Archive for the ‘Bodybuilding’ Category

“No pain, no gain.” So say those working out to build up their muscles, and on a cellular level it is a pretty accurate description of how muscle mass increases. Exercise causes tears in muscle membrane and the healing process produces an increased amount of healthy muscle. Implicit in this scenario is the notion that muscle repair is an efficient and ongoing process in healthy individuals. However, the repair process is not well understood. New University of Iowa research into two types of muscular dystrophy now has opened the door on a muscle repair process and identified a protein that plays a critical role.

The protein, called dysferlin, is mutated in two distinct muscular dystrophies known as Miyoshi Myopathy and limb-girdle muscular dystrophy type 2b. The UI study suggests that in these diseases, the characteristic, progressive muscle degeneration is due to a faulty muscle-repair mechanism rather than an inherent weakness in the muscle’s structural integrity. The research findings reveal a totally new cellular cause of muscular dystrophy and may lead to many discoveries about normal muscle function and to therapies for muscle disorders.

The research team led by Kevin Campbell, Ph.D., the Roy J. Carver Chair of Physiology and Biophysics and interim head of the department, UI professor of neurology, and a Howard Hughes Medical Institute (HHMI) Investigator, studied the molecular consequences of losing dysferlin and discovered that without dysferlin muscles were unable to heal themselves.

The UI team genetically engineered mice to lack the dysferlin gene. Just like humans with Miyoshi Myopathy and limb-girdle muscular dystrophy type 2b, the mice developed a muscular dystrophy, which gets progressively worse with age. However, treadmill tests revealed that the muscles of mice that lack dysferlin were not much more susceptible to damage than the muscles of normal mice. This contrasts with most muscular dystrophies of known cause where genetic mutations weaken muscle membranes and make muscles more prone to damage.

“This told us that the dystrophies caused by dysferlin loss were very different in terms of how the disease process works compared to other dystrophies we have studied,” Campbell said. “We were gradually picking up clues that showed we had a different type of muscular dystrophy here.”

Most muscular dystrophy causing genetic mutations have been linked to disruption of a large protein complex that controls the structural integrity of muscle cells. The researchers found that dysferlin was not associated with this large protein complex. Rather, dysferlin is normally found throughout muscle plasma membrane and also in vesicles, which are small membrane bubbles that encapsulate important cellular substances and ferry them around cells. Vesicles also are important for moving membrane around in cells.

Previous studies have shown that resealing cell membranes requires the accumulation and fusing of vesicles to repair the damaged site.

Using an electron microscope to examine muscles lacking dysferlin, the UI team found that although vesicles gathered at damaged membrane sites, the membrane was not resealed. In contrast, the team discovered that when normal muscle is injured, visible “patches” form at the damaged sites, which seal the holes in the membrane. Chemicals that tag dysferlin proved that these “patches” were enriched with dysferlin and the patches appeared to be formed by the fusion of dysferlin-containing vesicles that traveled though the cell to the site of membrane damage.

The researchers then used a high-powered laser and a special dye to visualize the repair process in real time.

Under normal conditions, the dye is unable to penetrate muscle membrane. However, if the membrane is broken the dye can enter the muscle fiber where it fluoresces. Using the laser to damage a specific area of muscle membrane, the researchers could watch the fluorescence increase as the dye flowed into the muscle fiber.

“The more dye that entered, the more fluorescence we saw,” Campbell explained. “However, once the membrane was repaired, no more dye could enter and the level of fluorescence remained steady. Measuring the increase in fluorescence let us measure the amount of time that the membrane stayed open before repair sealed the membrane and prevented any more dye from entering.”

In the presence of calcium, normal membrane repaired itself in about a minute. In the absence of calcium, vesicles gathered at the damaged muscle membrane, but they did not fuse with each other or with the membrane and the membrane was not repaired. In muscle that lacked dysferlin, even in the presence of calcium, the damaged site was not repaired.

Campbell speculated that dysferlin, which contains calcium-binding regions, may be acting as a calcium sensor and that the repair system needs to sense the calcium in order to initiate the fusion and patching of the hole. Campbell added that purifying the protein and testing its properties should help pin down its role in the repair process.

The discovery of a muscle repair process and of dysferlin’s role raises many new questions. In particular, Campbell wonders what other proteins might be involved and whether defects in those components could be the cause of other muscular dystrophies.

