Ask the Expert: Interview with Brad Schoenfeld Ph.D.

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If you have been keeping up with the evidence-based side of the fitness industry at all for the past couple of years, I’m sure you know who Brad Schoenfeld is.

If not, I don’t think it’s an overstatement to say he is THE go-to guy for the science of hypertrophy right now.  Certainly one of the preeminent people in the field.

He’s written for just about every major publication in the industry, so it’s an amazing honor for him to do an interview for Strength & Science.

He’s the Director of the Human Performance Lab at CUNY Lehman College in NYC, the Assistant Editor-in-Chief of the NSCA Strength and Conditioning Journal, on the Editorial Advisory Board for the Journal of the International Society of Sports Nutrition, and the President of Global Fitness Services.  You can check out his website here, and if you’re interested in gaining some size, I’d highly recommend his new book.  It’s an excellent introduction to the science of hypertrophy that’s accessible on every level, regardless of how much background knowledge you have in the subject.

Personally, the thing I respect the most about Brad is that he’s made it in the industry as a scientist, not a salesman.  He’ll be the first person to admit the limitations of his research and interpret results conservatively and skeptically, rather than exaggerating findings and sweeping details under the rug in order to sell products.

Before and after pictures of Ronnie Coleman. On the left was before he found out about Dr. Schoenfeld. On the right is after. …I think

So, without further ado, let’s jump in!

Sarcoplasmic vs. Myofibrillar hypertrophy has been a hot debate in the strength training community for as long as I can remember.  You’ve done some research on this topic, if I’m not mistaken.  Is sarcoplasmic hypertrophy a real thing, how much does it contribute to total hypertrophy, and does increased muscle hydration have any meaningful effect on myofibrillar hypertrophy?

“This topic has been very much overblown, IMO.

First things first: Yes, there is evidence that training does impact sarcoplasmic hypertrophy. There is no question that non-contractile elements such as collagen, mitochondria, and glycogen will increase pursuant to resistance training. Moreover, since each gram of glycogen attracts ~3 grams of water, there also will be an increase in fluid in the muscle.

I recently collaborated on a study showing that 16 weeks of bodybuilding-type training (i.e. multiple sets of multiple exercises working in a moderate rep range with fairly short rest intervals) resulted in significant increases in intracellular water content.

Whether this actually impacts myofibrillar hypertrophy is the million dollar question. There is compelling in vitro (i.e. in a test tube) evidence that increasing cellular hydration has the dual effect of increasing protein synthesis while decreasing protein breakdown. Whether this translates in vivo (translation: during actual exercising conditions) cannot be determined at this point. The logical basis is there, but sometimes logic doesn’t translate into practice.

It also is not clear the extent to which one type of training influences these effects more than another. I will be collaborating on a study that looks at the topic in bodybuilding- vs. powerlifting-type training that is slated to begin in the next few months so stay tuned.”

Type 1 muscle fibers have been neglected in the common consciousness of strength athletes for a long time.  But, as I understand it, you think they contribute to total muscle hypertrophy in a significant way.  What sort of evidence supports that idea, and how would you go about hypertrophy-ing a type 1 fiber?

“There is no question that type I fibers contribute to total muscle volume. People tend to discount the hypertrophic importance of type I fibers based on research showing that type II fibers have about 50% greater potential for growth.

However, this may be a function of the training studies that have investigated the topic to date. Specifically, almost all studies that have looked at fiber-type differences in CSA have employed intensities greater than ~70% 1RM. Recent work from my lab suggests that low-load training might preferentially stimulate the type I’s and thus be able to promote even greater growth in these fibers, although I do not have biopsy data to provide conclusive evidence.

The topic needs further study, but it does seem that including some high-rep sets (i.e. >20 reps or so) could be of benefit for maximizing muscle growth. I’m currently carrying out a longitudinal study as we speak that investigates muscular adaptations using 10 reps vs. 30 reps to failure in experienced lifters with all other variables controlled. This should provide further insight into the response of different loading ranges and their potential effects on different fiber types.”

You, Aragon, and Kreiger authored an epic meta-analysis casting doubt on the effectiveness of post-workout protein supplementation.  However, an issue in a lot of the studies you guys reviewed was that total protein intake was pretty low.  Do you know of any studies specifically examining peri-workout protein supplementation in guys getting 1.8g/kg or more?  And if not, what’s your gut reaction – is there really no benefit?

