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The Effect of the Female Reproductive Cycle on Metabolism - Literature review Example

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This literature review "The Effect of the Female Reproductive Cycle on Metabolism" quantifies differences in individual women at different points in their own reproductive cycle, focusing specifically on changes in metabolism, rather than comparing the women as a group to some other standard…
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The Effect of the Female Reproductive Cycle on Metabolism
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?The Effect of the Female Reproductive Cycle on Metabolism Unlike males, female mammals generally undergo reproductive cycles, which consist of a series of preparation steps for fertilization of the ovum, or egg cell. In humans and other primates, this is known as a menstrual cycle, because it involves menstruation, or periodic vaginal bleeding, as the uterine wall is shed; however, menstruation only happens if fertilization does not occur. In human women, the commonly accepted figure for the length of the cycle is approximately twenty-eight days, though this can vary widely between individuals and is also affected by in humans by the use of pharmaceutical contraceptives that interfere with the normal reproductive cycle (Barrett 2010). Much is known about the reproductive cycle and its effects on co-morbid conditions during normal function, the pathology of disease states specifically or indirectly affecting reproduction, and changes due to ageing. However, considerably less is understood about the effects of the reproductive cycle in healthy women on many individual factors, as this is their normal state and so there is no control against which to test, though there does exist some research into the differences in metabolism between healthy women with amenorrhoea and those with a regular reproductive cycle (Maughan 2000). No standard exists for the correct levels of bleeding at different ages, for example, which is becoming a fairly substantial public health issue (Harlow & Ephross 1995). However, this research hopes to quantify differences in individual women at different points in their own reproductive cycle, focusing specifically on changes in metabolism, rather than comparing the women as a group to some other standard. The hypothesis to be tested is that a woman's point in the reproductive cycle will have an effect on resting and post-exercise metabolism; the null hypothesis being used is that it will not have an effect. Declining conception rates combined with an increase in obesity among women of childbearing age make this research important to the future of reproductive medicine; it is vital that the connection between metabolism and reproduction is fully understood (Crain et al. 2008). In order to achieve this, metabolic rates will be measured at rest and after exercise using expired gas analysis weekly for four weeks. This timing has been chosen to ensure that a sample is taken during or close to each of the four stages of the reproductive cycle. These are the menstruation phase, the follicular phase, the ovulatory phase, and the luteal phase (Porter 2009). The different length of time for each phase in individual women make it extremely difficult to ensure samples are taken during each phase, but the day within the cycle can be monitored so that the data can be corrected for this factor. Additionally, algorithms do exist to monitor an individual's reproductive cycle and measure at which point a particular woman is in her cycle, allowing careful recording of this related data (Wactawski-Wende et al. 2009). Each of these phases has a different effect on the woman experiencing them. The menstruation phase, which traditionally marks the start of the next reproductive cycle, is the period of time during which the uterine wall is shed in response to a reduction in oestrogen and progesterone levels. Bleeding occurs, though usually only in a volume of about fifteen to seventy-five millilitres. Menstruation actually during the “next” phase of the cycle, the follicular phase, though they are being considered separately for purposes of this research. During this follicular phase, there is an increase in follicle-stimulating hormone, which causes several follicles to begin to grow in preparation for releasing an ovum, or egg cell. This follicle then begins to produce oestrogen, of which levels peak at the ovulation phase. The ovulation phase is the point where the ovum is released from the follicle and is precipitated by a surge in both lutenizing and follicle-stimulating hormone. As oestrogen levels plateau, progesterone levels begin to rise, indicating the beginning of the luteal phase. This leads to a thickening of the uterine walls, in preparation for fertilization of the ovum and a possible pregnancy. If this fertilization does not occur, the resulting drop in progesterone levels leads to a breakdown of the thickened wall and the individual re-enters the menstrual phase (Porter 2009). All of these hormonal changes likely have an effect on metabolism. Metabolism, as it is currently defined, is “the continuous conversion between structural molecules and energy” in a living organism. Without it, life as we know it would never have existed; in fact, it is nonsensical to think of “life” as separate from “metabolism” (Ruggiero & Ferrucci 2006). The rate of metabolism affects all parts of an organism's life cycle, and in fact may be intrinsically tied to lifespan (Haigis & Guarente 2006). Past research has shown that changing the hormonal status of post-menopausal women can have an effect on neural metabolism; oestrogen seems to increase brain metabolism