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  At Bangor Sam became interested in a particular clinical application of exercise science. As everyone knows, exercise builds the muscles. Certain diseases have the opposite effect. Sam wrote his dissertation on the effects of exercise on disease-related muscle wasting. He had a special motivation: His mother had been diagnosed with a rare kidney disease that caused muscle wasting. He wanted to find a way to help his cara madre and others in her sad situation.

  Possessing not only a sympathetic heart but also a keen mind with a special gift for perceiving the obvious thing that others miss, Sam focused his attention on a particular aspect of muscle-wasting disease that previously had been given zero attention.

  “Working with these patients,” he says, “and also with my mom, I noticed that what bothered them was not so much the muscle wasting itself as the fatigue that came with it.”

  In his efforts to gain an understanding of disease-related fatigue, Sam spent time with patients suffering from systemic lupus erythematosus, an autoimmune disease characterized by pervasive fatigue. Sam observed a curious feature in the fatigue associated with this particular illness: It fluctuated drastically from day to day. Although the tissue inflammation that supposedly caused the fatigue changed very slowly, becoming only slightly worse day by day, a patient might experience her bodily fatigue as paralyzing one day, barely noticeable the next, and halfway between those extremes the day after that.

  Sam asked himself what inside the body could possibly change quickly enough to explain such rapid fluctuations, knowing that the inflamed organs themselves could not. There was only one possibility: the brain.

  To test his hunch that disease-related fatigue is somehow regulated by the brain, Sam designed an eyebrow-raising experiment in which he subjected a group of breast cancer patients to a maximal exercise test immediately before and after chemotherapy treatments, which are known to cause disease-like muscle fatigue. As anyone would have expected, he found that the women had a much lower exercise capacity after chemotherapy. However, measurements of heart rate, oxygen consumption, and so forth revealed no changes in any of the physiological parameters typically associated with exercise capacity. From the neck down, the women seemed capable of working just as hard as they had before their treatments. Yet they could not. Sam suspected that a toxic effect of the drugs on the central nervous system caused the patients to feel more fatigued by the same level of physiological stress and thereby reduced their exercise performance. But this could be true only if the feeling of fatigue itself, not the body’s actual physiological capacity, determined the limits of exercise performance—a heretical idea.

  Throughout the previous century and into the present one, the prevailing model of exercise fatigue has been the so-called catastrophe model. According to this model, fatigue is an involuntary drop in performance caused by the loss of homeostasis (or balance) somewhere in the body. For example, lactic acid builds up in the muscles and makes them too acidic to function properly. Or the muscles become depleted of glycogen (their primary, carbohydrate-based fuel), so there’s no longer enough energy available to sustain performance. This model associates fatigue with a “catastrophic” functional breakdown in the muscles. In this model the brain is understood to have no influence whatsoever on exercise fatigue; it is merely along for the ride. But Sam’s observation of the effect of chemotherapy on exercise performance gave him a different idea—that the brain may in fact be the true source of limits on exercise capacity.

  As he pondered this idea Sam could not help but consider its relevance to endurance sports, since he was then serving as a scientific adviser to the now defunct Mapei professional cycling team. Could it be, he wondered, that the barriers to performance that cyclists, runners, triathletes, and others fight against day after day exist not in their muscles, blood, or hearts but inside their heads?

  Sam found a simple way to test his hypothesis. To pull it off he needed subjects who knew how to suffer. So he approached the Bangor University rugby team and asked for ten volunteers. One by one the willing athletes visited Sam’s exercise lab, where they were placed on a stationary bike equipped with a power meter and subjected to a grueling three-part test. First, the athletes were instructed to pedal as hard as they could for just five seconds. On average they were able to produce 1,075 watts in this brief all-out effort—an impressive number, as was to be expected from strong, well-trained athletes. Next, after a rest period, they were required to pedal at a fixed wattage as long as they possibly could, stopping only when they felt they could not complete a single additional pedal stroke at that power level. The fixed wattage was high but submaximal—something the athletes could sustain for ten to fifteen minutes before reaching exhaustion. On average the subjects were able to sustain only 242 watts for approximately twelve minutes in this second part of the test. Finally, as soon as the athletes quit part two and before they had any chance to recover, they were asked to repeat the original five-second all-out effort.

  What Sam was interested in was the difference in the amount of power the rugby players were able to put out in the first five-second maximal effort, when their legs were fresh, and the last, when their legs were tired. He knew the catastrophe model would predict a massive difference. Remember, according to this model exhaustion occurs when a functional breakdown occurs in the muscles. An athlete slows down involuntarily at the point of exhaustion because he physically cannot sustain the desired pace, his muscles having run up against some sort of hard physical limit such as lactic acid buildup. It’s like a car running out of gas. In the case of this study, proponents of the catastrophe model would say that the athletes stopped pedaling their bikes after roughly twelve minutes during the second part of the test because their muscles no longer had enough “gas” to sustain a power output of 242 watts (in the average case). Therefore, the catastrophe model would predict that in the second five-second maximal effort that immediately followed their capitulation, the volunteers would be able to produce no more than 242 watts. After all, how could anybody possibly produce more than 242 watts when a functional breakdown in his muscles has just forced him to stop pedaling at that very power level? It would be like a car driving without fuel.

