Once upon a time the understanding of exercise physiology was easy. The key to all forms of exercise performance was the heart, whose function determined how far and how fast humans can run, swim, or cycle. Once the heart’s limiting capacity is reached, the muscles become oxygen deficient, releasing poisonous lactic acid. The lactic acid interferes with normal muscle function, causing the anguish we recognize as fatigue. According to this explanation, the best athletes are those with the largest hearts, best able to pump the most blood to their active muscles and produce the highest rates of oxygen consumption during exercise.
It is a theory based on work done by the British Nobel Laureates Sir Frederick Gowland Hopkins in 1907 and Professor Archibald Vivian Hill in the 1920s. This idea has been widely promoted and vigorously defended by legions of exercise scientists ever since. Most humans with any interest in exercise science believe this theory to be the only possible truth.
But for the first time in 90 years, the past decade has witnessed the appearance of some cracks in the walls of this fortress of belief. We now know that some things are not easily explained by this traditional Hopkins-Hill model. If the model is the final truth, then there really is no need for athletic competitions. Medals can simply be given to those with the largest hearts and the greatest capacity to consume oxygen. But the problem is that the very best distance runners (the Kenyans and Ethiopians, for example) do not have any greater capacity to consume oxygen than do lesser runners who finish far, far behind. Thus something other than simply a big heart and a large capacity to consume oxygen must explain truly exceptional athletic performance.
Indeed, this theory invites the simplest question: If the heart limits all forms of endurance exercise performance, why do cyclists in the Tour de France or runners in the Olympic marathon race at submaximal levels of heart function? If the heart is indeed the factor limiting their performances, then those athletes’ hearts must begin to function at maximal effort the instant the race begins. But their hearts do not. Hence, something else is involved.
Probably the most damning evidence against this traditional theory is the simplest and most obvious—so obvious, in fact, that it has been ignored for the past 90 years: Can the Hopkins-Hill model explain how athletes pace themselves not just during races but also during training?
If the control of exercise performance resides in the exercising muscles under the action of this toxic lactic acid, then why do athletes begin races of different distances at different paces? If lactic acid is the sole determinant of an athlete’s pace, then there can be only one exercise pace for each individual regardless of the distance she plans to cover. The pace must be that at which the effect of the poisonous lactic acid is just being felt. Going any faster will cause more lactic acid to be produced, slowing the performance. But slowing down will cause a drop in lactic acid levels in the muscles, removing its inhibitory effect and leading to an immediate (but temporary) increase in performance. Soon, however, the higher intensity will lead to increased lactic acid production in the muscles, reversing the process.
If the model is completely unable to clarify how different paces are possible during exercise, it has even greater difficulty explaining what happens near the end of the exercise as athletes begin to speed up in anticipation of the finish—the classic end spurt. The end spurt is most obvious at the finish of each stage of the Tour de France but is present in all running races longer than 800 meters. How is it possible for an exhausted athlete to speed up at the end of a race when he is the most fatigued? This common phenomenon indicates that our understanding of fatigue—classically defined in all textbooks of exercise physiology as the inability to sustain the desired muscle force (or running speed)—is utterly incapable of explaining what happens in the real world of competitive sport. If athletes speed up at the end of races when they should be the most tired, they cannot be fatigued, according to this hallowed physiological definition.
And even more confusing is this: As they sprint for the line in the final moments of their end spurts, athletes do not activate all the available muscle fibers in their exercising limbs. They always finish with muscular reserve. Which raises these questions: Why not? What is holding them back? And even more intriguing is this: If an athlete finishes second, milliseconds behind the first athlete, what was holding her back? Why did she not risk death by exercising just a little harder in order to win the race? The conclusion must be that she chose to come in second rather than to go faster even if going faster would not have killed her.
Then the final piece of evidence against this purely peripheral control of exercise performance is that certain substances can have a marked effect on human exercise performance even though they act only on the brain. The most obvious example is amphetamines, a class of drugs that dramatically improve performance by acting on the brain to reduce the uncomfortable sensations of fatigue.
In the face of such compelling evidence, one could expect that supporters of this traditional explanation would acknowledge that their model might not be absolutely correct. Science is supposed to be a courteous activity conducted by decorous men and women according to time-honored principles of fair play and respect for differing opinions, all for a singular goal: the pursuit of a perfect truth. Sadly, the reality is sometimes different. Modern science, and perhaps even more so in exercise science, is a war waged on opposing sides by men and women with varying measures of self-importance. Those most certain of their opinions are usually also the most belligerent.
Those intrepid nonbelievers who question soon attract the scorn of the majority. The result is that it is much easier to stay quiet or to choose conformity. It is into this hostile arena that the genial Dr. Thomas Rowland and his sagacious book have made their entry.
