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Researchers at Albert Einstein College of Medicine of Yeshiva University have discovered a process that controls the amount of fat that cells store for use as a back-up energy source. Disruption of this process allows cellular fat to accumulate — a key factor in age-related metabolic diseases such as obesity and type 2 diabetes. The study is published today in the online version of Nature.

Discovery of this previously unknown fat-fighting pathway could lead to novel drugs for the treatment of metabolic syndrome (characterized by obesity, blood lipid disorders, and insulin resistance) and for a common liver disease known as “fatty liver” or steatohepatitis. Nonalcoholic steatohepatitis (NASH) is a common, often “silent” liver disease. Although NASH resembles alcoholic liver disease, it occurs in people who drink little or no alcohol. NASH affects 2 to 5 percent of Americans, according to the National Institute of Diabetes and Digestive and Kidney Diseases.

All cells store lipids, a type of fat, in the form of small droplets that can be broken down for energy when needed. In situations of excessive food intake or in certain diseases such as diabetes or obesity, these lipid droplets become so large that they interfere with normal cell function.

“In this study, we found that the amount of fat stored in these intracellular lipid droplets is controlled through autophagy, a process until now thought to help primarily in digesting and recycling damaged cellular structures,” says Mark Czaja, M.D., professor of medicine at Einstein whose team worked collaboratively on the research with the laboratory of Ana Maria Cuervo, M.D., Ph.D., associate professor of developmental & molecular biology, medicine, and anatomy & structural biology at Einstein.

Autophagy, or “self-eating,” is carried out by lysosomes, which function as the cell’s recycling center. In studies of liver cells in culture and in live animals, Dr. Czaja and his colleagues discovered that lysosomes do something never before observed: continuously remove portions of lipid droplets and process them for energy production.

“When food is scarce, autophagy becomes a main source of energy for the cells and this process of digesting lipid droplets is accelerated,” says Dr. Cuervo. “If autophagy slows down, as occurs in aging, the lipid droplets stored in cells keep growing and eventually become so big that they can no longer be degraded.”

This slowdown in fat control appears to trigger a vicious cycle in which the enlarging fat droplets impair autophagy, allowing even more fat to accumulate, and so on, which could eventually contribute to diseases such as diabetes. The researchers noted that therapies aimed at helping autophagy operate more efficiently might prevent disease by keeping fat droplets under control.

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Article adapted by MD Sports from original press release.
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Contact: Deirdre Branley
Albert Einstein College of Medicine

Drs. Cuervo and Czaja’s paper, “Autophagy regulates lipid metabolism” is published in the April 1 online version of Nature. Their co-authors at Einstein include Rajat Singh and Susmita Kaushik (primary co-authors), Yongjun Wang, Youqing Xiang, and Inna Novak; as well as Masaaki Komatsu and Keiji Tanaka of the Tokyo Metropolitan Institute of Medical Science, Bunkyo-ku, Tokyo, Japan.

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About Albert Einstein College of Medicine of Yeshiva University

Albert Einstein College of Medicine of Yeshiva University is one of the nation’s premier centers for research, medical education and clinical investigation. It is the home to some 2,000 faculty members, 750 M.D. students, 350 Ph.D. students (including 125 in combined M.D./Ph.D. programs) and 380 postdoctoral investigators. Last year, Einstein received more than $130 million in support from the NIH. This includes the funding of major research centers at Einstein in diabetes, cancer, liver disease, and AIDS. Other areas where the College of Medicine is concentrating its efforts include developmental brain research, neuroscience, cardiac disease, and initiatives to reduce and eliminate ethnic and racial health disparities. Through its extensive affiliation network involving five hospital centers in the Bronx, Manhattan and Long Island – which includes Montefiore Medical Center, The University Hospital and Academic Medical Center for Einstein – the College runs one of the largest post-graduate medical training program in the United States, offering approximately 150 residency programs to more than 2,500 physicians in training. For more information, please visit http://www.aecom.yu.edu.

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Consuming caffeine, whether in coffee of soft drinks, has been shown to delay fatigue during prolonged exercise. Studies have shown, for example, that ingesting three to nine mg/kg of caffeine can increase the amount of exercise time to achieve by as much as 50 percent. How caffeine achieves this effect has not been fully determined.