“This work has described a new physiological mechanism in muscle and identified a component of this repair process,” Campbell said. “What is really exciting for me is the feeling that this is just a little hint of a much bigger picture.”

In addition to Campbell, the UI researchers included Dimple Bansal, a graduate student in Campbell’s laboratory and the lead author of the paper, Severine Groh, Ph.D., and Chien-Chang Chen, Ph.D., both UI post-doctoral researchers in physiology and biophysics and neurology, and Roger Williamson, M.D., UI professor of obstetrics and gynecology. Also part of the research team were Katsuya Miyake, Ph.D., a postdoctoral researcher, and Paul McNeil, Ph.D., a professor of cellular biology and anatomy at the Medical College of Georgia in Augusta, Ga., and Steven Vogel, Ph.D., at the Laboratory of Molecular Physiology at the National Institute of Alcohol Abuse and Alcoholism, Rockville, Md.

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Article adapted by MD Sports from original press release.
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Contact: Jennifer Brown
University of Iowa 

The study was funded by a grant from the Muscular Dystrophy Association.

University of Iowa Health Care describes the partnership between the UI Roy J. and Lucille A. Carver College of Medicine and UI Hospitals and Clinics and the patient care, medical education and research programs and services they provide.

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Scientists have discovered that a group of chemicals known as Histone Deacetylase (HDAC) inhibitors stimulate growth and regeneration of adult skeletal muscle cells by increasing expression of the protein follistatin. The research, published in the May issue of Developmental Cell, may provide new avenues for developing effective means to promote regeneration in muscular dystrophies.

Dr. Vittorio Sartorelli from the Muscle Gene Expression Group in the Laboratory of Muscle Biology, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, in Bethesda, Maryland, and colleagues at the Salk Institute and the Dulbecco Telethon Institute in Rome report that HDAC inhibitors, which stimulate the formation of mature muscle cells from immature precursor cells, also cause a significant elevation of follistatin levels. When follistatin levels are reduced, then HDAC inhibitors no longer stimulate adult muscle growth. The regeneration activities of the HDAC inhibitors appear to function only in skeletal muscle, since follistatin is not stimulated in other cell types tested. In animal studies, administration of an HDAC inhibitor produced clear signs of muscle regeneration in regions of injured skeletal muscle tissues.

“Our findings establish for the first time that follistatin promotes the recruitment and fusion of immature muscle cells to pre-existing adult muscle fibers. These results suggest that follistatin is a promising target for future drug development of muscle regeneration. HDAC inhibitors, by stimulating follistatin, could well be pharmacologically useful as stimulants of muscle regeneration. We are investigating whether these inhibitors are a viable treatment to regenerate healthy new muscle tissues in animal models of muscular dystrophies,” explains Dr. Sartorelli. The functional link between HDAC inhibitors, follistatin, and adult muscle regeneration is especially provocative as an HDAC inhibitor is already being used clinically in humans as an anti-cancer therapeutic.

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Article adapted by MD Sports from original press release.
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Contact: Heidi Hardman
Cell Press 

Simona Iezzi, Monica Di Padova, Carlo Serra, Giuseppina Caretti, Cristiano Simone, Eric Maklan, Giulia Minetti, Po Zhao, Eric P. Hoffman, Pier Lorenzo Puri, and Vittorio Sartorelli: “Deacetylase Inhibitors Increase Muscle Cell Size by Promoting Myoblast Recruitment and Fusion through Induction of Follistatin”

 

Investigators in The Research Institute at Nationwide Children’s Hospital have identified the role of a protein that could potentially lead to new clinical treatments to combat musculoskeletal diseases, including Duchenne muscular dystrophy (DMD).

Results of these studies appear in the March 11, 2008 issue of the Proceedings of the National Academy of Sciences.

These studies, led by Brian Kaspar, PhD, a principal investigator in the Center for Gene Therapy at The Research Institute and an assistant professor of Pediatrics at The Ohio State University, focus on a protein called follistatin (FS). Using a single injection, gene-delivery strategy involving FS, investigators treated the hind leg muscles of mice. Results showed increased muscle size and strength, quadruple that of mice treated with proteins other than FS. The muscle enhancements were shown to be well-tolerated for more than two years.

According to Dr. Kaspar, increased muscle mass and strength were also evident when this strategy was tested using a model of DMD. Apart from the injected hind leg muscles, strengthening effects were also shown in the triceps. In addition, fibrosis, abnormal formation of scar tissue and a hallmark of muscular dystrophy, was decreased in FS-treated animals.