“There have been a number of studies that have investigated protein timing with higher levels of protein intake (>~1.8 g/kg). In particular, two of these studies were carried out in well-trained lifters. The first was by Cribb et al. (2006) who found that pre- and post-exercise supplementation significantly increased lean body mass and type II fiber type cross sectional area compared to protein consumed in the morning/evening.

The second, by Hoffman et al. (2009) used a similar design (i.e. immediate pre- and post vs. morning/evening) but saw no differences in body composition between groups.

My feeling is that provided protein intake is kept at or above levels needed for a non-negative protein balance (~1.8 g/kg/day) that there will be little if any hypertrophic differences from protein timing, particularly if protein is consumed throughout the day as is generally the case with most aspiring bodybuilders.

I have a study set to begin in the fall in collaboration with my colleague Alan Aragon that will address some of the methodological issues with the current body of literature and hopefully provide greater clarity on the topic.”

Exercise protocols showing a big spike in testosterone or growth hormone – how relevant are those results to the overall training effect you’ll get on those protocols?

“Short answer is not much, if at all. I actually wrote a review on the topic that was published in JSCR last year. There is some conflicting evidence on this topic, and I’m not yet prepared to completely discount that acute hormonal spikes might confer some hypertrophic benefits – perhaps specific to an impact on satellite cells – but I’m confident in saying that any effects, if they do indeed exist, would be quite small. Without question, a lifter shouldn’t design his workouts around trying to maximize elevations in testosterone or GH – that amounts to not seeing the forest from the trees IMO.”

You did a review about squatting.  What’s the best way to squat if I want to squat a house?  What about if I want to get huge legs or improve athletic performance?  Also squats and knee/back health – what’s the safest way to squat?

“To properly answer these questions would require a chapter in a book! There are simply too many variables to give cookie-cutter responses.”

(Note from Greg:  This is something I’ve been preaching for a while now, so I sort of hoped Brad would answer like this – though I hope the way I asked the question wasn’t too leading.  If someone’s claiming there’s only one way to squat, it’s a good indicator that they don’t know very much about biomechanics.)

NSAIDs – how much are they really going to affect my strength and size gains?

“This is a really interesting topic that is still not well understood.

The primary negative impact of NSAIDs appears to be a blunting of satellite cell activity. For those who don’t know, satellite cells are muscle stem cells that reside just outside the fiber membrane. Satellite cells remain largely quiescent until stimulated by mechanical tension or muscle damage. Once activated, satellite cells initiate immediate muscular repair and facilitate long-term growth by donating nuclei to existing fibers (and thus enhancing their ability to increase protein synthesis over time).

Interestingly, some studies show no negative impact on muscular adaptations and exercise performance from the use of NSAIDs and a recent study has actually shown a positive effect.

The confounding issue is that these longitudinal studies were carried out in elderly subjects. Two issues here: first, the simple fact of reducing pain in elderly subjects, who generally suffer from osteoarthritis and other musculoskeletal ailments, likely made it more feasible for them to train harder while taking NSAIDs. Second, it is highly probable that a majority of the elderly subjects suffered from chronic low-grade inflammation, which has been shown to impair muscle protein synthesis. Since NSAIDs reduce pain and inflammation, the ultimate benefits could potentially trump the negative effects on satellite cells in the elderly.

On the other hand, since young lifters – particularly those who are serious about training – would tend to discount the pain and not have issues with low chronic grade inflammation, the use of NSAIDs may very well be detrimental to long-term hypertrophy.

Practical recommendations are somewhat tricky. Taking an occasional NSAID for pain/discomfort isn’t going to have any significant negative effects and perhaps could help over the short-term. Long-term is another story. For the young hard-training lifter, I’d suggest avoiding consistent use of NSAIDs as it well may hinder gains. For the elderly it is a complex issue that becomes more of a medical concern. I would certainly suggest that anyone who takes NSAIDs on a consistent basis do so under regular medical supervision as there are other health issues that may arise from their persistent use.”

Your recent article comparing strength and hypertrophy responses to powerlifting-style and bodybuilding-style training generated quite a bit of buzz.  So is that the final word – more sets of fewer reps is better, period?  Or are there some caveats here?

There are a number of caveats here. On the surface the study showed similar gains in muscle from a volume-equated powerlifting-style routine versus a bodybuilding-style routine. However, it must be noted that it took the powerlifting group trained approximately 70 minutes to complete their sets while the bodybuilding group finished on average in 17 minutes.

Simply from an efficiency standpoint that’s a huge difference. Moreover, the powerlifting group was basically toast by the time the study was finished; all subjects in that group complained of general fatigue and sore joints. Two subjects had to drop out from injury.

