This is an excerpt from Running Science by Owen Anderson
The traditional view in running is that fatigue, or the inability to continue a desired running velocity, is caused by the accumulation of metabolites in the muscles, the depletion of intramuscular energy stores, or increased body temperature. In this well-accepted conception, the muscles are believed to be the center of fatigue. One theory is that muscle fibers allow calcium to leak from them as strenuous running proceeds, lessening the force of muscle contraction. This occurs because the flow of calcium into muscle cells is a key stimulus for muscle-fiber shortening. Another frequently cited hypothesis—that science has proved to be incorrect—is that a buildup of lactic acid inside muscle cells is the dominant cause of fatigue during intense running.
A fundamental problem with the lactic acid and calcium concentrations theories is that neither corresponds to the real world. An often-forgotten implication of these conventional conceptions is that runners would slow down continuously during challenging runs as the leakiness of muscle fibers gradually increased or as lactic acid continued to pile up. If lactic acid is the true cause of fatigue, running pace should slow rather steadily over the course of a 5K or 10K race as intramuscular lactic acid concentrations increased.
The actual performances of well-trained runners reveal that race velocities vary widely over the course of a competition and are not tightly linked with calcium leaking from muscles or lactic acid level. When Haile Gebrselassie set his 10K world record, for example, his calcium leakiness and lactate level surely advanced steadily over the course of 10,000 meters of hard running, but his fastest pace was actually achieved over the last kilometer (.62 mi), which he covered in 2:31.3; most of the prior 1,000-meter segments of the race were completed in 2:37 to 2:38.1 He was running fastest when lactic acid levels and calcium leakiness had reached their apices.
The theory that fatigue during running is caused by biochemical, intramuscular factors is clearly inadequate. If muscle biochemistry were the true source of fatigue, there would be a clear link between muscle metabolite concentrations and actual running velocity. Some other system must be at work to explain why runners slow down during workouts and races.
Brain Regulates Pace and Fatigue
A key point to remember is that running velocity during a workout or competition is always a direct function of the rate of work performed by the muscles, but the instructions the muscles receive to work at various rates are always provided by the brain. The brain must take into account a variety of factors in order to choose the velocity at which an athlete will run. The brain might monitor body temperature, muscle metabolites, distance left to run, and other variables in order to reach a decision about running pace. The brain might even create a sensation of fatigue in order to enforce its decision—to prevent a runner from exceeding certain physiological thresholds. The brain could regulate running pace by generating strong feelings of fatigue in order to prevent physiological failure.
Anecdotal evidence that the brain acts as a regulator of fatigue and running pace is abundant although usually ignored. A classic example of the brain’s anticipatory role in running performance, presented by sports scientist Ross Tucker, is the case of a 40-minute 10K runner who is transported to either high altitude or a venue with hot, humid conditions and then asked to run a 10K race. In both situations, the runner’s 10K pace is much slower than usual from the very beginning of the 10K, not at some point within the race when inadequate oxygen delivery to the muscles or high internal temperatures become physiologically limiting.
Traditional theory would indicate that the slowdown in these situations was the result of oxygen depletion or high body temperature, but this is clearly wrong since the slowing occurred before either of these events. The brain must be able to anticipate physiological failure and thus slows pace and creates fatigue in certain situations in order to prevent too great a disturbance in physiological equilibrium. Since the brain anticipates and regulates, the overall process is thus called anticipatory regulation of running velocity.
A clear example of the shift in thinking that has occurred from the old model of fatigue to the new anticipatory regulation schema can be found in research carried out on the role played by overheating in causing fatigue. Traditional investigations suggest that athletes run in the heat until core body temperature reaches a certain limit, usually thought to be approximately 40 degrees Celsius (104°F), at which point the brain stimulates the muscles to a lesser degree and heat-related fatigue occurs. Fatigue (i.e., the slowdown) is thus believed to be caused by a failure to maintain adequate coolness of the body during running.
However, such studies have been carried out in the unnatural situation in which athletes are required to continue exercising at a fixed rate until they are unable to continue. This is rarely the case during running workouts or races where pace varies considerably as the exertion proceeds. In fact, research carried out with athletes running in the heat when they are not forced to run at a single pace verifies the anticipatory regulation model by demonstrating that runners don’t slow down because they are overheated; rather, they decrease their pace in order to prevent themselves from getting too hot. The failure to run as quickly in the heat as would be the case under cool conditions is thus the result of anticipatory regulation by the brain, not an overheating phenomenon within the muscles or brain itself.
If the anticipatory regulation theory of fatigue is sound, there should be studies that show that the nervous system gradually reduces its stimulation of muscles during fatiguing exercise and that this reduction parallels the actual increases in fatigue. Such a finding would be in contrast with the traditional view of fatigue, which would suggest that the nervous system continues a high level of stimulation while the muscles simply fail to continue functioning. Such investigations do exist. In one inquiry, cyclists completed a 100K ride sprinkled with all-out 1-kilometer (.62 mi) sprints. The quality of the sprints declined over the duration of this 100K effort. In parallel with this drop-off in sprint power, integrated EMG (IEMG ) activity also fell, which indicated that the central nervous systems of the athletes were recruiting fewer and fewer motor units as the ride progressed. 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 even though there was an opportunity for the athletes’ nervous systems to bring more motor units into play—if they so desired.
