You Can’t Beat the Heat

Even when the body is able to maintain core body temperature, cardiovascular performance is decreased in the heat.

      Researchers from the American College of Sports Medicine conducted research in January 2010 that shows that environmental heat stress with only modest hyperthermia has a significant impact on aerobic endurance. This research is of importance to a military operating in a desert environment in which temperatures can exceed 120˚ F in the summer.

      Subjects were asked to perform fifteen minutes of cycling in a temperate (69˚F) or hot environment (104˚F). Core and skin temperature and heart rate were constantly monitored. Performance and pacing were analyzed by kJ of work completed. Core temperature was modestly elevated in both environments, with skin temperature being higher in the hot environment. While heart rate and fatigue level were consistent between the two environments, the total amount of work done in the hot environment was 17% less than in the temperate environment. Also, while the pace was maintained in the temperate climate, it dropped significantly over time in the hot environment.

      So, although excessive hyperthermia was avoided, performance was still impacted by the hot environment. While it has been established that marked hyperthermia leads to increased fatigue during exercise, it seems that a hot environment can increase fatigue even without significant increase in core temperature. There are a few theories about how this happens. One idea is that athletes use an anticipatory control mechanism during exercise to ensure maintenance of core body temperature by making unconscious adjustments in work rate. Increased cardiovascular strain resulting from the maintenance of high skin blood flow required to maintain core temperature may also explain the observed decrease in performance. So, impact aerobic ability in the heat may come from either an early modification of work output or an inability to maintain a desired work output over time. This study supported the idea that initial pace could not be maintained, as the participants in the hot group got much slower over time.

       It seems clear that cardiovascular performance is decreased in the heat even when the body is able to maintain core temperatures. Further research may elucidate whether an early modification of pace in the heat may minimize the overall decline in performance associated with environmental heat stress. This information can help athletes who must compete in the heat to pace themselves, and may also shed light on tactics the military can use to maintain optimum performance in hot climates.

 Nicole Myers

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Where can I get that gene “juice”?

By Abby Larson

Athletes are competitive by nature, and many will do whatever they can to win.  Steroid usage is heavily monitored in competitions, yet with the coming of the Winter Olympics, whispers of “gene doping” are becoming audible. There has been a craze by athletes for “gene juice” ever since a 2005 study performed by Dr. Ronald Evans, a geneticist at the Salk Institute for Biological Studies in San Diego, California, produced the “Marathon Mouse”.  Evans discovered a gene involved in muscle formation and altered it, producing a mouse that could run twice as far as normal mice.  This spurred the World Anti-Doping Agency (WADA) to list gene doping as illegal.

Evans was searching for a way to treat muscular dystrophy, characterized by muscle wasting and inability to build muscle.  His study was based on the idea of gene therapy: treating a disease caused by a mutated or malfunctioning gene by inserting copies of the normal gene into cells.  The cells essentially replace the non-functional gene with the normal one.  So, if you can use gene therapy to treat mutated genes, why can’t you use gene therapy to replace a “normal” athletic gene with a “high performance” athletic gene?

A review article by Dr. Craig Sharp that will be published in March, 2010, titled “The Human Genome and Sport, Including Epigenetics, Gene Doping, and Athleticogenomics,” discusses many athletic performance gene discoveries that may be possible targets for gene doping.   One example is a gene encoding myostatin, an inhibitor of muscle growth.  Exercise tears muscles, which results in increased expression of actin and myosin.  This increase in expression is eventually repressed by the protein myostatin, preventing excessive muscle growth.  In 2004, a boy was born with a mutated form of myostatin that disrupted some of the protein’s function.  The boy had significantly hypertrophied muscles, and was still unusually muscular at age 4.  Based on studies like this one, by injecting muscle cells with the mutated form of myostatin, Sharp believes that athletes and bodybuilders can create greater muscle mass than without the gene doping because inhibition of muscle production will be decreased following exercise.  Who knew genetic studies could lead to Schwarzenegger-sized people?

Death does not seem to scare overzealous coaches and athletes, who may bypass the risks of gene doping to achieve that extra edge.  In several gene therapy studies, some patients developed cancers or severe autoimmune responses to the product of the injected genes.  A 2008 report by Dr. E.B. Wheeldon showed that a patient went into an extreme immune response due to a reaction with a carrier virus used to transmit the gene of interest into his cells, causing death from organ failure.  This does not seem to discourage some athletes and coaches.

Have athletes started using gene doping to get ahead?  An experimental drug, Repoxygen, was developed to treat severe anemia due to a mutated gene.  As several Olympic coaches discovered, Repoxygen contained the gene for erythropoietin (EPO), which increases red blood cell production and performance.  EPO itself is a currently banned substance by WADA for performance enhancement—but how can one detect the gene for it?  There are no current established methods for gene doping detection aside from muscle biopsy, says Sharp, which is a painful and unappealing method of detecting changes in tissue development.  A rising technique commonly used in cancer genomics may be the key: DNA microarray.  A DNA microarray detects changes in gene expression in a person between two periods in time.  In order for anti-doping agencies to use this method in top competitions such as the Olympics, an athlete’s genetic file must be established as a reference.  WADA has already developed a “passport” program to keep blood and urine samples of athletes on file to use for future genomic comparisons.

Gene doping raises an ethical issue that surpasses steroid use due to its difficulty in detection, although gene doping has been banned for over 5 years for major competitions.  By the 2012 Summer Olympics in London, genetic testing could be a common procedure by anti-doping committees.  It seems that as we learn more about the way the body responds to exercise and why the world’s top athletes are so good, more daemons are unleashed from Pandora’s box.

Running in Genes

By Abby Larson

Can someone really be born to be an athlete?  Science says so.  The idea of a genetic basis to exercise is a fairly new area of science, but it makes sense based on how the human body works. The expression of genes controls the function of human physiology: muscle development, capillary growth, hemoglobin concentration in red blood cells, etc.   After strenuous exercise, gene expression fires up to control muscle tissue repair due to increased forces on the body and tissue metabolic demand.  Capillaries feeding the muscles grow and become more efficient at delivering oxygen to tissues.  All of this is controlled by gene expression, the cellular switchboard of the human body.

Recent studies have identified over 200 genes that can determine the body’s ability to adapt quickly to exercise.  Based on this, training and conditioning could only take an athlete up to his or her genetically predetermined potential.  Does this mean that children can be genetically tested to see if they will be good at sports?  Is there a gene that makes a good football player versus a good runner? It’s more complicated than saying if a person has a specific gene, he or she can be a top athlete.  Like all processes in the human body, multiple genes are involved in adaptation to exercise and gene interactions play a large role.   Gene products don’t interact in a linear fashion, but in pathways and networks.  This makes genes harder to understand, and our knowledge of the interactions is in its infancy.  Once these pathways are discovered, scientists can begin to understand the extent to genetic determination of athletic ability.

These studies on the genetic basis of exercise are not going to benefit  just athletes—physical activity is one of the greatest preventative medicines for obesity, diabetes, and heart disease.  It is likely that genes correlated with exercise response could be mutated in people that have obesity or heart disease, which proposes new options of drug and gene therapy as preventative medicine.  The more we understand the benefits and mechanisms of exercise, the better we can understand how exercise can be used to improve public health.  So next time you go to the gym or run outside, think to yourself, “this is science.”

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