the thing I don't like about the citation, is that it is labeled a "dysfunction" as if it is unnatural or not normal. My text, by Costill, said the same thing, and my professor, who studied under Costill, was pissed off royally by that label.
the thing I don't like about the citation, is that it is labeled a "dysfunction" as if it is unnatural or not normal. My text, by Costill, said the same thing, and my professor, who studied under Costill, was pissed off royally by that label.
Dogman wrote:
Basic, but nicely done. I believe my statements have supported everything you have said.
Sorry, that should have been a response from 1_Coach. I use a shared computer and I didn\'t notice an office mates name in the window.
I also want to point out that there is a HUGE variance in % body fat for various tests. You have to take your results with a grain of salt. I believe I've done them all, so here's my results, which were all done within a few months/weeks of each other:
Bod Pod: 20.1%
Dexa Scan: 19.7%
Underwater Weighing: 12.6%
Skin Calipers: 10.6%
Circumference measurements: 10.3%
Upper Body Bioelectrical Impedence: 16.5%
Plus, I get regular periods (with or without oral contraceptives) while running an average of 75 miles/week.
trackhead wrote:
the thing I don't like about the citation, is that it is labeled a "dysfunction"
Good point. A better term that should have been used is irregularities.
Here's something from Lore of Running, which is a generalization based all the research presented in the book:
The first is a short-term irregularity to which all women runners are prone especially during periods of heavy training, intensive competition, and associated weight loss.
.... The athlete with long-term menstrual irregularity is likely to be a young female who has not had children, who had a late menarche, and who experienced previous menstrual irregularity before she began running. She is likely to be a vegetarian of low body weight, and she may be on a calorie-restricted diet.... She is likely to train heavily and to be a better-than-average performer. Such a woman typically selects a stressful lifestyle, and this sustained level of stress, to which the running in part contributes, may be responsible for the irregular menstrual patterns.... All of these stresses act to suppress the hypothalamus, which then fails to release hormones necessary for cyclical menstruation."
SP wrote:
So, 11% is essential for a woman, so what is wrong with that??
My point was that for some women 11.5% is probably not healthy. Obviously, it was OK for you. By the same token, 25% may not be unhealthy for some men. Both numbers are on the borderline.
My exercise phys. prof at university did her master's reserach on amenorreah, and likened it to the swelling of an injured ankle. The swelling is not a dysfunction, but a rather a protective function so that you can use the ankle and have to let it rest to heal.
By the same token, amenorreah occurs because the body thinks a pregnancy at this time, under these conditions, would be a bad idea, so it suspends that system. When conditions change, menstruation resumes.
trackhead wrote:
Where are your CHO reserves at the end of a 2.5hr run? Or after 40min of hard running? They are not dependable reserves. They are constantly being replenished, yes, but reserves are always being tapped.
And this regular flux of glycogen stores would cause what, exactly? And why don't women on low carb diets get amenorrhea? I also have a hard time believing your underlying hypothesis that the fetus can only use glucose as a fuel source. Now, I've never studied fetal nutrition, but I'd need to see a credible source to believe that with all the lipids diffusing easily across the placental barrier.
Plus, my old exercise physiology texts gave the same stock answer on exercise-induced amenorrhea. It was written almost a decade before anyone knew about leptin and the manner in which it served as a surrogate signal of starvation that could regulate apetite, metabolic rate and reproductive function. Now we know a little more about this new endocrine system and the regulation of reproduction.
It isn't "total" body fat that disrupts reproductive function - its energy balance in the short term - i.e. an obese women who goes on a diet could stop getting her periods even though she still had 40% body fat. If you are really interested read this article:
"Energy Availability, Not Body Fatness, Regulates Reproductive Function in Women"
here is the link
http://www.acsm-essr.com/pt/re/essr/fulltext.00003677-200307000-00008.htm
;jsessionid=BzZkjTMVSkRsDapSxl1UTAPapQLwL1WAuI7CrrvtlduPz9nnuxhf!53808052!-949856032!9001!-1
posted link into URL field below
For the final answer, we turn to the journal of endocrinology:
"Hypothalmic dysfunction associated with strenuous exercise, and the resulting disturbance of GnRH pulsatility, can result in delayed menarche and disruption of menstrual cyclicity. ..An energy drain incurred by women whose energy expenditure exceeds dietary intake appears to be the primary factor effecting GnRH suppession in athletes engaged in sports emphasizing leaness; nutritional rstriction may be an important causal factor in the hypoestrogenism observed in these athletes."
from the Journal of Endocrinology and metabolism:
"Thus, amenorrheic athletes displayed a hormonal pattern in agreement with hypothalamic inhibition due to energy deficiency..."
I can't copy and paste on this computer but if you search for the Journal of endocrinology on google, then menustration and athlete on their web page, you'll find this article.
If you still want to be sorta right you can say that athletes restricting their caloric intake may have lower body fat than other athletes, but it isn't the causal factor.
Here's a journal for you. From a very recent New England Journal of Medicine:
"Recombinant human leptin in women with hypothalamic amenorrhea.
Welt CK, Chan JL, Bullen J, Murphy R, Smith P, DePaoli AM, Karalis A, Mantzoros CS.
Reproductive Endocrine Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
BACKGROUND: Disruptions in hypothalamic-gonadal and other endocrine axes due to energy deficits are associated with low levels of the adipocyte-secreted hormone leptin and may result in hypothalamic amenorrhea. We hypothesized that exogenous recombinant leptin replacement would improve reproductive and neuroendocrine function in women with hypothalamic amenorrhea. METHODS: Eight women with hypothalamic amenorrhea due to strenuous exercise or low weight were studied for one month before receiving recombinant human leptin and then while receiving treatment for up to three months. Six control subjects with hypothalamic amenorrhea received no treatment and were studied for a mean (+/-SD) of 8.5+/-8.1 months. RESULTS: Luteinizing hormone (LH) pulsatility, body weight, ovarian variables, and hormone levels did not change significantly over time in the controls and during a one-month control period before recombinant leptin therapy in the treated subjects. In contrast, recombinant leptin treatment increased mean LH levels and LH pulse frequency after two weeks and increased maximal follicular diameter, the number of dominant follicles, ovarian volume, and estradiol levels over a period of three months. Three patients had an ovulatory menstrual cycle (P<0.05 for the comparison with an expected rate of spontaneous ovulation of 10 percent); two others had preovulatory follicular development and withdrawal bleeding during treatment (P<0.05). Recombinant leptin significantly increased levels of free triiodothyronine, free thyroxine, insulin-like growth factor 1, insulin-like growth factor-binding protein 3, bone alkaline phosphatase, and osteocalcin but not cortisol, corticotropin, or urinary N-telopeptide. CONCLUSIONS: Leptin administration for the relative leptin deficiency in women with hypothalamic amenorrhea appears to improve reproductive, thyroid, and growth hormone axes and markers of bone formation, suggesting that leptin, a peripheral signal reflecting the adequacy of energy stores, is required for normal reproductive and neuroendocrine function."
Anyway, there are obviously multiple inputs into the hypothalamus that determine the reporoductive hormone output, and total fat stores are not the only influence. Stress, physical exertion etc. certainly help determine why one woman may be anovulatory while another woman with even less fat may not. However, the amount of fat stores obviously has an enormous influence on reprodctive function through the fat cell-secreted hormone leptin.