Brad Schoenfeld, MSc, CSCS | Sun July 24, 2011
Great job on this Anoop. Excellent points about the shortcomings of McGill’s lecture. Selective science is pseudoscience…
July 24 2011
National Strength & Conditioning Association (NSCA) is the world’s leading authority in strength & conditioning. They hold an annual conference every year which attracts conditioning & fitness professionals from all over the world. The conference includes presentations from leading fitness & conditioning experts, and was held in Las Vegas from July 6 till July 9, 2011. Here is the part 1 of my little review.
Dr. Stuart Mcgill is a professor of spine biomechanics at the University of Waterloo , Canada. His advice is often sought by governments, corporations, legal experts and elite athletes and teams from around the world. Difficult back cases are regularly referred to him for consultation.
Dr. Mcgill presented two topics. I attended the first and many people thought this was one of the best presentations. In the first presentation, he talked a lot of training concepts (titled ‘Lessons learned from the greatest athletes’). He talked about training the speed of contraction and relaxation, spending more time with asymmetric carries, learning to enhance stiffness in the core, avoiding spine flexion movements and so forth. In short, Dr. Stuart Mcgill’s work is basically about increasing performance and preventing low back injuries and pain largely by focusing on the core.
I was a bit concerned about how he makes so many absolute statements without too much evidence. When it comes to performance, I just think we are just over -emphasizing the role of core. Why are we so worried about the core? Has it been shown that just like strength, endurance, vo2 max, vertical jump and other proven variables, core strength is a major determinant of performance? No. Has it been shown that improving core strength can improve performance? No. Is there a general test for reliably measuring the core strength? No. So when Dr. Mcgill says that the great athletes fire this particular core muscle more than the others(or in a particular way) and hence we should all train that way, I would say that’s just another correlation. I just didn’t see many studies from him to support his statements either.
If we really want to say that this particular observation is really important for performance and it is what makes great athletes great, we need to do an intervention study. Find athletes from different disciplines, put them through his intervention, and show how they increased their time or distance or speed or strength and so forth than the control group.
When it comes to low back pain, I think it is pretty clear that the psychosocial component is very important, and maybe even more important than the biomechanical aspect. I have never heard or read Dr. Mcgill mentioning the psychosocial factors involved in pain. Even American College of Physicians recommend not to scan people with non-specific low back pain because what you find on a scan has very little to do with the onset, severity, prognosis, or duration of low back pain. Considering the bulk of evidence against the biomechanical model of pain, I think it’s a bit perplexing (and bothering) that he doesn’t even bother alluding to it and keeps ignoring it. Dr. Mcgill’s studies are a good example of studies which measure surrogate measures like EMG, spine models, compressive/shear stress instead of looking at meaningful outcomes to people like pain, performance or strength. There is nothing wrong with these studies, but you have to be careful about extrapolating your conclusions because you might be very well wrong. If you are not sure what I mean by surrogate measures, check my recent post on it.
I couldn’t attend his second presentation, but he seems to have changed his topic of his presentation because the presenter before him talked about how we don’t have much evidence about what causes low back pain or how to treat it. Unfortunately, it is true, and Dr. Mcgill disagreed to the extent that he felt he should change his presentation. If he had enough studies to show against, he wouldn’t have to talk so loud and so often and talk about so many anecdotal evidences, I thought.
Dr. Kerksick is an Assistant Professor of Exercise Physiology and Director of the Applied Biochemistry and Molecular Physiology Lab at the University of Oklahoma. Chad talked about Intensity vs volume in muscle growth. Chad spoke like a true researcher - he had data for everything he said and was very careful and hesitant about jumping into conclusions unlilike others.
He introduced his lecture by quoting the size principle and how the Type 2 fibers, which has the greatest potential for muscle growth, gets recruited at the end of a set. Then he talked about the infamous Dr. Phillips study which showed how low load, high volume protocol (30RM) showed greater protein synthesis compared to a high load, low volume (90% RM) protocol. He also showed another study by Wilborn et al., ( 2009) which showed molecular markers and proteins for muscle growth all increased significantly for both 18-20 reps and 8-10 reps. Both these studies lend some credence to the fact that high reps may be valuable for increasing muscle growth.
