Guys, I’m STOKED about this study I have for you all today. It’s by far the most interesting journal article I’ve read in a long time.
It touches on so many things that are relevant to all of us – fasted training, sprints vs(?) low-intensity cardio, gender differences, and insulin (so, by extension, peri-workout nutrition). On top of that, it’s a really well-controlled study that uses a really challenging protocol, so it should be more applicable than most. I’ll warn you up front, the beginning of this post will be pretty dry and scienc-y, but stick around and I promise it’ll get exciting by the end 🙂
What they were doing:
This was essentially a follow-up study. The same researchers had used a similar protocol in a 1996 study, and found a pretty substantial hypertrophy response in women after 4 weeks of doing sprints 3x per week (+25% in cross-sectional area of type IIB fibers), with NO hypertrophy response in men. Obviously that’s a puzzling result, since men tend to hypertrophy easier than women do, primarily – it’s generally assumed – due to differences in testosterone levels.
Since that 1996 study, more research had been done on gendered responses to sprinting protocols, examining the mechanisms that could explain the difference – primarily the via the mTOR pathway – which “…controls the initiation of protein translation and ultimately skeletal muscle growth.” In short, various protocols had shown that the mTOR pathway wasn’t activated in men due to sprinting, so Esbjörnsson wanted to repeat the original protocol that had produced gender differences in hypertrophy to see if women and men would have differing mTOR responses, which would then explain the differences in hypertrophy.
They recruited nine men and eight women, aged 20-30, who were active and healthy but didn’t compete in anything at the elite level.
The testing protocol was brutal – report to the lab fasted, then 3 successive Wingate tests with 20 minutes rest in between. The Wingate test is a 30 second, all-out sprint on a stationary bike to measure your anaerobic power. It may not sound difficult, but it’s generally considered one of the most crushingly hard research protocols in existence. Doing it three times is, for lack of a better term, insane.
They took muscle biopsies before the first sprint and 140 minutes after the last, and they drew blood before the first sprint, between sprints, and 9, 80, and 140 minutes after the last sprint.
What they found:
1) When controlling for fat free mass, there was no significant difference in power output between the men and the women. That’s a HUGELY important point, since that means, normalized to negate body fat differences, the men and women were exercising at the same relative intensities. So the potential contention that difference in response may be due to one gender or the other working harder simply isn’t founded.
2) There were also no significant fiber type differences between the men and the women. So it can’t be contended that the differences in outcome were actually due to fiber type differences. After ruling out fiber type and work rate as potential differences, it really seems like the influencing factor has to be gender – which is exactly what the authors were going for.
3) mTOR phosphorylation after exercise was increased about 120% on average, with no significant differences between men and women.
4) AMPK (a protein that, more-or-less, has an antagonistic with mTOR) phosphorylation was not different between men and women, or between pre- and post-exercise.
5) p70S6k, a downstream protein in the mTOR signalling pathway, was elevated in both men and women, but the increase was 230% in women and only 60% in men. (VERY important implications here that we’ll discuss later)
6) plasma leucine (the amino acid most associated with mTOR activation) was significantly higher in men pre-exercise, but decreased significantly more in men pre- to post-exercise, though it decreased significantly in women too.
7) lactate levels were the same at rest between genders, and plasma lactate increased significantly for both genders, but increased more in men than in women when measured between sprints.
8) glucose levels weren’t significantly different at rest and increased in both genders in response to the sprints, but the increase was larger in women.
9) serum insulin levels weren’t significantly different at rest, and increased in both genders, but the increase was roughly 3x over baseline in men, and 5x over baseline in women.
10) serum growth hormone levels were higher at rest for women, but increased to a larger degree in men, though peak values weren’t significantly different.
11) there was a pretty strong correlation (r = .68) between increase in p70S6k and increase in insulin in response to the sprints.
Making sense of it all:
I warned you that it would be a little science-heavy at first, but here’s the pay-off. There are a couple of really exciting implications here.
First and foremost – if you train and don’t get to eat right away, though it’s not optimal, you certainly don’t need to worry about getting “catabolic.” These people were training fasted, doing an absurd protocol, and didn’t eat for 2 hours after they worked out – and they STILL had elevated mTOR – one of the primary markers of anabolism.
Secondly (this is the important part) – energy status of your cells has a lot to do with hypertrophy response to the same stimulus.
Let me break it down for you
a. Women had a larger rise in blood glucose, so the liver was putting out more glucose to be used for the sprints.
b. Women had a larger increase in insulin, so there was a larger hormonal signal to drive glucose uptake into the muscle.
c. Women had a SMALLER increase in lactate. Lactate levels acutely decrease insulin sensitivity.
d. Women had a SMALLER decrease in plasma leucine
Add all this together, and the men’s muscles were in a much more depleted state post-exercise than the womens’. mTOR is, to a degree, a “fuel gauge” for the cell.
So, what you wind up with is the SAME activation of mTOR due to exercise, but significantly blunted downstream signalling in men, as evidenced by the much smaller increase in phosphorylation of p70S6k.
Implications (one serious, and one *sort of* joking, and one to make you go “hmmm”):
1. If either hypertrophy or the maintenance of muscle while dieting is your goal, consider eating or supplementing with some carbs before or during really depleting workout. Although the jury is definitely still out regarding pure resistance training and carbohydrate supplementation, this study seems to suggest that some carbs around your training would have a beneficial effect on workouts that are similarly challenging to your anaerobic energy systems.
Obviously the rest periods (20 minutes) make this a difficult study to generalize to traditional circuit training in general, but this at least seems to suggest that, as long as cellular energy status is maintained, HIIT may actually be anabolic. Of course, consuming carbs before or during the session would sort of defeat the purpose if your goal is fat loss, but at the very least, the type of training described in this articles is definitely NOT catabolic to muscle tissue, even when done in a fasted state with no food consumption for over 2 hours post-workout.
Interestingly, the authors of the study propose that one reason that the women may have had a larger spike in insulin is that men tend to have higher catecholamine output (epinephrine and norepinephrine) in response to sprint training, and catecholamines have been shown to blunt insulin secretion. Maybe that should call into question the SUPER JACKED HARDCORE preworkout you take, considering the correlation the authors found between rise in insulin and phosphorylation of p70S6k (and thus, hypertrophy) 😉
2. The differences in gender response here may help explain why CrossFit women are so freaking jacked. The physiological responses these women had to SEVERELY depleting training – elevated glucose, elevated insulin, blunted elevations in lactate, smaller decrease in insulin – might suggest that they’re more metabolically suited to this type of training than the average male. At the very least, we have mechanisms to explain a previously-observed hypertrophy response.
3. Hypertrophy is not just a man’s game. This study sheds some light on the fact that there’s a gendered response to various hypertrophy stimuli. I think it’s pretty well accepted that high muscular tension tends to cause more hypertrophy in men than in women. However, stressing the energetic capacity of the muscle cells invokes a larger response in women. What’s more, as was previously established, the primary response is in the most powerful fibers – type IIB!
Thanks for wading through this one with me. Not as clear-cut and straight-forward as my belt vs. beltless article, but I think this one gave us the opportunity to touch on a lot of interesting topics.
Share it around with your friends who like science, your female friends who want to get jacked, and people you’ve heard pondering why the average CrossFit girl can destroy the average gym bro.