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I’ve made it no secret that I think we’ve put the cart way too far in front of the horse when it comes to training for sarcoplasmic hypertrophy. What started out as a theory to explain increased muscle hypertrophy in the absence of strength gains in some early training texts (1,2) has morphed into complete training programs to target specific sub-cellular fractions (myofibrillar vs sarcoplasmic). In my previous posts, I’ve looked at some literature to explain how changes in metabolites alone (glycogen specifically) can’t explain hypertrophy, that bodybuilders aren’t that weak after all, how the approach to a rep can explain strength differences between bodybuilders and powerlifters and that even IF sarcoplasmic hypertrophy occurs we can’t call it non-functional.
After revisiting two recent papers (3,4) on the effects of load (%RM) on protein synthesis and hypertrophy in a discussion on Bret Contreras’s site, I had a light bulb moment about how these papers could relate to the idea of sarcoplasmic hypertrophy as well. You can find what I’ve previously written about these papers in my article entitled ‘30%‘ but it’s worth taking a specific look at the protein synthetic response of the myofibrillar and sarcoplasmic fractions following a single training session in Burd et al (3) with this idea in mind.
Does low load training have a preferential sarcoplasmic protein synthetic response?
If lower-load training preferentially targets the sarcoplasmic fraction, we would expect one of two effects when looking at the acute response to exercise: 1) a disproportionate sarcoplasmic response following lower-load relative to higher intensity training (either increased peak or sustained response) and that 2) the increase in sarcoplasmic protein synthesis may be greater than the myofibrillar fraction. Fortunately, Burd et al (3) took a look at both these fractions in groups of males who trained at either 90%-1RM to failure, 30%-1RM to failure or 30%-1RM work-matched to the 90%-1RM to failure condition. Lucky for us the paper has free full-text access online, so head over there to read the original, although for this discussion you can simply focus on figure one in the paper.
Looking at the acute protein synthetic response, we can see that training with 90%-1RM to failure resulted in a substantial increase in both myofibrillar and sarcoplasmic protein synthesis at four hours post-exericse (3.3 and 1.7 fold rest respectively). By 24 hours, protein synthesis was no longer elevated compared to rest with this training load. When looking at the group that trained with 30%-1RM to failure, there was increased myofibrillar protein synthesis at four hours (3.6x rest) only the response was sustained such that increased synthesis was detected at 24 hours post-exericse as well (2.9x rest). Conversely, while the 90%-1RM had increased sarcoplasmic synthesis at 4 hours, the increase in the 30%-1RM to failure group occurred at 4 and 24 hours post-exericse (1.4 and 1.5 fold rest respectively).
This sustained sarcoplasmic protein synthetic response in the low-load condition may seem supportive of the theory of sarcoplasmic hypertrophy, but given that myofibrillar protein synthesis was also sustained I still think that disproportionate sarcoplasmic growth is unlikely. We’ve met our first criteria from above and found that lower load training supported a longer synthetic response in the sarcoplasmic fraction, but fail to meet condition #2 as the myofibrillar fraction was also sustained. In fact, the authors of the paper make the case that this low-load training could be superior for overall hypertrophy training, and this is what ignited the hypertrophy blogosphere in a unified rage. It should be noted that the subsequent paper (4) failed to find increased hypertrophy as compared to high-load training despite the sustained synthetic response in the 30%-1RM group, so don’t throw out your heavy dumbbells just yet.
This isn’t the final nail in the coffin
This certainly isn’t the final nail in the coffin for the low-load training, sarcoplasmic hypertrophy theory. There’s no question that we can argue many more potential factors that could contribute to it, however the existing scientific literature just can’t support it right now. Can it contribute to overall muscle hypertrophy and occur following strength training? Sure it can! Can we say that it occurs preferentially or that we can target it with specific training programs? Absolutely not.
To date, I’ve still only found one paper (5) with a disproportionate sarcoplasmic response to training and it suggests that it was a consequence of strength training in general and not specific to bodybuilders or high-repetition training. If you’ve found some other resources, be sure to send them on to me because I LOVE reading and discussing anything hypertrophy-related. But at the very least this research still doesn’t support the idea that we can create strength training programs to engineer specific adaptations in these particular sub-cellular compartments (myofibrillar vs sarcoplasmic proteins).
All in all, sarcoplasmic hypertrophy remains a nice theory that needs more evidence in my mind, but I’m still not convinced that there are all these disproportionately weak bodybuilders waddling around with myofibril-deficient muscle. Are you?
How about Kaatsu-training ?
