Myostatin Lowered By Cardio, Follistatin

Myostatin is a protein that inhibits muscle cell growth. Animals lacking myostatin, or where myostatin activity is blocked, have significantly more muscle mass, also known as being ‘double muscled’. While this isn’t actually a doubling of muscle, mutations in cattle breeds where the myostatin gene is damaged have an increase in muscle of no more than 40%.

Animals treated with follistatin, which blocks the binding of myostatin to receptors, have significantly larger muscles, with even a 20% reduction in myostatin have an impact on the development of muscle. Reducing myostatin levels, or at least knowing when myostatin increases to its highest point is where our interest is most, unless we somehow remove the myostatin gene from our bodies.

Lowering myostatin can be achieved, funnily enough, by that catabolic activity that many hate so much – cardio. Myostatin declined by 37% in subjects after aerobic exercise. The study this was found in is actually really interesting as far as studies go. The results are visually represented on this nice graph. And even better, ‘improvements in insulin sensitivity and aerobic endurance in mice after short-term Mstn inhibition were as effective as four weeks of aerobic exercise training’.

So if your cardiac health and not dying of a heart attack or stroke at 35 is not enough reason to do your cardio on-cycle, here’s another great reason to do it.

Here’s the data that we’ve all been waiting for though: myostatin levels were significantly higher on day 56 compared to baseline in both young and older men. But the increases in myostatin were not sustained, and at day 140 they were back at baseline once more. If I squint and read the bar graph right, day 0 for young men has myostatin at around 7.8ng/ml, spiking to ~10ng/ml at day 56, and then falling back to baseline by day 140. Subjects received Test E at either 25, 50, 125, 300, or 600 mg doses over 20 weeks, though the Data and Safety Monitoring Board stopped the 600 mg TE dose group in December 2002 due to them being massive killjoys.

This data shows that myostatin levels are increased in response to the increase in skeletal muscle mass. It also shows that it’s only temporary, but for our purposes nobody here should be running a cycle 140 days long where it returned to baseline. Baseline mean for young men was 7.8ng/ml whereas the oldies were at 6.8ng/ml. and if you want to read the study referenced it is available here: https://imgur.com/a/5DMeJuZ

The biggest weakness of the study is that the data published is not raw – it does not include the myostatin changes by week or by dosage. So I can’t tell you that 300mg of test e resulted in a 30% increase in myostatin levels, compared to a 100mg dose which resulted in a 5% increase. For data on just how much myostatin increases over a PED cycle I’m still clueless.

Moving away from the study, myostatin inhibition does not directly increase strength, just size of the muscle. That’s in mice, and it’s not to say it won’t make humans stronger, since those lucky few with myostatin-related muscle hypertrophy are also significantly stronger than average, but just that size and strength and not going to be linearly related. Another way to say this is your muscle growth won’t necessarily translate into the same level of 1RM gained as you might ordinarily expect.

So what can we do with this information? Firstly, if you choose to run 12 week cycles, know you have the rise in myostatin working against you, and set your expectations accordingly in weeks 8 and 12, or just choose to run 8 week cycles. Second, you can opt for a compound to increase follistatin, such as YK11. Third, do your cardio, or get to work in the lab figuring out a way of removing the myostatin gene altogether.