Archive for the ‘Energy Balance’ 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.

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

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New study dispels belief that increasing the hormone level improves the sexual function

Bethesda, Md.— The American Journal of Physiology: Endocrinology and Metabolism, one of the 14 peer-reviewed journals published by the American Physiological Society (APS), spotlights recent research findings designed to improve and understand human well-being and health. A study in the December edition examines how different doses of testosterone affect body composition, muscle size, strength, and sexual functions.

Background

Testosterone regulates many physiological processes, including muscle protein metabolism, some aspects of sexual and cognitive functions, secondary sex characteristics, erythropoiesis, plasma lipids, and bone metabolism. However, testosterone dose dependency of various hormonal dependent functions has not been well understood in the scientific community. Previous studies reveal that administration of replacement doses of testosterone to hypogonadal men and of supraphysiological doses to eugonadal men increases fat-free mass, muscle size, and strength. Conversely, suppression of endogenous testosterone concentrations is associated with loss of fat-free mass and a decrease in fractional muscle protein synthesis.

What is not known is whether testosterone effects on the muscle are dose dependent, or the nature of the testosterone dose-response relationships. Animal studies suggest that different androgen-dependent processes have different androgen dose-response relationships. Sexual function in male mammals is maintained at serum testosterone concentrations that are at the lower end of the male range. However, it is not known whether the low normal testosterone levels that normalize sexual function are sufficient to maintain muscle mass and strength, or whether the higher testosterone concentrations required to maintain muscle mass and strength might adversely affect plasma lipids, hemoglobin levels, and the prostate.

The Study

The primary objective of this study was to determine the dose dependency of testosterone’s effects on fat-free mass and muscle performance. The authors hypothesized that changes in circulating testosterone concentrations would be associated with dose-dependent changes in fat-free mass, muscle strength, and power in conformity with a single linear dose-response relationship, and that the dose requirements for maintaining other androgen-dependent processes would be different.

Young men were treated with a long-acting gonadotropin-releasing hormone (GnRH) agonist to suppress endogenous testosterone secretion, and concomitantly also with one of five testosterone-dose regimens to create different levels of serum testosterone concentrations extending from subphysiological to the supraphysiological range. The lowest testosterone dose, 25 mg weekly, was selected because this dose had been shown to maintain sexual function in GnRH antagonist-treated men. The selection of the 600-mg weekly dose was based on the consideration that this was the highest dose that had been safely administered to men in controlled studies.

The authors of the study, “Testosterone Dose-Response Relationships in Healthy Young Men” are Shalender Bhasin, Linda Woodhouse, Connie Dzekov, Jeanne Dzekov, Indrani Sinha-Hikim, Ruoquing Shen, and Atam B. Singh, all from the Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA; Richard Casaburi, Dimple Bhasin, Nancy Berman, Rachelle Bross and Jeffrey Phillips, from the Harbor-University of California Los Angeles Medical Center, Torrance, CA; Xianghong Chen and Kevin E. Yarasheski at the Biomedical Mass Spectrometric Research Resource, Department of Internal Medicine, Washington University, School of Medicine, St. Louis, Missouri, Lynne Magliano and Thomas W. Storer, from the Laboratory for Exercise Sciences, El Camino College, El Camino, CA.

Protocol

This was a double-blind, randomized study consisting of a four-week control period, a 20-week treatment period, and a 16-week recovery period. The participants were healthy men, 18-35 years of age, with prior weight-lifting experience and normal testosterone levels. These men had not used any anabolic agents and had not participated in competitive sports events in the preceding year, and they were not planning to participate in competitive events in the following year. The participants were asked not to undertake strength training or moderate-to-heavy endurance exercise during the study. These instructions were reinforced every four weeks.

Sixty-one eligible men were randomly assigned to one of five groups. All received monthly injections of a long-acting GnRH agonist to suppress endogenous testosterone production. In addition, group 1 received 25 mg of testosterone enanthate intramuscularly weekly; group 2, 50 mg testosterone enanthate; group 3, 125 mg testosterone enanthate; group 4, 300 mg testosterone enanthate; and group 5, 600 mg testosterone enanthate. Twelve men were assigned to group 1, 12 to group 2, 12 to group 3, 12 to group 4, and 13 to group 5.

