Archive for the ‘Dietary supplements’ Category

Researchers at The University of Auckland have shown for the first time that the mere presence of carbohydrate solution in the mouth immediately boosts muscle strength, even before it is swallowed.

The results suggest that a previously unknown neural pathway is activated when receptors in the mouth detect carbohydrate, stimulating parts of the brain that control muscle activity and producing an increase in muscle strength.

Previous research had shown that the presence of carbohydrate in the mouth can improve physical performance during prolonged activity, but the mechanism involved was not known and it was unclear whether a person must be fatigued for the effect to be seen.

“There appears to be a pathway in the brain that tells our muscles when energy is on the way,” says lead researcher Dr Nicholas Gant from the Department of Sport and Exercise Science.

“We have shown that carbohydrate in the mouth produces an immediate increase in neural drive to both fresh and fatigued muscle and that the size of the effect is unrelated to the amount of glucose in the blood or the extent of fatigue.”

The current research has been published in the journal Brain Research and has also captured the attention of New Scientist magazine.

In the first of two experiments, 16 healthy young men who had been doing biceps exercises for 11 minutes were given a carbohydrate solution to drink or an identically flavored energy-free placebo. Their biceps strength was measured before and immediately afterward, as was the activity of the brain pathway known to supply the biceps.

Around one second after swallowing the drink, neural activity increased by 30 percent and muscle strength two percent, with the effect lasting for around three minutes. The response was not related to the amount of glucose in the bloodstream or how fatigued the participants were.

“It might not sound like much, but a two percent increase in muscle strength is enormous, especially at the elite level. It’s the difference between winning an Olympic medal or not,” says co-author Dr Cathy Stinear.

As might be expected, a second boost in muscle strength was observed after 10 minutes when carbohydrate reached the bloodstream and muscles through digestion, but no additional boost in neural activity was seen at that time.

“Two quite distinct mechanisms are involved,” says Dr Stinear. “The first is the signal from the mouth via the brain that energy is about to be available and the second is when the carbohydrate actually reaches the muscles and provides that energy,” says Dr Stinear.

“The carbohydrate and placebo solutions used in the experiment were of identical flavor and sweetness, confirming that receptors in the mouth can process other sensory information aside from the basic taste qualities of food. The results suggest that detecting energy may be a sixth taste sense in humans,” says Dr Gant.

In the second experiment, 17 participants who had not been doing exercise and were not fatigued simply held one of the solutions in their mouths without swallowing. Measurements of the muscle between the thumb and index finger were taken while the muscle was either relaxed or active.

A similar, though smaller effect was observed as in the first experiment, with a nine percent increase in neural activity produced by the carbohydrate solution compared with placebo. This showed that the response is seen in both large powerful muscles and in smaller muscles responsible for fine hand movements.

“Together the results show that carbohydrate in the mouth activates the neural pathway whether or not muscles are fatigued. We were surprised by this, because we had expected that the response would be part of the brain’s sophisticated system for monitoring energy levels during exercise,” says Dr Stinear.

“Seeing the same effect in fresh muscle suggests that it’s more of a simple reflex – part of our basic wiring – and it appears that very ancient parts of the brain such as the brainstem are involved. Reflexive movements in response to touch, vision and hearing are well known but this is the first time that a reflex linking taste and muscle activity has been described,” she says.

Further research is required to determine the precise mechanisms involved and to learn more about the size of the effect on fresh versus fatigued muscle.

———————————–

Article adapted by MD Sports from original press release.
———————————–
Contact: Pauline Curtis
The University of Auckland

Advertisements

Cereal and non-fat milk is as good as a commercially-available sports drink in initiating post-exercise muscle recovery.

Background

This study compared the effects of ingesting cereal and nonfat milk (Cereal) and a carbohydrate-electrolyte sports drink (Drink) immediately following endurance exercise on muscle glycogen synthesis and the phosphorylation state of proteins controlling protein synthesis: Akt, mTOR, rpS6 and eIF4E.

