Anatomy of a $12 Million Arm


Two guys in a bar: “Coney’s throwing batting practice up there. Man, I coulda hit that last fastball. Hell, you coulda hit that last fastball.” “Hey, whadya mean by that? [Knock—another hit] Yeah, Cone’s had a great career, but i think he’s lost it.”

That’s the kind of conversation that’s been taking place among baseball fans since the days of Mordecai “Three Finger” Brown. Yet no one ever asks the obvious question: What is the it that the pitcher in question has lost, and how and why did he lose it?

One reason, perhaps, is that the answers go well beyond the realm of tobacco juice and double knits. It’s about the tensile loads in the tendon, two kinds of molecular cross-linking, and the mysterious muscle-nerve interface. On the other hand, maybe it’s because the answers hit a little close to home. “The same inexorable aging process that is happening in all of us is happening in David Cone,” says Baylor University gerontologist Dr. George Taffet. “It’s just that for a Major League pitcher the yardstick is finer, and the decline is so much more obvious.”

OK, so why can’t Coney throw like he used to? Blame it on the tendons. While a lot of things happen to a pitcher by the time he’s reached 37—his maximum heart rate is probably 10 beats lower than it was a decade earlier, and for the last couple of years he’s lost some muscle mass: about 1 percent per year—if you’ve got to place the blame anywhere, blame it on the tendons.

Back up a second. What do tendons do, anyway? Simple—they are the connective tissues that attach muscles to bones. According to Dr. Vijay Vad, an orthopedic surgeon at New York’s Hospital for Special Surgery, it helps to think of a pitcher’s arm as a slingshot, and the tendon as being like the rubber band. The tendons in the shoulder and the elbow stretch, and that helps a pitcher throw a four-seam fastball hard or put spin on a slider.

So what’s the matter with Coney’s tendons? They’ve lost much of their tensile properties, or elasticity. Staying with the slingshot analogy, imagine one with a brand-new rubber band—that’s like a 20-year-old’s tendon. You can pull it back really far, it snaps back quickly, and the rock just flies out of there. Replace that shiny new rubber band with an old one that’s been sitting out in the sun too long—this is a tendon that’s pushing 40, and it’s got two problems. The first is that the rubber band—the tendon—won’t stretch as far, or rebound as fast, and thus won’t generate as much power. And of course, that lack of elasticity also makes the tendon liable to snap. Just ask 37-year-old Achilles-tendon victims Vinny Testaverde and Patrick Ewing.

So why do tendons lose their tensile properties? To the naked eye, an aging tendon appears kind of dried out and less pliable—a little like gum after you’ve chewed it, according to Vad. But the real action is happening at a microscopic level. The first degenerative change is that aged tendons exhibit less enzymatic cross-linking, a braiding of fibers that helps increase their tensile properties and keeps them supple. There’s significantly less cross-linking in a 40-year-old’s connective tissue than in a 20-year-old’s.

OK, we’re waiting for the other shoe to drop. . . . There’s another age-related pathology called Advanced Glycosylation End products, or AGEs, that’s also responsible for tissue deterioration (biogeeks will note that AGEs do their damage through non-enzymatic cross-linking). Essentially, AGEs are undesirable by-products of the sugar-burning metabolism that powers the body. AGEs are found in all body tissues, from nerve cells to blood vessels to muscles and connective tissue, and they interfere with the tissue’s flexibility and thus its ability to perform. “You know how meat hardens when you cook it?” says Ken Moch, CEO of Alteon, a biotech company doing research into AGEs. “Your whole body is cooking at 98.6 degrees.” In younger people, macrophages—essentially scavenger cells in the body’s immune system—get rid of AGEs before they do any damage. But as a person ages, this part of the immune system begins to deteriorate.

