Isegoria

For years, exercise physiologists thought that muscle fatigue was a result of lactic acid. Feel the burn. Now they have A New Explanation of Muscle Fatigue:

Muscle contraction and relaxation are controlled by the release and storage of calcium ions within muscle fibers. Scientists at Columbia University say thtat muscle fatigue, largely misunderstood for decades, is caused by calcium leaking into muscle cells.

Muscle Contraction
Calcium ions are released into the cell, causing filaments in the muscle fiber to contract.

Muscle Relaxation
Calcium ions are pumped into storage, allowing the muscle filaments to relax.

The discovery came while looking at heart disease:

As the damaged heart tries to deal with the body’s demands for blood, the nervous system floods the heart with the fight or flight hormones, epinephrine and norepinephrine, that make the heart muscle cells contract harder.

The intensified contractions, Dr. Marks and his colleagues discovered, occurred because the hormones caused calcium to be released into the heart muscle cells’ channels.

But eventually the epinephrine and norepinephrine cannot stimulate the heart enough to meet the demands for blood. The brain responds by releasing more and more of those fight or flight hormones until it is releasing them all the time. At that point, the calcium channels in heart muscle are overstimulated and start to leak.

What can be done about that?

When they understood the mechanisms, the researchers developed a class of experimental drugs that block the leaks in calcium channels in the heart muscle. The drugs were originally created to block cells’ calcium channels, a way of lowering blood pressure.

Dr. Marks and his colleagues altered the drugs to make them less toxic and to rid them of their ability to block calcium channels. They were left with drugs that stopped calcium leaks. The investigators called the drugs rycals, because they attach to the ryanodine receptor/calcium release channel in heart muscle cells. The investigators tested rycals in mice and found that they could prevent heart failure and arrhythmias in the animals. Columbia obtained a patent for the drugs and licensed them to a start-up company, Armgo Pharma of New York. Dr. Marks is a consultant to the company.
[...]
“If you go to the hospital and ask heart failure patients what is bothering them, they don’t say their heart is weak,” Dr. Marks said. “They say they are weak.”

So he and his colleagues looked at making mice exercise to exhaustion, swimming and then running on a treadmill. The calcium channels in their skeletal muscles became leaky, the investigators found. And when they gave the mice their experimental drug, the animals could run 10 to 20 percent longer.

It looks like it works on human cyclists too — so I have to assume human cyclists will be using it outside the lab.

Tim Layden of Sports Illustrated has written about Kevin Everett’s devastating injury and The Road Back from paralysis:

On the first weekend of the 2007 NFL season, Everett fell limply to the Ralph Wilson Stadium turf after making a tackle on the second-half kickoff. He did not get up. The stadium fell silent, an ambulance drove onto the field, and players from both teams formed a prayer circle, the nightmare tableau that can unfold in any football game but is thankfully rare. Everett, a third-year player, had suffered a fracture dislocation in his neck and severe spinal cord damage. He would be the subject of grim prognoses (many victims of his injury, indeed, do not walk again) but also exhaustive and controversial medical care, including the groundbreaking use of a hypothermia treatment that has both encouraged and divided the medical community.

The details:

As Hixon started upfield, he angled toward the middle. Just past the 15-yard line he planted his right foot and prepared to cut outside, to his left. As he made the move, Everett arrived, shoulders squared, his body in an athletic crouch. Just before impact, Everett bent his upper body forward; Hixon dropped his upper body. The players collided violently, the crown of Everett’s helmet meeting the side of Hixon’s. “I’ve seen the play so many times, and it was the timing of it,” says Everett. “I did the same thing I would do every time running down on kickoff team, got low to put my pads under his, and this one time he lowered his helmet.”

Hixon was driven sideways by the blow, staggering to his right, where Aiken finished the tackle. Everett never saw that. “My body went numb instantly,” he says. “I thought he kept going because it felt like he ran smack over me.”

Everett’s body went limp, and he crashed to the artificial turf, flat on his stomach, his head turned to the right. He was motionless except for a momentary twitch of his head and neck as he tried to lift his paralyzed body off the ground with the only muscles in his body still firing.

