Archive for October, 2007

Steroid use starts early, decreases as teens grow older

Participation in sports with real or perceived weight requirements, such as ballet, gymnastics, and wrestling, is strongly associated with unhealthy weight control behaviors and steroid use in teens, according to researchers at the University of Minnesota.

Research published in the March 2007 issue of the Journal of the American Dietetic Association found nearly 6 percent of males between the ages of 12 and 18 who participated in weight-related sports induced vomiting within the week prior to being surveyed, as compared to only 0.9 percent of males who did not participate in weight- related sports. The use of diuretics within the previous year was reported by 4.2 percent of males in a weight-related sport, as opposed to 0.8 percent who did not participate in a weight-related sport.

Steroid use was reported in 6.8 percent of females who reported participating in weight-related sports, compared to 2.3 percent of those that weren’t active in a weight-related sport. Vomiting and using laxatives were also more likely in girls who were active in weight-related sports.

“The link between unhealthy weight-control behaviors and weight-related sports, especially in boys, is alarming,” said Marla Eisenberg, Sc.D., M.P.H., assistant professor at the University of Minnesota Medical School Department of Pediatrics. “Parents and coaches should emphasize skill and talent instead of weight and body image and educate teens about the negative health effects of steroid use and extreme weight control.” Researchers surveyed over 4,500 middle and high school students from the Minneapolis/St. Paul metro area. The students were asked if they had engaged in self-induced vomiting, used diet pills or laxatives, or used steroids within the previous week and year.

Steroid use in teens peaks at young age, but overall use has not increasedIn a separate study, published in the March 2007 issue of Pediatrics, University of Minnesota researchers surveyed the same teen population again five years later. They found that steroid use among teens peaked at 5 percent in middle school boys and girls, but as they grew older, steroid use declined significantly.

“It is encouraging to see that the majority of young people who reported using steroids in 1999 stopped using them as they got older,” said Patricia van den Berg, Ph.D., lead author of the study from the University of Minnesota School of Public Health. “But even given this decline, between one and three in 100 teens still reported using steroids within the last year when asked again 5 years later.”

Researchers conducted the longitudinal study with more than 2,000 adolescents to examine changes in eating patterns, weight, physical activity, and related factors over five years. Participants completed two surveys, one in 1999 and one in 2004, to determine if there were changes in steroid use.

Overall, 1.7 percent of boys and 1.4 percent of girls between the ages of 15 and 23 reported steroid use in 2004. Those that reported use early on were 4 to 10 times more likely to use later in life.

Boys who reported wanting a larger body in 1999, as well as those who said they used healthy weight-control behaviors, were more likely to take steroids when they were older. In contrast, girls who were heavier, less satisfied with their weight, and who had limited knowledge of healthy eating and exercise habits were more likely to take steroids as they grew older.

The study found no significant change in steroid use overall among teens from 1999-2004. “Our research suggests that the increased media coverage surrounding steroid use among athletes in recent years hasn’t led to a huge rise in steroid use in young people,” said van den Berg.

Anabolic-androgenic steroids are synthetic derivatives of the male hormone, testosterone. They are typically taken to increase muscle mass and strength for either improved sports performance or enhanced appearance. These steroids have significant negative effects on the body’s muscles, bones, heart, reproductive system, liver, and psychological state.

Article adapted by MD Sports Weblog from original press release.

Contact: Liz Wulderk
University of Minnesota 

Project EAT: Eating Among Teens Both studies are part of Project EAT: Eating Among Teens, research designed to investigate the factors influencing the eating habits of adolescents, to determine if youth are meeting national dietary recommendations, and to explore dieting, physical activity patterns, and related factors among youth. The project is designed to build a greater understanding of the socio-environmental, personal, and behavioral factors associated with diet and weight-related behaviors during adolescence so more effective nutrition interventions can be developed.

The studies were supported by the Maternal and Child Health Program, Health Resources and Services Administration, the Department of Health and Human Services, and a training grant from the Centers for Disease Control.

