Isegoria

How little exercise can you get away with? Very little, I’ve been saying for years, as long as you make it count — and now the New York Times‘ “phys ed” columnist reports the same thing:

That minimum amount of exercise required to see a significant lowering of your risk of dying prematurely was, they concluded, 500 MET minutes of exercise a week. Of course, unless you’re an exercise scientist, there’s a good chance you don’t know what a MET minute is. A single MET, or Metabolic Equivalent of Task, is the amount of energy a person uses at rest. Two METs represent twice the energy burned at rest; four METs, four times the energy used at rest; and so on. Walking at three miles per hour is a 3.3-MET activity, while running at 6 miles an hour is a 10-MET activity. The committee concluded that a person needs to accumulate a weekly minimum of 500 MET minutes of exercise, which does not mean 500 minutes of exercise. Instead, 150 minutes a week (two and a half hours) of a moderate, three- to five-MET activity, such as walking, works out to be about 500 MET minutes. Half as much time (an hour and 15 minutes per week) spent on a 6-plus MET activity like easy jogging seems, according to the committee, to have similar health effects.

Interestingly, they did not find that exercise beyond a certain point conferred significant additional health benefits. Instead, the “dose response” for exercise, the committee found, is “curvilinear.” In other words, people who are the least active to start with get the most health benefit from starting to exercise. People who already are fit don’t necessarily get a big additional health benefit from adding more workout time to their regimens.

Apparently short heels and long toes are a surprising recipe for speed — if you don’t understand mechanical advantage:

Using ultrasound imaging, researchers compared the feet of 12 top college sprinters with those of 12 mere mortals. Surprisingly, the athletes had particularly short heels and longer-than-average toes — features that actually put them at a mechanical disadvantage when running.

“What we found is that sprinters actually had less mechanical advantage than the non-sprinter subjects that we tested,” said biomechanics researcher Stephen Piazza of Penn State University, co-author of the study published Friday in the Journal of Experimental Biology. “This was surprising to us because we expected that sprinters needed all the help they could get.”

Piazza and his co-author, kinesiology graduate student Sabrina Lee, launched their study after they happened to measure the Achilles’ tendon of a former NFL wide receiver, and were shocked by how little leverage his tendon provided.
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On average, top sprinters had heels that were 25 percent shorter than their non-athlete counterparts, as well as significantly longer toes.

To understand the paradox, the researchers set up a computer model of a sprinter’s push-off. The simulation revealed that despite providing a mechanical disadvantage, the short lever arm of a sprinter’s heel actually produced more force than the longer lever arm of a non-sprinter.

“It turns out that there’s a trade-off that we think is going on,” Piazza said. “The larger the lever arm of the Achilles tendon, the more the tendon has to travel up when you point your toes. What that means is that the calf muscles have to shorten more rapidly, and muscle that is shortening more rapidly can’t generate much force.”

In other words, sprinters sacrifice the mechanical advantage of a long lever for the benefit of a stronger push-off. Since quick acceleration over a short distance is the key to winning a short race, Piazza says the trade-off makes sense for sprinters. “He has to be able to generate a lot of force, but he also needs that leverage,” he said. “It turns out that by giving up some leverage, you actually gain more in terms of force generation and get a net benefit.”

Have these researchers ever driven a stick-shift? High-gear isn’t faster off the line.

Does exercise boost immunity? Yes, moderate exercise does, but, unsurprisingly, working to exhaustion does the opposite:

In general, and this is true in both mice and men, says Jeffrey A. Woods, a professor of kinesiology and community health at the University of Illinois and one of the scientists involved, viruses evoke an increase in what are called T1-type helper immune cells. These T1-helper cells induce inflammation and other changes in the body that represent a first line of defense against an invading virus. But if the inflammation, at first so helpful, continues for too long, it becomes counterproductive. The immune system needs, then, at some point to lessen the amount of T1-mediated inflammatory response, so that, in fighting the virus, it doesn’t accidentally harm its own host. The immune system does this by gradually increasing the amount of another kind of immune cell, T2-helper cells, which produce mostly an anti-inflammatory immune response. They’re water to the T1 fire. But the balance between the T1- and T2-helper cells must be exquisitely calibrated.