Methods

Trained cyclists or triathletes (8 male: 28.0+/-1.6 yrs, 1.8+/-0.0 m, 75.4+/-3.2 kg, 61.0+/-1.6 ml O2 * kg-1 * min-1; 4 female: 25.3+/-1.7 yrs, 1.7+/-0.0 m, 66.9+/-4.6 kg, 46.4+/-1.2 mlO2 * kg-1 * min-1) completed two randomly-ordered trials serving as their own controls. After 2 hours of cycling at 60-65% VO2MAX, a biopsy from the vastus lateralis was obtained (Post0), then subjects consumed either Drink (78.5 g carbohydrate) or Cereal (77 g carbohydrate, 19.5 g protein and 2.7 g fat). Blood was drawn before and at the end of exercise, and at 15, 30 and 60 minutes after treatment. A second biopsy was taken 60 minutes after supplementation (Post60). Differences within and between treatments were tested using repeated measures ANOVA.

Results

At Post60, blood glucose was similar between treatments (Drink 6.1+/-0.3, Cereal 5.6+/-0.2 mmol/L, p<.05), but after Cereal, plasma insulin was significantly higher (Drink 123.1+/-11.8, Cereal 191.0+/-12.3 pmol/L, p<.05), and plasma lactate significantly lower (Drink 1.4+/-0.1, Cereal 1.00+/-0.1 mmol/L, p<.05). Except for higher phosphorylation of mTOR after Cereal, glycogen and muscle proteins were not statistically different between treatments. Significant Post0 to Post60 changes occurred in glycogen (Drink 52.4+/-7.0 to 58.6+/-6.9, Cereal 58.7+/-9.6 to 66.0+/-10.0 mumol/g, p<.05) and rpS6 (Drink 17.9+/-2.5 to 35.2+/-4.9, Cereal 18.6+/-2.2 to 35.4+/-4.4 %Std, p<.05) for each treatment, but only Cereal significantly affected glycogen synthase (Drink 66.6+/-6.9 to 64.9+/-6.9, Cereal 61.1+/-8.0 to 54.2+/-7.2%Std, p<.05), Akt (Drink 57.9+/-3.2 to 55.7+/-3.1, Cereal 53.2+/-4.1 to 60.5+/-3.7 %Std, p<.05) and mTOR (Drink 28.7+/-4.4 to 35.4+/-4.5, Cereal 23.0+/-3.1 to 42.2+/-2.5 %Std, p<.05). eIF4E was unchanged after both treatments.

Conclusion

These results suggest that Cereal is as good as a commercially-available sports drink in initiating post-exercise muscle recovery.

Author: Lynne Kammer, Zhenping Ding, Bei Wang, Daiske Hara, Yi-Hung Liao and John L. Ivy

Credits/Source: Journal of the International Society of Sports Nutrition 2009, 6:11

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.

 —————————-
Article adapted by MD Sports from original press release.
—————————-

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.

Lower muscle mass and an increase in body fat are common consequences of growing older.

While exercise is a proven way to prevent the loss of muscle mass, a new study led by McMaster researcher Dr. Mark Tarnopolsky shows that taking a combination of creatine monohydrate (CrM) and conjugated linoleic acid (CLA) in addition to resistance exercise training provides even greater benefits.

The study to be published on Oct. 3 in PLoS One, an international, peer-reviewed online journal of the Public Library of Science, involved 19 men and 20 women who were 65 years or older and took part in a six-month program of regular resistance exercise training.

In the randomized double blind trial, some of the participants were given a daily supplement of creatine (a naturally produced compound that supplies energy to muscles) and linoleic acid (a naturally occurring fatty acid), while others were given a placebo. All participants took part in the same exercise program.

The exercise training resulted in improvements of functional ability and strength in all participants, but those taking the CrM and CLA showed even greater gains in muscle endurance, an increase in fat-free mass and a decrease in the percentage of body fat.

“This data confirms that supervised resistance exercise training is safe and effective for increasing strength and function in older adults and that a combination of CrM and CLA can enhance some of the beneficial effects of training over a six month period,” said Tarnopolsky, a professor of pediatrics and medicine.

