ONLINE DRIVERS MEDIA

Its nice to be lean, but is it really worth ruining your health? I dont think so, but everyone is the architect of his / her own future.

I want to say in advance that youd 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) dont 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!
Its 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, its 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 its 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 its 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).

Resistance training alone wont make up for a sloppy diet - no matter if you do it before or after meals.

I am not sure how feasible this is going to be for you, but if you are a type II diabetic or anyone concerned about the potential detrimental health effects of the rise in glucose and triglycerides after a meal, working out 45 minutes after dinner is the way to go.

Abnormally elevated postprandial glucose and triacylglycerol (TAG) concentrations are strong risk factors for cardiovascular disease (CVD) in patients with type-2 diabetes. Therefore, scientists expect that interventions that reduce postprandial glucose and TAG concentrations should lower the risk of CVD (Krook. 2003; OGorman. 2008).
Previous studies have shown that acute exercise typically lowers postprandial glucose and TAG concentrations (Tobin. 2008) in patients with type-2 diabetes, but as Timothy D. Heden et al. point out, there is considerable heterogeneity in the responses with some individuals not experiencing beneficial changes in these risk factors (Gill. 2007; van Dijk. 2012).

"One potential explanation why some patients with type-2 diabetes do not have beneficial changes in postprandial glucose and TAG with acute exercise is because of the timing of the acute exercise session relative to meal consumption. Limited evidence suggests that the timing of aerobic exercise around a meal may be important and might explain why some individuals are exercise “insensitive” or “non responders”." (Heden. 2014) 

The only study to directly compare the effect of pre-meal and post-meal aerobic exercise on postprandial glucose concentrations in patients with type-2 diabetes showed that post-dinner, but not pre-dinner walking, lowered postprandial glucose concentrations (Colberg. 2009).

Figure 1: Previous studies indicate that aerobic workouts after meals have more beneficial effects on the potentially unhealthy increases in glucose or triglycerides (Collberg. 2009)

Although no study has directly examined the effect of exercise timing on postprandial TAG in patients with type-2 diabetes, there is evidence that exercise performed the day prior to a high fat meal has no effect on postprandial TAG responses (Dalgaard. 2004; Gill. 2007), while post-breakfast aerobic exercise reduced the postprandial TAG response (Tobin. 2008). Taken together, it appears that aerobic exercise may have its most powerful effect to lower postprandial glucose and TAG responses when performed after a meal, possibly because of slowed gastric emptying and/or greater skeletal muscle glucose and TAG uptake and utilization at this time.

The question that remained was: Is the same true for resistance training?

Since resistance exercise (RE) has a more pronounced long(er)-lasting effect on ones metabolism than aerobic training, the researchers from the University of Missouri tested the hypothesis that post-dinner RE, compared to pre-dinner RE, would in fact be more effective at improving two clinically important postprandial risk factors (glucose and 109 TAG) for CVD at a time of day when they are typically highest in obese patients with type-2 diabetes.

The standardized test workout consisted of the following exercises (in this order): leg press, seated calf raises, seated chest flyes, seated back flyes, back extensions, shoulder raises, leg curls, and abdominal crunches. All exercises were performed for three sets (1-2 min rest between sets) of 10-repetitions for each RE. During this session, the first set for each exercise was a warm-up set and the weight used was 50% of the participants 10-RM. After the warm-up set, the weight for the next two sets was the participants previously determined 10-RM.

Figure 2: Postrandial lipid response in the obese type II diabetics (Heden. 2014)

As you can see in Figure 2 the scientists suspicion was right, the postprandial workout (M-RE) had significantly more pronounced beneficial effects on the lipid metabolism of the type II diabetic subjects who consumed a standardized breakfasts (English muffin, cheddar cheese, one large egg, ham, hash brown, ketchup, and apple or orange juice) lunch (white bread, ham, mayonnaise, cheddar cheese, a granola bar, and apple or orange juice) and dinner meals (spaghetti noodles, spaghetti sauce with beef added, garlic bread, a lemon lime flavored soda, and 1.5 g of acetaminophen (to assess gastric emptying)) containing ~50% carbohydrate, 35% fat, and 15% protein.

Similar effects were observed for the insulin and glucose responses (see Figure 3) which were significantly improved and should thus complement the beneficial effects of the reduced triglyceride and very low density lipoprotein (VLDL) levels.
References:

• Colberg, Sheri R., et al. "Postprandial walking is better for lowering the glycemic effect of dinner than pre-dinner exercise in type 2 diabetic individuals." Journal of the American Medical Directors Association 10.6 (2009): 394-397. 
• Dalgaard, Marian, Claus Thomsen, and Kjeld Hermansen. "Effects of one single bout of low-intensity exercise on postprandial lipaemia in type 2 diabetic men." British Journal of Nutrition 92.03 (2004): 469-476.
• Gill, Jason MR, et al. "Effect of prior moderate exercise on postprandial metabolism in men with type 2 diabetes: heterogeneity of responses." Atherosclerosis 194.1 (2007): 134-143.
• Heden, Timothy D., et al. "Post-dinner resistance exercise improves postprandial risk factors more effectively than pre-dinner resistance exercise in patients with type 2 diabetes."
  Journal of Applied Physiology (2014). Ahead of print.
• Krook, Anna, et al. "Reduction of risk factors following lifestyle modification programme in subjects with type 2 (non?insulin dependent) diabetes mellitus." Clinical physiology and functional imaging 23.1 (2003): 21-30.
• OGorman, Donal J., and Anna Krook. "Exercise and the treatment of diabetes and obesity." Endocrinology and metabolism clinics of North America 37.4 (2008): 887-903.
• Tobin, L. W. L., Bente Kiens, and Henrik Galbo. "The effect of exercise on postprandial lipidemia in type 2 diabetic patients." European journal of applied physiology 102.3 (2008): 361-370.
• van Dijk, Jan-Willem, et al. "Exercise and 24-h glycemic control: equal effects for all type 2 diabetic patients?." Medicine and science in sports and exercise (2012).