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TPT
04-14-2010, 07:33 PM
just published for more chatter.


Single vs. Multiple Sets of Resistance Exercise for Muscle Hypertrophy: A Meta-Analysis (http://journals.lww.com/nsca-jscr/Fulltext/2010/04000/Single_vs__Multiple_Sets_of_Resistance_Exercise.36 .aspx)

Krieger, James W
The Journal of Strength & Conditioning Research. 24(4):1150-1159, April 2010.
doi: 10.1519/JSC.0b013e3181d4d436

Abstract:

Krieger, JW. Single vs. multiple sets of resistance exercise for muscle hypertrophy: a meta-analysis. J Strength Cond Res 24(4): 1150-1159, 2010-Previous meta-analyses have compared the effects of single to multiple sets on strength, but analyses on muscle hypertrophy are lacking. The purpose of this study was to use multilevel meta-regression to compare the effects of single and multiple sets per exercise on muscle hypertrophy. The analysis comprised 55 effect sizes (ESs), nested within 19 treatment groups and 8 studies. Multiple sets were associated with a larger ES than a single set (difference = 0.10 +/- 0.04; confidence interval [CI]: 0.02, 0.19; p = 0.016). In a dose-response model, there was a trend for 2-3 sets per exercise to be associated with a greater ES than 1 set (difference = 0.09 +/- 0.05; CI: -0.02, 0.20; p = 0.09), and a trend for 4-6 sets per exercise to be associated with a greater ES than 1 set (difference = 0.20 +/- 0.11; CI: -0.04, 0.43; p = 0.096). Both of these trends were significant when considering permutation test p values (p < 0.01). There was no significant difference between 2-3 sets per exercise and 4-6 sets per exercise (difference = 0.10 +/- 0.10; CI: -0.09, 0.30; p = 0.29). There was a tendency for increasing ESs for an increasing number of sets (0.24 for 1 set, 0.34 for 2-3 sets, and 0.44 for 4-6 sets). Sensitivity analysis revealed no highly influential studies that affected the magnitude of the observed differences, but one study did slightly influence the level of significance and CI width. No evidence of publication bias was observed. In conclusion, multiple sets are associated with 40% greater hypertrophy-related ESs than 1 set, in both trained and untrained subjects.
(C) 2010 National Strength and Conditioning Association

Go to Full Text of this Article (http://journals.lww.com/nsca-jscr/Fulltext/2010/04000/Single_vs__Multiple_Sets_of_Resistance_Exercise.36 .aspx)

TPT
04-17-2010, 01:32 PM
this was a valuable study because most of the previous studies and meta-analyses were on strength. this was a study on muscle hypetrophy. something that should be discriminated as strength and hypertrophy are not one and the same. thus, should not be interpretated as such.

multiple sets per exercise were associated with significantly greater modifications in muscle size during resistance programs. specifically, multiple sets had 40% greater hypertrophy-related effect sizes than a single set. there was a trend toward dose effects. i.e., increasing muscle size with increasing number of sets.

thus, the study suggests that we should be performing a minimum of 2-3 sets per exercise. possibly, 4-6 sets would be more effective in achieving maximal hypertrophy.

Abraxas
04-21-2010, 05:37 AM
You know,im curious to know how going to failure fits in all of this.
Especially since going to failure efficiently, takes time to develop.

I would like to see some studies where they use athletes
who are trained to efficiently go to failure,let them do one all out set.

And see if those people get a just as significant growth response as the subjects who did multiple sets in this study,and see if the ''failure'' group did more sets,if that would have any significant benefit over doing one set as far as hyperthrophy goes.

Abraxas
04-21-2010, 05:45 AM
I believe,high intensity,low volume,high frequency coupled with a periodisation scheme were each workout the muscles are subjected to maximum yet substantially different loads,as far as weight and rep execution goes,is they way to go.

Just a theory..

ob205
04-21-2010, 11:06 AM
Mike Mentzer would be pissed! I would like to see this study done on identical twins, where one trains 1 set to failure and the other multiple. Ideally, they would be say 21, with no previous weight training experience and similar athletic backgrounds. Assuming all things being equal (diet, rest, extra ciricular activities), our greatest variable would be intensity of EFFORT. If you give 2 people 80% of the 1rm and say go to failure, you are going to get some very different results, based on their motivation and ability to generate emotional intensity. This is where I find the study, although useful, not completely accurate.

I trained for several years Heavy Duty style and made great gains, while at the same time being told my the Ivory Tower types in the Exercise Phys dept that it is not possible to stimulate hypertrophy with only 1 set.

Looking around any commercial gym I see most people doing a great number of sets, but hardly any of them look productive. 1 all out set from a person trained in the high intensity techniques and motivated easily exceeds 4-6 sets of an individual half assing the work.

Good Post, love the topic and the debate!

Costco77
04-21-2010, 12:51 PM
How can a study really judge intensity and going past mental and physical failure?

Abraxas
04-22-2010, 04:23 AM
How can a study really judge intensity and going past mental and physical failure?