Caffeine and the Central Nervous System (CNS) Study

No previous research effort has examined the possible direct central nervous system (CNS) effects of caffeine on fatigue during prolonged exercise. Now, a team of researchers from the University of South Carolina has hypothesized that the blockade of adenosine receptors by caffeine may be the most likely mechanism of CNS stimulation and delayed fatigue.

Their theory is based on the fact that adenosine is produced within the body and inhibits neuronal excitability and synapse transmission. Adenosine also inhibits the release of most brain excitatory neurotransmitters, particularly dopamine (DA), and may reduce DA synthesis. Decreases in dopamine (DA), along with increases in 5-HT (serotonin, which is generally associated with behavioral suppression), have been linked to central fatigue during exercise. In addition, adenosine has been shown to reduce arousal, induce sleep, and suppress spontaneous activity, which are all behaviors associated with increases in 5-HT.

The researchers’ hypothesis is the foundation of a new study to determine the effects of intracerebroventricular injection of caffeine and the adenosine A1 and A2 receptor agonist 5′-N-ethylcarboxamidoadenosine (NECA) on treadmill run time to fatigue in rats. NECA was chosen for the study because caffeine is a nonselective adenosine receptor antagonist, and it is not known which of the four subtypes of adenosine receptors may be involved in an effect of caffeine on fatigue. However, A2b and A3 receptors are relatively less active than A1 and A2a receptors under normal physiological conditions. If the researchers were correct, the CNS administration of caffeine will increase run time to fatigue, whereas NECA will reduce run time to fatigue. Furthermore, pretreatment with caffeine before NECA will weaken the fatigue-inducing effects of NECA.

The authors of “Central Nervous System Effects of Caffeine and Adenosine on Fatigue,” are J. Mark Davis, Zuowei Zhao, Howard S. Stock, Kristen A. Mehl, James Buggy, and Gregory A. Hand, all from the Schools of Public Health and Medicine, University of South Carolina, Columbia, SC. Their findings appear in the February 2003 edition of the American Journal of Physiology –Regulatory, Integrative and Comparative Physiology. The journal is one of 14 peer-reviewed publications produced monthly by the American Physiological Society (APS).

Methodology

Male Wistar rats, five weeks old and weighing 200-250 grams, were used in this study, and randomly assigned to intracerebroventricular or intraperitoneal injection groups. Rats were given two weeks of treadmill acclimation of running for 15 minutes a day. The treadmill speed was slowly increased from eight meters a minute, 7.5 percent grade at the beginning, progressing to 20 meters a minute at the end of the acclimation period. Gentle hand prodding and mild electric shock were combined to encourage the animals to run throughout the study.

After the first two weeks of acclimation, rats assigned to the intracerebroventricular group were anesthetized with pentobarbital sodium, and tubes were implanted bilaterally into the lateral ventricles. After seven days of recovery from surgery, the rats were again acclimated to treadmill running for another one to two weeks, until they were able to run easily for at least 15 minutes per day for 5 consecutive days at a speed of 20 meters a minute at a 7.5 percent grade. Animals that were unable to run at that pace were excluded.

Four drug treatments were used in the study: NECA, caffeine, caffeine plus NECA, and a vehicle solution (Normosol-R). The vehicle solution has been used as a control solution in other studies involving intracerebroventricular infusions of drugs and tissue microdialysis. In the CNS groups (n = 10), each rat was injected intracerebroventricularly with one of the four drugs (NECA, caffeine, caffeine plus NECA, or vehicle) in one testing session. The other drugs were then given in successive testing sessions at one-week intervals to allow full recovery from the exercise bout and washout of the drugs. On two days during the recovery period, all rats were exercised for 15 minutes to maintain acclimation to the treadmill protocol. All rats received all four-drug treatments in a randomized and counterbalanced design to minimize possible order effects.