Nutritional Intake

Energy and protein intakes were standardized at 36 kcal/kg. The standardized diet was initiated two weeks before treatment started; dietary instructions were reinforced every four weeks. The nutritional intake was verified by analysis of three-day food records and 24-hour food recalls every four weeks.

Outcome Measures

Body composition and muscle performance were assessed at baseline and during week 20. Fat-free mass and fat mass were measured by underwater weighing and dual-energy X-ray absorptiometry. Total thigh muscle and quadriceps muscle volumes were measured by MRI scanning.

For estimation of total body water, the men ingested 10 g of 2H2O, and plasma samples were drawn at 0, 120, 180, and 240 min. A measurement of 2H abundance in plasma was made by nuclear magnetic resonance spectroscopy, with a correction factor of 0.985 for exchangeable hydrogen. Another measure of bilateral leg press strength was taken by use of the one-repetition maximum (1-RM) method. A seated leg press exercise with pneumatic resistance was used for this purpose. Subjects performed 5-10 min of leg cycling and stretching warm-up and received instruction and practice in lifting mechanics before performing progressive warm-up lifts leading to the 1-RM. Seat position and the ensuing knee and hip angles, as well as foot placement, were measured and recorded for use in subsequent testing. To ensure reliability in this highly effort-dependent test, the 1-RM score was reassessed within seven days, but not sooner than two days, after the first evaluation. If duplicate scores were within five percent, the higher of the two values was accepted as the strength score. If the two tests differed by greater than five percent, additional studies were conducted.

Sexual function was assessed by daily logs of sexual activity and desire that were maintained for seven consecutive days at baseline and during treatment by use of a published instrument. Spatial cognition was assessed by a computerized checkerboard test and mood by Hamilton’s depression and Young’s mania scales.

Adverse experiences, blood counts and chemistries, prostate-specific antigen (PSA), plasma lipids, total and free testosterone, luteinizing hormone (LH), sex steroid-binding globulin (SHBG), and insulin-like growth factor I (IGF-I) levels were measured periodically during control and treatment periods. Serum total testosterone was measured by an immunoassay.

Results

Of 61 men enrolled, 54 completed the study: 12 in group 1, 8 in group 2, 11 in group 3, 10 in group 4, and 13 in group 5. One man discontinued treatment because of acne; other subjects were unable to meet the demands of the protocol. The five groups did not significantly differ with respect to their baseline characteristics. Key findings included:

– Compliance: All evaluable subjects received 100percent of their GnRH agonist injections, and only one man in the 125-mg group missed one testosterone injection.

– Nutritional intake: Daily energy intake and proportion of calories derived from protein, carbohydrate, and fat were not significantly different among the five groups at baseline. There was no significant change in daily caloric, protein, carbohydrate, or fat intake in any group during treatment.

– Hormone levels: Serum total and free testosterone levels, measured during week 16, one week after the previous injection, were linearly dependent on the testosterone dose (P = 0.0001). Serum total and free testosterone concentrations decreased from baseline in men receiving the 25- and 50-mg doses and increased at 300- and 600-mg doses. Serum LH levels were suppressed in all groups. Serum SHBG levels decreased dose dependently at the 300- and 600-mg doses but did not change in other groups. Serum IGF-I concentrations increased dose dependently at the 300- and 600-mg doses.

– Body composition: Fat-free mass, measured by underwater weighing, did not change significantly in men receiving the 25- or 50-mg testosterone dose, but it increased dose dependently at higher doses. The changes in fat-free mass were highly dependent on testosterone dose (P = 0.0001) and correlated with log total testosterone concentrations during treatment (r = 0.73, P = 0.0001). Fat mass, measured by underwater weighing, increased significantly in men receiving the 25- and 50-mg doses, but did not change in men receiving the higher doses of testosterone. There was an inverse correlation between change in fat mass by underwater weighing and log testosterone concentrations.

– Muscle size: The thigh muscle volume and quadriceps muscle volume did not significantly change in men receiving the 25- or 50-mg doses but increased dose-dependently at higher doses of testosterone. The changes in thigh muscle and quadriceps muscle volumes correlated with log testosterone levels during treatment.