I agree,there should be some way though..

JamesKrieger
04-23-2010, 12:21 PM
You know,im curious to know how going to failure fits in all of this.
Especially since going to failure efficiently, takes time to develop.


I am the author of this paper.

I used a random effects model to analyze the data. When combining the results of different studies, you can't account for all possible sources of variation between studies. A random effects model essentially takes this into consideration. What that means is that it's harder to see significant differences with a random effects model, because you are automatically building in more uncertainty.

What I'm saying here, is that my statistical model automatically accounts for small variations among studies in regards to training to failure.

Also, all the studies included in this analysis involved subjects training to failure, so the point is moot.




And see if those people get a just as significant growth response as the subjects who did multiple sets in this study,and see if the ''failure'' group did more sets,if that would have any significant benefit over doing one set as far as hyperthrophy goes.

This was a meta-analysis of studies comparing single sets to multiple sets, so there are no people in this study, per se. The experimental units in this study are the studies and treatment groups.




I would like to see some studies where they use athletes
who are trained to efficiently go to failure,let them do one all out set.


What do you mean, "efficiently go to failure?"

What I've never understood is why failure is considered some sort of "magical" or "holy grail" concept. It only means that the muscles, as a whole, can no longer produce enough force to move the resistance. That's it. However, from the concept of stimulating protein synthesis (which is the entire goal if you're trying to get bigger), it doesn't mean much.

JamesKrieger
04-23-2010, 01:11 PM
Assuming all things being equal (diet, rest, extra ciricular activities), our greatest variable would be intensity of EFFORT.


Intensity of effort is a subjective quantity that cannot be directly measured. While there are self-reported ratings of intensity of effort (like Rate of Perceived Exertion or RPE), you are essentially taking the subject's word for it.

Second, intensity of effort is not the greatest variable. This is easily illustrated by looking at someone doing a 100-RM set. Doing 100 reps to failure certainly will require a great intensity of effort, but it will do little to change muscle size.



If you give 2 people 80% of the 1rm and say go to failure, you are going to get some very different results, based on their motivation and ability to generate emotional intensity.


You are going to get different results based on a variety of factors, including genetics and diet. This is where measures of variation (standard deviations and standard errors) and statistics come into play. Basically, statistics tell you whether the magnitude of a difference between groups (1 set and multiple sets, in this case) is greater than the variability observed in those groups.



This is where I find the study, although useful, not completely accurate.


The statistics automatically take into consideration the variability, so yes, the study is accurate in that sense.




I trained for several years Heavy Duty style and made great gains, while at the same time being told my the Ivory Tower types in the Exercise Phys dept that it is not possible to stimulate hypertrophy with only 1 set.


My paper showed that you do stimulate hypertrophy with 1 set. It's just that the effects of multiple sets were greater.

TPT
04-24-2010, 06:28 PM
I am the author of this paper.

I used a random effects model to analyze the data. When combining the results of different studies, you can't account for all possible sources of variation between studies. A random effects model essentially takes this into consideration. What that means is that it's harder to see significant differences with a random effects model, because you are automatically building in more uncertainty.

What I'm saying here, is that my statistical model automatically accounts for small variations among studies in regards to training to failure.

Also, all the studies included in this analysis involved subjects training to failure, so the point is moot.


'repetitions to failiure' is a relevant variable and should be controlled as such.

especially, as it fits into the study of single vs multiple sets. or the arguments of high intensity/heavy duty vs volume training. i.e., single sets with repetitions to failure might be argued as more effective for muscle strength or hypertrophy than multiple sets without repetitions to failure.

im suspicious of whether many of the cited studies actually controlled repetitions to failure as they stated since i didnt see any reliability measures and some studies appeared to discriminate 'failure' more than others. e.g., rhea et al. (2002) described a much more explicit training program with undulating periodization with no supervision. while others including ronnestead et al. (2007) used a different program with initial supervision. i understand this was part of a meta-analysis and will not be so critical of the inherrent limitations of meta-regressions. however, speaking of implicit confounds should still be appreciated.



This was a meta-analysis of studies comparing single sets to multiple sets, so there are no people in this study, per se. The experimental units in this study are the studies and treatment groups.



What do you mean, "efficiently go to failure?"

What I've never understood is why failure is considered some sort of "magical" or "holy grail" concept. It only means that the muscles, as a whole, can no longer produce enough force to move the resistance. That's it. However, from the concept of stimulating protein synthesis (which is the entire goal if you're trying to get bigger), it doesn't mean much.

nothing magical, but relevant as it may have differential effects on muscular endurance, strength, hypertrophy, and the central nervous system.

Will Brink
04-24-2010, 06:35 PM
multiple sets are associated with 40% greater hypertrophy-related ESs than 1 set, in both trained and untrained subjects.


That was established a long time ago. If they have funding, too bad they didn't look to answer a new question. :no:

JamesKrieger
04-24-2010, 07:49 PM
especially, as it fits into the study of single vs multiple sets. or the arguments of high intensity/heavy duty vs volume training. i.e., single sets with repetitions to failure might be argued as more effective for muscle strength or hypertrophy than multiple sets without repetitions to failure.