  This was not what Sam expected, however. Sam expected that the athletes would quit the second part of the test not because they actually ran out of gas but because the suffering required to continue pedaling at the required intensity would become unbearable, causing them to quit voluntarily. Although the athletes would feel as if they had run out of gas, in fact their muscles would be perfectly capable of continuing—not forever, of course, but for some time. The voluntary nature of their quitting would be revealed (Sam anticipated) when the athletes discovered they were able to crank out significantly more than 242 watts for five seconds in the third and final part of the test.

  Any triathlete familiar with the phenomenon of the finishing kick would probably make the same prediction. It happens all the time in races. An athlete starts to tire and slow down inexorably in the closing miles of the run leg of a race, only to find that he is able to unleash a full sprint to the finish line in the final 100 yards or so. Mark Allen was the victim of such a finishing kick in the 1988 USTS championship race at Hilton Head, South Carolina. Young Mike Pigg, the strongest cyclist the sport had ever seen, got off the bike with a three-minute lead on Mark. Knowing Grip was coming at him from behind “like a bullet,” as he later described it, Pigg ran as hard as he could, but in the last mile he began to falter. Mark nearly caught him with half a mile to go. But Pigg dug deep and sprinted ahead of Mark in the homestretch to take the victory. According to the catastrophe model, that should have been impossible. If Mike had begun to slow with a mile to go because he was running out of gas—if his slowing was completely physical and involuntary—then he simply could not have increased his speed again. Yet he did.

  And guess what? In their second five-second bike sprint, the subjects of Sam’s experiment managed to crank out 731 watts, on average—more than
three times the power they had felt unable to sustain a second longer immediately prior to that sprint.

  Those five seconds unraveled 100 years of exercise science doctrine. The catastrophe model was dead, just like that. A car cannot drive without fuel, and a rugby player who has stopped pedaling his bike at 242 watts after twelve minutes because his muscles have broken down cannot immediately thereafter produce 731 watts for five seconds. The only reasonable explanation for this rebound was that the subjects of Sam’s experiment did not, in fact, break down in the middle part of the test; they gave up. They quit the sustained submaximal effort after twelve minutes because they could not bear the open-ended suffering anymore. Sure, they were physically able to persist a little longer, but their misery was great and was only going to become greater, and they had to draw a line somewhere. They were then able, for five seconds, to blast out three times more power than the amount they supposedly could no longer sustain because, well, it was only five seconds. It would hurt, but only briefly, so without a thought the athletes tapped into the reserve capacity that they had hidden from themselves just moments earlier.

  In his published report on this study, Sam proposed that fatigue in endurance exercise is always voluntary and always occurs as a response to an intolerable level of suffering, or what exercise scientists call perceived effort. The problem is never lactic acid buildup or muscle glycogen depletion or any other form of running out of gas. These things happen, but they never become so extreme that they directly stop the muscles from working. They merely force the brain to make a greater and greater effort to keep the muscles working at a desired level until this effort becomes so unpleasant that continuing no longer seems worth the agony.

  Sam calls this idea the psychobiological model of exercise tolerance. It is based on an old and simple psychological construct called motivational intensity theory, which understands persistence in challenging tasks as being determined by a weighing of cost and reward. As long as the reward remains attainable and outweighs the cost, we persist. When the reward comes to seem unattainable, or the cost becomes more significant than the reward, we quit.

  In endurance exercise the cost is suffering, or perceived effort. The potential rewards are many and vary between individuals, but the satisfaction of proving one’s toughness seems to be almost universal among these rewards. The more meaningful the rewards are, the more motivated the athlete will be to tolerate suffering. Perceived effort increases slowly and steadily throughout a race, whereas the motivation level is fixed before the race begins. If the increasing burden of perceived effort eclipses the fixed weight of motivation before the finish line is reached, the athlete raises a white flag, one way or another. He either quits or slows down. Defeat is never death but always surrender.

  In reality, quitting is rare because endurance athletes learn through experience, by feel, how to start each race at a pace that, if held steadily all the way through (with small adjustments along the way), will cause their perception of effort to reach the maximal tolerable level just when they reach the finish line. This perception-based art of pacing is how endurance athletes finish races in the shortest time possible. But even the athlete who masters this art must fight against a desire to quit in the last part of each race. If you don’t want to quit, you’re not doing it right.

  MOST EXERCISE PHYSIOLOGISTS don’t like Sam’s model, but they’re having a hard time disproving it, even though he has told them exactly how to do so. Sam enjoys issuing the following challenge to his many doubters:

  “If you can show me a treatment that can change performance without changing either perception of effort or motivation, I will say that my psychobiological model is wrong.”

