The last NFL season was dominated by worries about concussions and other head injuries more than any before, but it ended on an upbeat note when Green Bay Packers quarterback Aaron Rodgers shook off two regular season concussions to win Super Bowl MVP honors. But after the bright lights go down, the long-term effects of brain injuries linger in the dark. And no one, it seems, knew that better than Dave Duerson.
Duerson played 11 seasons as a battering ram, a safety for the Chicago Bears and New York Giants. Last week he committed suicide, thrusting the worries about the long-term consequences of repeated blows to the head back into the spotlight.
When the 50-year-old former NFL safety and successful entrepreneur shot himself in the chest, there was another purpose: so that his brain could be donated to Boston University researchers and studied to assess the life-long neurological effects of playing in the National Football League. [Wired]
According to reports, Duerson made sure to get his final message across. He texted family members on the day of his death that he wanted his brain to go to the center, and to be sure he was heard, he left behind a paper note reading “Please, see that my brain is given to the NFL’s brain bank.”
Steroids. Human growth hormone. EPO. The cast of characters implicated in major athletic doping scandals are familiar to fans who follow major sports. Nor are accusations of doping anything new to Lance Armstrong, the seven-time champion of the Tour de France and most famous American participant in a sport constantly marred by scandal.
Armstrong has always denied the doping charges, and he continues to in the wake of a major investigation published this week by Sports Illustrated. But this time around, reporters Selena Roberts and David Epstein allege something new: That Armstrong illegally acquired and took an experimental drug called HemAssist, which never got beyond clinical trials.
So what is this stuff? HemAssist, developed by Baxter Pharmaceuticals, belongs to a group of drugs called hemoglobin-based oxygen carriers, or HBOC. Simply, they are blood substitutes, ones that mimic the structure of hemoglobin—the protein in red blood cells that transports oxygen. According to a scientific source we spoke to, who researched these drugs for years but preferred to provide background anonymously, the drugs mimic the structure of hemoglobin to more than 99 percent, and can deliver oxygen the way natural hemoglobin does.
Biotech researchers have been developing HBOCs for decades because of their exciting potential applications. For example, these blood substitutes could be taken out on a battlefield where stocks of real blood could not be refrigerated and preserved, and given to wounded soldiers to send a rush of oxygen to their critical organs like the brain and the heart. That ability to pack an oxygen punch is what makes HBOCs a tempting target for a doper.
About two-fifths of marathon runners “hit the wall” on the big day. That means they completely deplete their body’s stash of readily available energy, which makes them feel wiped out and severely limits their running pace; it sometimes forces people out of the run completely.
Marathoner and biomedical engineer Benjamin Rapoport has been physically and mentally struggling with this phenomenon for years, and had the bright idea to turn it into a research project. He published a mathematical theory in the journal PLoS Computational Biology describing how and why runners hit the wall–and how they can avoid it.
By taking into account the energy it takes to run a marathon, the body’s energy storage capacity and the runner’s power, the researchers were able to accurately calculate how many energy-rich carbohydrates a runner needed to eat before race day and how fast to run to complete all 26.2 miles (42 kilometers). [LiveScience]
Rapoport’s studies of marathoners were prompted by his desire to run in the Boston Marathon in 2005, and his teacher’s desire for him to be in class. In return for missing class, Rapoport was tasked with giving a class lecture on the physiology of the marathoner. That same year, Rapoport himself hit the wall while running the New York Marathon.
We’re coming off the first weekend of the NFL season, full of the bone-crunching hits and brain-rattling tackles that fans have come to love. But never before have fans been so attuned to the consequences of that violence, with concussions and other brain injuries in particular gathering more attention than ever at the start of this autumn’s season. And it’s not just at the professional level.
Owen Thomas killed himself this spring. He was 21, a defensive lineman and captain for the University of Pennsylvania football team, and he hanged himself in his apartment. Any out-of-nowhere suicide by a seemingly happy person leaves those left behind grappling for an explanation. But when doctors completed their autopsy of Thomas, they found something startling: evidence of incipient chronic traumatic encephalopathy (CTE), the condition caused by repetitive brain trauma that’s been showing up in many former NFL players.
That may seem a strange question, akin to asking who’s buried in Grant’s tomb. But a new study proposes that some athletes diagnosed with Lou Gehrig’s disease may in fact have a different fatal disease that is set off by concussions.
Researchers have previously investigated the link between athletes and this neurodegenerative disease, more technically known as amyotrophic lateral sclerosis (ALS). A recent study examined what seemed to be a higher than usual incidence of Lou Gehrig’s disease among soccer players, and, of course, the disease bears the name of a New York Yankee who was famously undaunted by the hard knocks of his sport. Though it’s impossible to determine now whether Lou Gehrig suffered from ALS or a different condition (Gehrig was cremated), the study’s lead author speculates that Lou Gehrig’s disease might be a misnomer:
“Here he is, the face of his disease, and he may have had a different disease as a result of his athletic experience,” said Dr. Ann McKee, the director of the neuropathology laboratory for the New England Veterans Administration Medical Centers, and the lead neuropathologist on the study. [The New York Times]
Players complaining about the new ball: It’s one of the traditions that returned like clockwork with this World Cup, along with egregious diving, English misery, and American fans perking up when the team performs and then swearing off soccer for another four years when USA crashes out.