In a separate study, experienced cyclists completed a 60-minute time trial that included six maximal sprints. As predicted by the anticipatory regulation hypothesis, there was a eduction in power output and IEMG activity from the second through the fifth sprint as the nervous system cautiously tempered intensity in order to avoid physiological failure. However, both power and IEMG magically revived—and increased significantly—during the sixth sprint, which took place during the last minute of the overall ride. There was no real magic in the revival, however. Rather, the nervous system simply took the brakes off and allowed nonfatigued muscles to operate at high levels. The muscles were not fatigued during the second through fifth intervals—they were simply reined in by the nervous system.
Nervous system control of training intensity is a familiar phenomenon to many runners even though the dominant role is often not clearly grasped. Faced with an interval workout consisting of 6 × 800 meters, runners find the first interval to be fast and the second through fifth intervals to be progressively slower. The sixth interval, however, is often the quickest of the entire workout even though peripheral (i.e., muscular) fatigue should be the greatest and body temperature the highest. As the last work interval is reached, the brain is anticipating the ending of the workout and recognizing that physiological limits will not be exceeded even if a high running intensity is maintained. Thus the running pace over that last interval is fastest even though peripheral fatigue should be at its highest point.
The anticipatory regulation model of fatigue may help explain the dominance of Kenyan endurance runners. Various studies have shown that elite Kenyan athletes can sustain a higher percentage of VO2max in their races than runners from the rest of the world. While most highly competitive runners toil away at about 90 to 92 percent of VO2max during their 10K races, elite Kenyans have the ability to complete the distance at an intensity of 94 to 95 percent of VO2max. Traditionally, this difference has been explained as being due to greater resistance to fatigue, but the actual, physiological nature of this heightened resistance has never been detected or adequately explained.
Swiss researcher Bengt Kayser suggests that in elite competition, the difference between the winner and loser may not be the result of differences in VO2max but “rather in how big a safety margin the CNS (central nervous system) imposes in order for the organism to stay clear of serious damage (to the heart and muscles).” Kayser postulates that one reason Kenyans do so well is that “they are able to push the limits imposed by the CNS closer to the danger zone . . .” To put it another way, the Kenyans’ governor of exercise intensity is more permissive.
Training the Brain for Racing
If the central nervous system regulates performance, it begs this question: “Can you train your brain to allow you to go faster?” To answer this question, first note that anticipatory regulation is of more than esoteric interest to the serious endurance runner: It should also shape racing strategies and training-program creation. It is clear that fatigue and thus distance-running performance are influenced not just by factors related to oxygen consumption, body temperature increases, and muscle metabolite accumulation but also by muscle recruitment by the nervous system and the consequent production of propulsive force—and in which the nervous system anticipates unwanted disturbances in overall physiological equilibrium.
It is also certain that when runners move up to higher speeds, their nervous systems are recruiting more motor units in their leg muscles and recruiting those motor units more quickly. When runners slow down, they are using fewer motor units and recruiting those units less quickly. Electromyographic studies reveal that EMG values go up during 5Ks as runners speed up and drop as runners decelerate. Since EMG recordings reflect neural input to the muscles, it is clear that pace changes during the race are not the result of fatigue within the muscles but rather are the outcome of changes in stimulation of the muscles by the nervous system. Thus, training that teaches the nervous system to sustain higher outputs, and thus greater inputs to the muscles, should help improve race performances. It is doubtful that this teaching can be best accomplished by long, slow distance training, which features and rehearses low neural inputs.
Runners who can keep their muscle recruitment by the nervous system at the highest-possible levels fare the best in endurance competition. Based on past experience of running, a runner develops the capacity to set the optimal velocity for a competitive effort. This again points to the importance of high-quality training, as well as to specific training. That is, those runners who have religiously practiced goal race paces over suitable interval distances during training will have nervous systems that are most ready and willing to lock in those paces during actual race situations.
High-speed training improves motor-unit recruitment and also advances the synchronization of motor units; it is best for promoting neuromuscular attributes and for enhancing nervous system tolerance of high-quality running. High-intensity strength training with challenging resistance also enhances neural output to the muscles during activity. Contrary to popular belief, high-quality training is also optimal for advancing aerobic attributes since high training speeds are generally closer to VO2max than long-run pacings. The constant proximity to VO2max forces the heart to become a better oxygen pump and the leg muscles to become better oxygen users, raising aerobic capacity and even vVO2max since fast-pace training also enhances economy.
These findings should lead to changes in the overall planning of workouts. The time-honored routine of the weekly Sunday long run should be replaced with a long run every third Sunday and explosive routines on the other two Sundays. These Sunday explosive days, featuring plyometric drills, highspeed and running-specific strength training, and high-velocity running intervals, would force the runner’s anticipatory regulation system to reset and would create a nervous system that would be much more permissive to high running intensities, allowing greater speeds to be maintained for longer periods. Such training recognizes the dominating impact of the brain in anticipating the velocity that is manageable for each quality workout and race and then regulating that speed throughout the overall exertion.
From Running Science by Owen Anderson
Copyright © 2013 by Human Kinetics Publishers, Inc. Excerpted by permission of Human Kinetics, Champaign, IL. Available to order from Human Kinetics Canada at www.HumanKinetics.com or by calling 1-800-465-7301.
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by Owen Anderson, PhD
Available June 2013 - Paperback - 560 pp
ISBN 978-0-7360-7418-6 - $29.95