while progesterone seems to have a down-regulation effect (Silverman et al. 2011). Though this research has been performed using synthetic hormone treatments, it is likely that such effects are the same with naturally-produced hormones and that these effects carry over into other cells of the body. Neurons and neural activity, after all, are simply specialized body cells; there is no reason that such changes in metabolism would not be the same in other somatic cells. Humans are of course not the only animals to have reproductive cycle, and humans are not the only ones for whom the phase of the reproductive cycle might affect metabolism. One example of this effect is in the much simpler organism the scallop. The development of the gamete and the spawning process reduces the metabolism of the adductor muscle, which reduces the ability of the scallop to escape from danger. This research also determined that mitochondrial activity alone was not to blame for this performance reduction, but that it was related to enzyme and protein levels of the scallop (Kraffe et al. 2008). While the features of the reproductive cycle of this creature are profoundly different from those of the human reproductive cycle, the fact remains that the energy expended in the growth of a gamete is then not available for use by other areas of the body. This re-distribution of energy and resources could potentially reduce the metabolism of the somatic cells during the follicular stage of the human reproductive cycle (Becker 2001). Conversely, the added energy requirements for this process could increase the total body metabolism during the follicular or luteal phases (Maughan 2000). Other studies have shown that excretion of glutamine, glycine, alanine, lysine, serine and creatinine are greatly decreased during the luteal phase, which could indicate that the body is making use of more of these proteins than normal (Wallace et al. 2010) There are also many connections between weight, metabolism, and reproductive health (Pasquali et al. 2006). It has been difficult to determine in many cases if the hormonal condition, such as poly-cystic ovary syndrome, is a cause or a symptom of obesity and resultant co-morbidities. Obesity results in a hyper-androgenic state, or an excess of male hormones, which leads to fertility difficulties even without another condition being present. PCOS also leads to an increase in the production of male hormones in women that would otherwise be of reproductive age, making it difficult to pin down the cause and the effect in this link. The existence of evidence that obesity during pregnancy can lead to PCOS of a female child after she reaches childbearing age indicates that there is a connection between these abnormal hormone levels in the obese woman, the abnormal metabolic state that led her to become obese originally, and abnormal uterine function (Samuelsson et al. 2008). This link between maternal metabolic health and the future health of the offspring has been shown in several animal models and is indicated to exist in humans (Pasquali et al. 2006). PCOS is also linked to changes in the metabolism of lipids and lipoproteins, again indicating a link between somatic cellular metabolism and the state of the reproductive cycle (Thomson et al. 2008). Similarly to the study mentioned above, much of the existing research on a link between hormone levels and metabolism has been done on disease states such as PCOS and in women with extremely high levels of body fat and total body weight, though not on the addition of exercise to the treatment regimen (Crunkhorn & Patti 2008). The new research being proposed on the reproductive cycle and metabolism may be among the first to analyse such ties in healthy and normal-weight women. The proposed exclusion criteria include such conditions as diabetes, as a connection has already been proven between this disorder, hormone levels, and metabolism (University of Waterloo Department of Research Ethics; Sowers et al. 2008). Cardiovascular disease is being excluded for the same reason, as well as for the safety of the participants (Warren & Perlroth 2001; Volek et al. 1997). Use of these criteria will help ensure that the data from this research remains uncontaminated with contributing factors from pathological states. The second point of interest in this study, besides the direct effect of reproductive cycle on resting metabolic rate, is the changes seen in the metabolism after exercise and how those relate to the reproductive cycle. It is well-known that intense exercise can have an effect on the female reproductive system and on hormone levels throughout the body; what is less well understood is the reverse condition of how the reproductive system can affect exercise (Rumbold et al. 2011). An obvious difficulty of collecting such data is the increase in metabolism and perceived hunger after exercise irrespective of any other contributing factors (Thomas et al. 2010). In order to collect this data without contamination, the exertion level of the exercise period used to gather the post-exercise data needs to be carefully controlled (Maughan 2000). An additional possible point of contamination exists in the fitness level of the participants. If the exercises they perform as part of this study increase their fat-free body mass, their resting metabolic rate will also increase with no connection to their reproductive cycle (Maughan 2000). For this reason, the period of exercise is to be only five minutes long. Research at this point does indicate that the hypothesis of this study will be upheld. Resting metabolic rate has been found to fluctuate with relation to reproductive cycle phase, though these results are sometimes in disagreement with each other (Maughan 2000). This