Sulforaphane from Cruciferous Vegetables Inhibits Myostatin and Increases Cell Viability in Skeletal Muscle Satellite Cells

Chicken Egg Rolls with Red Cabbage, Mango & Lime (CleanEatingMag); small inset shows sulforaphane content (µg/ml) of a juice made cauliflower, broccoli, red and white cabbage and brussel sprouts (based on Totušek. 2011).

When I am looking at the currently top-rated posts (see box "Most Popular (last 30 days)" on in the right navigation bar), it appears as if someone must have found my older article on the myostatin boosting effects of clenbuterol and told all his facebook friends about it.
In case this hypothesis is right, he (or she?) and all the friends will probably be happy to hear that there is a virtually side-effect free over-the-counter alternative that can suppress myostatin and thus make your muscles grow faster: Broccoli, cauliflower, cabbage and co (see image on the right and realize Red Cabbare, not broccoli is the King!) - the sulforaphane in these cruciferous vegetables appears to make that possible.

Muscle building veggies... yamyol!

Back in the day Popeye was invented to convince children that it would be worth eating their spinach (unfortunately this advise was based on the false assumption that it was a good source of iron and would thus help build the kids' stamina). I guess when the inventors of Popeye get wind of the soon to be published paper we are going to look at, today, we are soon going to see a digital avatar of Mr. O. munching broccoli in a 3D animated cartoon.

Whether the digital broccoli munching Mr. O Popey will be able to bring more scientifically sound arguments to the table than his predecessor, popeye does however still have to be determined. After all, the scientists from the Animal Breeding and Husbandry Group at the University of Bonn in Germany did not study the real-world effects of sulforaphane (SFN), but only the in vitro effects the exposition of porcine satellite cells to, of which every SuppVersity reader knows that they function as skeletal muscle stem cells and support muscle growth and regeneration following injury or disease, when they found that...

"[...] SFN treatment significantly represses MSTN expression, accompanied by strongly attenuated expression of negative feedback inhibitors of the MSTN signaling pathway. miRNAs targeting MSTN are not implicated in posttranscriptional regulation of MSTN." (Fan. 2012)

If you take a closer look at the data in figure you may notice that this increase in myostatin went hand in hand with a decrease in MyoD expression. With MyoD being a protein that is involved in the very first step of satellite cell recruitment (it stops the proliferation of stems cells and initiates their transformation to muscle cells) this may seem awkward at first.

In view of the MyoD promoting effects of trichostatin A,which basically stops cell development in its tracks it can however be explained by the fact that less new satellite cells are needed, because their survival is increased so that the proliferation rate does not actually suffer (figure 1, left).

Figure 1: Cell viability, proliferation, MyoD, Myostatin and (total) Follistatin mRNA expression in porcine stem cells (satellite cells) from semimembranosus muscles from 6 purebred Pietrain piglets after exposure to DMSO (control),  trichostatin A or different concentrations of sulforaphane (SFN; data based on Fan. 2012)

This explanation does not only stand in line with the previously reported increase in MyoD expression in aging muscle (in this case unfortunately in the absence of increased cell viability; Alway. 2012), but is also supported by the concomitant downregulation of the pro-apoptotic (=initiating cell death) caspase enzymes (not shown in figure 1) in the SFN treated satellite cells.

In conjunction with the decrease in myostatin, which is, as I am sure you all know the 'myocyte hypertrophy break' of your body, the data from this in vitro study clearly suggests that SFN treatment could well have a growth promoting effect on skeletal muscle, which is -- and this may be one of the most important messages here -- more prononce at lower concentration used in the study.

Figure 2: Appearance of SFN in serum (triangles) and its metabolite in the urin of one of 10 healthy, normal-weight adult (34 +/-13 y) male volunteers after the ingestion of 200g of raw (top) or cooked (bottom) as part of a warm meal (Vermeulen. 2008)

Bottom line: After you have read about the potent anti-adiposity effect of antibiotics which are used in poultry fattening, yesterday, and today's news about the myostatin inhibiting effects of cruciferous vegetables, or more precisely, their sulforphane content, the infamous 'chicken breast, broccoli and rice diet' does actually begin to shine in new splandor! I mean, if only 50% of the aforementioned in vitro effects could actually be achieved by eating like this day in and day out, these recent findings could well explain, why generations of bodybuilders thrived on these spartan foods. And in case you wondered why the guys get freakier year by year - that's simply the availability of broccoli extracts and the increased use of antibiotics in poultry fattening... ;-)

I am obviously just kidding. If we go by the bioavailability data of raw (figure 2, top) and cooked (figure 2, bottom) broccoli, 200g of broccoli served as part of a warm meal will get your blood SFN levels up to only 2.5% or 1.2% of the most effective dose (5µM) used in the study. So, it's pretty certain that you'd have to gobble copious amounts of red cabbage juice (see picture on top of the article) to get there.

In view of the fact that lower concentrations yielded greater effects, it is however not totally unlikely that even concentrations as low as 1µM would yield results. With additional supplements, it does therefore not appear to be unrealistic to achieve blood levels like that (although you should not expect the increase to be linear).... anyway, I will let you know as soon as the first pertinent rodent or even human trials are available.


References:

• Alway SE, Degens H, Lowe DA, Krishnamurthy G. Increased myogenic repressor Id mRNA and protein levels in hindlimb muscles of aged rats. Am J Physiol Regul Integr Comp Physiol. 2002 Feb;282(2):R411-22.
• Fan H, Zhang R, Tesfaye D, Tholen E, Looft C, Hölker M, Schellander K, Cinar MU. Sulforaphane causes a major epigenetic repression of myostatin in porcine satellite cells. Epigenetics. 2012 Oct 23;7(12).
• Totušek J, Tříska J, Lefnerová D, et al. Contents of Sulforaphane and Total Isothiocyanates, Antimutagenic Activity, and Inhibition of Clastogenicity in Pulp Juices from Cruciferous Plants. Czech J. Food Sci. 2011; 29(5): 548–556.
• Vermeulen M, Klöpping-Ketelaars IW, van den Berg R, Vaes WH. Bioavailability and kinetics of sulforaphane in humans after consumption of cooked versus raw broccoli. J Agric Food Chem. 2008 Nov 26;56(22):10505-9.