Results
The major findings of this study revealed that:

  • CNS administration of caffeine at a dose of 200 µg/rat (0.6 mg/kg), which is much less than the effective dose given peripherally (6 mg/kg), does increase treadmill run time to fatigue in rats by approximately 60 percent;
  • the same dose of caffeine given peripherally (intraperitoneally) is ineffective.
  • the results supported the researchers’ hypothesis that intracerebroventricular CNS administration of the selective adenosine A1 and A2 receptor agonist NECA significantly reduced run time to fatigue, whereas intracerebroventricular caffeine increased run time to fatigue.
  • inhibitory effects of NECA on run time to fatigue were also reversed by intracerebroventricular pretreatment with caffeine, suggesting that the ergogenic effects of intracerebroventricular caffeine are mediated through blockade of the adenosine receptors.
  • CNS administration of the adenosine receptor agonist NECA inhibited treadmill run time to fatigue and spontaneous locomotor activity in rats.
  • pretreatment with caffeine blocked the inhibitory effects of NECA on exercise performance, although not on spontaneous behavioral activity.
  • peripheral (intraperitoneal) administration of the same drugs at the same doses had no effect on treadmill run time to fatigue.

Conclusions

These results indicate that caffeine can act specifically within the CNS to delay fatigue, at least in part by blocking adenosine receptors. Because caffeine easily crosses the BBB, these results also suggest that the CNS also plays an important role in the ergogenic effect of caffeine ingestion.

The precise independent contribution of caffeine at the central (behavioral) and peripheral (metabolic) levels awaits further research. The researchers argue that some interaction at both levels is likely.

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Article adapted by MD Only Sports Weblog from original press release.
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Contact: Donna Krupa
American Physiological Society

Source: February 2003 edition of the American Journal of Physiology– Regulatory, Integrative and Comparative Physiology

The American Physiological Society (APS) was founded in 1887 to foster basic and applied science, much of it relating to human health. The Bethesda, MD-based Society has more than 10,000 members and publishes 3,800 articles in its 14 peer-reviewed journals every year.

Although it’s too soon to recommend dropping by Starbucks before hitting the gym, a new study suggests that caffeine can help reduce the post-workout soreness that discourages some people from exercising.In a study to be published in the February issue of The Journal of Pain, a team of University of Georgia researchers finds that moderate doses of caffeine, roughly equivalent to two cups of coffee, cut post-workout muscle pain by up to 48 percent in a small sample of volunteers.

Lead author Victor Maridakis, a researcher in the department of kinesiology at the UGA College of Education, said the findings may be particularly relevant to people new to exercise, since they tend to experience the most soreness.

“If you can use caffeine to reduce the pain, it may make it easier to transition from that first week into a much longer exercise program,” he said.

Maridakis and his colleagues studied nine female college students who were not regular caffeine users and did not engage in regular resistance training. One and two days after an exercise session that caused moderate muscle soreness, the volunteers took either caffeine or a placebo and performed two different quadriceps (thigh) exercises, one designed to produce a maximal force, the other designed to generate a sub-maximal force. Those that consumed caffeine one-hour before the maximum force test had a 48 percent reduction in pain compared to the placebo group, while those that took caffeine before the sub-maximal test reported a 26 percent reduction in pain.

Caffeine has long been known to increase alertness and endurance, and a 2003 study led by UGA professor Patrick O’Connor found that caffeine reduces thigh pain during moderate-intensity cycling. O’Connor, who along with professors Kevin McCully and the late Gary Dudley co-authored the current study, explained that caffeine likely works by blocking the body’s receptors for adenosine, a chemical released in response to inflammation.

Despite the positive findings in the study, the researchers say there are some caveats. First, the results may not be applicable to regular caffeine users, since they may be less sensitive to caffeine’s effect. The researchers chose to study women to get a definitive answer in at least one sex, but men may respond differently to caffeine. And the small sample size of nine volunteers means that the study will have to be replicated with a larger study.

O’Connor said that despite these limitations, caffeine appears to be more effective in relieving post-workout muscle pain than several commonly used drugs. Previous studies have found that the pain reliever naproxen (the active ingredient in Aleve) produced a 30 percent reduction in soreness. Aspirin produced a 25 percent reduction, and ibuprofen has produced inconsistent results.

“A lot of times what people use for muscle pain is aspirin or ibuprofen, but caffeine seems to work better than those drugs, at least among women whose daily caffeine consumption is low,” O’Connor said.

Still, the researchers recommend that people use caution when using caffeine before a workout. For some people, too much caffeine can produce side effects such as jitteriness, heart palpitations and sleep disturbances.