“We believe this new FS strategy may be more powerful than other strategies due to its additional effects, including its ability to reduce inflammation,” said Dr. Kaspar.

The strategy showed no negative effects on the heart or reproductive ability of either males or females. The results were also replicated in older animals, suggesting that this strategy could be useful in developing clinical treatments for older DMD patients.

“This research provides evidence of multiple potential treatment applications for muscle diseases including, but not limited to, muscular dystrophy,” said Jerry Mendell, MD, director of the Center for Gene Therapy at The Research Institute, a co-author on the study, and professor of Pediatrics in Neurology and Pathology at The Ohio State University. “These results offer promise for treatment of potentially any muscle-wasting disease, including muscle weakness due to other illnesses, aging, and inflammatory diseases such as polymyositis. Our next step is to pursue clinical trials.”

The Research Institute at Nationwide Children’s Hospital has a patent pending on the FS technique due to the major role it may play for muscular dystrophy treatment and other muscle-wasting diseases.

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Article adapted by MD Sports from original press release.
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Contact: Pam Barber/Mary Ellen Fiorino
Nationwide Children’s Hospital

USC study finds combining resistance training and androgens gives more muscular bang for the buck

PHILADELPHIA (June 19, 2003)-Men who take supplemental androgens-the male hormone testosterone or similar medications-increase their strength by adding muscle mass, but androgens alone do not pack more might into the muscles, according to studies presented today by University of Southern California researchers.

Treatment with androgens increases lean body mass-which encompasses everything in the body but bone and fat-and strength increases proportionately with the amount of muscle added, says E. Todd Schroeder, Ph.D., postdoctoral fellow in the Department of Medicine at the Keck School of Medicine of USC and adjunct assistant professor in the USC Department of Biokinesiology and Physical Therapy. Schroeder presented his findings at the Endocrine Society’s 85th Annual Meeting.

However, when men use androgen therapy combined with resistance training, such as weightlifting, their gains in strength may far outpace the amount of muscle that can be added with androgens alone. Each muscle cell packs a bigger punch, a concept known as improved muscle quality.

“The results of androgen therapy alone on muscle and strength are not necessarily bad, but they are not optimal,” Schroeder says. “The men did improve their strength, but it was proportional to the muscle mass they added.”

The findings wield health implications beyond the stereotypes of muscle-bound bodybuilders. Schroeder and his colleagues are studying the usefulness of androgens and exercise in helping maintain muscle strength, muscle power and physical function among seniors, for example. They also have studied androgen therapy’s effectiveness in battling wasting among HIV-positive patients.

In their recent study, Schroeder and USC colleagues Michael Terk, M.D., and Fred R. Sattler, M.D., looked at both young men and seniors. They followed two groups: 33 seniors ranging from their mid-60s to late 70s, and 23 HIV-positive men ranging from their early 30s to late 40s.

The younger men were randomly assigned to get 600 milligrams (mg) each week of nandrolone alone or in combination with resistance training. The older men were randomly assigned to receive 20 mg a day of oxandrolone or a placebo. These pharmacologic androgen doses were given over 12 weeks.

Researchers determined maximal strength-the most weight a participant could safely lift or push-using leg press, leg extension and leg flexion machines.

The researchers also measured the cross-sectional area of participants’ thighs and the lean body mass of their lower extremities by magnetic resonance imaging, or MRI. They then determined the strength that participants exerted for each unit of muscle (muscle quality) and how muscle quality changed over time.

Androgens alone increased lean body mass and maximum strength in both groups of men, but “gains were modest,” Schroeder says, and muscle quality did not change, since the muscle size and strength both increased proportionately. However, among those using nandrolone and undergoing resistance training, muscle quality improved significantly: Gains in strength were much greater than the gains that could occur from muscle-mass increase alone.

“It is clear from our studies and others that resistance training is critical for increasing muscle quality, but the effects can probably be augmented with androgens,” Schroeder says. “In addition, not everyone can do resistance training, and a short course of androgens can help get people stronger and more functional.”

Finally, results provide researchers insight into how to better design future studies to test strategies to best preserve and even improve muscle strength and physical function among seniors. Similar studies will be important for other types of patients who experience muscle loss and frailty, such as those with cancer, chronic lung disease, chronic renal failure and other conditions.

