Exercise-Associated Menstrual Dysfunction Can Be Treated W/ Carbohydrates: Add. 30% Glucose or Oligosaccharide Reverse Amenorrhea, Ovarian & Hormonal Abnormalities

It's nice to be lean, but is it really worth ruining your health? I don't think so, but everyone is the architect of his / her own future.

I want to say in advance that you'd better not read this article if you belong to the ever-increasing number of carbophobs (people who are afraid of carbohydrates) who have been so indoctrinated by the confusing information on the Internet that they are willing to close their eyes to all objective data.

In view of the fact that you kept reading, I assume that you (a) don't belong to this group of blockheads or are (b) a blockhead who is about to scroll down to the comment section to start raving about how bad carbohydrates are, pointing out that "you just have to eat a ketogenic diet to live happily ever after" - spare me this bullshit, please!
It's scaremongering bullshit like that due to which more and more non-athletes develop what Can Zhao et al. describe in their latest paper in the peer-reviewed scientific Journal of Sport and Health Science as "exercise-associated menstrual dysfunction" aka EAMD (Zhao. 2014).

For those who have read the SuppVersity Athlete Triad Series, it's no news that menstrual irregularities and amenorrhea in female athletes is closely linked to the imbalance between energy intake and exercise-associated energy requirement (Williams. 2001). Accordingly Zhao et al. wanted to investigate, ...

"[...]whether carbohydrate supplements can reverse EAMD and protect against exercise-induced impairment in ovary as an important part of HPO axis regulation and rebalances the energy intake and energy expenditure to support the reproductive function" (Zhao. 2014).

Now the bad news is that they did this in rodents. 45 healthy mature 2-month-old female Spraguee Dawley rats, to be precise. This sounds idiotic, but in view of the fact that the experimental procedure required that "subjects" are sacrificed in the course of the study it's quite reasonable to use rodents, not ladies.

Figure 1:  Treadmill running schedules show the specific timeline and various treatments of each groups (Zhao. 2014)

Figure 1 shows a graphical overview of the study protocol which involved an identical initial exercise period in the course of which the speed of the treadmill was continuously increased for six weeks.

At the end of this initial 6-week study period, the female rats, the ovary epithelial cells of the rodents showed significant abnormalities. At the end of week 9, the follicular cells of the rodents in group E contained swollen mitochondria with broken cristae.

Similar exercise-induced mitochondrial damages were also observed in the EAMD rats with post-exercise rest. In the rodents in group O and G, however, Zhao et al. observed a significant recovery of exercise-induced mitochondria impairment. They showed significant reduction of swollen endoplasmic reticulum and Golgi complex, and increases in abundant organelles, irrespective of whether they had been fed a 30% glucose or 30% oligosaccharide diet.

Normalization of organ changes and hormones w/out increase in energy intake

In contrast to the previously hinted at prejudices, the addition of simple sugars to the rodent diet did not lead to an increase in energy intake - in spite of the fact that the goal was a 30% increase in energy intake from glucose / oligosaccharide supplements, the total energy intake was not higher than in the non-exercised control group (see Figure 2).

Figure 2: Changes in energy intakes in each group throughout 9 weeks study (Zhao. 2014).

In conjunction with the significant improvement in GnRH, LH, FSH and estrogen it's thus more than unlikely that a comparable increase in "sugar" intake in human females would trigger the increase in body fat many women fear so much that they are willing to run around tired and infertile for years, although most of them know that reducing the exercise volume and normalizing their eating behavior would solve the problem once and for all.

Figure 3: Relative levels (% of control) of GnRH, FSH, LH, E2 and Progesterone (P) after 9 weeks (Zhao. 2014)

Interestingly, the saccharide polymers (oligosaccharides), which are also commonly found on the plasma membrane of animal cells, where they can play a role in cell–cell recognition, did a slightly better job than glucose, when it comes to the restoration of normal hormone levels (see Figure 3).
Reference:

• Qiang, Xu, Chao YongLie, and Wan QianBing. "Health benefit application of functional oligosaccharides." Carbohydrate Polymers 77.3 (2009): 435-441. 
• Tomten, S. E., and A. T. Høstmark. "Energy balance in weight stable athletes with and without menstrual disorders." Scandinavian journal of medicine & science in sports 16.2 (2006): 127-133. 
• Williams, Nancy I., et al. "Longitudinal Changes in Reproductive Hormones and Menstrual Cyclicity in Cynomolgus Monkeys during Strenuous Exercise Training: Abrupt Transition to Exercise-Induced Amenorrhea 1." Endocrinology 142.6 (2001): 2381-2389. 
• Zhao, Can, et al. "Effects of carbohydrate supplements on exercise-induced menstrual dysfunction and ovarian subcellular structural changes in rats." Journal of Sport and Health Science (2014).