– Muscle performance: The leg press strength did not change significantly in the 25- and 125-mg-dose groups but increased significantly in those receiving the 50-, 300-, and 600-mg doses. Leg power did not change significantly in men receiving the 25-, 50-, and 125-mg doses of testosterone weekly, but it increased significantly in those receiving the 300- and 600-mg doses. The increase in leg power correlated with log testosterone concentrations and changes in fat-free mass and muscle strength.

– Behavioral measures: The scores for sexual activity and sexual desire measured by daily logs did not change significantly at any dose. Similarly, visual-spatial cognition and did not change significantly in any group.

– Adverse experiences and safety measures: Hemoglobin levels decreased significantly in men receiving the 50-mg dose but increased at the 600-mg dose; the changes in hemoglobin were positively correlated with testosterone concentrations. Changes in plasma HDL cholesterol, in contrast, were negatively dependent on testosterone dose and correlated with testosterone concentrations. Total cholesterol, plasma low-density lipoprotein cholesterol, and triglyceride levels did not change significantly at any dose. Serum PSA, creatinine, bilirubin, alanine aminotransferase, and alkaline phosphatase did not change significantly in any group, but aspartate aminotransferase decreased significantly in the 25-mg group. Two men in the 25-mg group, five in the 50-mg group, three in the 125-mg group, seven in the 300-mg group, and two in the 600-mg group developed acne. One man receiving the 50-mg dose reported decreased ability to achieve erections.

Discussion

The researchers found that GnRH agonist administration suppressed endogenous LH and testosterone secretion. Therefore, circulating testosterone concentrations during treatment were proportional to the administered dose of testosterone enanthate. This strategy of combined administration of GnRH agonist and graded doses of testosterone enanthate was effective in establishing different levels of serum testosterone concentrations among the five treatment groups. The different levels of circulating testosterone concentrations created by this regimen were associated with dose- and concentration-dependent changes in fat-free mass, fat mass, thigh and quadriceps muscle volume, muscle strength, leg power, hemoglobin, circulating IGF-I, and plasma HDL cholesterol.

Serum PSA levels, sexual desire and activity, and spatial cognition did not change significantly at any dose. The changes in fat-free mass, muscle volume, leg press strength and power, hemoglobin, and IGF-I were positively correlated, whereas changes in plasma HDL cholesterol and fat mass were negatively correlated with testosterone dose and total and free testosterone concentrations during treatment.

There were no significant changes in overall sexual activity or sexual desire in any group, including those receiving the 25-mg dose. Testosterone replacement of hypogonadal men improves frequency of sexual acts and fantasies, sexual desire, and response to visual erotic stimuli. The data demonstrate that serum testosterone concentrations at the lower end of male range can maintain some aspects of sexual function.

Conclusions

This study demonstrates that an increase in circulating testosterone concentrations results in dose-dependent increases in fat-free mass, muscle size, strength, and power. The relationships between circulating testosterone concentrations and changes in fat-free mass and muscle size conform to a single log-linear dose-response curve. The data do not support the notion of two separate dose-response curves reflecting two independent mechanisms of testosterone action on the muscle.

In addition, the study could not determine if responsiveness to testosterone is attenuated in older men. Testosterone dose-response relationships might be modulated by other muscle growth regulators, such as nutritional status, exercise and activity level, glucocorticoids, thyroid hormones, and endogenous growth hormone secretory status. Serum PSA levels decrease after androgen withdrawal, and testosterone replacement of hypogonadal men increases PSA levels into the normal range.

The data demonstrate that different androgen-dependent body functions respond differently to different testosterone dose-response relationships. Some aspects of sexual function and spatial cognition, and PSA levels, were maintained by relatively low doses of testosterone in GnRH agonist-treated men and did not increase further with administration of higher doses of testosterone. In contrast, graded doses of testosterone were associated with dose and testosterone concentration-dependent changes in fat-free mass, fat mass, muscle volume, leg press strength and power, hemoglobin, IGF-I, and plasma HDL cholesterol.