In the mice at the University of Illinois, moderate exercise subtly hastened the shift from a T1 response to a T2-style immune response — not by much, but by just enough, apparently, to have a positive impact against the flu. “Moderate exercise appears to suppress TH1 a little, increase TH2 a little,” Woods says.

On the other hand, intense or prolonged exercise “may suppress TH1 too much,” he says. Long, hard runs or other workouts may shut down that first line of defense before it has completed its work, which could lead, Woods says “to increased susceptibility to viral infection.”

Is the exercise cool-down really necessary? No.

Scientists discover clues to what makes human muscle age:

Working in collaboration with Dr. Michael Kjaer and his research group at the Institute of Sports Medicine and Centre of Healthy Aging at the University of Copenhagen in Denmark, the UC Berkeley researchers compared samples of muscle tissue from nearly 30 healthy men who participated in an exercise physiology study. The young subjects ranged from age 21 to 24 and averaged 22.6 years of age, while the old study participants averaged 71.3 years, with a span of 68 to 74 years of age.

In experiments conducted by Dr. Charlotte Suetta, a post-doctoral researcher in Kjaer’s lab, muscle biopsies were taken from the quadriceps of all the subjects at the beginning of the study. The men then had the leg from which the muscle tissue was taken immobilized in a cast for two weeks to simulate muscle atrophy. After the cast was removed, the study participants exercised with weights to regain muscle mass in their newly freed legs. Additional samples of muscle tissue for each subject were taken at three days and again at four weeks after cast removal, and then sent to UC Berkeley for analysis.

Morgan Carlson and Michael Conboy, researchers at UC Berkeley, found that before the legs were immobilized, the adult stem cells responsible for muscle repair and regeneration were only half as numerous in the old muscle as they were in young tissue. That difference increased even more during the exercise phase, with younger tissue having four times more regenerative cells that were actively repairing worn tissue compared with the old muscle, in which muscle stem cells remained inactive. The researchers also observed that old muscle showed signs of inflammatory response and scar formation during immobility and again four weeks after the cast was removed.

“Two weeks of immobilization only mildly affected young muscle, in terms of tissue maintenance and functionality, whereas old muscle began to atrophy and manifest signs of rapid tissue deterioration,” said Carlson, the study’s first author and a UC Berkeley post-doctoral scholar funded in part by CIRM. “The old muscle also didn’t recover as well with exercise. This emphasizes the importance of older populations staying active because the evidence is that for their muscle, long periods of disuse may irrevocably worsen the stem cells’ regenerative environment.”

At the same time, the researchers warned that in the elderly, too rigorous an exercise program after immobility may also cause replacement of functional muscle by scarring and inflammation. “It’s like a Catch-22,” said Conboy.

The researchers further examined the response of the human muscle to biochemical signals. They learned from previous studies that adult muscle stem cells have a receptor called Notch, which triggers growth when activated. Those stem cells also have a receptor for the protein TGF-beta that, when excessively activated, sets off a chain reaction that ultimately inhibits a cell’s ability to divide.

The researchers said that aging in mice is associated in part with the progressive decline of Notch and increased levels of TGF-beta, ultimately blocking the stem cells’ capacity to effectively rebuild the body.

This study revealed that the same pathways are at play in human muscle, but also showed for the first time that mitogen-activated protein (MAP) kinase was an important positive regulator of Notch activity essential for human muscle repair, and that it was rendered inactive in old tissue. MAP kinase (MAPK) is familiar to developmental biologists since it is an important enzyme for organ formation in such diverse species as nematodes, fruit flies and mice.

For old human muscle, MAPK levels are low, so the Notch pathway is not activated and the stem cells no longer perform their muscle regeneration jobs properly, the researchers said.

When levels of MAPK were experimentally inhibited, young human muscle was no longer able to regenerate. The reverse was true when the researchers cultured old human muscle in a solution where activation of MAPK had been forced. In that case, the regenerative ability of the old muscle was significantly enhanced.

“The fact that this MAPK pathway has been conserved throughout evolution, from worms to flies to humans, shows that it is important,” said Conboy. “Now we know that it plays a key role in regulation and aging of human tissue regeneration. In practical terms, we now know that to enhance regeneration of old human muscle and restore tissue health, we can either target the MAPK or the Notch pathways. The ultimate goal, of course, is to move this research toward clinical trials.”

(Hat tip to FuturePundit.)