But for all the studies included, training protocols were identical other than the number of sets. Any studies that compared 1-set-to-failure to multiple-sets-not-to-failure were excluded.




im suspicious of whether many of the cited studies actually controlled repetitions to failure as they stated since i didnt see any reliability measures and some studies appeared to discriminate 'failure' more than others. e.g., rhea et al. (2002) described a much more explicit training program with undulating periodization with no supervision. while others including ronnestead et al. (2007) used a different program with initial supervision. i understand this was part of a meta-analysis and will not be so critical of the inherrent limitations of meta-regressions. however, speaking of implicit confounds should still be appreciated.


As I mentioned in my previous post, it is impossible to include covariates in the model for every single potential source of variance between studies. This is why a random effects model is used; the statistical model automatically accounts for unaccounted sources of variance between studies.

Also, the Rhea paper did not specify whether there was supervision or not. Thus, it cannot be stated that the subjects were not supervised.





nothing magical, but relevant as it may have differential effects on muscular endurance, strength, hypertrophy, and the central nervous system.

In regards to hypertrophy, why?

If I I do 9 repetitions of a 10 RM weight (hence stopping 1 rep short of failure), why would that 1 repetition really make that much of a difference in regards to stimulation of protein synthesis? I think people tend to "micromanage" this aspect of training too much, when it probably makes little to no difference in the grand scheme of things.

The only thing that happens at "failure" is the fact the muscle can no longer produce enough force to move the weight. There's nothing that significant about it. I've always found the statements by HITers a bit incredulous, because they'll say that if someone does multiple sets to failure, they aren't reaching "true" failure. Or if a study happens to find multiple sets to produce superior results, they'll make an excuse like "the single set group wasn't really reaching full mental and physical failure." Then they offer up some vague definition of what "true" failure really means. To me, that's just an excuse to ignore data that doesn't fit with their beliefs.

It's similar to people that believe in ESP. There have been dozens of studies that fail to support the existence of ESP. The ESP believers will then say, "Well, the researchers hostile thoughts are interfering with ESP transmission which is why they're getting negative results." Basically, they've constructed a non-falsifiable hypothesis. They've already made up their minds, and no amount of conflicting data will overturn that.

Essentially, the hardcore HITers have developed a non-falsifiable hypothesis. For every study that shows multiple sets to produce better results, they'll always say, "Well, the single set group isn't REALLY going to failure."

JamesKrieger
04-24-2010, 07:53 PM
That was established a long time ago. If they have funding, too bad they didn't look to answer a new question. :no:

In what study was this established?

Abraxas
04-25-2010, 01:47 PM
But for all the studies included, training protocols were identical other than the number of sets. Any studies that compared 1-set-to-failure to multiple-sets-not-to-failure were excluded.




As I mentioned in my previous post, it is impossible to include covariates in the model for every single potential source of variance between studies. This is why a random effects model is used; the statistical model automatically accounts for unaccounted sources of variance between studies.

Also, the Rhea paper did not specify whether there was supervision or not. Thus, it cannot be stated that the subjects were not supervised.





In regards to hypertrophy, why?

If I I do 9 repetitions of a 10 RM weight (hence stopping 1 rep short of failure), why would that 1 repetition really make that much of a difference in regards to stimulation of protein synthesis? I think people tend to "micromanage" this aspect of training too much, when it probably makes little to no difference in the grand scheme of things.

The only thing that happens at "failure" is the fact the muscle can no longer produce enough force to move the weight. There's nothing that significant about it. I've always found the statements by HITers a bit incredulous, because they'll say that if someone does multiple sets to failure, they aren't reaching "true" failure. Or if a study happens to find multiple sets to produce superior results, they'll make an excuse like "the single set group wasn't really reaching full mental and physical failure." Then they offer up some vague definition of what "true" failure really means. To me, that's just an excuse to ignore data that doesn't fit with their beliefs.

It's similar to people that believe in ESP. There have been dozens of studies that fail to support the existence of ESP. The ESP believers will then say, "Well, the researchers hostile thoughts are interfering with ESP transmission which is why they're getting negative results." Basically, they've constructed a non-falsifiable hypothesis. They've already made up their minds, and no amount of conflicting data will overturn that.

Essentially, the hardcore HITers have developed a non-falsifiable hypothesis. For every study that shows multiple sets to produce better results, they'll always say, "Well, the single set group isn't REALLY going to failure."

How do you quantify intensity if not going to failure? (you could say minus one rep to failure, fine by me)

Im not a HIT proponent,im just trying to make all the pieces fit together.

What im postulating is,whether you go to failure or not,there will always be variables in the amount of force someone can produce relative to their own strength, in a set. (or in multiple ones for that matter)

Since most people (since most people do bodybuilder-type volume routines) do not ever subject themselves to training themselves to produce a maximum effort in a single set,it would be natural for them not to be good at it,and would need more sets to illicit a maximal hypertrophic response because of that fact alone.