But, mind you, both these studies are acute studies in beginners and measure surrogate measures not muscle growth. Chad also mentions this and how we have to be careful since this an acute design. I asked him about how this could be muscle-specific since both the studies were done on leg musculature and we have heard plenty of stories about 20 rep squats and how people grow better with high reps for legs.
The second half of the presentation was by Dr. Coil Wilborn about training to failure which I will cover in the next part.
It is very important to draw lines between what we know, what we do not know and what we need to know. Unlike what most people think, things aren’t as black and white and are mostly shades of grey. Anyway, that’s all I have for the first part.
Brad Schoenfeld, MSc, CSCS | Sun July 24, 2011
Great job on this Anoop. Excellent points about the shortcomings of McGill’s lecture. Selective science is pseudoscience…
Anoop | Sun July 24, 2011
Thanks Brad for the comment! And thanks for introducing me to people at the conference.
I am waiting for your article on spinal flexion to get published.
Love your comments about “being over the core”. I agree 100%!
Anoop, what was a conclusion of Chad Kerksick on subject (Intensity vs volume)?
Yeah, it’s good to see some criticism of Stuart Mcgill. He’s often held up as the ultimate guru of the back. But I think this “guru” has no clothes.
Anoop | Mon July 25, 2011
Thanks for the comments. Jon Cissik had an excellent presentation questioning the concept of “core strengthening”. I will write about in the next part.
From the acute studies, I don’t think we can conclude much. And I don’t think he had a slide with conclusions. He was a bit cautious since it kind of goes against some of the studies and what we believe.
Thanks Bill! He is rightly the ultimate guru on low back. But what we care about is pain and performance, not what an EMG says or what some observational data shows about our low back. And that is the problem with is data and his studies. His studies lack some meaningful outcomes.
I think McGill is mostly focused on the mechanical aspects of the low back. I’ve read his book “low back disorders” and it was very educational. It will teach you how injuries can mess up the muscles in the lower back and how he thinks you can fix it. I have no doubt that his methods work for correcting the mechanical faults that can occur after a back injury (for example, if the space between two vertebra is shortened, the muscles will have to adjust to this). However, the mechanical aspects are not always well correlated with pain, but I think they can be important nonetheless, specially if you want to avoid further injury.
I learned a lot about the anatomy and biomechanics of the lower back from reading his book. Specially with regards to injury mechanics.
Also, it is not like he ignores the psychological aspects of back pain. If you read his book he has written about it, so it’s not like he is not aware
Without being an expert on the low back, I would think that most back injuries result from some kind of mechanical fault, like an injured muscle, ligament, disc, or what ever.. and that the resulting pain often comes from this as well, which would mean that fixing this physical injury would be important, not only to regain function, but to become pain free as well. However, often the pain will persist when the mechanical issues are healed. McGill doesn’t focus. If you want to heal your back you obviously need both and I think Mcgill does an excellent job in dealing with the mechanical and anatomical side of things, but his expertise does not lie in the neurological/psychological pathology behind pain that goes on when the reason for the pain has subsided.
Anoop | Tue July 26, 2011
Thanks for the comment. As always, good questions.
I don’t think I ever said his stuff on the biomechanics is not excellent or there is no role for the biomechanical model in pain. There is a good reason why it is called the biopsychosocial model of pain. What is clear is that the biomechanical part is becoming less and less relevant though. And I have read both his books. He mentions the psychological aspects, but very clearly says that it is “often greatly exaggerated”.