“It can reduce pain,” Maridakis said, “but you have to apply some common sense and not go overboard.”

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Article adapted by MD Only Sports Weblog from original press release.
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Contact: Sam Fahmy
University of Georgia

The serious athlete knows better than to rely just on a famous cereal to provide additional energy in preparation of a sporting event. Supplements have assumed an important role in today’s training regimen. Some – such as anabolic steroids — have been deemed illegal by most sports authorities. Others – such as caffeine and creatine — are controversial yet presently allowed.Background
Caffeine, the primary ingredient of coffee, is used as a central nervous system stimulant, diuretic, circulatory and respiratory stimulant, and as an adjunct in the treatment of headaches. Evidence shows that caffeine intensifies muscle contractions, masks the discomfort of physical exertion, and even speeds up the use of the muscles’ short-term fuel stores. Some exercise physiologists believe that caffeine might improve performance by increasing fat oxidation and conserving muscle glycogen.

Creatine is used by athletes to increase lean body mass and improve performance in single and repetitive high-intensity, short-duration exercise tasks such as weightlifting, sprinting, and cycling. It is a popular nutritional supplement that is used by physically active people – from recreational exercisers to Olympic and professional athletes. According to a recent survey, 28 percent of athletes in an NCAA Division IA program reported using creatine. The creatine that is normally present in human muscle may come from two potential sources: dietary (animal flesh) and internally manufactured.

The purpose of creatine supplementation is to increase either total creatine stores or phosphocreatine (PCr) stores within muscle. Supplementation increases the rate of resynthesis of creatine phosphate following exercise. Various studies have shown increased muscle PCr levels after supplementing with 20-30 grams of creatine monohydrate daily.

Creatine supplementation has also been known to shorten relaxation time during intermittent maximal iosometric muscle contraction. This shortened time, coupled with a creatine loaded muscle facilitates calcium absorption into the sarcoplasmic reticulum (the endoplasmic reticulum of skeletal and cardiac muscle). However, some believe that caffeine intake enhances calcium release from the sarcoplasmic reticulum.

The Study
This has lead a research team from Belgium to suggest that the combined effects of creatine and caffeine supplementation may be counterproductive to creatine’s effect on muscle relaxation time. The authors of the study, “Opposite Actions of Caffeine and Creatine on Muscle Relaxation Time in Humans” are P. Hespel, B. Op ‘T Eijnde, and M. Van Leemputte, all from the Department of Kinesiology, Katholieke Universiteit Leuven, Leuven, Belgium. Their findings appear in the February 2002 edition of the Journal of Applied Physiology.

Methodology
Ten physical education students (nine men and one woman) participated in the study. They were told to abstain from medication and caffeine intake one week prior to the experiment. The subjects were additionally asked to avoid changes in their level of physical activity and diet during the 25-week duration of the study. In this double blind experiment, the subjects performed the exercise test before and after creatine supplementation, short-term caffeine intake, creatine supplementation in the short term, acute caffeine intake, or a placebo.

This study required the random assignment of the students into five experimental protocols, each lasting eight days. Three elements were measured during an experiment consisting of 30 intermittent contractions of quadriceps entailing two seconds of stimulation and two seconds of rest. Measurements included maximum torque (Tmax), contraction time (CT) from 0.25 to 0.75 of Tmax, and relaxation time (RT) from 0.75 to 0.25 of max.

Results
Key findings of this study included:

· a confirmation of the fact that oral creatine supplementation shortens muscle relaxation time in humans: relation time was reduced by five percent and was significantly shorter than after the placebo;

· discovery that the intake of caffeine, combined with a daily creatine supplement, counteracted the beneficial effects of creatine intake on relaxation time and fatigue enhanced this inhibitory effect; and

· the observation that caffeine reduces the functional capacity of sacroplasmic reticulum calcium ATPase.

Conclusion The researchers believe that the findings from this experiment offer indirect evidence that suggests that facilitation of muscle relaxation may be important to the ergogenic action of creatine supplementation as well as power production during sprint exercises.

However, for the athlete in training, the key finding is that sustained caffeine intake, over a three-day period, negates the benefits of creatine supplements.

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Article adapted by MD Only Sports Weblog from original press release.
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Contact: Donna Krupa
American Physiological Society