Athlete at Age

Scientists discover clues to what makes human muscle age

2009-10-08T08:07:34-04:00

MAPK and Notch pathways apparently age human (and all other) muscle

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."

Solution for Tennis Elbow!

2009-08-28T11:54:30-04:00

The NY Times just ran a short piece on a new treatment for tennis elbow: PhysEd: A New Treatment for Tennis Elbow .

...researchers from the Nicholas Institute of Sports Medicine and Athletic Trauma at Lenox Hill Hospital in New York City announced last month that they’ve developed an effective and supremely cheap treatment for chronic tennis elbow. Huddling a while back to brainstorm about inexpensive methods for combating the injury, the scientists glanced around their offices and noticed a homely, low-tech rubber bar, about 8 inches long, which, at the time, was being used for general physical therapy programs. The researchers wondered whether the ribbed, pliable bars, available for less than $20, might be re-purposed to treat tennis elbow. The answer, it soon become clear, was a resounding yes.

...
in the past two or three years, doctors and researchers have begun focusing on a particular kind of exercise that has shown promise against other achy tendons, especially the Achilles. The program involves eccentric exercises, which aren’t oddball moves but those in which the muscle lengthens as it tenses. Think of a biceps curl. When you raise the dumbbell, your bicep shortens and tightens. That’s a concentric contraction. When you lower the weight, the muscle lengthens, straining against the force of the weight. That’s eccentric.
...

“There’s a growing body of research showing that eccentric exercises are quite effective in treating Achilles tendonosis” and other tendon problems, Tyler says.

One of those studies was a well-designed 2007 experiment centered on tennis elbow. Conducted in Belgium, it found that eccentric exercises provided considerable relief. But the exercises had to be performed on expensive machines under medical supervision during repeated office visits. “We looked at those results and thought, there has to be an easier, more cost-effective way,” Tyler says.

Which is how they arrived at the rubber bar technique. He and his colleagues realized that a single, unhurried exercise using a tensile bar that looks like an oversized licorice stick could create an eccentric contraction all along the forearm. In the exercise, a person holds the bar upright at his or her side using the hand connected to the sore elbow, then grasps it near the top with the good hand. The top hand twists as the bar is brought around in front of the body and positioned perpendicular to the ground; the sore hand then takes over, slowly untwisting the bar by flexing the wrist. “Afterward, you should be sore,” Tyler says. “That’s how we know it’s effective.”

Eccentric contractions require the muscle to work against a force, in this case the coiled bar. “You can load a tendon so much more eccentrically” than with concentric exercises, Tyler says. “So we think the process may be remodeling the tendon.” Ultrasound studies by other researchers, including the group in Belgium, have shown that damaged tendons typically become less thick, indicating they are less damaged, after a course of strenuous eccentric exercise.

Tyler reported his findings at the July annual meeting of the American Orthopedic Society for Sports Medicine and has been deluged ever since with requests from doctors, physical therapists and patients for more information about how to perform the exercise and where to buy the bar. (Called the Thera-Band Flexbar, it’s available on Amazon.com; the manufacturer donated products for the study, but didn’t otherwise fund it; Tyler is not affiliated with the company.) “It’s not a difficult exercise but it is unique, so I would advise people to be taught by a physical therapist, if possible,” Tyler says. If not, proceed on your own — after, of course, an examination by a doctor; elbow pain can have many causes, not just tennis elbow. “In my opinion, you’re not going to hurt yourself,” Tyler continues, although you should be prepared for a commitment. His patients did three sets of fifteen repetitions every day. Beginners should start with three sets of five repetitions, adding more as the repetitions get easier, Tyler says.

The article has an instructional video, also available on YouTube Isolated eccentrics with flexbar:

I ordered a flexbar at Amazon. $17.17 + shipping. Given the tendonitis I've worked around for years, it seems like a bargain.

Can we get some CrossFitters or other trainers to apply this idea of "isolated eccentrics" to other tendons?

Alpha^2

Can Your Brain Fight Fatigue?

2009-07-15T14:05:18-04:00

The NY Times has an article out today with the intriguing title: Can Your Brain Fight Fatigue?:

Recently, researchers in England discovered that simply rinsing your mouth with a sports drink may fight fatigue. In the experiment which was published online in February in the Journal of Physiology, eight well-trained cyclists completed a strenuous, all-out time trial on stationary bicycles in a lab. The riders were hooked up to machines that measured their heart rate and power output. Throughout the ride, the cyclists swished various liquids in their mouths but did not swallow. Some of the drinks contained carbohydrates, the primary fuel used during exercise. The other drinks were just flavored, sugar-free water.