And why are you so sure that ‘fixing’ the injury would be ‘important’ when the American College of Physicians guidelines for physicians recommend not to scan people with non-specific low back pain which constitutes about 80% of the low back pain? So do you think we should screen everyone just like we do for blood pressure and fix the ‘injuries’ since it has been shown that 30-6o% of asymptomatic (no pain) people have gross injuries on their back scans? And do you think every study for back pain should have an MRI scan as the outcome measure to see if the abnormality got fixed, even if the back pain has been resolved? Has Dr. Mcgill shown that with his methods the findings on a scan can be been reversed or normalized after the treatments? There are a lot of questions that has no answers from studying the biomechanical aspects of the spine. So when you talk about ‘back pain’ to a 100’s of trainers and conditioning experts, you have to make atlaeast a passing reference to the glaring limitations of his type of research on pain. His talk is totally justified if it was a spine biomechanics conference.
I don’t know if you have read my article on pain, Karky. Check it out please when you get a chance: http://bretcontreras.com/2011/03/a-revolution-in-the-understanding-of-pain-and-treatment-of-chronic-pain/
You don’t actually have to scan your low back with an MRI to do the exercises he recommends.
Why do they recommend not scanning people? Is it because they think they might find something that is worse than the pain would indicate, and then make the patient worse in a psychological manner when telling them. Or is it simply because often you find nothing and they don’t want to waste money?
We shouldn’t routinely scan people with an MRI, no.
As far as I know, muscle weakness doesn’t really show up on an MRI (unless you count cross sectional area). Many of the mechanical injuries will stay for life or there is very little you can do about them. For example if you have a herniated disc, the disc will become smaller. Now the muscles in the back are used to the size of the disc before the accident and they could become loose and not be able to properly adjust the spine under load. This would need to be addressed and I think that for a muscle to get used to the new distance it would have to be used (eg, exercised). Unfortunately these things are very theoretical and hard to measure.
I still believe we should exercise after a back injury to overcome muscle weakness, whether it was a result of, or a cause of the injury. I still believe that stability exercises are better than flexing exercises. And that is basically what McGill is saying.
Obviously, often fixing muscle weaknesses or what ever the resulting faults of the back injury are does not fix the pain, but that doesn’t mean it isn’t important, because it can probably help the pain and I would think it can help avoid further injury.
Sometimes you can have big mechanical “faults” that aren’t really faults anymore because the body has adjusted to them, for example by readjusting muscle lengths, but I think this can be achieved by exercising, not laying in bed dozing off from pain killers.
Also, I would like to point out, that just because many people show injuries on their MRI but no pain, doesn’t mean that the injury can’t have consequences, like increasing the risk of future injury. This doesn’t mean I think we should scan everyone, I’m just saying, pain isn’t necessarily everything.
I’ve read your article on pain, and pain, both “normal” and pathological, have been covered in my education, so I know what it is. Truth is, we don’t really know that much about it.
The point of my previous post was that we shouldn’t not treat back injuries just because a lot of the time the pain is psychological. Maybe training your lower back won’t help your pain, maybe it will, it is worth a try.
Also, isn’t psychological pain mostly just a result from a mechanical pain? In that the body is oversensitive to stimuli or feels pain in the absence of stimuli. The mechanical/anatomical reason for the pain might be gone, but there have been changes in the CNS that makes the body still feel it or unable to adjust to the new mechanical situation (in the cases where the faults can’t be fixed)
McGill has his role, others have theirs, and I think he fills his role nicely. No single person fills the entire spectrum when it comes to something as complex as the low back. If a trainer only reads McGill, or any other single expert on the low back and thinks he is ready to treat low back pain, then someone should welcome that trainer to the real world. However, if McGill doesn’t really mention the psychological/or really neurological aspects of chronic pain, then he should.
It might also be worth distinguishing acute from chronic low back pain. Without having seen research, I would think that the latter is more susceptible to be pathological pain.
Also, something to think about. Since most people have actually experienced acute lower back pain, but many people who show injuries on an MRI are not experiencing low back pain. Couldn’t it be that they did experience acute pain when the injury happened, but they got over it, their body adjusted to it and luckily for them, the pain didn’t become psychological/pathological or what ever the correct term is.