Myostatin (MSTN) is a transforming growth factor-ß (TGF-ß) family member that plays a critical role in regulating skeletal muscle mass [1]. Mice engineered to carry a deletion of the Mstn gene have about a doubling of skeletal muscle mass throughout the body as a result of a combination of muscle fiber hyperplasia and hypertrophy [2]. Moreover, loss of myostatin activity resulting either from postnatal inactivation of the Mstn gene [3], [4] or following administration of various myostatin inhibitors to wild type adult mice [5][7] can also lead to significant muscle growth. Hence, myostatin appears to play as least two distinct roles, one to regulate the number of muscle fibers that are formed during development and a second to regulate growth of muscle fibers postnatally. The function of myostatin appears to have been conserved across species, as inactivating mutations in the myostatin gene have been demonstrated to cause increased muscling in cattle [8][11] , sheep [12], dogs [13] and humans [14]. As a result, there has been considerable effort directed at developing strategies to modulate myostatin activity in clinical settings where enhancing muscle growth may be beneficial. In this regard, loss of myostatin activity has been demonstrated to improve muscle mass and function in dystrophic mice [15][17] and to have beneficial effects on fat and glucose metabolism in mouse models of obesity and type II diabetes [18].

Myostatin is synthesized as a precursor protein that undergoes proteolytic processing to generate an N-terminal propeptide and a C-terminal dimer, which is the biologically active species. Following proteolytic processing, the propeptide remains bound to the C-terminal dimer and maintains it in an inactive, latent complex [6], [19], [20], which represents one of the major forms of myostatin that circulates in the blood [21], [22]. In addition to the propeptide, other binding proteins are capable of regulating myostatin activity in vitro, including follistatin [19], [21], FLRG [22], and Gasp-1 [23]. We previously showed that follistatin can also block myostatin activity in vivo; specifically, we showed that follistatin can ameliorate the cachexia induced by high level expression of myostatin in nude mice [21] and that transgenic mice expressing follistatin in muscle have dramatic increases in muscle mass [19]. Here, I show that overexpression of follistatin can also cause substantial muscle growth in mice lacking myostatin, demonstrating that other TGF-ß related ligands normally cooperate with myostatin to suppress muscle growth and that the capacity for enhancing muscle growth by targeting this signaling pathway is much larger than previously appreciated.


Increased muscle mass in transgenic mice expressing FLRG

Previous studies have identified several proteins that are normally found in a complex with myostatin in the blood [22], [23]. One of these is the follistatin related protein, FLRG, which has been demonstrated to be capable of inhibiting myostatin activity in vitro. To determine whether FLRG can also inhibit myostatin activity in vivo, I generated a construct in which the FLRG coding sequence was placed downstream of a myosin light chain promoter/enhancer. From pronuclear injections of this construct, a total of four transgenic mouse lines (Z111A, Z111B, Z116A, and Z116B) were obtained containing independently segregating insertion sites. Each of these four transgenic lines was backcrossed at least 6 times to C57 BL/6 mice prior to analysis in order to control for genetic background effects. Northern analysis revealed that in three of these lines the transgene was expressed in skeletal muscles but not in any of the non-skeletal muscle tissues examined (Figure 1); in the fourth line, Z111B, the expression of the transgene was below the level of detection in these blots. As shown in Table 1, all four lines exhibited significant increases in muscle weights compared to wild type control mice. These increases were observed in all four muscles that were examined as well as in both sexes. Moreover, the rank order of magnitude of these increases correlated with the rank order of expression levels of the transgene; in the highest-expressing line, Z116A, muscle weights were increased by 57–81% in females and 87–116% in males compared to wild type mice. Hence, FLRG is capable of increasing muscle growth in a dose-dependent manner when expressed as a transgene in skeletal muscle.

The research was funded by grants from the NIH and the Muscular Dystrophy Association and by a gift from Merck Research Laboratories.

See for more information.
Citation: Lee S-J (2007) Quadrupling Muscle Mass in Mice by Targeting TGF-ß Signaling Pathways. PLoS ONE 2(8): e789. doi:10.1371/journal.pone.0000789


Source: Nick Zagorski
Johns Hopkins Medical Institutions

Athletes for years have found that the the low-glycemic carbohydrate Glycoose™ promotes utilization of body fat as energy source and thus improves metabolic fat oxidation in comparison to other carbohydrates. Glycose™ helps provide a sustained supply of energy from low glycemic carbloyhdrates , while at the same time supporting fat mobilization.