By the end of the time trials, the cyclists who had rinsed with the carbohydrate drinks — and spit them out — finished significantly faster than the water group. Their heart rates and power output were also higher. But when rating the difficulty of the ride, on a numerical scale, their feelings about the effort involved matched those for the water group.

In a separate portion of the experiment, the scientists, using a functional M.R.I., found that areas within the brain that are associated with reward, motivation and emotion were activated when subjects swished a carbohydrate drink. It seems that the brains of the riders getting the carbohydrate-containing drinks sensed that the riders were about to get more fuel (in the form of calories), which appears to have allowed their muscles to work harder even though they never swallowed the liquid.

I wonder how soon they'll start to market carbhydrate laden mouth washes to the low-carb set? Interesting stuff!

Alpha^2

To Improve Fitness, Try Sleep

2009-06-17T18:29:35-04:00

Tara Parker-Pope writes about a small study on sleep and fitness for the NY Times.

To Improve Fitness, Try Sleep

Most people training for a race or sport focus on adding more miles, workouts or weight training to improve their fitness. But new research suggests that simply getting more sleep can improve athletic performance.

The small study included five members of the Stanford women’s tennis team. For two to three weeks, the athletes maintained their regular schedules, sleeping and working out as usual. They took part in sprinting and hitting drills to measure their performance. Then the players were told to extend their sleep to 10 hours a night for five to six weeks.

After increasing sleep, the athletes performed better on all the drills. Sprinting drill times dropped on average to 17.56 seconds from 19.12 seconds. Hitting accuracy, measured by valid serves, improved to 15.61 serves, up from 12.6 serves, and a hitting depth drill improved to 15.45 hits, up from 10.85 hits.

Nice to see these ideas hitting the mainstream press.

Alpha^2

Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance

2009-02-20T00:16:17-05:00

From the abstract of "Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance"

Background: Exercise practitioners often take vitamin C supplementsbecause intense muscular contractile activity can result inoxidative stress, as indicated by altered muscle and blood glutathioneconcentrations and increases in protein, DNA, and lipid peroxidation.There is, however, considerable debate regarding the beneficialhealth effects of vitamin C supplementation.

Objective: This study was designed to study the effect of vitaminC on training efficiency in rats and in humans.

Design: The human study was double-blind and randomized. Fourteenmen (27–36 y old) were trained for 8 wk. Five of the menwere supplemented daily with an oral dose of 1 g vitamin C.In the animal study, 24 male Wistar rats were exercised under2 different protocols for 3 and 6 wk. Twelve of the rats weretreated with a daily dose of vitamin C (0.24 mg/cm² body surfacearea).

Results: The administration of vitamin C significantly (P =0.014) hampered endurance capacity. The adverse effects of vitaminC may result from its capacity to reduce the exercise-inducedexpression of key transcription factors involved in mitochondrialbiogenesis. These factors are peroxisome proliferator–activatedreceptor co-activator 1, nuclear respiratory factor 1, and mitochondrialtranscription factor A. Vitamin C also prevented the exercise-inducedexpression of cytochrome C (a marker of mitochondrial content)and of the antioxidant enzymes superoxide dismutase and glutathioneperoxidase.

Conclusion: Vitamin C supplementation decreases training efficiencybecause it prevents some cellular adaptations to exercise.

The "Discussion" section continues:

Vitamin C modulates endurance capacity but not maximal oxygen uptake after training
The maximal rate of oxygen consumption (O₂max)increased significantly after 8 wk of training in both the nonsupplementedmen (22.0% increase) and the men supplemented with vitamin C(10.8% increase). In 1999, Nielsen et al (29) found no effectof antioxidant supplementation on O₂maxin triathletes. We found a very similar result in our animalstudy—ie, a significant increase in O₂maxafter 6 wk of training in both the nonsupplemented (17.0% increase)and the vitamin C–supplemented (4.7% increase) groups.Endurance capacity is dependent mainly on the mitochondrialcontent of skeletal muscle (muscle oxidative capacity), noton the cardiovascular factors previously mentioned (20). Forobvious ethical reasons, we could not perform an endurance laboratorytest in our volunteers. Thus, to determine the effect of theantioxidant administration and exercise in the mitochondrialmuscle content, we performed another series of experiments inrats. We divided our animals into 2 training groups: endurance-trainedfor 3 wk and endurance-trained for 6 wk. Six weeks is approximatelythe period required to achieve a new steady state mitochondrialcontent in response to endurance training (15), although changesin mitochondrial protein and mRNA content can be apparent atmuch earlier time points (22). In our study, endurance-trainedrats showed a clear increase (186.7%) in their endurance capacity.However, the administration of vitamin C dramatically decreasedthis adaptation to only 26.5%. This finding is in keeping witha previous study in which it was shown, using endurance-trainedrats, that O₂max increased only 14%despite a 100% increase in muscle oxidative capacity (21). Oneof the main conclusions from that study was that the mitochondrialcontent of muscle is a major determinant of endurance capacity,whereas the maximal aerobic workload capacity appears to beregulated by O₂max (21). We offera molecular explanation for this result (ie, that vitamin Cdecreases exercise-induced mitochondrial biogenesis and theantioxidant capacity in skeletal muscle). We have found thatexercise training up-regulates the following mitochondriogenicpathway: PGC-1" border="0" src="http://www.ajcn.org/math/rarr.gif" /> NRF-1" border="0" src="http://www.ajcn.org/math/rarr.gif" /> mTFA" border="0" src="http://www.ajcn.org/math/rarr.gif" /> cytochrome C. All of these adaptationsare prevented by vitamin C administration.