So im using the term failure here as a way of confirming a high intensity effort.

TPT
04-25-2010, 05:29 PM
That was established a long time ago. If they have funding, too bad they didn't look to answer a new question. :no:


not sure what youre speaking to.

TPT
04-25-2010, 06:01 PM
But for all the studies included, training protocols were identical other than the number of sets. Any studies that compared 1-set-to-failure to multiple-sets-not-to-failure were excluded.

yes. i appreciated the rigid inclusion criteria. thus, the sample studied was small. however, id be suspicious on whether the protocols were 'identical' as i said in the previous post.


As I mentioned in my previous post, it is impossible to include covariates in the model for every single potential source of variance between studies. This is why a random effects model is used; the statistical model automatically accounts for unaccounted sources of variance between studies.

of course its impossible. but, that doesnt mean we dont discuss relevant variables not accounted for or potential confounds.


Also, the Rhea paper did not specify whether there was supervision or not. Thus, it cannot be stated that the subjects were not supervised.

that was just one example for questioning the validity of the experimental control of studies you analyzed. meta-analyses are only as helpful as the sample the studies reviewed.


In regards to hypertrophy, why?

If I I do 9 repetitions of a 10 RM weight (hence stopping 1 rep short of failure), why would that 1 repetition really make that much of a difference in regards to stimulation of protein synthesis? I think people tend to "micromanage" this aspect of training too much, when it probably makes little to no difference in the grand scheme of things.

The only thing that happens at "failure" is the fact the muscle can no longer produce enough force to move the weight. There's nothing that significant about it. I've always found the statements by HITers a bit incredulous, because they'll say that if someone does multiple sets to failure, they aren't reaching "true" failure. Or if a study happens to find multiple sets to produce superior results, they'll make an excuse like "the single set group wasn't really reaching full mental and physical failure." Then they offer up some vague definition of what "true" failure really means. To me, that's just an excuse to ignore data that doesn't fit with their beliefs.

It's similar to people that believe in ESP. There have been dozens of studies that fail to support the existence of ESP. The ESP believers will then say, "Well, the researchers hostile thoughts are interfering with ESP transmission which is why they're getting negative results." Basically, they've constructed a non-falsifiable hypothesis. They've already made up their minds, and no amount of conflicting data will overturn that.

Essentially, the hardcore HITers have developed a non-falsifiable hypothesis. For every study that shows multiple sets to produce better results, they'll always say, "Well, the single set group isn't REALLY going to failure."


i do understand the dogmatic behaviors of hiters as youve described. oberved them plenty as they reference arthur jones as if he used the literature to determine training. and hit should be more concerned with strength than hypertrophy.

im not a hiter and certainly hypertrophy still occurs without repetitions to failure. but, this doesnt mean we shouldnt examine it and its effects. we do have data to suggest failure is related to increased motor unit activation, mechanical stress with associated gene expression and damage, and a number of anabolic hormonal responses. these variables are all related to hypertrophy.

ob205
04-26-2010, 11:56 AM
James,
First, I would like to thank you for contributing here. What I would like to know is, was progressive overload taken into account?

Also, you stated "why is failure so important anyways?" So your conclusion would be that we could do mulitple sets of 8 with our say 10RM and get greater hypertrophy than someone going all out on 1 set and doing 10 reps with the 10rm?

It seems that the major consideration is volume, period. Is this a correct assumption?

Also, what were the markers for hypretrophy? Was it strictly anthropometric or were there biochemical or muscle biopsies which showed greater response from the volume?

JamesKrieger
04-26-2010, 08:23 PM
yes. i appreciated the rigid inclusion criteria. thus, the sample studied was small. however, id be suspicious on whether the protocols were 'identical' as i said in the previous post.


But as I stated before, my statistical model automatically accounts for any unknown sources of variance between studies. So even if the protocols aren't absolutely identical, it would have no bearing on the results.




of course its impossible. but, that doesnt mean we dont discuss relevant variables not accounted for or potential confounds.


But unaccounted variables are actually accounted for in the statistical model.




do have data to suggest failure is related to increased motor unit activation,


Motor unit activation is maximal from the first repetition if you're using weights heavier than 40-60% 1-RM, so training to failure won't improve motor unit recruitment if you're using reasonably heavy weights.




mechanical stress with associated gene expression and damage,


But there are question marks as to whether damage is necessary to increase muscle size, or even desirable. In fact, there is some research showing superior results for hypertrophy with concentric-only training (which does little tissue damage) compared to eccentric-only training (which is damaging to tissue), although data is not consistent in this area.



and a number of anabolic hormonal responses.


Recent research has shown that the acute anabolic hormonal response to a training session plays no role in the hypertrophy process.

JamesKrieger
04-26-2010, 08:27 PM
James,
First, I would like to thank you for contributing here. What I would like to know is, was progressive overload taken into account?


All of the studies used systems of progression for increasing the weights used as the subjects improved in strength.




