This web page was produced as an assignment for an undergraduate course at Davidson College.


The Endurance Gene

Why are long distance runners in such good shape? How does one increase endurance? Why does exercise help people get/stay thin? The answers may be found in current research being done on a transcription factor that increases endurance and also, gives resistance to obesity and diabetes. A gene that can control these physiological aspects of human life could have a huge impact on the athletic and health world. A major issue concerning the genetic manipulation of this gene is how the public perceives gene therapy and what the lay public reads about genetic experiments that create "super" mice. If scientific journalists do not convey the correct information in their public press articles then the public may be turned off to any of the benefits of gene therapy.

Genomics and the Popular Press

The role of the scientific journalist is becoming increasingly important as complex topics like gene therapy and genomics are starting to become more prevalent in the world of medicine and science. In order for a scientific journalist to fulfill their role as a communicator between the scientific world and the lay public, he/she must be three things: an "intermediary", a "watch dog", and a "tool giver". As an intermediary, the journalist must translate the scientific jargon in a scientific paper into language that the public can understand, and if a scientific term is used, then the journalist must give a simple, concise definition. In order to fulfill the role of "watch-dog" the journalist has to arouse interest in the readers by giving the social and moral issues associated with the topic he/she is discussing. The last role the scientific journalist must fulfill is that of the "tool-giver" or one who can prepare the reader to evaluate the current or future issues that the public press article implies (Kua et al., 2004). I will evaluate an article found on that describes a gene that gives resistance to obesity and gives athletes an extra boost. Before I evaluate the article, though, I first look at the scientific paper the journalist based his/her article on.

The Scientific Paper: Regulation of Muscle Fiber Type and Running Endurance by PPARdelta


In the study, genetically engineered mice had a significant increase in endurance and a resistance to obesity. In these mice a transcription factor, peroxisome proliferator-activated receptor delta (PPARdelta), was targeted for expression in skeletal muscle. The effect of expression of PPARdelta in skeletal muscle is increased conversion of fast twitch muscle fiber (type II) into slow twitch muscle fiber (type I). Because type I are mitochondria-rich and use oxidative metabolism as an energy source, type I muscle fibers resist fatigue much more readily than does type II muscle fiber, which has low levels of mitochondria and uses glycolytic metabolism, a mechanism that creates a limited energy source. Skeletal muscle in adults can convert type II muscle fiber into type I through specific training programs. Besides influencing endurance, specific muscle fibers play a role in obesity and diabetes, as rodents that have more type II muscle gain the most weight on high-fat diets. (Evans et al., 2004)


The transgenic mice created in the experiment showed an increase not only in the amount of type I muscle fiber present in their skeletal muscle but also in the endogenous muscle PPARdelta protein. Besides the PPARdelta protein, all proteins associated with skeletal muscle were at the same level of abundance in both wild-type and transgenic mice. From this one can make the obvious conclusion that increase in type I muscle fiber increases the amount of endogenous PPARdelta.(Evans et al., 2004)

In order to observe the increased amount of type I muscle fiber generated in the transgenic mice the researchers simply looked at their muscles. Because of higher levels of mitochondrial biogenesis (creation of mitochondria) and myoglobin content in type I muscle, type I muscle appears much redder than type II. The transgenic mice had a much redder muscle appearance than did the wild-type mice and this can be observed in Fig. 1. (Evans et al., 2004)


Figure 1. Comparison of muscle appearance between wild-type and transgenic mice. (A and B) The transgenic mice have much redder muscles than do the wild-type (gasrocnemius muscle is a mixture of type I and type II muscle). (C) This a slide containing muscles cells that have been stained for type I and type II muscle cells. Dark blue staining signifies type I muscle fiber. Image used courtesy of

The increased mitochondrial biogenesis in the transgenic muscle cells confirms the presence of a muscle fiber switch. Through a western blot (technique used to identify proteins in particular cells) the researchers show the increase of proteins associated with type I muscle fiber in the muscle cells of the transgenic mice. Results of the western blot are found in figure 2.(Evans et al., 2004)

Figure 2. Western blot of proteins found in muscle cells of both wt and tg mice. Proteins associated with type I muscle fiber are more abundant in transgenic mice. Image used courtesy of

In order to test the hypothesis that individuals with a higher abundance of oxidative muscle fibers resist obesity more readily, the mice were fed a high fat diet for 97 days. The control littermates became obese, while the transgenic mice maintained a normal body mass. Also, the transgenic mice expressed an increased tolerance to glucose, which implies a resistance to diabetes as well as obesity.(Evans et al., 2004)

Because untrained mice with similar body weights were used, the increased endurance phenotype observed in the transgenic mice can be attributed to the increase in PPARdelta expression. This rules out the idea that the transgenic mice were simply in better shape than the wild-type pre-experiment. Also, the daily activity levels of the mice were not significantly different during the experiment and the muscle mass of the transgenic and wild-type did not change throughout the experiment. These ideas further strengthen the hypothesis that there is a muscle fiber switch that can be genetically manipulated. To strengthen the idea that PPARdelta contributes to the high endurance phenotype PPARdelta-null mice were genetically created that could not run for as long a time as their wild-type littermates. (Evans et al., 2004)