But while equipment discontent typically fades as the tournament enters its final stages, anger toward World Cup 2010’s Jabulani ball won’t subside. So Caltech scientists decided to find out for themselves: They took the ball into their lab’s wind tunnel to see if it’s really so bad.
If you’ve spent any time kicking around a soccer ball, you’ll remember that it isn’t a perfect sphere, but rather is made of geometric panels with grooves in between. But while a traditional ball contains 32 panels, the Jabulani contains only 8, which made the team led by Beverly McKeon suspect there could be something to the complaints about its erratic behavior.
If you relax and concentrate, you’re more likely to make a goal. Seems pretty logical, but researchers at Britain’s Exeter University have tracked soccer players eye-movements to make sure. They have confirmed that players who ignore goalies’ distracting antics are more likely to make the shot.
The latest in the why-Britain-hasn’t-won-the-World-Cup-since-1966 line of research–which has also looked at the ball’s surface (smooth is good but some grooves necessary) and the psychological benefits of playing on your home field (it’s better)–Greg Wood’s study will appear in the Journal of Sports Medicine. Hopefully it will be available in time for the World Cup‘s start on June 11th.
Wood says that goalies can make use of a biological instinct to screw up a kicker’s shot.
“We focus on things in our environment that are threatening. In a penalty kick, that threat is a goalkeeper,” Wood said. “If he (the goalkeeper) can make himself more threatening, he can distract the kicker even more. By doing (certain) behaviors, he can make it so the kicker will kick (the ball) near the goalie.” [AP]
After years of denial, Floyd Landis–the cyclist who was stripped of his winning title to the 2006 Tour de France after failing a drug test–admitted last week that he did take performance enhancing drugs. And his confession is causing a stir, partly because he also implicated former teammate Lance Armstrong, seven-time-winner of the Tour de France (Armstrong denies the accusation), and partly because of the particular drugs he fessed up to taking:
Mr. Landis said in [several emails to cycling officials] that during his career, he and other American riders learned how to conduct blood transfusions, take the synthetic blood booster Erythropoietin, or EPO, and use steroids. All these practices are banned in cycling. Mr. Landis said he started using testosterone patches, then progressed to blood transfusions, EPO, and a liquid steroid taken orally. [Wall Street Journal]
EPO shook the cycling community in the 1990s, when police raids during the 1998 Tour de France (dubbed the “Tour de Dopage“) found that several riders were using EPO. It looks like the drug, believed to be thwarted by drug tests, has returned.
As we slowly slide out of the steroid era in baseball, human growth hormone (HGH) lingers as the next doping trend in major sports. Players like the New York Yankees’ Andy Pettitte have been implicated as HGH users already, and teammate Alex Rodriguez in currently one of many players being questioned in a federal investigation into the substance. However, until now there was no hard evidence that athletes gained a competitive edge by taking it. Researchers say a new study changes that.
“This is the first demonstration that growth hormone improves performance and justifies its ban in sport,” said Dr. Ken Ho, who led the study [AP].
The new research shows that the gains for athletes cheating with HGH could be staggering—but uneven and fraught with side effects. In the study published in the Annals of Internal Medicine, researchers divided 96 athletes into groups that received either placebo, HGH, testosterone, or a testosterone/HGH mix:
After eight weeks, researchers found that growth hormone improved sprint capacity in men and women by an average of 3.9% over the placebo group — which would trim 0.4 of a second from a 10-second time in the 100-meter dash, said study lead author Dr. Kenneth Ho at St. Vincent’s Hospital in Sydney, Australia. In the 2008 Olympics, the top three male finishers had times of 9.69, 9.89 and 9.91 seconds.
That same 3.9% improvement could cut 1.2 seconds from a 30-second time in a 50-meter swim, Ho said [Los Angeles Times].
We’re a week into the Vancouver Olympics, and if you haven’t had your fill of world-class athletes frolicking on the ice in frilly clothing, playing ice shuffleboard with 4o-plus-pound stones, or hurtling downhill at terrifying speed, don’t worry: There’s more than a week left to go. And there will be feats of dizzying daring and velocity, since Olympians don’t settle for just terrifying speed when there’s a chance to attain ridiculous speed, or even ludicrous speed. Thankfully, the Olympics are a bastion of technology, not just sport.
Take bobsledding. Team USA has been working with the Exa Corporation to develop the most aerodynamic sled possible, by computationally mapping fluid dynamics of air rushing past the sled. Says Exa’s Brad Duncan, “We’ve heard that some other countries are using more traditional processes where they do testing in wind tunnels…. That’s where the U.S. team was able to leapfrog the competition, was to do digital testing” [LiveScience]. The sleds could reach up to 95 miles an hour in the race, and designer Bob Cuneo says the sled design is a huge factor. Ultimately, Cuneo estimates that about a third of the team’s success in Vancouver comes down to engineering [Popular Mechanics].