Sorry this post got very long and messy.
Also, I haven’t really read anything on low back pain in quite a while. So I’m really just speculating here.
Anoop | Wed July 27, 2011
Lot of good questions and thoughts.
About scans: Check these articles: http://www.exercisebiology.com/index.php/site/articles/scans_for_low_back_pain_good_or_bad/
And I have a lot of good videos, podcasts and references in that pain article. You should check it out.
The more and more you stress the bio-mechanical factors in pain, the more you raise the threat level in the brain which will amplify and maintain pain. It is the implicit perception of threat to the tissues that causes pain and this implicit threat is influenced by many inputs including sensory input, belief, previous experience, expectations and such. Nociception is just one of them, and nociception is not required nor sufficient to output pain. . And this is based on the Neuromatrix theory proposed by Melzack. if anybody knows about pain, it is probably Melzack and Patrick Wall.
And Karky start a new thread in the forum if you want to discuss more about pain.
Just so that you know, Dr. Mcgill’ stance about avoiding flexion is a good example of his extreme stance without enough evidence. I know there will be an excellent article published soon in SCJ by Brad Schoenfeld questioning the validity of his statements.
Anoop | Thu July 28, 2011
Here the article which critically looks at Dr. Mcgill’s extreme stance about we should avoid spine flexion:
This is a good example of fear mongering by experts without sufficient evidence. There are number of examples where this type of fear mongering has happened in the past (albeit to a much larger extent) like whole power lines will give you tumor, DDT and breast cancer, radon and cancer and so forth.
I always find it funny to read how scientists and trainers focus on type 2 muscle fibers, because they have (or should have) the greatest growth potential. Meanwhile there are also some studies that show many bodybuilders have more type 1 than type 2 fibres. I don’t know how this is possible, but it seems to me that more is going on.
Also: I find the research surrounding the ‘size principle’ confusing. (not the principle itself) For instance, animal motor units seem to fire in another order as human motor units/muscle fibers. Some people are shown to be able to “conciously” contract more muscle fibres or even selectively (probably an overstatement) contract type 2 fibres. Also faster contractions would involved more fibres including more type 2 apparently.
Some people (read: Chad Waterbury and some others) even comment that if the ‘size principle’ is correct that would mean that one would get stronger during a set after the type 1 fibres are fatigued and the bigger/stronger type 2 fibres are recruited. (in some set and/or individuals off course) Instead, contraction speed and strength gradually become less and less during a set, which would mean less and less fibres are contracting. (I would say motor unit firing is not the same as actual muscle contraction and fatigue, but hé, would am I)
I don’t know if these comments and study results are correct or correctly presented, but they do confuse a lot of people, me included. (although personally I don’t care which muscle fibres I am recruiting and/or fatiguing as long as I am getting stronger and bigger)
What research is the ‘size principle’ really based on? How solid is this principle really?
Oh, and good comments on Mcgill’s statements.
The size principle is pretty sound. And you can’t really selectively recruit fast twitch fibers. There is one study showing that eccentric contraction can selectively recruit fast twitch fibers, but more studies say no, and the one study can be explained by the phenomenon that sometimes neighbouring (in recruitment threshold) motor units can sort of switch so order. (I have a review on this if anyone is interested)
I don’t know of any studies that have found selective recruitment in fast contractions.
And the size principle being correct does not mean you would get stronger as the set goes on. Let’s say you start out with type 1 muscle fiber recruitment (lifting slowly and controlled, since if you lifted explosively you’d recruit type 2 fibers also) only and as the type 1 fatigues you start recruiting type 2 fibers, you’re not stronger now, because the type I’s are fatigued. At the beginning of the set you had pretty much all your type I AND type II fibers without fatigue that you could use if you wanted to suddenly lift explosively. While as the set goes on and more and more muscle fibers fatigue, this potential (your real “strength” so to speak) goes down.