Time after time athletes report sustained energy to compete and finish their event in the absence of muscle fatique and cramps.

In comparing the effects of a Glycose™ -to a high fructose corn syrup and sucrose -based energy drinks, after consumption, athletes found they had longer sustained energy for competition and training and noticed lower body fat percentages after a few weeks. Moreover, a higher glycogen storage rate of energy production from carbohydrates was noted, along with the fat burning effect.

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).


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.

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.


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.

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

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.”

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

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.

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.

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.

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

Contact: Donna Krupa
American Physiological Society

A new study investigating the potential of a circadian rhythm in athletic performance adds further confirmation that it exists. The finding is being published in the Journal of Applied Physiology. The authors of “Circadian Variation in Swim Performance,” are Christopher E. Kline, J. Larry Durstine, J. Mark Davis, Teresa A. Moore, Tina M. Devlin, Mark R. Zielinski, and Shawn D. Youngstedt, all from the Department of Exercise Science, Arnold School of Public Health, University of South Carolina, Columbia, SC. Background

Circadian rhythms are generated within the body, and are “re-set” almost every 24 hours. Human circadian rhythms originate from the tiny hypothalamus residing in the back of the brain. The hypothalamus, working with the endocrine system, drives many of our behavioral and physiological rhythms.

Researchers have speculated that there may be a circadian rhythm inherent in athletic performance and point to research showing that athletic performance varies based on time-of-day. Other studies have shown that peak performance occurs in early evening, at approximately the peak of the body temperature rhythm. Additional studies have found that morning is the worst time for athletic performance.

These findings, however, have limitations. For example, the studies failed to identify the other factors that could cause time-of-day differences that are independent of circadian rhythm. For example, worse performance in the morning could be attributed to nutritional status, joint stiffness following bed-rest, sleep inertia upon arising, lower ambient temperature, and a lack of “warm up” in the muscles.


To better understand the potential existence of a circadian rhythm in swimming performance, researchers assessed 25 highly trained swimmers over 50-55 consecutive hours while who were adhering to a 180-minute ultra-short sleep/wake schedule, specifically one hour of sleep in darkness and two hours of wakefulness in dim light, repeated throughout the length of observation. This study design distributed multiple masking factors equally across the 24-hour day and allowed multiple performance assessments to be conducted over a short period of time with relatively little sleep loss.

Each swimmer performed six scheduled maximal-effort 200-meter swim trials that were distributed equally across eight times of day, with nine hours between each trial. Data from the sleep/wake schedules, swim performances, states of sleepiness, physical/mental energy, and physical/mental fatigue and body temperature measurements were collected. The statistical comparisons were performed using SPSS software. All results were presented as mean plus or minus standard error; with significance set at P<0.05.


The primary findings of the study showed:

  • swimming performance had significant circadian variation when expressed relative to the time of day (Tmin). Specifically, swim performance was impaired between 2:00 – 8:00 AM, compared to all other times of day. Peak performance was at 11:00 PM;
  • there was a clear superiority of swim performance in the afternoon/evening compared to in the morning. (The results confirm previous findings of a significant time-of-day variation in swimming performance.);
  • the ultra-short sleep/wake cycle provided the first clear evidence of circadian regulation in athletic performance.

Implications of the Study’s Results

These data suggest a circadian rhythm in athletic performance exists. The circadian range from best to worst performance in this study — 5.84 seconds — could have considerable importance in athletic competition. For example, among females competing in the 200-meter freestyle final at the 2004 Olympics, first and third place were separated by only 0.42 seconds, and first and eighth place were separated by only 1.17 seconds. Among the men, 0.61 seconds separated the winner from third place, and 3.69 seconds separated first from eighth place.

By demonstrating a circadian rhythm in athletic performance, the research provides a stronger theoretical rationale for expecting decrements in performance following circadian desynchronization (multiple time zone travel). However, by knowing the circadian time of peak performance, athletes may be better able to shift their circadian systems so that the peaks of their performance rhythms coincide with the time of desired peak competition.

In the highly competitive sports environment, where financial stakes are often high, team managers will find it useful to add the study of physiological concepts such as circadian rhythms to provide a potential edge for victory.

Contact: Donna Krupa
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.