Also, you stated "why is failure so important anyways?" So your conclusion would be that we could do mulitple sets of 8 with our say 10RM and get greater hypertrophy than someone going all out on 1 set and doing 10 reps with the 10rm?


On average, I would say yes, you would get better results with multiple sets. Of course, there will be variation in individual responses.



It seems that the major consideration is volume, period. Is this a correct assumption?


No, because many other variables play a role as well (frequency and intensity are a couple key ones).



Also, what were the markers for hypretrophy? Was it strictly anthropometric


Anthropometric and regional body composition measurements

TPT
04-27-2010, 08:53 PM
But as I stated before, my statistical model automatically accounts for any unknown sources of variance between studies. So even if the protocols aren't absolutely identical, it would have no bearing on the results.


But unaccounted variables are actually accounted for in the statistical model.

one should always be suspicous anytime a summation of data are presented including group designs, meta-analyses, and multilevel models. as they might 'hide' interindividual variablity.



Motor unit activation is maximal from the first repetition if you're using weights heavier than 40-60% 1-RM, so training to failure won't improve motor unit recruitment if you're using reasonably heavy weights.

that is inconclusive. unless you have a recent citation im unaware of.



But there are question marks as to whether damage is necessary to increase muscle size, or even desirable. In fact, there is some research showing superior results for hypertrophy with concentric-only training (which does little tissue damage) compared to eccentric-only training (which is damaging to tissue), although data is not consistent in this area.

of course.

however, the overall data shows that eccentric-only training performed at high intensities are more effective in muscle strength and hypertrophy. and especially for eccentric strength.

the key is for us to discriminate the 'optimal' dosing of those variables that induce optimal muscle damage. besides anecdote, we dont know that yet.


Recent research has shown that the acute anabolic hormonal response to a training session plays no role in the hypertrophy process.

what research?

i wouldnt believe it.

JamesKrieger
04-28-2010, 05:36 PM
one should always be suspicous anytime a summation of data are presented including group designs, meta-analyses, and multilevel models. as they might 'hide' interindividual variablity.


Of course, but the point of summary statistics aren't to know what happens in every single individual...it's to know what happens in most individuals most of the time.

Will certain individuals get equivalent results from single set training? Of course. But that doesn't mean most individuals will.




what research?


http://www.ncbi.nlm.nih.gov/pubmed/19736298

http://www.ncbi.nlm.nih.gov/pubmed/19910330




i wouldnt believe it.

Why wouldn't you believe it? The post-training hormonal response is very short-lived, yet post-exercise protein synthesis is elevated for 24-48 hours.

TPT
04-28-2010, 06:13 PM
Of course, but the point of summary statistics aren't to know what happens in every single individual...it's to know what happens in most individuals most of the time.

Will certain individuals get equivalent results from single set training? Of course. But that doesn't mean most individuals will.

yes. of course.




http://www.ncbi.nlm.nih.gov/pubmed/19736298

http://www.ncbi.nlm.nih.gov/pubmed/19910330 (http://www.ncbi.nlm.nih.gov/pubmed/19910330)

J Appl Physiol. (http://javascript<b></b>:AL_get(this, 'jour', 'J Appl Physiol.');) 2010 Jan;108(1):60-7. Epub 2009 Nov 12.
Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors.

West DW (http://www.ncbi.nlm.nih.gov/pubmed?term=%22West%20DW%22%5BAuthor%5D), Burd NA (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Burd%20NA%22%5BAuthor%5D), Tang JE (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Tang%20JE%22%5BAuthor%5D), Moore DR (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Moore%20DR%22%5BAuthor%5D), Staples AW (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Staples%20AW%22%5BAuthor%5D), Holwerda AM (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Holwerda%20AM%22%5BAuthor%5D), Baker SK (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Baker%20SK%22%5BAuthor%5D), Phillips SM (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Phillips%20SM%22%5BAuthor%5D).
Exercise Metabolism Research Group, Dept. of Kinesiology, McMaster Univ., Hamilton, ON L8S4K1 Canada.
Abstract

The aim of our study was to determine whether resistance exercise-induced elevations in endogenous hormones enhance muscle strength and hypertrophy with training. Twelve healthy young men (21.8 +/- 1.2 yr, body mass index = 23.1 +/- 0.6 kg/m(2)) trained their elbow flexors independently for 15 wk on separate days and under different hormonal milieu. In one training condition, participants performed isolated arm curl exercise designed to maintain basal hormone concentrations (low hormone, LH); in the other training condition, participants performed identical arm exercise to the LH condition followed immediately by a high volume of leg resistance exercise to elicit a large increase in endogenous hormones (high hormone, HH). There was no elevation in serum growth hormone (GH), insulin-like growth factor (IGF-1), or testosterone after the LH protocol but significant (P < 0.001) elevations in these hormones immediately and 15 and 30 min after the HH protocol. The hormone responses elicited by each respective exercise protocol late in the training period were similar to the response elicited early in the training period, indicating that a divergent postexercise hormone response was maintained over the training period. Muscle cross-sectional area (CSA) increased by 12% in LH and 10% in HH (P < 0.001) with no difference between conditions (condition x training interaction, P = 0.25). Similarly, type I (P < 0.01) and type II (P < 0.001) muscle fiber CSA increased with training with no effect of hormone elevation in the HH condition. Strength increased in both arms, but the increase was not different between the LH and HH conditions. We conclude that exposure of loaded muscle to acute exercise-induced elevations in endogenous anabolic hormones enhances neither muscle hypertrophy nor strength with resistance training in young men.



