Bodybuilders, power lifters and other strength athletes may be able to build up more muscle if they eat a portion of cabbage-related vegetables every day. Brassicas such as cauliflower, broccoli and sprouts all contain the compound sulforaphane. Molecular scientists at the University of Bonn have discovered that this deactivates the muscle growth inhibitor myostatin in satellite cells – and therefore may also have an anabolic effect. The results of their study have been published in Epigenetics.
Sulforaphane & muscles
It’s nothing new that sulforaphane is of interest to strength athletes. The popular scientific website Ergo-Log – modest ahem – speculated a year ago already about this after Italian researchers had discovered that sulforaphane improved the survival chances of one type of stem cell that is capable of developing into muscle cells.
The Italian findings were unexpected. Nutritionists have had their eye on sulforaphane for a while, but had been concentrating on a different health effect: on its ability to boost detoxification and possible anti-carcinogenic effect.
Well, the researchers in Bonn did experiments on satellite cells taken from the muscles of pigs. Pigs’ cells bear a remarkable resemblance to human cells. Satellite cells are found in muscle tissue and develop into adult muscle cells when given the right stimuli.
The researchers exposed the pig satellite cells to sulforaphane [SFN] in test tubes, using concentrations of 5, 10 and 15 micromoles, and observed that the lowest dose [SFN 5] increased the vitality of the cells and reduced the synthesis of suicide proteins such as caspase-3 and -9. This is interesting, because in cancer cells sulforaphane has completely the opposite effect: sulforaphane actually reduces vitality in cancer cells and activates the suicide mechanism.
Sulforaphane dramatically reduced the production of myostatin [MSTN] in the satellite cells, as shown above. The researchers are not sure why this was the case. They did check whether sulforaphane boosted the synthesis of follistatin [FST], a protein that can deactivate myostatin, but this was not the case.
The researchers have high expectations of the muscle strengthening effect of sulforaphane. “If its effects are verified and applied to in vivo models, sulforaphane may have therapeutic benefits in the treatment of human skeletal muscle disorders and practical value in meat production”, they write.
The best natural sources of sulforaphane are fresh broccoli and Brussels sprouts. Tinned cabbage and prepared cabbage in plastic packaging do not contain much sulforaphane. Bodybuilders who want to start experimenting with sulforaphane right away can of course use natural supplements.
Strictly speaking cabbage-type vegetables don’t contain sulforaphane, but do contain glucoraphanin [structural formula shown below]. Cutting up, chewing and digesting cabbage-type vegetables converts glucoraphanin into sulforaphane [structural formula on right below].
Sulforaphane causes a major epigenetic repression of myostatin in porcine satellite cells.
Satellite cells function as skeletal muscle stem cells to support postnatal muscle growth and regeneration following injury or disease. There is great promise for the improvement of muscle performance in livestock and for the therapy of muscle pathologies in humans by the targeting of myostatin (MSTN) in this cell population. Human diet contains many histone deacetylase (HDAC) inhibitors, such as the bioactive component sulforaphane (SFN), whose epigenetic effects on MSTN gene in satellite cells are unknown. Therefore, we aimed to investigate the epigenetic influences of SFN on the MSTN gene in satellite cells. The present work provides the first evidence, which is distinct from the effects of trichostatin A (TSA), that SFN supplementation in vitro not only acts as a HDAC inhibitor but also as a DNA methyltransferase (DNMT) inhibitor in porcine satellite cells. Compared with TSA and 5-aza-2′-deoxycytidine (5-aza-dC), 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. Nevertheless, a weakly enriched myoblast determination (MyoD) protein associated with diminished histone acetylation in the MyoD binding site located in the MSTN promoter region may contribute to the transcriptional repression of MSTN by SFN. These findings reveal a new mode of epigenetic repression of MSTN by the bioactive compound SFN. This novel pharmacological, biological activity of SFN in satellite cells may thus allow for the development of novel approaches to weaken the MSTN signaling pathway, both for therapies of human skeletal muscle disorders and for livestock production improvement.
PMID: 23092945 [PubMed – indexed for MEDLINE] PMCID: PMC3528693