When supplementing with vitamin C, there is the possibilitythat it may act as a prooxidant in vivo. These prooxidativereactions of vitamin C readily occur in vitro, and it has beenshown that they also may have relevance in vivo (30). A highintake of iron along with ascorbic acid could increase in vivolipid peroxidation of LDL and therefore could increase the riskof atherosclerosis (31). However, another study showed that,in iron-overloaded plasma, ascorbic acid acts as an antioxidantand prevents oxidative damage to lipids in vivo (32). In thepresent study, we measured different variables of oxidativestress, eg, blood glutathione oxidation and plasma malondialdehyde,in rats and men (data not shown); we did not find an indicationof an in vivo prooxidant effect of vitamin C in any of the experimentalgroups.

Free radicals as signals in muscle cell metabolism: potential interference by antioxidant vitamins
It is important to consider that free radicals are not alwaysdamaging to cells; in many cases, they serve as signals to adaptmuscle cells to exercise via modulation of gene expression (9,33). We have found that training causes an increase in 2 majorantioxidant enzymes (Mn-SOD and GPx) in skeletal muscle. Wewere surprised to see that vitamin C prevents these beneficialeffects of training. On the basis of the paradigm that enzymaticantioxidant systems such as Mn-SOD and GPx provide a first-linedefense against ROS, it is expected that exercise may inducethese protective mechanisms. Moderate exercise increases lifespan and decreases disability in rats (12) and humans (15).We report here that exercise training causes an increase inthe expression of antioxidant enzymes, which is prevented bythe administration of vitamin C.

Moderate exercise as an antioxidant
A major conclusion that can be drawn from our experiments isthat exercise itself is an antioxidant, because training increasesthe expression of 2 antioxidant enzymes related with longevity—namely,SOD and GPx. We provide evidence that the continuous presenceof small stimuli, such as low concentrations of ROS, in factinduces the expression of antioxidant enzymes as a defense mechanism.Low concentrations of radicals may be considered to be beneficial,because they act as signals to enhance defenses, rather thanbeing deleterious, as they can be when they are at higher concentrations.

Antioxidant vitamins impair training efficiency
The second major conclusion that can be drawn from our experimentsis that supplementation with vitamin C lowers training efficiency.Endurance capacity is directly related to the mitochondrialcontent. This variable is seriously hampered by antioxidantsupplementation, whereas O₂max, whichis dependent also on the cardiovascular system adaptations,is not significantly affected. This information is helpful fornutritionists who must prepare diets for athletes whose performanceis dependent on their endurance capacity. It should be takeninto account that some of the world's best marathon runnersexhibit rather modest measures of O₂max(34). Antioxidant supplementation is very popular among athletes,but data showing any beneficial effects on muscle function ofthis type of widespread practice are elusive. In fact, severalreports have shown deleterious effects of antioxidant treatment.As early as 1971, it was shown that vitamin E supplementation(400 IU/d for 6 wk) caused unfavorable effects on enduranceperformance (35). In 1996 and 1997, a Scandinavian journal published2 reports showing the deleterious effects of ubiquinone-10 supplementationon the performance of humans after a high-intensity trainingprogram (36, 37). In 2001, Coombes et al (38) reported that,in the muscles of unfatigued rats, supplementation with vitaminE and -lipoic acid depressed muscle tetanic force at low stimulationfrequencies. One year later, it was shown that supplementationof racing greyhounds with 1 g vitamin C/d for 4 wk significantlyslowed their speed (39). Taking into account that a high fitnesslevel is associated with a lower risk of premature death fromany cause, the effect of vitamin C administration on endurancecapacity has important implication for nutritionists, physicians,and exercise trainers and practitioners. Thus, the common practiceof taking vitamin C supplements during training (for both health-relatedand performance-related physical fitness) should be seriouslyquestioned.

