Interviewees: John Faulkner and Chris Mendias
Sports journalist and author Matt Chaney has no doubt that his college steroid use was behind his football career-ending knee injury.
“I had slight ligament damage four years before,” says Chaney, but the knee hadn’t given him any trouble until he got huge on steroids. Then, in a practice scrimmage, “my knee exploded, without being touched.”
“It was definitely the ‘roids,” he says.
Chaney, who is writing a book on doping in professional football, says it’s generally but silently understood in the sports world that increases in steroid use have been accompanied by increases in devastating injuries like tendon ruptures. “Think about it, it’s common sense,” he says. “You have people on steroids alone — never mind the next-generation stuff like gene doping — nearing 300 pounds. But their tendons don’t grow, their bones don’t grow along with their mass.
Now researchers at the University of Michigan have found that muscle-building substances may actually make tendons smaller and weaker. They say the finding is a disappointment to those hoping to treat muscle-wasting diseases like Muscular Dystrophy — as well as another strike against any artificial muscle-builders.
John Faulkner and Chris Mendias were studying a new class of drugs that block myostatin, the protein our bodies use to break down muscle. Animals and rare people lacking myostatin are extraordinarily muscular, and it’s hoped that drugs that inhibit it could help treat muscle-wasting diseases.
But their studies of myostatin-deficient mice showed how myostatin is needed to promote the growth of tendons–the tissue that connects muscle to bone.
“There’s been a great deal of interest in muscle but this was the first study that indicated that it had a very different action in tendon,” Faulkner says.
They wrote in the “Proceedings of the National Academy of Sciences” that the myostatin-deficient mice had much higher muscle mass than normal mice, but their tendon mass was only half of normal. They also found that the myostatin-deficient tendons were less flexible, more brittle, and could withstand much less force. That’s troubling because bigger muscles need bigger tendons.
“Tendon is an important link in the musculoskeletal system,” explains Mendias. “They link the motors within muscle that actually generate force, out into the external world. They link it to bone and allow you actually move. So tendons, also in addition to providing that link, they can protect the muscle from injury.”
“With regard to the myostatin inhibitors, it looks like the risks are serious enough to make it not a very promising way to go with treatment of any of the debilitating diseases, or with aging, or any way of treating atrophied muscle,” says Faulkner.
And the researchers say it’s likely that steroids work the same way to weaken tendons.
“We’ve known for some time that athletes who’ve used anabolic steroids are much more likely to rupture their tendons, and it wasn’t really clear why that was,” Mendias says. “We actually think that myostatin plays a role in that process.”
“When you go to the gym and you lift weights what happens is, you actually damage the motors within your muscle that allow your muscle to generate force,” he explains. “So what the body has to do is break down those damaged proteins, damaged motors, first, to allow you to build more stronger motors. So myostatin plays an important role in that process that allows the body to break down those muscle motor proteins, but at the same time, myostatin also appears to signal the tendon actually to become much larger.”
“If you’re taking anabolic steroids, you’re short-circuiting that breakdown process, so you’re actually synthesizing new motor proteins without first breaking down existing motor proteins, and there’s no release of myostatin in that case, and no tendon adaptation,” he says. “So because athletes who take steroids, their muscles get bigger but that signal for the tendons to get bigger isn’t present, that’s why these athletes are more prone to actually rupture their tendons.”
In fact, when the researchers added myostatin back into tendon cells in the lab, they saw that the signaling mechanism for tendon growth was restored.
Mendias points out that not only are there substances that claim to block myostatin for sale on the internet, there are also reports of athletes getting their hands on drugs designed to inhibit myostatin from Korea and China. “Currently in the United States there are no approved myostatin inhibitors for sale,” he adds.
He worries that athletes may find the temptation irresistible, and warns “if you’re an athlete who’s taking a myostatin inhibitor, your muscles might get bigger but its not actually going to increase your performance. It may actually lead to a career-ending injury if your tendon ruptures.”
Chaney agrees that the temptation to use is overwhelming just to stay competitive. At the time of his tendon blowout, he had every intention of continuing “on the juice.” “If I had not been injured, I was definitely moving into a higher competition level, I was going to be a much better football player, and I was going to be that through anabolics like steroids in particular.”
So, is it all bad news? Actually, Mendias is now experimenting with using myostatin to grow tendons from adult stem cells in the lab– hoping to engineer replacement tissues for our injured troops. “We’re testing this technology in terms of taking some of the stem cells from these soldiers and actually making engineered muscle and tendon tissues in a dish,” he says.
“It’s really hard to get tendon, the cells that control tendons, to actually increase their numbers and actually become bigger,” he says. “So we’re taking these cells from tendons and adding myostatin to them to make them grow bigger. And the thought is, we can take these tendons that we’ve created and attach them to the muscle that we’ve also created in a dish, and use them to replace muscles that are lost from some sort of traumatic injury.”
‘We’re especially excited about the potential use for treating our soldiers that are coming back from Iraq that have a massive loss of tissue due to explosions and losing entire muscle groups,” Mendias says.
This research was published in Proceedings of the National Academy of Sciences, January 8, 2008, and was funded by the National Institute on Aging and the National Institute of Diabetes and Digestive and Kidney Diseases.
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