J Physiol. (http://javascript<b></b>:AL_get(this, 'jour', 'J Physiol.');) 2009 Nov 1;587(Pt 21):5239-47. Epub 2009 Sep 7.
Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young men.

West DW (http://www.ncbi.nlm.nih.gov/pubmed?term=%22West%20DW%22%5BAuthor%5D), Kujbida GW (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Kujbida%20GW%22%5BAuthor%5D), Moore DR (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Moore%20DR%22%5BAuthor%5D), Atherton P (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Atherton%20P%22%5BAuthor%5D), Burd NA (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Burd%20NA%22%5BAuthor%5D), Padzik JP (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Padzik%20JP%22%5BAuthor%5D), De Lisio M (http://www.ncbi.nlm.nih.gov/pubmed?term=%22De%20Lisio%20M%22%5BAuthor%5D), Tang JE (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Tang%20JE%22%5BAuthor%5D), Parise G (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Parise%20G%22%5BAuthor%5D), Rennie MJ (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Rennie%20MJ%22%5BAuthor%5D), Baker SK (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Baker%20SK%22%5BAuthor%5D), Phillips SM (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Phillips%20SM%22%5BAuthor%5D).
Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, 1280 Main Street West, Hamilton, ON L8S 4K1, Canada.
Abstract

We aimed to determine whether exercise-induced elevations in systemic concentration of testosterone, growth hormone (GH) and insulin-like growth factor-1 (IGF-1) enhanced post-exercise myofibrillar protein synthesis (MPS) and phosphorylation of signalling proteins important in regulating mRNA translation. Eight young men (20 +/- 1.1 years, BMI = 26 +/- 3.5 kg m(-2)) completed two exercise protocols designed to maintain basal hormone concentrations (low hormone, LH) or elicit increases in endogenous hormones (high hormone, HH). In the LH protocol, participants performed a bout of unilateral resistance exercise with the elbow flexors. The HH protocol consisted of the same elbow flexor exercise with the contralateral arm followed immediately by high-volume leg resistance exercise. Participants consumed 25 g of protein after arm exercise to maximize MPS. Muscle biopsies and blood samples were taken as appropriate. There were no changes in serum testosterone, GH or IGF-1 after the LH protocol, whereas there were marked elevations after HH (testosterone, P < 0.001; GH, P < 0.001; IGF-1, P < 0.05). Exercise stimulated a rise in MPS in the biceps brachii (rest = 0.040 +/- 0.007, LH = 0.071 +/- 0.008, HH = 0.064 +/- 0.014% h(-1); P < 0.05) with no effect of elevated hormones (P = 0.72). Phosphorylation of the 70 kDa S6 protein kinase (p70S6K) also increased post-exercise (P < 0.05) with no differences between conditions. We conclude that the transient increases in endogenous purportedly anabolic hormones do not enhance fed-state anabolic signalling or MPS following resistance exercise. Local mechanisms are likely to be of predominant importance for the post-exercise increase in MPS.


cool shit.

and just published.



Why wouldn't you believe it? The post-training hormonal response is very short-lived, yet post-exercise protein synthesis is elevated for 24-48 hours.

i was speaking to not only acute responses, but transient responses including overnight. anyway, these data were counterintuitive and present possible paradigm shifts in how we view the role of exericise-induced hormone respones.

im curious of whether the elevated anabolic responses function different beyond small muscles such as the elbow flexors. they must function for reasons we yet know. something. possibly, systemic wide functions that are muscle group specific. i assume west and collegues are already measuring cross sectional areas of the legs in current experiments.

thoughts?

ob205
04-29-2010, 11:33 AM
[/quote] im curious of whether the elevated anabolic responses function different beyond small muscles such as the elbow flexors. they must function for reasons we yet know. something. possibly, systemic wide functions that are muscle group specific. i assume west and collegues are already measuring cross sectional areas of the legs in current experiments.

thoughts?[/quote]

Good point TPT, why would they choose an isolation exercise to elicit a hormonal response. Any gym rat would be able to tell you that there is far more whole body stimulation from Deads or squats as opposed to a curl. I too would like to see that study done with a whole body lift with sets of 5-8 reps, 2-3 minutes rest between sets.

JamesKrieger
04-29-2010, 12:36 PM
im curious of whether the elevated anabolic responses function different beyond small muscles such as the elbow flexors. they must function for reasons we yet know.


I'm not sure though that we should assume that acute hormone responses must have a function, at least in terms of adaptations to resistance exercise. IMO they are simply a correlational phenomenon.