Unfortunately no studies come to my mind on occlusion training that look specifically at sarcoplasmic fractions specifically, but I need to take a look through the literature again on this as it has been awhile. I've been thinking about putting an article together on this, thanks for reminding me!
Really enjoyed reading this article Dan keep them coming buddy!
Thanks Andrew, glad you liked it, and don't worry there will be more!
I think the distinct difference in the two training modalities (Heavy loads- low repetitions / higher repetitions 90% and above ) recruit more total muscle fibres and significantly larger proportions of the Type II fibres which have greater capacity for strength and size increases in the myofibrils themselves. When you recruit the high threshold fibres , you have recruited all the smaller / medium size fibres also so myofibril activation is significant. However, once the rep range is increased and lighter loads are lifted the size principle tells us that we are recruiting less neurons and not engaging as many of the high threshold muscle fibres, so we have smaller muscle fibres doing more work ( Unless of course each repetition is being completed with maximum force,however many bodybuilders utilise slower repetition tempos which further recruit less fibres .Of course there is still muscle fibre strength and size gains, however the biggest fibres are being left out of the action and therefore creating a completely differently look to the muscles,lacking in density with increased oedema, trauma and glycogen storage which all contribute to temporary size gains, hence the superman type of feeling you have the day proceeding a high volume workout where you feel bigger. You are bigger thanks to significant cell oedema brought on by muscle exhaustion.However a day or two off and you start to feel small again, because you are, the swelling is going down and so too is your size. Sarcoplasmic hypertrophy which does occur creates a swollen soft , puffy and less defined looking musculature and definitely significantly less gains in near maximal strength. So for performance , power, max strength , speed and agility , fat burning and conditioning it makes more sense to lift heavy weights as fast as you can(heavy loads will only move so fast anyway, but it is the intention to move a weight as fast as possible which creates more force and recruits maximum fibres. If maximum hypertrophy is your goal, then of course sarcoplasmic hypertrophy will add to the muscle gains you are making by contributing a bulky, puffy looking muscle. Of course you cannot have one without the other, they are intertwined and support one another, however low rep heavy training will lead to less sytemic fatigue, less oedema and fatigue, which = training more often which = increased frequency of stimulus which =, to me atleast, increased potential for improved performance. I think that if higher rep ranges are to be utilised you can have the best of both world's by utilising fast contractions which increase force which recruit more fibres, that coupled with the higher rep range which leads to further increases in cell volume and therefore linear gains hypertrophy and strength.
KEEP THE AWESOME ARTICLES COMING DAN.
Hi Simon,
Glad you enjoyed the article and you may enjoy my previous posts on the site about sarcoplasmic hypertrophy. You'll see that while I think sarcoplasmic hypertrophy is an interesting theory we don't have the evidence to assume subcellular adaptations based on training parameters.
Also regarding recruitment differences between loading conditions, sure the size principle may dictate recruitment order, but the amount of muscle recruited is not just a passive process dictated by the load on the bar. We know that even untrained people can recruit a large proportion of the muscle for many large muscle groups voluntarily, likely including high threshold motor units, and speaks to what you mentioned regarding effort (attempting to contract as hard and fast as possible irrespective of load).
Motor unit recruitment is also influenced by fatigue such that while the load may be initially insufficient to maximize activation, as fatigue sets in higher-threshold motor units will be progressively recruited. This is why the relationship between load and time-under-tension is more important than either variable alone in my opinion.
My hypertrophy programs emphasize multiple intensity ranges, although while I acknowledge the super low-load hypertrophy research (30%-1RM), I have to admit that I'm biased towards the heavy end of the spectrum. If anything, I find I use these 30% papers opposite to everyone else, to encourage people to go heavier in their hypertrophy training than the often recommended 60-75%-1RM range.
I just stumbled upon this article and i love it.
im also a sucker for hypertrophy related articles, but
i just can't seem to find enough of them on the net that
arent' trying to sell readers something (except ones like this).
quick question though, my Traps have not been growing
no matter what i tried (high reps, low reps, heavy weight etc)
even though i shrug (DB,BB), deadlift, and row consistently.
how can i use those scientific findings to increase hypertorphy in my trapezius? i want super high upper trapezius.
Great article,
just recently I also wrote an article based on the Burd et al. papers (http://scifit.com.au/2013/10/24/never-lift-heavy-weights-againalmost/). The focus was generalised to muscle growth and volume as a whole though – rather than a discussion on sarcoplasmic hypertrophy.
Check it out if you have some time.