This might be a bit of a simplification, but I think it should explain pretty well why you won’t get stronger as your set goes on.
I would love to see that review and any other reviews about this matter if you have them!
Waterbury mentions that (in a set of several fast contractions with enough load) the type 2 fibres will fatigue first and then the more fatigue resistant type 1 fibres. This is how he explains the loss of strength (and speed). First type 1 plus 2 and then only type 1.
I don’t know who is right. Or maybe the results change with faster contractions. I don’t know, but I sure would love to see some actual reseach done on human for either vision.
If you could do that I would be very happy.
Well, it’s possible that the fast twitch fibers will fatigue first in a contraction where they are recruited from the start. I was just talking about if you start with only type I recruitment and just trying to explain why you wouldn’t get stronger as the set goes on.
I have a review on selective recruitment in eccentric contractions, but nothing else.
Dunno if you’ll get access to the full text.
How does local hypoxia/occlusion affect the fiber recruitment? Studies using low loads either with tonic cadence(are fast contractions needed?)or Kaatsu demonstrate increases in CSA. What is the recruitment in this environment? Does the effect cause a rapid shift to type two fibers?
Anoop | Sun July 31, 2011
Good point about how we get so focused on Type 2 fibers and how bodybuilders seems to have more Type 1. I think in humans the type 2 and type 1 fibers are of the same size, but not sure.
I don’t think there are any major questions about the validity of the the size principle. This is one of the basic foundational theories of neurophysiology. And it was shown in cats first, so I am not sure about the animal thing you say.
Oh sorry, I did not mean that the type 2 fibres were bigger, but that the motor units would involve much more total paralel contractile protein per unit. Now, my only source for this is Waterbury and I don’t know if I should that guy seriously. He has been know to ignore some research and so on according to critics. I will have to re-read some of his articles to get a clearer picture.
I guess most of those questions about the size-principle come mostly from the articles of cherry-picking writers I have read in the past. (I try not too read that stuff anymore and be critical, but sometimes this is hard to do) The review Karky linked to (thanks by the way) shows to me that a lot of writers have been cherry-picking that one study that showed different fibre recruitment during eccentric contractions even though 9! others showed no difference compared to concentric contractions.
By the way, Karky, if understand it correctly you are saying that no matter if a muscle contracts quickly or slowly (or against a heavy or lighter load) all muscle fibres types in that muscle will be recruited and fatigued when the muscle is taken to failure. Am I assuming correctly?
(note that I did not say: ‘set to failure’. I guess short heavy sets will only fatigue part of the fibres untill the concentric action is not possible anymore against a heavy load)
Found Waterbury’s comments, source: http://chadwaterbury.com/the-science-of-motor-unit-recruitment-part-2/
““The last few reps of a set is where the results happen,” has long been the dogma in resistance training circles. The theoretical reason why some coaches said this was true is because they figured that additional motor units were recruited at the end of a long, agonizing set to failure. However, if you look at the neuroscience research it’s clear that this postulate holds no water.
If you recruited more motor units in the last few reps to failure, the set would get easier and the speed would increase. Since this doesn’t happen it’s time to look at a more progressive way of training. Lift heavy, lift fast, keep the sets shorts, and avoid failure. Those are the keys to maximum motor unit recruitment.”
Joe Cannon | Mon August 01, 2011
FullDeplex, that is a very good use of logic thanks for passing it and Chads website along. I people say that stuff about the last few reps alot also.
Yeah that statement by Waterbury doesn’t make sense, speed won’t increase for the reasons I mentioned above, assuming a submaximal lifting speed (like maybe a 3 second concentric or something). But if you were to lift a weight explosively (so using all your strength and probably all your motor units too, despite it being a submaximal load) then speed would definitely decrease as your set goes on since you’re MUs start to fatigue. In the submaximal speed scenario the MUs will also fatigue, and new MUs will be activated (the fatigued MUs don’t have to stop fireing, but they will develop a reduced amount of force due to being fatigued), but speed won’t increase all on it’s own by that reason, even though you’re now using bigger and faster MUs than you were before. The newly recruited units will produce enough force to cover only what was lost from the fatigue in the already recruited units. That is, unless you consciously make a choice to lift the weight faster, then you will recruit more of the MUs that were not recruited in the beginning of the lift, produce more force, and accelerate the weight.