Testosterone doses associated with significant gains in fat-free mass, muscle size, and strength were associated with significant reductions in plasma HDL concentrations. Further studies are needed to determine whether clinically significant anabolic effects of testosterone can be achieved without adversely affecting cardiovascular risk. Selective androgen receptor modulators that preferentially augment muscle mass and strength, but only minimally affect prostate and cardiovascular risk factors, are desirable.

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

Source: American Journal of Physiology: Endocrinology and Metabolism, December 2001

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.

Experts at The University of Nottingham are to investigate the effect of nutrients on muscle maintenance in the hope of determining better ways of keeping up our strength as we get old.

The researchers, based at the School of Graduate Entry Medicine and Health in Derby, want to know what sort of exercise we can take and what food we should eat to slow down the natural loss of skeletal muscle with ageing.

The team from the Department of Clinical Physiology, which has over 20 years experience in carrying out this type of metabolic study, need to recruit 16 healthy male volunteers in two specific age groups to help in it’s research.

Skeletal muscles make up about half of our body weight and are responsible for controlling movement and maintaining posture. However, at around 50 years of age our muscles begin to waste at approximately 0.5 per cent to one per cent a year. It means that an 80 year old may only have 70 per cent of the muscle of a 50 year old.

Since the strength of skeletal muscle is proportional to muscle size, such wasting makes it harder to carry out daily activities requiring strength, such as climbing stairs and leads to a loss of independence and an increased risk of falls and fractures.

In order for skeletal muscles to maintain their size, the large reservoirs of muscle protein require constant replenishment in the way of amino acids from protein contained within the food we eat. In fact, amino acids from our food act not only as the building blocks of muscle proteins but also actually ‘tell’ our muscle cells to build proteins.

Recent research from the clinical physiology team has shown that the cause of muscle wasting with ageing appears to be an attenuation of muscle building in response to protein feeding. In other words, as we age we lose the ability to covert the protein in the food we eat in to muscle tissue. The proposed research will investigate the mechanisms responsible for this deficit.

Dr Philip Atherton, who is currently recruiting volunteers, said: “I am really excited to be involved in this project because if we can determine ways to better maintain muscle mass as we age it will greatly benefit us all.”

The researchers are looking for 16 healthy, non-smoking, male volunteers aged 18 to 25 and 65 to 75.

Initially, the volunteers will undergo a health screening and then on a different day, under the supervision of a doctor, will be infused with an amino acid mixture to simulate feeding along with a ‘tagged’ amino acid that allows them to assess muscle building. To make these measures, blood samples will be taken from the arm and muscle biopsies from the thigh muscle under local anaesthesia. Volunteers will receive an honorarium to cover their expenses.

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Article adapted by MD Sports from original press release.
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Contact: Lindsay Brooke
University of Nottingham

 

The study will take place at The University of Nottingham’s Medical School which based at the City Hospital in Derby.

It’s an inevitable truth: as we get older, our muscles deteriorate and we become weaker. Not only can this be an immensely frustrating change, but it can also have many other, more serious implications. We become clumsier and begin to have more falls, often resulting in broken bones or even more severe injuries. There is wide interest in this phenomenon, but to date, the majority of research has focussed on therapies for older patients with advanced symptoms. Now one study, led by Dr Alexandra Sänger from the University of Salzburg, is taking a new approach: scientists are examining the effects of different exercise regimes in menopausal women, with the aim of developing new strategies for delaying and reducing the initial onset of age related muscle deterioration. Results will be presented on Monday 7th July at the Society for Experimental Biology’s Annual Meeting in Marseille [Poster Session A5].

Dr Sänger’s research group has investigated two particular methods of physical training. Hypertrophy resistance training is a traditional approach designed to induce muscle growth whereas ‘SuperSlow®’ is a more recently devised system which involves much slower movement and fewer repetitions of exercises, and was originally introduced especially for beginners and for rehabilitation. “Our results indicate that both methods increase muscle mass at the expense of connective and fatty tissue, but contrary to expectations, the SuperSlow® method appears to have the greatest effect,” reveals Dr Sänger. “These findings will be used to design specific exercise programmes for everyday use to reduce the risk of injury and thus significantly contribute to a better quality of life in old age.”