If this holds up it should cause many of us to rethink supplementation (or at least certain supplements). Any counter science out there?

Alpha^2

Sprints may be best for diabetes prevention

2009-02-18T22:58:00-05:00

The title may overstate the case, but Reuters Health reports via Yahoo's Sprints may be best for diabetes prevention:

A few minutes of intense exercise a week is just as good as a half-hour of moderate physical activity a day for reducing a person's risk of developing type 2 diabetes -- and may actually be even more effective, new research hints.

"It is possible to gain significant health benefits from only 7.5 minutes of exercise each week -- if that is all that you find the time to do," Dr. James A. Timmons of Heriot-Watt University in Edinburgh, one of the researchers on the study, told Reuters Health.

"This is a dramatically different view from current thinking," he admitted.

Timmons and his team found that young sedentary men who did just 15 minutes of all-out sprinting on an exercise bike spread out over two weeks substantially improved their ability to metabolize glucose (sugar). Traditional aerobic exercise programs can boost sensitivity to the key blood-sugar-regulating hormone insulin. The high-intensity program did this too, but it also directly reduced the men's blood sugar levels -- something that standard exercise programs have not been shown to do.

Current exercise guidelines recommend at least 30 minutes of exercise a day at least five days a week, but "the general population fails to follow such regimes due to lack of time, motivation and adherence," the investigators note in the journal BMC Endocrine Disorders. They hypothesized that high intensity exercise might improve insulin sensitivity more efficiently.

Alpha ^2

A Promising Treatment for Athletes, in the Blood

2009-02-17T19:05:40-05:00

The New York Times reports in A Promising Treatment for Athletes, in the Blood on a new treatment for injuries:

Two of the Pittsburgh Steelers’ biggest stars, Hines Ward and Troy Polamalu, used their own blood in an innovative injury treatment before winning the Super Bowl. At least one major league pitcher, about 20 professional soccer players and perhaps hundreds of recreational athletes have also undergone the procedure, commonly called platelet-rich plasma therapy.

Experts in sports medicine say that if the technique’s early promise is fulfilled, it could eventually improve the treatment of stubborn injuries like tennis elbow and knee tendinitis for athletes of all types.

The method, which is strikingly straightforward and easy to perform, centers on injecting portions of a patient’s blood directly into the injured area, which catalyzes the body’s instincts to repair muscle, bone and other tissue. Most enticing, many doctors said, is that the technique appears to help regenerate ligament and tendon fibers, which could shorten rehabilitation time and possibly obviate surgery.

Research into the effects of platelet-rich plasma therapy has accelerated in recent months, with most doctors cautioning that more rigorous studies are necessary before the therapy can emerge as scientifically proven. But many researchers suspect that the procedure could become an increasingly attractive course of treatment for reasons medical and financial.

“It’s a better option for problems that don’t have a great solution — it’s nonsurgical and uses the body’s own cells to help it heal,” said Dr. Allan Mishra, an assistant professor of orthopedics at Stanford University Medical Center and one of the primary researchers in the field. “I think it’s fair to say that platelet-rich plasma has the potential to revolutionize not just sports medicine but all of orthopedics. It needs a lot more study, but we are obligated to pursue this.”

I've struggled for months with tendinitis in both elbows (not to mention, knee surgery for a torn meniscus last summer). This "...platelet-rich plasma therapy..." could prove a great boon in keeping us aging athletes in the game(s)/gym.

Alpha^2

At 85, More Peaks to Conquer and Adventures to Seek

2008-12-16T08:01:25-05:00

The New York Times reports on Fred Beckey - 85 years old and going strong.

SEATTLE — He had been called a vagabond, a recluse and a schemer, a cantankerous mountain man hiding his little black book of secret climbing techniques from the world. In seven decades, he had claimed more virgin ascents than any mountaineer alive. Some ascribed his feats to vengeance of a long-ago slight, others to the murder of his own fears. He was said to howl at tourists. His past was the stuff of lore, his plans the stuff of mystery.

Then, this fall, word of his next expedition spread among the worldwide network of contacts whose telephone numbers he kept scribbled on notecards wrapped with rubber bands in the gearbox pocket of his station wagon. The plan was announced in disarmingly casual fashion.