The bodybuilding group on the other hand had no such issues and expressed they could have handled a lot more volume.

Bottom line: the study provides insight that the potential mechanisms from hypertrophy might be redundant between the two types of protocols provided an equal volume of training. But the bodybuilding type routine provides a more feasible way to accomplish maximizing hypertrophic gains by allowing for a greater volume of training without bodily resources being overtaxed.”

The million dollar question – what actually causes hypertrophy?  Of the contributing factors, which seem to be the most important ones, and how would you go about eliciting those responses?

“In a previous review, I described the three primary mechanisms of hypertrophy as mechanical tension, metabolic stress, and muscle damage.

Evidence indicates that mechanical tension is the driving stimulus, and that the other factors provide an additive response (this is somewhat simplistic as there is evidence of at least attenuating catabolism simply by employing an ischemic/hypoxic stimulus that induces metabolic stress).

The practical applications are somewhat murky given that it is difficult to tease out whether a threshold exists for mechanical tension above which the other factors are synergistic or redundant (my recent study suggests they may in fact be redundant).

That said, here are some basics. It certainly seems important to train throughout the spectrum of rep ranges as this will ensure all of the mechanisms are covered. It also is important to utilize both concentric and eccentric actions, and perhaps employ techniques that enhance the responses to such actions (i.e. heavy negatives). Optimizing the effects of variables in program design is not a cookie-cutter process, however, and it is clear that inter-individual differences can and should dictate be taken into account to customize the approach.

Studies by Marcus Bamman’s lab at the University of Alabama (Bamman et al. 2007; Petrella et al. 2008; Thalacker-Mercer et al. 2013) show clear evidence that there are “responders” and “non-responders” to resistance exercise and that these responses are dictated by the ability to express various genes. It gives credence to the principle of individual differences and indicates that substantial fine-tuning must be done to derive best results on an individual basis.”

I see you posting on facebook about new studies you’re conducting all the time.  Can you give us a sneak peak at some of the research we can expect from you in the next year or two?

“There are so many. In addition to the ones mentioned earlier, I currently have a number of studies in review including two meta-analyses (one on muscle strength and hypertrophy high- vs. low-load lifting, the other on the effects of meal frequency on body composition), a couple of EMG studies (one on muscle activation in low- vs. high-load training, the other on hamstrings activation in SLDs vs. leg curls), and a training frequency study in pro bodybuilders. Moreover, I’m currently finishing up a study on muscular adaptations in low- vs. high-load training in well-trained lifters (the first study to investigate this topic in experienced trainees) and another on the effects of fasted cardio on body composition. Over the next few months I’ll be starting research on a study comparing split- vs total-body training routines and another looking at protein timing – both studies in well-trained men. Suffice to say, I should have a lot of info to share over the coming months.”

More studies on trained subjects!  Brad, your research is a godsend to people like me who care about getting big and strong, but who want to understand the scientific underpinnings of training to make our training more efficient and effective.  Thanks so much for taking the time, and I’ll definitely be watching out for many more high-quality studies from you in the future.

If you’re like to check out more of Brad’s research, you can do so here.

References

  1. Bamman MM, Petrella JK, Kim JS, Mayhew DL, Cross JM. Cluster analysis tests the importance of myogenic gene expression during myofiber hypertrophy in humans. J Appl Physiol (1985). 2007 Jun;102(6):2232-9.
  2. Cribb PJ, Hayes A. Effects of supplement timing and resistance exercise on skeletal muscle hypertrophy. Med Sci Sports Exerc. 2006 Nov;38(11):1918-25.
  3. Hoffman JR, Ratamess NA, Tranchina CP, Rashti SL, Kang J, Faigenbaum AD. Effect of protein-supplement timing on strength, power, and body-composition changes in resistance-trained men. Int J Sport Nutr Exerc Metab. 2009 Apr;19(2):172-85.
  4. Petrella JK, Kim JS, Mayhew DL, Cross JM, Bamman MM. Potent myofiber hypertrophy during resistance training in humans is associated with satellite cell-mediated myonuclear addition: a cluster analysis. J Appl Physiol (1985). 2008 Jun;104(6):1736-42
  5. Thalacker-Mercer A, Stec M, Cui X, Cross J, Windham S, Bamman M. Cluster analysis reveals differential transcript profiles associated with resistance training-induced human skeletal muscle hypertrophy. Physiol Genomics. 2013 Jun 17;45(12):499-507
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