Why is it that Cone is more effective on long rest? Cone ain’t what he used to be. Literally. “Individual cells have a life span,” says Vad. “They die out and then they’re replaced.” But this process, called remodeling, slows down as we get older, and by age 40, on average, it takes twice as long to remodel a tendon as at age 20. Thus it takes a veteran pitcher longer to recover from both the microtrauma of throwing 85 to 100 pitches and a major injury like a torn rotator cuff tendon in the shoulder.

So why can a few pitchers still be effective well into their forties? Not all athletes age at the same rate, and different systems in a single individual also do not age at the same rate. Some 40-year-olds have tendons that are as flexible as a teenager’s, while others, well, don’t.

Why do only good pitchers seem to have these problems? Call it natural selection—all the mediocre pitchers have retired by the time they’re 32. Basically, it’s the Nolan Ryan Factor. If you throw 98 miles an hour when you’re 25 and you lose 5 percent off your fastball by the time you’re 35, you’re still bringing it at 93 and that’s above the Major League average. But if you’re throwing 91 in your prime and lose that same 5 percent over the next decade, you’re now down to 86—and you’ve probably lost some movement. Now you’re throwing batting practice.

But old guys have better control, right? Well, yes and no. If an older pitcher has better control numbers, it could be because he’s more disciplined, or because his pitches are slower and have less break on them. But physiologically, control is also a problem for older pitchers. This is because of the deterioration of the nerve-muscle interface. Starting at about age 18, according to Dr. Barry Jordan, neurologist and director of the brain injury program at Burke Rehabilitation Hospital, nerve cells, or neurons, start dying off. This gives the remaining neurons more responsibility. “When you look at the number of muscle fibers that are stimulated by one neuron, in a younger person, it might be 40,” says Taffet. “In an older person, it may be 70 or even 90. It clearly decreases your level of control.”

What about a guy’s reflexes? The ability to form complex reactions is also affected by aging. “The speed of information processing slows down,” says Jordan. A simple test of reaction time—say, catching a throw back from the catcher—is relatively unaffected by age. But make the problem more complex—fielding a screaming liner off Mike Piazza’s bat—and “the age effect explodes,” says Taffet. Cone needs to see the ball, decide if it’s headed for him, decide if he should catch it or move out of the way, and decide which parts of the body he has to move in order to do so. With fewer neurons than in his earlier years, the 37-year-old Cone just ain’t as quick to react.

Boy, this is all depressing. Is there anything you can do about any of this? While you can’t stop the deterioration that’s going on at a molecular level, you can minimize the effect that it has on performance through training. “You can actually improve the tensile properties of a tendon by slow, sustained stretching,” says Vad. “And weight training doesn’t only strengthen muscles, it strengthens tendons and bones, too.”

What about down the road? There’s lots of exciting stuff on the horizon, but while it won’t be around soon enough to help Cone, some might be available to prolong, say, Kerry Wood’s career. Vad suggests that within five to 15 years, doctors will be able to attack tissue degeneration with hormonal growth agents and/or gene therapy—essentially tricking the body into building tissues that have the characteristics of a 20-year-old’s. And Alteon has a drug in human clinical trials which is purported to break AGE cross-links and restore cells “to a more youthful state.” While the study is focusing on the cardiac benefits, it could be a breakthrough for orthopedics as well.

What’s Coney’s prognosis? From a baseball point of view, his slide has been pretty predictable. Most pitchers who get into late middle age have a season like this, where their ERA doubles and they lose twice as many games as they win. What happens next is an open question. Some guys, like Jack Morris, who went from 21-6 with a 4.04 ERA in 1992 to 7-12 with a 6.19 ERA the next year, are basically done. Others, like Tom Seaver, who went from 14-2 and 2.54 to 5-13 and 5.50 in one season, stick around for quite a while longer (Seaver pitched for four more seasons) at a considerably reduced effectiveness (he went 47-49). But if you want the David Cone of 1988, you’d better tune in to ESPN Classic, pedaling your stationary bike while you do. To paraphrase that great baseball fan John Donne: “Ask not for whom the fastball slows, it slows for thee.”

This article from the Village Voice Archive was posted on July 18, 2000

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