I’d agree that now a days the end of the set isn’t really where it happens as far as MU recruitment goes, I think the last part of the set is more about fatigue. You recruit the MUs of major muscles at about 80-85% of 1RM and even less than that if you lift as fast as you can in the concentric phase (which most of us do). And even if you were to drop the weight down to maybe 70% and don’t lift with max concentric speed, there still aren’t that many more MUs left to recruit.
Hope that makes sense. It’s awkward to try to explain why Chad is wrong in saying that speed should increase at the end of a set if orderly recruitment holds true, but I hope it made sense.
Perhaps these can help?
Benefits of forced reps?
Load necessary for MU recruitment?
Don’t thank me yet, Joe. Waterbury may turn out to be wrong in some of his statements. I just passed it along so people could see where the comments on the (interpretation of) the ‘size principle’ were coming from.
I could comment on his “strength increase during a set”-statement that for this to occur a muscle needs to consist for a large part of muscle fibres connected to the large high treshold motor units (say 50%). Else the “switch” for small to big motor units would not be noticed by an increase in strength.
Also, if his statements about the recruitment of large motor units are correct it would mean that these motor units are not recruited in a slow speed, light weight set take to failure. This, however, means that you could extend such a set for 10 seconds if you increased your speed or effort by the recruitment of the (still fresh) big motor units.
Seeing that, by Waterbury’s logic, the involvement of the large motor units would result in more strength/speed and (most of the time) a slow set taken to failure would have people increasing their effort in the last rep(s), it would mean that such actions would result in same phenomenon he says would occur if the ‘size principle’ were true.
Then again, logic is not enough to disprove or prove anything biologic. We need studies to show that type 2 fibres also can get recruited (and fatigued) AFTER the type 1 fibres were recruited during low treshold muscle actions (slow speed/low weight) taken to failure.
Waterbury’s “logic” is flawed. I can’t believe he said that, he used to be one of my go to guys for info about the nervous system back when I started lifting.
There are studies showing recruitment of new MUs in isometric contractions. Can’t find anything with regular lifting, though, probably because EMG readings in dynamic contractions can be really difficult.
This one doesn’t find new recruitment:
But these ones do:
I’ve only read the abstracts, but I’ll look at the full studies during the day today I think.
Thanks for the studies, Karky. (you too, sixty) It is interesting to read that even in submaximal constant (isometric) contraction the recruitment threshold decreases during the set. Something Waterbury does not to mention.
Without this little fact you “need” Waterbury’s routines to recruit the type 2 fibres. Pretty smart, actually.
Joe Cannon MS CSCS | Thu August 04, 2011
If anything you got me thinking about a topic I normally dont research too much and for that I thank you
I’ve read his article before and he does raise several valid concerns.. However, I’ve never seen that article published in a peer reviewed journal, and with good reason. Look at his conclusion, it seems like he actually has all the answers, when people who look at things more objectively, the conclusions are never that certain.
I haven’t critiqued the entire article, and I’m not gonna, but when the first reference I look up end up being pulled way out of proportion, that’s usually a bad sign. He writes this ” A recent study has demonstrated that as much as 70% MVC is needed to promote strength gains in abdominal muscle . It is unlikely that during CS exercise abdominal muscle would reach this force level .”
If you look at  (http://www.spinegateway.net/ArticlePage.aspx?DOI=10.1007/s00586-006-0181-1) it’s a study of just a few exercises done on all four. And to use that to say that core stability exercises don’t activate the muscles enough is simply terrible. To be able to say that you need to cite a large amount of studies testing many different core exercises or different difficulties.