The study focussed on groups of menopausal women aged 45-55 years, the age group in which muscle deterioration first starts to become apparent. Groups undertook supervised regimes over 12 weeks, based on each of the training methods. To see what effect the exercise had, thigh muscle biopsies were taken at the beginning and end of the regimes, and microscopically analysed to look for changes in the ratio of muscle to fatty and connective tissue, the blood supply to the muscle, and particularly for differences in the muscle cells themselves. “The results of our experiments have significantly improved our understanding of how muscles respond to different forms of exercise,” asserts Dr Sänger. “We believe that the changes that this new insight can bring to current training systems will have a considerable effect on the lives of both menopausal and older

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Article adapted by MD Sports from original press release.
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Notes to editors

  • Hypertrophy resistance training is a method of strength training that is designed to induce muscle growth, also known as hypertrophy.
  • SuperSlow® resistance training was developed by Ken Hutchins and is based on the same principle as hypertrophy resistance training, but involves slower movement and fewer repetitions of exercises, which is thought to improve the quality of muscle contraction and thereby strength.

Contact: Holly Astley
Society for Experimental Biology

And it increases endurance to run a mile and decreases inflammation

The Salk Institute scientist who earlier discovered that enhancing the function of a single protein produced a mouse with an innate resistance to weight gain and the ability to run a mile without stopping has found new evidence that this protein and a related protein play central roles in the body’s complex journey to obesity and offer a new and specific metabolic approach to the treatment of obesity related disease such as Syndrome X (insulin resistance, hyperlipidemia and atherosclerosis).

Dr. Ronald M. Evans, a Howard Hughes Medical Investigator at The Salk Institute’s Gene Expression Laboratory, presented two new studies (date) at Experimental Biology 2005 in the scientific sessions of the American Society for Biochemistry and Molecular Biology. The studies focus on genes for two of the nuclear hormone receptors that control broad aspects of body physiology, including serving as molecular sensors for numerous fat soluble hormones, Vitamins A and D, and dietary lipids.

The first study focuses on the gene for PPARd, a master regulator that controls the ability of cells to burn fat. When the “delta switch” is turned on in adipose tissue, local metabolism is activated resulting in increased calorie burning. Increasing PPARd activity in muscle produces the “marathon mouse,” characterized by super-ability for long distance running. Marathon mice contain altered muscle composition, which doubles its physical endurance, enabling it to run an hour longer than a normal mouse. Marathon mice contain increased levels of slow twitch (type I) muscle fiber, which confers innate resistance to weight gain, even in the absence of exercise.

Additional work to be reported at Experimental Biology looks at another characteristic of PPARd: its role as a major regulator of inflammation. Coronary artery lesions or atherosclerosis are thought to be sites of inflammation. Dr. Evans found that activation of PPARd suppresses the inflammatory response in the artery, dramatically slowing down lesion progression. Combining the results of this new study with the original “marathon mouse” findings suggests that PPARd drugs could be effective in controlling atherosclerosis by limiting inflammation and at the same time promoting improved physical performance.

Dr. Evans says he is very excited about the therapeutic possibilities related to activation of the PPARd gene. He believes athletes, especially marathon runners, naturally change their muscle fibers in the same way as seen in the genetically engineered mice, increasing levels of fat-burning muscle fibers and thus building a type of metabolic ‘shield” that keeps them from gaining weight even when they are not exercising.

But athletes do it through long periods of intensive training, an approach unavailable to patients whose weight or medical problems prevent them from exercise. Dr. Evans believes activating the PPARd pathway with drugs (one such experimental drug already is in development to treat people with lipid metabolism) or genetic engineering would help enhance muscle strength, combat obesity, and protect against diabetes in these patients.

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Article adapted by MD Sports Weblog from original press release.
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Contact: Sarah Goodwin
Federation of American Societies for Experimental Biology

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.