This study provides functional outcomes that build on an earlier mechanistic study co-led by Tarnopolsky and Dr. S. Melov at the Buck Institute of Age Research, published in PLoS One this year, which provided evidence that six months of resistance exercise reversed some of the muscle gene expression abnormalities associated with the aging process.
—————————-
Article adapted by MD Sports Weblog from original press release.
—————————-

Contact: Veronica McGuire
McMaster University

Trying to reap the health benefits of exercise? Forget treadmills and spin classes, researchers at the Salk Institute for Biological Studies may have found a way around the sweat and pain. They identified two signaling pathways that are activated in response to exercise and converge to dramatically increase endurance.

The team of scientists, led by Howard Hughes Medical Investigator Ronald M. Evans, Ph.D., a professor in the Salk Institute’s Gene Expression Laboratory report in the July 31 advance online edition of the journal Cell that simultaneously triggering both pathways with oral drugs turned laboratory mice into long-distance runners and conferred many of exercise’s other benefits.

In addition to their allure for endurance athletes, drugs that mimic the effects of exercise have therapeutic potential in treating certain muscle diseases, such as wasting and frailty, hospital patients unable to exercise, veterans and others with disabilities as well as obesity and a slew of associated metabolic disorders where exercise is known to be beneficial.

Previous work with genetically engineered mice in the Evans lab had revealed that permanently activating a genetic switch known as PPAR delta turned mice into indefatigable marathon runners. In addition to their super-endurance, the altered mice were resistant to weight gain, even when fed a high-fat diet that caused obesity in ordinary mice. On top of their lean and mean physique, their response to insulin improved, lowering levels of circulating glucose.

“We wanted to know whether a drug specific for PPAR delta would have the same beneficial effects,” says Evans. “Genetic engineering in humans, commonly known as gene doping when mentioned in connection with athletic performance, is certainly feasible but very impractical.”

An investigational drug, identified only as GW1516 (and not commercially available), fit the bill. When postdoctoral researcher and lead author Vihang A. Narkar, Ph.D., fed the substance to laboratory mice over a period of four weeks, the researchers were in for a surprise.

“We got the expected benefits in lowering fatty acids and blood glucose levels but no effect, absolutely none, on exercise performance,” says Narkar. Undeterred, he put mice treated with GW1516 on a regular exercise regimen and every day had them run up to 50 minutes on a treadmill.

Now the exact same drug that had shown no effect in sedentary animals improved endurance by 77 percent over exercise alone and increased the portion of “non-fatiguing” or “slow twitch” muscle fibers by 38 percent. The result, while very dramatic, gave rise to a vexing question: Why is exercise so important?

First and foremost, exercise depletes muscles’ energy store, a chemical known as ATP. In times of high demand, ATP releases all its energy and forms AMP. Rising AMP levels alert AMPK, a metabolic master regulator, which acts like a gas gauge that the cell is running on empty and revs up the production of ATP. “That led us to consider whether AMPK activation was the critical trigger that allowed PPAR delta to work,” recalls Narkar.

Usually, AMPK can be found in the cytoplasm, the compartment that surrounds the nucleus, but the Salk researchers’ experiment revealed that some exercise-activated AMPK molecules slip into the nucleus. There they physically interact with PPAR delta and increase its ability to turn on the genetic network that increases endurance.

“It essentially puts a turbo charge on PPAR delta, which explains why exercise is so important,” says Evans.

Then came the ultimate couch potato experiment. The researchers fed untrained mice AICAR, a synthetic AMP analog that directly activates AMPK. After only four weeks and without any prior training, these mice got up and ran 44 percent longer than untreated, untrained mice. “That’s as much improvement as we get with regular exercise,” says Narkar.

“Exercise in a pill” might sound tempting to couch potatoes and Olympic contenders alike, but the dreams of the latter might be cut short. Evans developed a test that can readily detect GW1516 and its metabolites as well as AICAR in blood and urine and is already working with officials at the World Anti-Doping Association, who are racing to have a test in place in time for this year’s Summer Olympics.

—————————-
Article adapted by MD Sports Weblog from original press release.
—————————-

Contact: Gina Kirchweger
Salk Institute

The study was supported by the Howard Hughes Medical Institute, the Hillblom Foundation and the National Institute of Health.