Fifty yards from Everett, on the Buffalo sideline, stood Andrew Cappuccino, 45, an orthopedic surgeon with specialty training in disorders of the spine and for 13 years a member of the Bills’ staff under the team’s medical director, John Marzo. Eleven days earlier, on Aug. 29, Marzo and head trainer Bud Carpenter had led a 1 1/2-hour spinal cord injury refresher drill at the Bills’ field house in Orchard Park, N.Y. Cappuccino had nearly begged off — “I told Bud, ‘That scenario is never going to happen,’ ” recalls Cappuccino, who’d yet to encounter a spinal cord injury at a Bills game in his time with the team — but Carpenter insisted. Now that drill would form the foundation for the seminal moment in Cappuccino’s career. And in Everett’s life.
[...]
Cappuccino knew there was a flicker of hope. On the field he had applied forceful pressure to Everett’s lower extremities, from his ankles to his groin, and had detected a response that was absent with a sharp sensation such as a pinprick. This told Cappuccino that Everett had suffered an incomplete spinal cord injury, probably meaning that the cord was severely damaged but not severed.

Cappuccino then made two decisions, one that has reverberated through the medical world and one that has gone largely unnoticed but might have been just as critical.

First, he introduced mild hypothermia as a part of Everett’s care. In November 2006, Cappuccino had attended a seminar of the Cervical Spine Research Society and sat in on a talk by Dalton Dietrich, scientific director of The Miami Project to Cure Paralysis. Dietrich devoted the last 10 minutes of his presentation to the potential benefits of induced hypothermia for neuroprotection — the rapid cooling of the body to reduce metabolic demand and to prevent further damage from swelling and other inflammatory mechanisms. It is a controversial treatment that has not been established as a standard of care in spinal cord injuries and is the subject of considerable debate in the field. Partly motivated by that talk, Cappuccino had instructed the EMTs at Bills games to stock their ambulance with three bags of saline solution in a cooler. [...]
Second, Cappuccino instructed Lengel to drive to Millard Fillmore Gates Circle Hospital. Normally a player injured in a Bills game would be taken to Buffalo General, about a mile closer, but Cappuccino knew that Gates has magnetic resonance imaging (MRI) technicians on duty 24 hours a day. This is rare, and with Gates’s in-house CT scanning capability it would enable swift diagnosis of Everett’s injury. The hospital also is the only one in Buffalo with a neurosurgical intensive care unit, under the direction of Dr. Kevin Gibbons, 47.

Everett arrived at the hospital about 35 minutes after the hit. X-rays and CT scans showed a fracture dislocation of Everett’s cervical vertebrae at the C3/C4 level, meaning that one vertebra had slipped out of alignment and was compressing against its adjacent vertebra and the spinal cord in the neck. An MRI showed that Everett’s spinal cord was 70% to 75% compromised, or pinched, by the dislocation.

Cappuccino and Gibbons, assisted by senior neurosurgical resident Ken Snyder, worked to reduce the dislocation. A halo device was screwed into Everett’s skull, and while he remained awake, manual pressure and traction weights were used to realign the vertebrae and remove pressure from the pinched spinal cord. Next would come 4 1/2 hours of surgery to stabilize Everett’s vertebrae and further decompress the spinal cord. Both the reduction and the stabilization surgery are common practices in spinal cord injuries and clearly were vital elements of Everett’s care. [,,,]
Everett was placed on the CoolGard in the predawn hours of Monday, Sept. 10, and within two hours his body had cooled to a temperature of 91.5°. That morning Everett was able to squeeze his thighs against Cappuccino’s hands. “Everybody was stunned,” says Cappuccino, “including me.”
[...]
Twelve days after an injury that could have left him in a wheelchair for life, Everett flew to Houston to begin rehab. Less than a month later he would be walking with assistance.

Soda, sweet drinks main source of calories in U.S.:

Tufts researchers recently reported that while the leading source of calories in the average American diet used to be from white bread, that may have changed. Now, according to preliminary research conducted by scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Americans are drinking these calories instead.
[...]
Among respondents to the 1999-2000 National Health and Nutrition Examination Survey (NHANES), more than two thirds reported drinking enough soda and/or sweet drinks to provide them with a greater proportion of daily calories than any other food. In addition, obesity rates were higher among these sweet drink consumers. Consumers of 100% orange juice and low fat milk, on the other hand, tended to be less overweight, on average.

