[This is a guest blog by Jenna Burnett. Jenna has a Bachelors degree in physics and mathematics from Purdue University and is working on her Masters in kinesiology at Iowa State University. She is currently working as a Sports Science Research Intern at Athletic Lab.]

Capture-TIME-MAGAZINE-COVEREpigenetics is an area of genetic research that is becoming increasingly popular in science circles. But what exactly is it? If we break the word down to its roots, ‘epi’ means ‘above’ or ‘in addition to,’ while ‘genetic’ is ‘of or referring to origin.’ Putting these together, we get the basic definition of epigenetics, something that is above or in addition to the origin. The origin in this case refers to the DNA sequence that is the basis of all the things we are. As every biology teacher can tell you, your genetics determine your basic abilities and define what you look like and what you can do. So your epigenetics, at a general understanding, are structural changes to your DNA sequences that cause increased or decreased gene expression. This means that certain genes will be more expressed, leading to increased protein and cell components or it also means they could be decreased, leading to decreased proteins and cell components. Whether the expression is increased or decreased is determined by the different environments your body is put into and the structural changes that result. This means anything that changes your body’s homeostasis may also change your epigenetics and gene expression, including stress, nutrition, chemical exposure and a host of other factors. While a lot of environments will cause detrimental changes, there are also choices you can make that will cause “healthy” changes to your gene expression.

One such example of a healthy choice is exercise. As anyone can tell you, exercise will help you maintain your weight, equilibrate your hormones, increase your metabolism, and generally lead to a happier and healthier state of being. But what actually causes these changes within your body? At the nuclear level, these changes are driven by the chemical environment created within your body by the exercise state. For example, the hypoxia or lack of oxygen you experience in your muscles during an exercise drives specific epigenetic changes after 2 or 3 repeated exercise bouts (Pareja-Galeano, Sanchis-Gomar, & Garcia-Gimenez, 2014). The changes are so drastic that when 23 previously sedentary individuals completed a 6 month exercise protocol, changes in DNA methylation, a type of epigenetic change, were found on 7,663 different genes (Rönn et al., 2013)!  These changes include both the addition and deletion of methyl groups across the 7,663 genes, leading to decreased and increased gene expression respectively within at least 1/3 of these genes(Rönn et al., 2013).

epigeneticsThe changes in your muscles include increased glucose transporters, increased fat breakdown, increased muscle cell growth and differentiation, as well as increased glucose storage in the muscles (Pareja-Galeano et al., 2014; Rönn et al., 2013). The increase in glucose transporters also have a secondary effect on the muscle; they not only increase the amount of glucose that can move into your cell for energy breakdown, but they also will help you maintain your glucose homeostasis during both resting and exercising states. This means that your cells will be more sensitive to insulin and maintain healthy blood sugar or glucose levels, contributing to why exercise has been shown to reduce diabetic problems in obese individuals (Atkinson et al., 2013; Rönn et al., 2013).

epigenomeThere also are several adaptations to your fat tissue that are the result of the epigeneticchanges. One big change found in a study using rats was that exercise made their fat cells smaller(Giles et al., 2016). The rats also experienced increased dietary fat metabolism, as noted by their Respiratory Exchange Ratio or RER, as well as by tracers in their food. Your RER tells you what ratio of fat and glucose your body is using to create fuel based on the amount of oxygen consumed and carbon dioxide expelled. The closer your RER gets to 0.7, the more fat you are breaking down for energy. For the rats in the study, their RER was found to drop when they lost weight from a low fat diet, whether they exercised or not. However, when compared to the sedentary rats, the RER was significantly lower in the exercising rats when they relapsed into weight gain. The exercising rat’s dietary fat metabolism was also significantly higher when compared to the sedentary rats both before and after the relapse into weight gain, implying that the RER isn’t the only thing that determined their fat breakdown (Steig et al., 2011). This means that not only are your fat cells smaller, but you are using them preferentially for energy creation when you lose weight and when you exercise. As a result of the increased fat breakdown, your body is using a more efficient energy strategy and relies less on your “quick” energy storage.

But epigenetical changes don’t just decide the health state of your body; there has been some evidence to suggest that some of your epigenetic settings could be passed onto your children and your children’s children. When a fetus is going through development, there are two points at which the epigenetics are “reprogrammed” within the fetus, as well as in the fetus’ germ cell. Some scientists believe that certain epigenetic markers slip past this reprogramming and are maintained within the developing fetus (Daxinger & Whitelaw, 2010). Several studies have been done with other animals, as well as in plants and it has yet to be shown definitively in humans for most epigenetic settings (Daxinger & Whitelaw, 2010). However, just because it hasn’t been shown in a study yet doesn’t mean that it isn’t a possibility! This could have drastic influences on your children’s base gene expression and state of health right off the bat! So remember, you aren’t just working out for your health, but you may also be working out to set your children’s health too!

References

  • Atkinson, B. J., Griesel, B. A., King, C. D., Josey, M. A., Olson, A. L., Ikemoto, S., … Cheatham, B. (2013). Moderate GLUT4 overexpression improves insulin sensitivity and fasting triglyceridemia in high-fat diet-fed transgenic mice. Diabetes, 62(7), 2249–58.https://doi.org/10.2337/db12-1146
  • Daxinger, L., & Whitelaw, E. (2010). Transgenerational epigenetic inheritance: More questions than answers. Genome Research, 20(12), 1623–1628. https://doi.org/10.1101/gr.106138.110
  • Giles, E. D., Steig, A. J., Jackman, M. R., Higgins, J. A., Johnson, G. C., Lindstrom, R. C., & MacLean, P. S. (2016). Exercise Decreases Lipogenic Gene Expression in Adipose Tissue and Alters Adipocyte Cellularity during Weight Regain After Weight Loss. Frontiers in Physiology, 7, 32. https://doi.org/10.3389/fphys.2016.00032
  • Pareja-Galeano, H., Sanchis-Gomar, F., & Garcia-Gimenez, J. L. (2014). Physical exercise andepigenetic modulation: Elucidating intricate mechanisms. Sports Medicine, 44(4), 429–436.https://doi.org/10.1007/s40279-013-0138-6
  • Rönn, T., Volkov, P., Davegårdh, C., Dayeh, T., Hall, E., Olsson, A. H., … Ling, C. (2013). A Six Months Exercise Intervention Influences the Genome-wide DNA Methylation Pattern in Human Adipose Tissue. PLoS Genetics, 9(6). https://doi.org/10.1371/journal.pgen.1003572
  • Steig, A. J., Jackman, M. R., Giles, E. D., Higgins, J. A., Johnson, G. C., Mahan, C., … Lane, M. (2011). Exercise reduces appetite and traffics excess nutrients away from energetically efficient pathways of lipid deposition during the early stages of weight regain. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 301(3), R656–67.https://doi.org/10.1152/ajpregu.00212.2011