It’s a bit scary to read articles like that since the author can argue for his own viewpoints and be very convincing since he can choose to only cite the research that favours his opinions or draw invalid conclusions based on his references. I’m not saying this can’t occur in a peer reviewed journal, but it’s probably much less likely. In addition, in a journal people can send in comments on the articles if they find something wrong with them.
Good points overall. Anytime you read a review article (minus the systematic) the assumption is that the author will be imparting his/her own views and biases on the subject. I have a moderate familiarity with the literature on this subject and my take is that Lederman is mostly accurate. Some of the support for his opinions is a little weak however the same can be said for those on the other side of the fence. The main take home would seem to be that there is an equally (if not more valid) alternative view on the core stabilization model.
To your point on the 70% MVC,,I think his point goes to the overload theory. As you know the evidence suggests that a certain intensity is needed to stimulate strengthening (past neuro) and many of the core exercises are probably below that threshold (data lacking).
I am also curious as to why you think he “has all the answers” in his conclusions. I did not read it that way. The article was about calling into question the core stab model not promoting his method or theory. Also, the article was published in the “Journal of Bodywork and Movement Therapies” which I don’t know much about but it appears to be peer reviewed. I do know of a few people on the editorial board however the topics covered in the journal seem a bit on the CAM side.
The nice thing about articles like Lederman’s is that it challenges the “common knowledge” and gets us to question our beliefs. And that questioning either leads to improved confidence in our beliefs or increased exploration for different models. Either way it is good.
I know what the overload model is and I know his point about 70% of MVC. He then goes on to say that core stability exercises don’t put enough load on the abdominal muscles by citing one study showing pretty low % of MVC. However, that study used pretty easy exercises, and I doubt the results would have been the same with harder exercises. If he wants to actually make that point he needs to cite research for a wide range of exercises using a wide range of loads or difficulties. Tried ab-rollouts, for example? Pretty tough. I don’t have data saying they go over 70% MVC, but I wouldn’t be surprised if they did (would depend on your strength level, of course)
And he had some pretty firm statements in his conclusion, which i dislike in research as things are pretty much never that clear.
I agree that it’s good people are questioning the common models and he does make some pretty good points. For example the one about the low level of activity in the core muscles during everyday tasks, saying that you don’t really need a lot of core strength. However, he doesn’t really mention endurance, since you sometimes need to hold these low levels of muscle activity for a very long time, could that play in? I don’t know. That being said, I really think that what’s most important in the muscles helping stabilize the spine is motor control. They need to “know” how much to contract and they need to do it at the right time.
He is not stating that there isn’t any abdominal exercises which work the muscles at a high MVC. He is stating that many of the common spinal stabilization exercises used in the rehab setting (and are claimed to increase strength)don’t actually meet the known criteria for strengthening. I am sure he would say, if you truly believe that strengthening is what a patient needs make sure you are not doing low MVC exercises.
You mention endurance which I think is a good point. However the problem becomes how do train endurance in a muscle that pretty much contracts at a low MVC throughout the entire day. It would seem that any endurance exercise done in the gym or clinic would be grossly underwhelming. Working 30 minutes on endurance of the spinal stabs would be like running 5 miles a day and expecting it to prepare you for an ultra-marathon.
“They need to know how much to contract and they need to it at the right time” That is exactly the point. No one really knows how much these muscle should contract and when the right time is. People think they know but the data does not support most of what is taught.
Also you mention that you don’t like his strong conclusions. This article is not a research paper. No experiment was performed. You are right that in a research paper the authors are not expected to obviously inject their opinion. However, this was a review article which is by definition an author putting forth his opinion on a topic and then supporting it. You can decide to agree or disagree but his statements were not inappropriate for the medium. It is kind of like the editorial page of a newspaper. It is not meant to be hard objective news.
Copyright 2008-2012 Anoop Balachandran. All rights reserved.