Dr. Rowland, a pediatric cardiologist, is lean and athletic—a lifetime athlete. His small, linear frame identifies him as an ectomorph. According to 1940s Harvard psychologist William Sheldon, the defining characteristic of the ectomorph is cerebrotonia—a greater capacity for deep thinking than for urgent acting. Shakespeare understood that their need to think and to understand more deeply places the ectomorph on the social edge. Of Cassius who plotted his assassination, Julius Caesar is allowed to observe this:
Yond Cassius has a lean and hungry look,
He thinks too much; such men are dangerous.
Much better to surround oneself with the soft bellied:
Let me have men about me that are fat,
Sleek-headed men and such as sleep a-nights.
In The Athlete’s Clock, Rowland plots the assassination not of an autocratic emperor. Instead, he invites us to question some of our most hallowed concepts of human athleticism. He wishes to understand how research in sport science helps us better understand how time, aging, our internal biological clocks, and associated controls like the central pattern generator (CPG) influence human athletic performance.
His overarching questions are these: Is the control of physical effort over time—sporting performance—under the conscious control of the athlete? Or do subconscious controls of which we have little knowledge really determine how well we can perform in sport? Thus he poses this question: Are the forces of destiny—or the finish time in a 10K road race—under our conscious control?
Rowland begins by providing evidence from laboratory studies showing that the pacing strategy during more prolonged endurance exercise may be regulated by subconscious controls that produce the uncomfortable symptoms that we recognize as fatigue. He wonders whether these sensations arise “from the unconscious portions of the brain, which, having sensed physiological information indicating high-exercise stress, depress force of muscle contraction and block the desire to continue, all in the name of preserving safety?” He acknowledges that few exercise scientists and even fewer athletes are impressed by any explanation that proposes that human athletes are not in exclusive control of their own sporting performances. In answer, he provides a body of current evidence that allows readers to arrive at a more informed opinion.
The function of those controls is to regulate the frequency and power of the muscle contractions, expressed in running as stride frequency and stride length. Runners achieve this by acting on a CPG that sets the stride frequency and stride length and hence the pace. This simple explanation is revolutionary. Defenders of the Hopkins-Hill model speak not in terms of how a CPG might regulate exercise performance but exclusively in terms of how the heart’s nutrient supply to the exercising muscles regulates their function and therefore establishes the runner’s pace.
Not that this CPG is a novel evolutionary development unique to athletic humans. Instead, a similar controller subtends the identical function in the more primitive brains of the most ancient creatures like the lowly cockroach. The magic of this CPG is that it will always choose the most efficient combination of contraction frequency and contraction power regardless of the activity—running, swimming, or cycling—and the conditions of exercise. The CPG does its work without requiring any input from conscious thought, although there may be some limited capacity for conscious choice to influence the actions of the CPG in the short term.
What of sprinting speed? Could the peak rate of firing of the (subconscious) CPG determine how fast humans can sprint over 100 meters? Probably not that simple, since this excludes the role of the sprinter’s muscles in producing the force necessary to propel the body between strides. Weak muscles and a superfast CPG will still produce a slow 100-meter time. But like distance runners, even 100-meter sprinters must pace themselves. According to Caribbean sprinter Steven Headley in an interview with Rowland, “You can’t run all out for more than about 4 or 5 seconds. . . . I really don’t know what causes me to slow at the finish. Sometimes I’m not even aware of it.” Is this another example of the subconscious control of human athletic performance?
Clear evidence for well-defined subconscious controls is provided by the diurnal (24-hour) variations in human athletic performance. Even better examples are the responses of players in fast ball sports like baseball, tennis, and cricket, in which the ball must be struck on the basis of advanced cues occurring in the very earliest portion of its flight and in which conscious actions can play no part. In all these sports, the ball striker must hit the ball at a time when he does not know the ball’s precise position in space (since he does not see it). Nor does he know precisely when the ball will reach the point at which he wishes to strike it. The marvel is that few humans are ever able to make these seemingly improbable actions successfully, let alone most of the time.
Thomas Rowland has written a magical book that is both timely and revolutionary. My wish is that it will open minds to a new possibility: that we know much less about the factors that regulate human athletic performance than in our simple ignorance we may believe. That is the hidden message of this rebellious, indeed heretical, book. It is a message that exercise scientists need to take seriously if we are to advance our profession as a solemn science that aims to detect, rather than to conceal, truth.
Tim Noakes, OMS, MD, DSc
Discovery Health Professor of Exercise and Sports Science, University of Cape Town and Sports Science Institute of South Africa