For example, with the post-training hormonal response to testosterone, I know some researchers have suggested that it's not increased testosterone output, but simply reduced clearance by the liver. Also, this elevation in testosterone is very short lived, lasting only 15 minutes or so. It doesn't seem logical to think that this would play any role in hypertrophic adaptations.

Regarding the post-training growth hormone response, it's established that the likely cause is drop in pH in the blood, as other things that cause drop in blood pH (like breath holding) also stimulate gH release. This is why short rest training dramatically increases the gH response. However, this is more a correlational phenomenon and doesn't have an impact on the hypertrophic response. This is supported by research which shows no difference in hypertrophy when long rest training is compared to short rest training. In fact, there is one study where hypertrophy gains were non-significantly worse in a group taking short rests.

JamesKrieger
04-29-2010, 12:42 PM
Good point TPT, why would they choose an isolation exercise to elicit a hormonal response.


They didn't. They used a leg exercise to elicit the hormonal response.




Any gym rat would be able to tell you that there is far more whole body stimulation from Deads or squats as opposed to a curl.


But gym rats are basing this off of conjecture and not scientific data.

The researchers got a sizeable hormone response from the leg exercise, and it had no impact on protein synthesis or changes in muscle size in the arms. That was the point of the study....to stimulate a hormonal response with a large muscle group exercise, and see if the whole body hormone response enhanced the gains observed in the arms. It didn't.

Will Brink
04-29-2010, 03:28 PM
In what study was this established?

The studies you used for you a meta-analysis no? Multi set vs single set protocols have been compared since what, the early 90s? As you are the author, and did all the digging, I will refer to you feedback.

Will Brink
04-29-2010, 03:44 PM
I'm not sure though that we should assume that acute hormone responses must have a function, at least in terms of adaptations to resistance exercise.

Perhaps the initiating factor to the "downstream" effects that leads to the adaptations from resistance training, or purely correlational as you mention. Regardless, Personally, I have never put much stock in the acute hormonal effects as short lived spikes in various hormones are easy to achieve minus any effects on strength or bodycomp.

ob205
04-29-2010, 08:25 PM
Perhaps the initiating factor to the "downstream" effects that leads to the adaptations from resistance training, or purely correlational as you mention. Regardless, Personally, I have never put much stock in the acute hormonal effects as short lived spikes in various hormones are easy to achieve minus any effects on strength or bodycomp.


Will,
Do you feel that short spikes of insulin have little effect on body comp too? Insulin seems to have had a profound affect on the physiques of todays champions.

TPT
04-29-2010, 09:08 PM
im curious of whether the elevated anabolic responses function different beyond small muscles such as the elbow flexors. they must function for reasons we yet know. something. possibly, systemic wide functions that are muscle group specific. i assume west and collegues are already measuring cross sectional areas of the legs in current experiments.

thoughts?


Good point TPT, why would they choose an isolation exercise to elicit a hormonal response. Any gym rat would be able to tell you that there is far more whole body stimulation from Deads or squats as opposed to a curl. I too would like to see that study done with a whole body lift with sets of 5-8 reps, 2-3 minutes rest between sets.


just to clarify- west et al. (2010) had subjects train each arm on separate days for 15 weeks. in the low hormone condition, one arm performed preacher curl exercise only and consisted of 3-4 sets of 8-12 repetitions at a load that was 95% of their 10 rm and failure occurred during the final set.

while in the high hormone condition the other arm performed the same curl exercise followed immediately by leg resistance exercises designed to elicit large increases in hormones. exercises were performed in the other arm and consisted of the same curl exercise, but followed by 5 sets of 10 repetitions of leg press, 3 sets of 12 repetitions of superset leg extension/leg curl i.e., 1 set of each exercise back-to-back with no rest 90% of 10 rm. between-set rest intervals for arm and leg exercises were 130 and 60 s, respectively.

in weeks 1-6 the subjects trained each arm three times over two weeks. they allowed 72 h between low hormone and high hormone training days. e.g., monday was high hormone training, tuesday low, friday high and wee 2 alternatedly training days the same.

in weeks 7-15, a fourth training session was added. e.g., high on monday, low on tuesday, high on thursday, and low on friday.

keep in mind that each subject performed both conditions. this should raise some concerns.

TPT
04-29-2010, 09:21 PM
I'm not sure though that we should assume that acute hormone responses must have a function, at least in terms of adaptations to resistance exercise. IMO they are simply a correlational phenomenon.

For example, with the post-training hormonal response to testosterone, I know some researchers have suggested that it's not increased testosterone output, but simply reduced clearance by the liver. Also, this elevation in testosterone is very short lived, lasting only 15 minutes or so. It doesn't seem logical to think that this would play any role in hypertrophic adaptations.