“Hi everyone, Fred Beckey called yesterday and he is going to northern Spain in early to mid-December,” began one posting this autumn at an online rock climbing forum. “Might be a long shot, but he’s looking for a partner to hook up with in Barcelona.”

Quoting Fred himself:

“You’ve got to be physically pretty strong to be any good at it at all,” Beckey said. “You’ve got to have a hard-core mental attitude. You’ve got to have the right mantra. You’ve got to have dedication, a sense of security, safety and sensitivity with your partners, and a good sense of balance. It’s a combination of many, many things. You need to have the capability or desire to accept a certain amount of risk. A lot of it is maybe spiritual, not a religious type, but you have to have an affinity with the outdoors.”

I'll follow his exploits with interest.

Alpha^2

Research on mice links fast food to Alzheimer's

2008-12-01T09:40:06-05:00

Reuters reports that Research on mice links fast food to Alzheimer's:

LONDON (Reuters) - Mice fed junk food for nine months showed signs of developing the abnormal brain tangles strongly associated with Alzheimer's disease, a Swedish researcher said on Friday.

The findings, which come from a series of published papers by a researcher at Sweden's Karolinska Institutet, show how a diet rich in fat, sugar and cholesterol could increase the risk of the most common type of dementia.

No surprise to readers of this (or many other blogs), but then we get what seems like an ingrained and not particularly scientific comment from the researcher:

"On examining the brains of these mice, we found a chemical change not unlike that found in the Alzheimer brain," Susanne Akterin, a researcher at the Karolinska Institutet's Alzheimer's Disease Research Center, who led the study, said in a statement.

"We now suspect that a high intake of fat and cholesterol in combination with genetic factors ... can adversely affect several brain substances, which can be a contributory factor in the development of Alzheimer's."

Whoa! What happened to sugar? Where did the refined carbohydrates go? TheScientist.com reported:

Alzheimer's: Type3 Diabetes?
Neurodegeneration research turns to insulin for answers

In 2005, while testing the effects of impaired insulin signaling on the brain, Suzanne de la Monte at Brown University and her colleagues observed several unexpected phenomena in her experimental mice. Hallmarks of neurodegenerative disease had surfaced: oxidative stress, amyloid fibrils, and cell loss. "It was the craziest thing," de la Monte says. Glucose metabolism and Alzheimer's had been linked previously, says de la Monte, and perhaps her findings explained why.

I grant that someone should ban transfats (Mayor Bloomberg in NY has started to do so), but the problem looks more like insulin regulation than it does cholesterol intake.

One wonders about how little researchers in the same fields pay attention to what others have discovered.

Alpha^2

Potentially Universal Mechanism Of Aging Identified

2008-11-29T09:07:29-05:00

ScienceDaily (Nov. 27, 2008) reports

Researchers have uncovered what may be a universal cause of aging, one that applies to both single cell organisms such as yeast and multicellular organisms, including mammals. This is the first time that such an evolutionarily conserved aging mechanism has been identified between such diverse organisms.

The mechanism probably dates back more than one billion years. The study shows how DNA damage eventually leads to a breakdown in the cell's ability to properly regulate which genes are switched on and off in particular settings.

Like our current financial crisis, the aging process might also be a product excessive deregulation.

Researchers have discovered that DNA damage decreases a cell's ability to regulate which genes are turned on and off in particular settings. This mechanism, which applies both to fungus and to us, might represent a universal culprit for aging.

"This is the first potentially fundamental, root cause of aging that we've found," says Harvard Medical School professor of pathology David Sinclair. "There may very well be others, but our finding that aging in a simple yeast cell is directly relevant to aging in mammals comes as a surprise."

These findings appear in the November 28 issue of the journal Cell.

...

"It is remarkable that an aging mechanism found in yeast a decade ago, in which sirtuins redistribute with damage or aging, is also applicable to mammals," says Leonard Guarente, Novartis Professor of Biology at MIT, who is not an author on the paper. "This should lead to new approaches to protect cells against the ravages of aging by finding drugs that can stabilize this redistribution of sirtuins over time."

Both Sinclair and Oberdoerffer agree with Guarente's sentiment that these findings may have therapeutic relevance.

"According to this specific mechanism, while DNA damage exacerbates aging, the actual cause is not the DNA damage itself but the lack of gene regulation that results," says Oberdoerffer. "Lots of research has shown that this particular process of regulating gene activity, otherwise known as epigenetics, can be reversed—unlike actual mutations in DNA. We see here, through a proof-of-principal demonstration, that elements of aging can be reversed."

Alpha^2