Researchers who contributed to the work include postdoctoral researchers Michael Downes, Ph.D., Ruth T. Yu, Ph.D., doctoral candidate Emi Embler, B.S., research associates Michael C. Nelson, B.S., Yuhua Zou, M.S., Ester Banayo, and Henry Juguilon, in the Gene Expression Laboratory, doctoral candidate M. Mihaylova, and assistant professor Reuben Shaw, Ph.D., in the Molecular and Cell Biology Laboratory, assistant professor Yong-Xu Wang, Ph.D., at the University of Massachusetts Medical School, Massachusetts, and professor Heonjoon Kang, Ph.D., at the School of Earth and Environmental Sciences, Seoul National University, South Korea.

By studying the genes of a German child born with unusually well developed muscles, an international research team has discovered the first evidence that the gene whose loss makes “mighty mice” also controls muscle growth in people.

Writing in the June 24 issue of the New England Journal of Medicine, German neurologist Markus Schuelke, M.D., and the team show that the child’s extra-large muscles are due to an inherited mutation that effectively silences the myostatin gene, proving that its protein normally keeps muscle development in check in people.

People with muscle-wasting conditions such as muscular dystrophy, and others just wanting to “bulk up,” have eagerly followed work on myostatin, hoping for a way to counteract the protein’s effects in order to build or rebuild muscle mass. But while research with mice has continued to reveal myostatin’s role and the effects of interfering with it, no one knew whether any of the results would be relevant to humans.

“This is the first evidence that myostatin regulates muscle mass in people as it does in other animals,” says Se-Jin Lee, M.D., Ph.D., professor of molecular biology and genetics in the Institute for Basic Biomedical Sciences at Johns Hopkins and co-author on the study. “That gives us a great deal of hope that agents already known to block myostatin activity in mice may be able to increase muscle mass in humans, too.”

Lee and his team discovered in 1997 that knocking out the myostatin gene led to mice that were twice as muscular as their normal siblings, lending them the moniker “mighty mice.” Later, others showed that naturally bulky cattle, such as Belgian Blues, got their extra muscles from lack of myostatin, too.

An unusual opportunity to examine myostatin’s role in humans arose when Schuelke examined a newborn baby boy, almost five years ago, and was struck by the visible muscles on the infant’s upper legs and upper arms. When ultrasound proved that the muscles were roughly twice as large as other infants’, but otherwise normal, Schuelke realized that a naturally occurring mutation in the child’s myostatin gene might be the cause.

Sequencing the myostatin gene from the boy and his mother, who had been a professional athlete, revealed a single change in the building blocks of the gene’s DNA. Surprisingly, the change was not in the gene regions that correspond to the resulting protein, but in the intervening regions that are used only to create protein-making instructions, thus changing the gene’s protein-building message.

“The mutation caused the gene’s message, the messenger RNA, to be wrong,” says Hopkins

neurologist Kathryn Wagner, M.D., Ph.D., who tested the genetic mutation’s effect in laboratory studies. “If the message had been used to make a protein, it would be much shorter than it should be. But we think the process doesn’t even get that far; instead the cells just destroy the message.”

Co-authors from Wyeth Research, Cambridge, Mass., analyzed samples of the child’s blood for evidence of the myostatin protein and found none. “Both copies of the child’s myostatin gene have this mutation, so little if any of the myostatin protein is made,” says Schuelke. “As a result, he has about twice the muscle mass of other children.”

Completely lacking myostatin, the boy is stronger than other children his age, and fortunately has no signs of problems with his heart so far, Schuelke says. But he adds that it’s impossible to know whether the lack of myostatin in that crucial muscle might lead to problems as the boy gets older.

While other family members — the boy’s mother and her brother, father and grandfather — were also reported to have been usually strong, only the mother’s DNA was available for analysis along with her son’s. Schuelke discovered that only one copy of the mother’s myostatin gene had the mutation found in both copies of her son’s myostatin gene. (We have two copies of each gene; one inherited from the mother and one inherited from the father.)

—————————-
Article adapted by MD Sports Weblog from original press release.
—————————-

 Contact: Joanna Downer
Johns Hopkins Medical Institutions

 

The Johns Hopkins researchers were funded by the National Institutes of Health and the Muscular Dystrophy Association. The German researchers were funded by the parents’ self-help group (Helft dem muskelkranken Kind).

