is minimized.14 Running-specific strengthening techniques are provided in chapter 14.
One potential problem with the stretch-shorten theory is that it predicts that runners with similar physiological characteristics (e.g., O2max and maximal treadmill speed) would start their races at a very similar pace, with the runners who experience greater damage subsequently falling off the pace as the race proceeds. However, the existing research indicates that runners with greater resistance to fatigue actually run more quickly than their more fatigue-prone peers, right from the opening gun.15 It’s possible that runners who have less resistance to fatigue carry more muscle damage accrued during prerace training into their races and thus are able to run with their more fatigue-resistant peers for only short periods of time.
Neural Governor
Although the muscle-damage hypothesis is appealing, a considerably more powerful and better-tested theory suggests that resistance to fatigue is actually a function of neural output, the extent to which the nervous system is willing to stimulate the leg muscles. Runners with the greatest fatigue resistance would be the ones whose nervous systems pour out and maintain a greater flow of stimulatory messages to the leg muscles. Under this theory, the functioning of the nervous system explains fatigue during long-distance running, a far cry from traditional conceptions that limitations in oxygen usage and the extent of leg-muscle damage are the foundations of fatigue.
Neural output during running would necessarily be controlled by a neural governor, a region of the brain’s motor cortex that determines appropriate exercise intensity. Scientific support is strong for the presence of an active neural governor that tightly controls neural output. For example, research reveals that individuals undergoing a O2max test in an exercise physiology laboratory often become exhausted and stop exercising prior to attaining a maximal rate of oxygen consumption, a maximal heart rate, or even a high level of blood lactate.16 Fatigue in such cases cannot be well explained by oxygen limitation, cardiac fatigue, or excessive lactic acid in the muscles; rather, it would appear to be caused by a neural-output setting in the neural governor that does not permit exercise of high intensity to continue beyond a fixed duration.
If the neural governor theory of fatigue is correct, there should be studies showing that the nervous system gradually reduces its stimulation of muscles during fatiguing exercise and that this reduction parallels the actual increases in fatigue. In fact, such investigations do exist. In one inquiry, cyclists completed a 100K ride that included a series of 1K sprints at maximal speed.17 Over the duration of the 100K effort, the quality of the sprints declined. Paralleling this drop-off in sprint power, integrated electromyography (IEMG) activity also fell, which indicated that the athletes’ central nervous systems were recruiting fewer and fewer motor units as the ride progressed (an IEMG is a recording of the electrical activity produced by muscles in response to stimulation by the nervous system). This was true even though less than 20 percent of the available motor units in the cyclists’ leg muscles were being recruited at any one time. There was an opportunity for the athletes’ nervous systems to bring more motor units into play, but that opportunity was not taken, apparently because of the tight control exerted by the athletes’ neural governors.
In a separate study, experienced cyclists completed a 60-minute time trial that included six sprints at maximal speed.18 Over the course of the trial, there was a reduction in power output and IEMG activity from the second through fifth sprint. However, both power and IEMG activity almost magically revived—and even increased significantly—during the sixth sprint, which took place during the last minute of the overall ride. In this study, it is impossible to explain the fatigue that occurred during the second through fifth sprints as being the result of either cardiac or muscular shortcomings. If there were true problems in the cardiac or muscle tissue, the sixth sprint could not have been carried out at such a fast pace. A more reasonable explanation is that the nervous system tightly controlled cycling intensity during the second through fifth sprints, maintaining a built-in reserve of neural output and preserving a capacity to recruit that reserve during the sixth sprint. In other words, fatigue and overall performance during the 60-minute time trial were controlled by the nervous system, not by the muscles.
Some runners may believe that the neural governor theory cannot possibly explain the crippling fatigue, and thus lack of fatigue resistance, that occurs toward the end of a marathon. During a marathon, runners simply run out of carbohydrate fuel, muscle glycogen is depleted, and no amount of increased neural activity seems able to restore running pace to its usual level over the last stage of the race. Although this argument is compelling, it overlooks the simple fact that fewer than 20 percent of motor units are recruited in a marathoner’s legs at any time during the competition. Figuring out a way to recruit at least some of the 80 percent of missing motor units might indeed fight fatigue and even increase running velocity over the last 6 miles of the big race. When fatigue strikes severely at the 20-mile point of a marathon, it might be time to begin recruiting more muscle fibers instead of ramping down running speed.
Two conclusions emerge from these kinds of investigations. First, there is strong evidence that a type of neural governor creates fatigue during intense or prolonged running and attempts to limit performances. Studies reveal that runners who sustain a higher level of IEMG activity during races perform significantly better in those races compared with runners with lower levels of IEMG activity.19 Second, there is also evidence that the neural governor is trainable. After all, experienced athletes stop their exertion at higher fractions of maximal heart rate and O2max compared with untrained individuals. Training that makes the neural governor more permissive should improve performances.
Endurance athletes hoping to achieve optimal levels of performance can no longer simply worry about their hearts and muscles; rather, they must also advance neural output to its highest level. Research on optimizing neural output is limited, but it is known that high-intensity, explosive strength training upgrades neural output compared with other forms of strengthening.20 This is not surprising since explosive training calls for high levels of neural output; thus, the specific, desired result is being rehearsed in training, perhaps teaching the nervous system that high levels of output are safe and manageable.
In the running arena, it would certainly appear that intense, high-quality running would enhance neural output to a greater extent compared with prolonged submaximal running with its lower required level of neural stimulation. An important finding is that East African runners tend to conduct more training at high intensity (>80 percent of O2max) compared with American and European elites, which should set the East-African governors at higher running velocities.1
Techniques of explosive and high-speed training are outlined in chapter 28 and 29.
Neural governor activity is the best explainer of fatigue resistance, but the setting on the neural governor would not be the only factor that determines performances. In addition to having a high neural governor set point, a runner would also require a high metabolic capacity in the muscles, a strong vO2max, a high lactate-threshold speed, an enhanced running economy, and an elevated maximal running velocity in order to reach his or her true potential. An overly restrictive neural governor, however, could potentially stop such superb physiological attributes from being expressed. An important point for runners to remember is that fatigue during running is to a significant extent a mental construct that may not accurately reflect what is really happening in the heart and muscles. In races and challenging workouts, it makes sense to treat fatigue as a sensory message rather than as a crippling crisis in the muscles, and not as a dictator of how the remainder of the competition or training session will proceed.
Conclusion
Scientific research on fatigue resistance is still developing, but that should not stop runners and coaches from conducting workouts that have the best chance of optimizing this important performance predictor. Workouts that involve high levels of neural drive, including sessions in which high neural output must be sustained over an extended period, should have the greatest effect on fatigue resistance. This means that explosive strength sessions and high-speed running workouts with short intervals conducted at close to maximal speed will be helpful, as will longer runs at very high quality tempos. Continuous 2.5K runs at 5K race pace, 4K runs at 8K race speed, and 5K runs at 10K pace should also lead to increases in neural drive, relaxation of the neural governor, and improvements in resistance to fatigue.
Running Science Page 18