  So far, nothing. Meanwhile, researchers have identified a variety of “treatments” that enhance endurance performance by changing perception of effort and without affecting any part of the body except the brain, which is something else that is not possible according to the catastrophe model. For example, a team of English scientists has shown that both cycling and running performance are improved when athletes periodically swish a sports drink around their mouths and spit it out. The carbohydrates in the drink never enter their bloodstream to provide energy to the muscles. Instead they stimulate receptors on the tongue that in turn activate a “pleasure center” in the brain, reducing perceived effort—that is, causing exercise to feel easier.

  It’s not only Sam’s professional peers who greet his model with skepticism. The relatively few endurance athletes who know something about it do too. They hate being called quitters. Nor do they feel like quitters. When an endurance athlete experiences exhaustion in a workout or race, he certainly feels as though his body has broken down and that his slowing is completely involuntary. But perceptions frequently deceive. Look no further than the Bangor University rugby team, whose mentally tough members felt certain they had held 242 watts as long as they possibly could, only to betray the illusoriness of this feeling by tripling that power output immediately after having given up in seeming total exhaustion.

  Another source of the skepticism with which athletes greet Sam’s explanation of endurance fatigue is less experiential and more conceptual and can be expressed in the following question: If fatigue is caused by a mere perception, why can’t athletes simply override it by an act of will?

  This objection reflects a common misunderstanding about the nature of mental phenomena. Intuitively, most people regard perceptions as nonphysical and therefore as lacking the power to exert deterministic control over physical functions. But perceptions are physical—they are specific patterns of electrical and chemical activity in the brain—and they have as much causal power as a punch to the gut. The drug addict’s need for drugs and the starving man’s hunger are perceptions against which the force of will may be impotent. Exercise fatigue is much the same. We certainly have some power to push through suffering—some of us more than others, all of us in some moments more than in others—but even the Dave Scotts and Mark Allens among us have only so much capacity to suffer.

  When people think “voluntary,” they think “conscious,” but a behavior can be voluntary without being conscious. For example, it has been demonstrated that baseball players “decide” to swing at good pitches before they are consciously aware of the speed and direction of the pitch at which they are aiming. The act of swinging is voluntary, but it is initiated unconsciously. Exercise fatigue is like that. A marathon runner who begins to lose pace after mile twenty-two despite trying his best to hang on is not consciously slowing down. But he is slowing down voluntarily, as we could easily demonstrate if we were to place a false finish line at the twenty-three-mile mark, upon seeing which the runner would suddenly find himself able to sprint. Fiendish, but it makes the point.

  But why would nature choose to make a species incapable of approaching its true physical limits in sustained exertion? What sort of survival advantage could possibly be conferred by experiencing sustained exertion as so unpleasant that the animal gives up while its muscles remain capable of continuing?

  “The reason perception of effort evolved is to limit energy expenditure,” Sam says. “Forty thousand years ago it was very difficult to find food. So you didn’t want people running around and wasting energy for no reason. Perception of effort evolved to make us avoid spending energy unnecessarily. We run around only if we have a very strong motivation to do so. People exert effort only when they believe that effort is worthwhile. It’s also why most people don’t exercise at all.”

  Not every athlete is skeptical of Sam’s theory. Interestingly, the very best endurance athletes—including Dave Scott and Mark Allen—have always believed that performance limitations are more psychological than physiological.

  “I have the ability to concentrate on the task at hand,” Dave said concerning his Ironman dominance in 1984. “I just don’t think some contestants out there have developed the ability to concentrate for that race.”

  Dave was often asked how he did it,
and he always, in one way or another, pointed at his head.

  MUCH IS KNOWN about the perceptions of pain and hunger. Not much is known about perception of effort. Neither psychologists nor exercise physiologists had seriously studied perceived effort before Samuele Marcora became interested in the phenomenon.

  Some researchers have proposed that feedback signals sent to the brain from the muscles and other organs during exercise are responsible for perception of effort. Sam believes otherwise. He thinks it all happens inside the brain, and he is able to adduce some compelling evidence against a role for feedback from the body. For example, researchers at the University of Zurich measured the effect of injections that interrupted the transmission of somatosensory signals from the legs to the brains of cyclists engaging in a simulated five-kilometer time trial. In plain English, the subjects could not feel their legs while they pedaled. If the brain depended on this type of feedback to perceive effort, then the injections should have sharply reduced their ratings of perceived effort compared to a control trial. They did not.

  Sam also points out that perceived effort during exercise is not affected by heart transplantation. The brain has no nerve connections to a transplanted heart. If the brain relied on somatosensory awareness of heart rate to perceive effort, as some have proposed, then heart transplant patients would exhibit a reduced perception of effort. Again, not so.