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

Female athletes often lose their menstrual cycle when training strenuously, but researchers have long speculated on whether this infertility was due to low body fat, low weight or exercise itself. Now, researchers have shown that the cause of athletic amenorrhea is more likely a negative energy balance caused by increasing exercise without increasing food intake.”A growing proportion of women are susceptible to losing their menstrual cycle when exercising strenuously,” says Dr. Nancy I. Williams, assistant professor of kineseology and physiology at Penn State. “If women go six to 12 months without having a menstrual cycle, they could show bone loss. Bone densities in some long distance runners who have gone for a prolonged time period without having normal menstrual cycles can be very low.”

In studies done with monkeys, which show menstrual cyclicity much like women, researchers showed that low energy availability associated with strenuous exercise training plays an important role in causing exercise-induced amenorrhea. These researchers, working at the University of Pittsburgh, published findings in the Journal of Clinical Endocrinology and Metabolism showing that exercise-induced amenorrhea was reversible in the monkeys by increasing food intake while the monkeys still exercised.

Williams worked with Judy L. Cameron, associate professor of psychiatry and cell biology and physiology at the University of Pittsburgh. Dana L. Helmreich and David B. Parfitt, then graduate students, and Anne Caston-Balderrama, at that time a post-doctoral fellow at the University of Pittsburgh, were also part of the research team. The researchers decided to look at an animal model to understand the causes of exercise-induced amenorrhea because it is difficult to closely control factors, such as eating habits and exercise, when studying humans. They chose cynomolgus monkeys because, like humans, they have a menstrual cycle of 28 days, ovulate in mid-cycle and show monthly periods of menses.

“It is difficult to obtain rigorous control in human studies, short of locking people up,” says Williams.

Previous cross-sectional studies and short-term studies in humans had shown a correlation between changes in energy availability and changes in the menstrual cycle, but those studies were not definitive.

There was also some indication that metabolic states experienced by strenuously exercising women were similar to those in chronically calorie restricted people. However, whether the increased energy utilization which occurs with exercise or some other effect of exercise caused exercise-induced reproductive dysfunction was unknown.

“The idea that exercise or something about exercise is harmful to females was not definitively ruled out,” says Williams. “That exercise itself is harmful would be a dangerous message to put out there. We needed to look at what it was about exercise that caused amenorrhea, what it was that suppresses ovulation. To do that, we needed a carefully controlled study.”

After the researchers monitored normal menstrual cycles in eight monkeys for a few months, they trained the monkeys to run on treadmills, slowly increasing their daily training schedule to about six miles per day. Throughout the training period the amount of food provided remained the standard amount for a normal 4.5 to 7.5 pound monkey, although the researchers note that some monkeys did not finish all of their food all of the time.

The researchers found that during the study “there were no significant changes in body weight or caloric intake over the course of training and the development of amenorrhea.” While body weight did not change, there were indications of an adaptation in energy expenditure. That is, the monkeys’ metabolic hormones also changed, with a 20 percent drop in circulating thyroid hormone, suggesting that the suppression of ovulation is more closely related to negative energy balance than to a decrease in body weight.

To seal the conclusion that a negative energy balance was the key to exercise-induced amenorrhea, the researchers took four of the previous eight monkeys and, while keeping them on the same exercise program, provided them with more food than they were used to. All the monkeys eventually resumed normal menstrual cycles. However, those monkeys who increased their food consumption most rapidly and consumed the most additional food, resumed ovulation within as little as 12 to 16 days while those who increased their caloric intake more slowly, took almost two months to resume ovulation.

Williams is now conducting studies on women who agree to exercise and eat according to a prescribed regimen for four to six months. She is concerned because recreational exercisers have the first signs of ovulatory suppression and may easily be thrust into amenorrhea if energy availability declines. Many women that exercise also restrict their calories, consciously or unconsciously.

“Our goal is to test whether practical guidelines can be developed regarding the optimal balance between calories of food taken in and calories expended through exercise in order to maintain ovulation and regular menstrual cycles,” says Williams. “This would then ensure that estrogen levels were also maintained at healthy levels. This is important because estrogen is a key hormone in the body for many physiological systems, influencing bone strength and cardiovascular health, not just reproduction.”

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Article adapted by MD Sports Weblog from original press release.
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Contact: A’ndrea Elyse Messer
Penn State