The data confirm that PPARdelta is a component in the muscle fiber switch. Increased expression of PPARdelta does several things in skeletal muscle tissue: increases the number of oxidation enzymes, the amount of mitochondrial biogenesis, and the production of type I muscle fiber. The physiological effects of increased expression of PPARdelta resembles the physiological effects associated with training and exercise that are needed to normally convert type II muscle into type I in adult skeletal muscles. The multiple physiological aspects that PPARdelta influences, increased stamina, resistance to obesity, and insulin sensitivity, suggests that it is a viable option for genetic manipulation.(Evans et al., 2004)

The Popular Press Article: 'Marathon' Mice Engineered for Extra Endurance

The scientific journalist who wrote this article does a below average job of fulfilling the roles of a scientific journalist. At the beginning of the article the journalist falls into a common trap that most scientific journalist fall into: the journalist uses a superlative to describe the effects of the gene. He/she says that: "'Schwarzenegger mice', rodents that bulked up after getting injected with muscle building genes" were created in the experiment. Clearly, this statement is supposed to grab the readers attention, yet it distorts the results in the scientific paper and thus, the reader is given a false impression of what the gene actually does. The transgenic mice gained no muscle mass and were not "ripped" or "cut". The only difference between the transgenic mice and the wild-type was the type of muscle the mice had. The author goes on to mention the increased endurance and the resistance to obesity. In describing the resistance to obesity effect caused by the gene the journalist uses the term "fat switch", and how if the "fat switch" genes are turned on, even a person who does nothing would have increased endurance. Later in the article, he/she says the "fat switch" gene is involved in converting type II muscle into type I. Nowhere in the scientific paper is there mention of a "fat switch" and I don't know how genes that have anything to do with fat would, if turned on or off, make a person have more endurance. This mistake severely limits the journalist's role as an intermediary as he/she has given incorrect information in regards to what was manipulated in the mice. The term the journalist should've used is "fiber switch", which is a term repeated many times throughout the scientific paper. The journalist does convey the ideas of slow twitch and fast twitch muscle well giving the example that sprinters need fast twitch (type II) and long distance runners need slow twitch (type I). The journalist makes another mistake (hopefully a typo rather than an actual misunderstanding of the information) when he/she talks about slow twitch being converted to fast twitch and how the genes must be turned on through a promoter. The journalist does a mediocre job of describing the process by which the scientists increase the expression of the endurance gene, but he says slow twitch is being converted into fast twitch through the increased expression. As an intermediary the journalist translates the information into a language the public can understand, yet he/she leaves out several details and actually changes the name of an important idea in the original paper.

The journalist fulfills his/her role as a "watch-dog" better than he/she fulfills her role as an intermediary. The author mentions the impact the gene would have on the athletic world as gene therapy would be near undetectable to officials, whereas drug testing is a reliable way to test athletes for an enhancer. The journalist conveys another issue surrounding gene therapy saying that a gene can have different effects in different organisms, but rather than back it up with another study he/she just mentions that someone died five years ago from gene therapy. The journalist could have mentioned that in another study increased PPARdelta in the intestines of mice increased polyp size and the number of polyps, which means PPARdelta is essential in the regulation of intestinal adenoma growth(Gupta et al., 2004).

The journalist completely ignores his/her role as a tool-giver. He/she simply goes along with the data never questioning the research methods or giving context as to the body of knowledge surrounding PPARdelta.

In conclusion, the journalist fulfills his/her role of giving the public pseudo-correct information, while oversimplifying the research done in the study. This journalist needed to give more context to the topic he/she was discussing rather than use space filling quotations to try and make it seem as if the researchers gave an official approval of the article's information. In order to truly understand a scientific article in a journal one must analyze the data and try to interpret the graphs and figures in a thoughtful way.


The scientific article:

The article on 'Marathon' mice engineered for extra endurance

Physical representation of the PPARdelta protein: go here and click on quick pdb to see backbone of protein


1.Evans, Ronald M., et al.2004. Regulation of Muscle Fiber Type and Running Endurance by PPARdelta. PLoS Biology 2,10: 1-8.


2.Gupta, R. A.; Wang, D.; Katkuri, S.; Wang, H.; Dey, S. K.; DuBois, R. N. :

Activation of nuclear hormone receptor peroxisome proliferator-activated receptor-delta accelerates intestinal adenoma growth. Nature Med. 10: 245-247, 2004.

3. Wang, Y.-X.; Lee, C.-H.; Tiep, S.; Yu, R. T.; Ham, J.; Kang, H.; Evans, R. M. :

Peroxisome-proliferator-activated receptor delta activates fat metabolism to prevent obesity. Cell 113: 159-170, 2003.

4. 2004. 'Marathon' mice engineered for extra endurance. Accessed on 9/02/04. <>



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