indicates the need for further studies such as this one, to fill in the gaps in the existing knowledge base on this topic. References Barrett, K., 2010. Ganong’s review of medical physiology 23rd ed., New York: McGraw-Hill Medical. Becker, K.L., 2001. Principles and practice of endocrinology and metabolism, Lippincott Williams & Wilkins. Bhutta, Z.A. et al., 2010. Linkages Among Reproductive Health, Maternal Health, and Perinatal Outcomes. Seminars in Perinatology, 34(6), p.434-445. Available at: http://www.seminperinat.com/article/S0146-0005(10)00102-3/abstract [Accessed April 5, 2011]. Crain, D. et al., 2008. Female reproductive disorders: the roles of endocrine-disrupting compounds and developmental timing. Fertility and Sterility, 90(4), p.911-940. Available at: http://www.fertstert.org/article/S0015-0282(08)03555-3/abstract [Accessed April 5, 2011]. Crunkhorn, S. & Patti, M.-E., 2008. Links between thyroid hormone action, oxidative metabolism, and diabetes risk? Thyroid: Official Journal of the American Thyroid Association, 18(2), p.227-237. Available at: http://www.ncbi.nlm.nih.gov/pubmed/18279023 [Accessed April 5, 2011]. Haigis, M.C. & Guarente, L.P., 2006. Mammalian sirtuins—emerging roles in physiology, aging, and calorie restriction. Genes & Development, 20(21), p.2913 -2921. Available at: http://genesdev.cshlp.org/content/20/21/2913.abstract [Accessed April 1, 2011]. Harlow, S.D. & Ephross, S.A., 1995. Epidemiology of menstruation and its relevance to women’s health. Epidemiologic Reviews, 17(2), p.265-286. Available at: http://www.ncbi.nlm.nih.gov/pubmed/8654511 [Accessed April 5, 2011]. Kraffe, E. et al., 2008. Effect of reproduction on escape responses, metabolic rates and muscle mitochondrial properties in the scallop Placopecten magellanicus. Marine Biology, 156(1), p.25-38. Available at: http://www.springerlink.com/content/l3jh753h26x02610/ [Accessed April 5, 2011]. Maughan, R.J., 2000. Nutrition in sport, Wiley-Blackwell. Pasquali, R., Gambineri, A. & Pagotto, U., 2006. Review article: The impact of obesity on reproduction in women with polycystic ovary syndrome. BJOG: An International Journal of Obstetrics & Gynaecology, 113(10), p.1148-1159. Available at: http://onlinelibrary.wiley.com/doi/10.1111/j.1471-0528.2006.00990.x/full [Accessed April 5, 2011]. Porter, R., 2009. The Merck manual home health handbook [3rd ed.]., Whitehouse Station NJ: Merck Research Laboratories. Ruggiero, C. & Ferrucci, L., 2006. The Endeavor of High Maintenance Homeostasis: Resting Metabolic Rate and the Legacy of Longevity. The journals of gerontology. Series A, Biological sciences and medical sciences, 61(5), p.466-471. Rumbold, P.L.S. et al., 2011. Energy intake and appetite following netball exercise over 5 days in trained 13-15 year old girls. Appetite, 56(3), p.621-628. Available at: http://www.sciencedirect.com/science/article/B6WB2-527PRDX-2/2/36ee31e101b33760751e5df2f0f2376a [Accessed April 5, 2011]. Samuelsson, A.-M. et al., 2008. Diet-Induced Obesity in Female Mice Leads to Offspring Hyperphagia, Adiposity, Hypertension, and Insulin Resistance: A Novel Murine Model of Developmental Programming. Hypertension, 51(2), p.383-392. Available at: http://hyper.ahajournals.org/cgi/content/abstract/51/2/383 [Accessed April 5, 2011]. Silverman, D.H.S. et al., 2011. Differences in regional brain metabolism associated with specific formulations of hormone therapy in postmenopausal women at risk for AD. Psychoneuroendocrinology, 36(4), p.502-513. Available at: http://www.sciencedirect.com/science/article/B6TBX-50X9SGV-2/2/ae46887dc54e214a1cc5348d502ed957 [Accessed April 5, 2011]. Sowers, M.R. et al., 2008. Levels of Sex Steroid and Cardiovascular Disease Measures in Premenopausal and Hormone-Treated Women at Midlife: Implications for the “Timing Hypothesis.” Arch Intern Med, 168(19), p.2146-2153. Available at: http://archinte.ama-assn.org/cgi/content/abstract/168/19/2146 [Accessed April 5, 2011]. Thomas, J., Nelson, J. & Silverman, S., 2010. Research Methods in Physical Activity, Human Kinetics. Thomson, R.L. et al., 2008. The Effect of a Hypocaloric Diet with and without Exercise Training on Body Composition, Cardiometabolic Risk Profile, and Reproductive Function in Overweight and Obese Women with Polycystic Ovary Syndrome. J Clin Endocrinol Metab, 93(9), p.3373-3380. Available at: http://jcem.endojournals.org/cgi/content/abstract/93/9/3373 [Accessed April 5, 2011]. University of Waterloo Department of Research Ethics, SAMPLE B14: INFORMATION LETTER AND CONSENT FORM FOR RESEARCH INVOLVING NON-INVASIVE PHYSIOLOGICAL ASSESSMENTS AND MEDICAL SCREENING OF PARTICIPANTS. Available at: http://iris.uwaterloo.ca/ethics/human/application/samples/B14_InfoLetter_NonInvasivePhys.htm [Accessed April 5, 2011]. Volek, J.S. et al., 1997. Testosterone and cortisol in relationship to dietary nutrients and resistance exercise. Journal of Applied Physiology (Bethesda, Md.: 1985), 82(1), p.49-54. Available at: http://www.ncbi.nlm.nih.gov/pubmed/9029197 [Accessed April 2, 2011]. Wactawski-Wende, J. et al., 2009. BioCycle study: design of the longitudinal study of the oxidative stress and hormone variation during the menstrual cycle. Paediatric and perinatal epidemiology, 23(2), p.171-184. Wallace, M. et al., 2010. Effects of menstrual cycle phase on metabolomic profiles in premenopausal women. Human Reproduction, 25(4), p.949 -956. Available at: http://humrep.oxfordjournals.org/content/25/4/949.abstract [Accessed April 5, 2011]. Warren, M. & Perlroth, N., 2001. The effects of intense exercise on the female reproductive system. J Endocrinol, 170(1), p.3-11. Available at: http://joe.endocrinology-journals.org/cgi/content/abstract/170/1/3 [Accessed April 5, 2011]. Read More
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