Fitness trumps fatness in longevity study:

Men and women who were fit, as judged by a treadmill test, but were overweight or obese had a lower mortality risk than those of normal weight but low fitness levels, the study in the Journal of the American Medical Association showed.

Exercise expert Steven Blair of the University of South Carolina and colleagues tracked about 2,600 people age 60 and up, examining how physical fitness and body fat affected their death rates over 12 years.

Those in the lowest fifth in terms of fitness had a death rate four times higher than participants ranked in the top fifth for fitness.
[...]
The researchers assessed the fitness of the participants using a treadmill test, seeing how long they could walk while the treadmill’s incline increased. They measured body mass index — calculated from a person’s weight and height — as well as waist circumference and body fat percentage.

The study showed that even a modest effort to improve physical activity can provide health benefits, the researchers said. Those in the bottom fifth in terms of fitness were about twice as likely to die than those in the next fifth.

Protein found to turn up metabolism in mice — and increase their average lifespan:

Tricking muscle tissue to burn rather than store fat has succeeded in increasing the average life span of mice and staved off some age-related diseases, U.S. researchers said on Tuesday.

Mice bred to make too much of a protein known as uncoupling protein 1 released food energy as heat instead of storing it as fat.

“What we’re uncoupling is the process of burning energy from storing energy,” said Dr. Clay Semenkovich of Washington University School of Medicine in St. Louis, Missouri whose research appears in the journal Cell Metabolism.

“Normally when you metabolize food, you take the energy that comes from that food and you store it. In essence, you are coupling the energy in the food into a stored form,” Semenkovich said in a telephone interview.

Mice that overproduced this uncoupling protein in their muscle tissue weighed less and had less fat tissue, even though they ate the same amount as normal mice in the study.

“They lived about three months longer on average, which translates into six or seven years in human life, which is pretty good,” Semenkovich said.

The protein did not extend the maximum life span of the mice, but it did increase their average life span, perhaps because they were less prone to age-related diseases, Semenkovich said.

Mice in the study had a lower incidence of vascular disease, hypertension and lymphoma, a type of cancer.

Semenkovich said these same uncoupling proteins occur in humans, and genetic variations in the proteins have been linked with people weighing more or less.

“It may be possible to accelerate metabolism and find an alternative way of treating diseases,” he said.

Soda, sweet drinks main source of calories in U.S.:

Tufts researchers recently reported that while the leading source of calories in the average American diet used to be from white bread, that may have changed. Now, according to preliminary research conducted by scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Americans are drinking these calories instead.
[...]
Among respondents to the 1999-2000 National Health and Nutrition Examination Survey (NHANES), more than two thirds reported drinking enough soda and/or sweet drinks to provide them with a greater proportion of daily calories than any other food. In addition, obesity rates were higher among these sweet drink consumers. Consumers of 100% orange juice and low fat milk, on the other hand, tended to be less overweight, on average.

Protein found to turn up metabolism in mice — and increase their average lifespan:

Tricking muscle tissue to burn rather than store fat has succeeded in increasing the average life span of mice and staved off some age-related diseases, U.S. researchers said on Tuesday.

Mice bred to make too much of a protein known as uncoupling protein 1 released food energy as heat instead of storing it as fat.

“What we’re uncoupling is the process of burning energy from storing energy,” said Dr. Clay Semenkovich of Washington University School of Medicine in St. Louis, Missouri whose research appears in the journal Cell Metabolism.

“Normally when you metabolize food, you take the energy that comes from that food and you store it. In essence, you are coupling the energy in the food into a stored form,” Semenkovich said in a telephone interview.

Mice that overproduced this uncoupling protein in their muscle tissue weighed less and had less fat tissue, even though they ate the same amount as normal mice in the study.

“They lived about three months longer on average, which translates into six or seven years in human life, which is pretty good,” Semenkovich said.

The protein did not extend the maximum life span of the mice, but it did increase their average life span, perhaps because they were less prone to age-related diseases, Semenkovich said.

Mice in the study had a lower incidence of vascular disease, hypertension and lymphoma, a type of cancer.

Semenkovich said these same uncoupling proteins occur in humans, and genetic variations in the proteins have been linked with people weighing more or less.

“It may be possible to accelerate metabolism and find an alternative way of treating diseases,” he said.