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Article adapted by MD Sports from original press release.
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Contact: Jon Weiner
University of Southern California

Grants by the National Institute of Diabetes & Digestive & Kidney Diseases and the National Center for Research Resources (General Clinical Research Center) supported the research. Bio Technology General Corp., which makes Oxandrin (oxandrolone), also supported part of the research.

Edward T. Schroeder, Michael Terk and Fred R. Sattler, “Pharmacological Doses of Androgen Do Not Improve Muscle Quality in Young or Older Men: Results from Two Studies,” Endocrine Society’s 85th Annual Meeting, poster P3-212, presentation 11 a.m., June 21. Findings released at news conference 1:30 p.m., June 19.

Recipe to recover more quickly from exercise: Finish workout, eat pasta, and wash down with five or six cups of strong coffee.

Glycogen, the muscle’s primary fuel source during exercise, is replenished more rapidly when athletes ingest both carbohydrate and caffeine following exhaustive exercise, new research from the online edition of the Journal of Applied Physiology shows. Athletes who ingested caffeine with carbohydrate had 66% more glycogen in their muscles four hours after finishing intense, glycogen-depleting exercise, compared to when they consumed carbohydrate alone, according to the study, published by The American Physiological Society.

The study, “High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is co-ingested with caffeine,” is by David J. Pedersen, Sarah J. Lessard, Vernon G. Coffey, Emmanuel G. Churchley, Andrew M. Wootton, They Ng, Matthew J. Watt and John A. Hawley. Dr. Pedersen is with the Garvan Institute of Medical Research in Sydney, Australia, Dr. Watt is from St. Vincent’s Institute of Medical Research, Fitzroy, Victoria, Australia. All others are with the Royal Melbourne Institute of Technology University (RMIT) in Bundoora, Victoria, Australia.

A fuller audio interview with Dr. Hawley is available in Episode 11 of the APS podcast, Life Lines, at www.lifelines.tv. The show also includes an interview with Dr. Stanley Schultz, whose physiological discovery of how sugar is transported in the gut led to the development of oral rehydration therapy and sports drinks such as Gatorade and Hi-5.

Caffeine aids carbohydrate uptake  

It is already established that consuming carbohydrate and caffeine prior to and during exercise improves a variety of athletic performances. This is the first study to show that caffeine combined with carbohydrates following exercise can help refuel the muscle faster.

“If you have 66% more fuel for the next day’s training or competition, there is absolutely no question you will go farther or faster,” said Dr. Hawley, the study’s senior author. Caffeine is present in common foods and beverages, including coffee, tea, chocolate and cola drinks.

The study was conducted on seven well-trained endurance cyclists who participated in four sessions. The participants first rode a cycle ergometer until exhaustion, and then consumed a low-carbohydrate dinner before going home. This exercise bout was designed to reduce the athletes’ muscle glycogen stores prior to the experimental trial the next day.

The athletes did not eat again until they returned to the lab the next day for the second session when they again cycled until exhaustion. They then ingested a drink that contained carbohydrate alone or carbohydrate plus caffeine and rested in the laboratory for four hours. During this post-exercise rest time, the researchers took several muscle biopsies and multiple blood samples to measure the amount of glycogen being replenished in the muscle, along with the concentrations of glucose-regulating metabolites and hormones in the blood, including glucose and insulin.

The entire two-session process was repeated 7-10 days later. The only difference was that this time, the athletes drank the beverage that they had not consumed in the previous trial. (That is, if they drank the carbohydrate alone in the first trial, they drank the carbohydrate plus caffeine in the second trial, and vice versa.)

The drinks looked, smelled and tasted the same and both contained the same amount of carbohydrate. Neither the researchers nor the cyclists knew which regimen they were receiving, making it a double-blind, placebo-controlled experiment.

Glucose and insulin levels higher with caffeine ingestion
The researchers found the following:  
  • one hour after exercise, muscle glycogen levels had replenished to the same extent whether or not the athlete had the drink containing carbohydrate and caffeine or carbohydrate only
  • four hours after exercise, the drink containing caffeine resulted in 66% higher glycogen levels compared to the carbohydrate-only drink
  • throughout the four-hour recovery period, the caffeinated drink resulted in higher levels of blood glucose and plasma insulin
  • several signaling proteins believed to play a role in glucose transport into the muscle were elevated to a greater extent after the athletes ingested the carbohydrate-plus-caffeine drink, compared to the carbohydrate-only drink

 Dr. Hawley said it is not yet clear how caffeine aids in facilitating glucose uptake from the blood into the muscles. However, the higher circulating blood glucose and plasma insulin levels were likely to be a factor. In addition, caffeine may increase the activity of several signaling enzymes, including the calcium-dependent protein kinase and protein kinase B (also called Akt), which have roles in muscle glucose uptake during and after exercise.