Authors on the paper are Schuekle, Christoph Hubner, Thomas Riebel and Wolfgang Komen of Charite, University Medical Center Berlin, Germany; Wagner and Lee of Johns Hopkins; Leslie Stolz and James Tobin of Wyeth Research, Cambridge, Ma.; and Thomas Braun of Martin-Luther-University, Halle-Wittenberg, Germany.

*Under a licensing agreement between MetaMorphix Inc. and The Johns Hopkins University, Lee is entitled to a share of royalty received by the University on sales of products described in this article. Lee also is entitled to a share of sublicensing income from arrangements between MetaMorphix and American Home Products (Wyeth Ayerst Laboratories) and Cape Aquaculture Technologies. Lee and the University own MetaMorphix Inc. stock, which is subject to certain restrictions under University policy. Lee owns Cape Aquaculture Technologies stock, which is subject to certain restrictions under University policy. Lee has served as a paid consultant to MetaMorphix Inc. The terms of these arrangements are being managed by The Johns Hopkins University in accordance with its conflict of interest policies.

Energy bars, touted for improving athletic performance while providing the right combination of essential nutrients, may not always give endurance athletes the boost they expect.An Ohio State University researcher compared two popular energy bars and found that one of the bars didn’t give the moderate increase in blood sugar known to enhance performance in endurance athletes. Instead, its effect was much like a candy bar – giving a big rush of sugar to the blood, followed by a sharp decline.

“Theoretically, energy bars produce more moderate increases and decreases in blood sugar levels than a typical candy bar,” said Steve Hertzler, an associate professor of medical dietetics at Ohio State. “But these claims aren’t necessarily valid.” His study appears in a recent issue of the Journal of the American Dietetic Association.

Hertzler wanted to know how energy bars affected blood glucose levels. Glucose is a sugar that provides energy to the body’s cells – for example, red-blood cells and most parts of the brain derive most of their energy from glucose.

“Athletes – especially those involved in endurance sports – want to enhance performance, and energy bars claim to help keep blood sugar levels at a moderate level,” Hertzler said.

Volunteers had to fast for at least 12 hours before taking part in each of four experiments. Then, they ate one of four experimental “meals” consisting of either four slices of white bread; a Snickers bar; an Ironman PR Bar; or a PowerBar. Each experimental meal provided the same amount of carbohydrates (50 grams.)

Hertzler then tested the effects these foods had on blood glucose levels at 15-minute intervals for up to two hours after each experimental meal. The volunteers had to wait at least 24 hours between each experimental meal.

Hertzler measured each subject’s blood samples for glucose levels, to determine which food most raised blood sugar levels.

Both energy bars caused blood glucose levels to peak at 30 minutes, while levels peaked at 45 minutes after the bread and candy bar were consumed. Blood glucose levels declined steadily throughout the duration of testing for all foods but the Ironman PR Bar. This bar caused blood glucose rates to remain fairly steady, probably because of the moderate carbohydrate level of the bar, according to Hertzler.

“Though blood glucose rates peaked at 30 minutes with both bars, the high-carbohydrate energy bar – the PowerBar – caused a much sharper decline,” Hertzler said. “In fact, the decline was sharper than with the candy bar.” Much of the energy derived from the bread and the candy bar came from carbohydrate and the same was true for the PowerBar. While the bar is low in protein and fat, more than 70 percent of it is made up of carbohydrate (such as high-fructose corn syrup; oat bran; and brown rice). In contrast, 40 percent of the Ironman PR is comprised of carbohydrate (high fructose corn syrup and fructose.) The rest of the bar was comprised of 30 percent fat and 30 percent protein.

“The composition of this bar may have been responsible for the diminished blood glucose response,” Hertzler said. “Athletes involved in short-duration events who want a quick energy boost should eat a high-carbohydrate energy bar or a candy bar,” he suggests. “However, endurance athletes would do well to consume an energy bar with a moderate carbohydrate level.”

Hertzler conducted this study while at Kent State University in Kent, Ohio. He is continuing similar research at Ohio State.

—————————-
Article adapted by MD Sports Weblog from original press release.
—————————-

Contact: Steve Hertzler
Ohio State University

Editor’s note: This research was funded by a grant from Kent State University. The researcher received no funding from either energy bar manufacturer.