Lower dose is next step  

In this study, the researchers used a high dose of caffeine to establish that it could help the muscles convert ingested carbohydrates to glycogen more rapidly. However, because caffeine can have potentially negative effects, such as disturbing sleep or causing jitteriness, the next step is to determine whether smaller doses could accomplish the same goal.

Hawley pointed out that the responses to caffeine ingestion vary widely between individuals. Indeed, while several of the athletes in the study said they had a difficult time sleeping the night after the trial in which they ingested caffeine (8 mg per kilogram of body weight, the equivalent of drinking 5-6 cups of strong coffee), several others fell asleep during the recovery period and reported no adverse effects.

Athletes who want to incorporate caffeine into their workouts should experiment during training sessions well in advance of an important competition to find out what works for them.

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Article adapted by MD Sports from original press release.
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Contact: Christine Guilfoy
American Physiological Society

Physiology is the study of how molecules, cells, tissues and organs function to create health or disease. The American Physiological Society (APS) has been an integral part of this scientific discovery process since it was established in 1887.

A University of Colorado at Boulder study of a space-age, low-gravity training machine used by several 2008 Olympic runners showed it reduced impacts on muscles and joints by nearly half when subjects ran at the equivalent of 50 percent of their body weight.

The new study has implications for both competitive runners rehabilitating from injuries and for ordinary people returning from knee and hip surgeries, according to Associate Professor Rodger Kram of CU-Boulder’s integrative physiology department.

Known as the “G-Trainer,” the machine consists of a treadmill surrounded by an inflatable plastic chamber that encases the lower body of the runner, said Kram. Air pumped into the chamber increases the pressure and effectively reduces the weight of runners, who are sealed in the machine at the waist in a donut-shaped device with a special zipper and “literally lifted up by their padded neoprene shorts,” he said.

Published in the August issue of the Journal of Applied Biomechanics, the study is the first to quantify the effects of running in the G-Trainer, built by Alter-G Inc. of Menlo Park, Calif., using technology developed at NASA’s Ames Research Center in California. The paper was authored by Kram and former CU-Boulder doctoral student Alena Grabowski, now a postdoctoral researcher at the Massachusetts Institute of Technology.

Although G-Trainers have been used in some sports clinics and college and professional sports training rooms since 2006, the new study is the first scientific analysis of the device as a training tool for running, said Grabowski.

“The idea was to measure which levels of weight support and speeds give us the best combination of aerobic workout while reducing the impact on joints,” said Kram. “We showed that a person can run faster in the G-Trainer at a lower weight and still get substantial aerobic benefits while maintaining good neuromuscular coordination.”

The results indicated a subject running at the equivalent of half their weight in the G-Trainer at about 10 feet per second, for example — the equivalent of a seven-minute mile — decreased the “peak” force resulting from heel impact by 44 percent, said Grabowski. That is important, she said, because each foot impact at high speed can jar the body with a force equal to twice a runner’s weight.

Several former CU track athletes participating in the 2008 Olympics in Beijing have used the machine, said Kram. Alumna Kara Goucher, who will be running the 5,000- and 10,000-meter races in Beijing, has used the one in Kram’s CU-Boulder lab and one in Eugene, Ore., for rehabilitation, and former CU All-American and Olympic marathoner Dathan Ritzenhein also uses a G-Trainer in his home in Oregon. Other current CU track athletes who have been injured have tried the machine in Kram’s lab and found it helpful to maintain their fitness as they recovered, Kram said.

For the study, the researchers retrofitted the G-Trainer with a force-measuring treadmill invented by Kram’s team that charts vertical and horizontal stress load on each foot during locomotion, measuring the variation of biomechanical forces on the legs during running. Ten subjects each ran at three different speeds at various reduced weights, with each run lasting seven minutes. The researchers also measured oxygen consumption during each test, Kram said.

Grabowski likened the effect of the G-Trainer on a runner to pressurized air pushing on the cork of a bottle. “If you can decrease the intensity of these peak forces during running, then you probably will decrease the risk of injury to the runner.”

The G-Trainer is a spinoff of technology originally developed by Rob Whalen, who conceived the idea while working at NASA Ames as a National Research Council fellow to help astronauts maintain fitness during prolonged space flight. While the NASA technology was designed to effectively increase the weight of the astronauts to stem muscle atrophy and bone loss in low-gravity conditions, the G-Trainer reverses the process, said Grabowski.

In the past, sports trainers and researchers have used climbing harnesses over treadmills or flotation devices in deep-water swimming pools to help support the weight of subjects, said Kram. Harnesses are cumbersome, while pool exercises don’t provide sufficient aerobic stimulation and biomechanical loading on the legs, he said.

Marathon world-record holder Paula Radcliffe of Great Britain is currently using a G-Trainer in her high-altitude training base in Font-Remeu, France. Radcliffe is trying to stay in top running shape while recovering from a stress fracture in her femur in time for the 2008 Olympic women’s marathon on Aug. 17, according to the London Telegraph.

Kram and Grabowski have begun a follow-up study of walking using the G-Trainer. By studying subjects walking at various weights and speeds in the machine, the researchers should be able to quantify its effectiveness as a rehabilitation device for people recovering from surgeries, stress fractures and other lower body injuries, Kram said.

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Article adapted by MD Sports from original press release.
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Contact: Rodger Kram
University of Colorado at Boulder

Neuroscience researchers at the Duke-NUS Graduate Medical School in Singapore have shown for the first time what happens to the visual perceptions of healthy but sleep-deprived volunteers who fight to stay awake, like people who try to drive through the night.

The scientists found that even after sleep deprivation, people had periods of near-normal brain function in which they could finish tasks quickly. However, this normalcy mixed with periods of slow response and severe drops in visual processing and attention, according to their paper, published in the Journal of Neuroscience on May 21.

“Interestingly, the team found that a sleep-deprived brain can normally process simple visuals, like flashing checkerboards. But the ‘higher visual areas’ – those that are responsible for making sense of what we see – didn’t function well,” said Dr. Michael Chee, lead author and professor at the Neurobehavioral Disorders Program at Duke-NUS. “Herein lies the peril of sleep deprivation.”

The research team, including colleagues at the University of Michigan and University of Pennsylvania, used magnetic resonance imaging to measure blood flow in the brain during speedy normal responses and slow “lapse” responses. The study was funded by grants from the DSO National Laboratories in Singapore, the National Institutes of Health, the National Institute on Drug Abuse, the NASA Commercialization Center, and the Air Force Office of Scientific Research.

Study subjects were asked to identify letters flashing briefly in front of them. They saw either a large H or S, and each was made up of smaller Hs or Ss. Sometimes the large letter matched the smaller letters; sometimes they didn’t. Scientists asked the volunteers to identify either the smaller or the larger letters by pushing one of two buttons.

During slow responses, sleep-deprived volunteers had dramatic decreases in their higher visual cortex activity. At the same time, as expected, their frontal and parietal ‘control regions’ were less able to make their usual corrections.

Scientists also could see brief failures in the control regions during the rare lapses that volunteers had after a normal night’s sleep. However, the failures in visual processing were specific only to lapses that occurred during sleep deprivation.

The scientists theorize that this sputtering along of cognition during sleep deprivation shows the competing effects of trying to stay awake while the brain is shutting things down for sleep. The brain ordinarily becomes less responsive to sensory stimuli during sleep, Chee said.

This study has implications for a whole range of people who have to struggle through night work, from truckers to on-call doctors. “The periods of apparently normal functioning could give a false sense of competency and security when in fact, the brain’s inconsistency could have dire consequences,” Chee said.

“The study task appeared simple, but as we showed in previous work, you can’t effectively memorize or process what you see if your brain isn’t capturing that information,” Chee said. “The next step in our work is to see what we might do to improve things, besides just offering coffee, now that we have a better idea where the weak links in the system are.”

 

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Article adapted by MD Sports from original press release.
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Contact: Mary Jane Gore
Duke University Medical Center

Other authors of the study include Jiat Chow Tan, Hui Zheng, and Sarayu Parimal of the Cognitive Neuroscience Lab at the Duke-NUS Graduate Medical School; Daniel Weissman of the University of Michigan Psychology Department; David Dinges of the University of Pennsylvania School of Medicine; and Vitali Zagorodnov of the Computer Engineering Department of the Nanyang Technological University in Singapore.