Regarding the post-training growth hormone response, it's established that the likely cause is drop in pH in the blood, as other things that cause drop in blood pH (like breath holding) also stimulate gH release. This is why short rest training dramatically increases the gH response. However, this is more a correlational phenomenon and doesn't have an impact on the hypertrophic response. This is supported by research which shows no difference in hypertrophy when long rest training is compared to short rest training. In fact, there is one study where hypertrophy gains were non-significantly worse in a group taking short rests.

understood. id still tread lightly in assuming that acute anabolic responses dont serve any strength or hypertrophic functions. especially, test.

though could the alternating training conditions with alternating anabolic responses set the occasion for similar strength and hypertrophic effects of both arms?

the next step in design would be to conduct a between-subjects design to rule out some sort of cross education effect or something similar where the anabolic responses to training one arm/leg doesnt confound outcomes of the contralateral arm.

Abraxas
04-30-2010, 03:49 AM
The effect of resistive exercise rest interval on hormonal response,
strength, and hypertrophy with training.

Buresh R (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Buresh%20R%22%5BAuthor%5D), Berg K (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Berg%20K%22%5BAuthor%5D), French J (http://www.ncbi.nlm.nih.gov/pubmed?term=%22French%20J%22%5BAuthor%5D).
Department of Health, Kennesaw State University, Kennesaw, Georgia, USA. rburesh@nebrwesleyan.edu
Abstract

The purpose of this study was to compare the effects of different between-set rest periods (1 and 2.5 minutes) on changes in hormone response, strength, arm cross-sectional area (CSA), thigh muscular cross-sectional area (MCSA), and body composition during a 10-week training period. Twelve untrained males (24.8 +/- 5.9 years) engaged in resistance training using either 1 minute (short rest [SR], n = 6) or 2.5 minutes (long rest [LR], n = 6) of rest between sets, with a load that elicited failure on the third set of each exercise. Body composition, thigh MCSA, arm CSA, and five-repetition maximum (RM) squat and bench press were assessed before and after training. Blood samples were collected after exercise in weeks 1, 5, and 10. In week 1, postexercise plasma testosterone levels were greater in SR (0.41 +/- 0.17 mmolxL) than in LR (0.24 +/- 0.06 mmol x L, p < 0.05), and postexercise cortisol levels were greater in SR (963 +/- 313 mmol x L) than in LR (629 +/- 127 mmol x L, p < 0.05). Week 1 postexercise GH levels were not different (p = 0.28). The differences between hormone levels in weeks 5 and 10 were not significant. Arm CSA increased more with LR (12.3 +/- 7.2%) than with SR (5.1 +/- 2.9%, p < 0.05). There were no differences in strength increases. These results show that in healthy, recently untrained males, strength training with 1 minute of rest between sets elicits a greater hormonal response than 2.5-minute rest intervals in the first week of training, but these differences diminish by week 5 and disappear by week 10 of training. Furthermore, the hormonal response is highly variable and may not necessarily be predictive of strength and lean tissue gains in a 10-week training program.

http://www.ncbi.nlm.nih.gov/pubmed/19077743


Short vs. long rest period between the sets in hypertrophic resistance training: influence on muscle strength, size, and hormonal adaptations in trained men.

Ahtiainen JP (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Ahtiainen%20JP%22%5BAuthor%5D), Pakarinen A (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Pakarinen%20A%22%5BAuthor%5D), Alen M (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Alen%20M%22%5BAuthor%5D), Kraemer WJ (http://www.ncbi.nlm.nih.gov/pubmed?term=%22Kraemer%20WJ%22%5BAuthor%5D), Häkkinen K (http://www.ncbi.nlm.nih.gov/pubmed?term=%22H%C3%A4kkinen%20K%22%5BAuthor%5D).
Department of Biology of Physical Activity & Neuromuscular Research Center, University of Jyväskylä, Jyväskylä, Finland. ahtiainen@sport.jyu.fi
Abstract

Acute and long-term hormonal and neuromuscular adaptations to hypertrophic strength training were studied in 13 recreationally strength-trained men. The experimental design comprised a 6-month hypertrophic strength-training period including 2 separate 3-month training periods with the crossover design, a training protocol of short rest (SR, 2 minutes) as compared with long rest (LR, 5 minutes) between the sets. Basal hormonal concentrations of serum total testosterone (T), free testosterone (FT), and cortisol (C), maximal isometric strength of the leg extensors, right leg 1 repetition maximum (1RM), dietary analysis, and muscle cross-sectional area (CSA) of the quadriceps femoris by magnetic resonance imaging (MRI) were measured at months 0, 3, and 6. The 2 hypertrophic training protocols used in training for the leg extensors (leg presses and squats with 10RM sets) were also examined in the laboratory conditions at months 0, 3, and 6. The exercise protocols were similar with regard to the total volume of work (loads x sets x reps), but differed with regard to the intensity and the length of rest between the sets (higher intensity and longer rest of 5 minutes vs. somewhat lower intensity but shorter rest of 2 minutes). Before and immediately after the protocols, maximal isometric force and electromyographic (EMG) activity of the leg extensors were measured and blood samples were drawn for determination of serum T, FT, C, and growth hormone (GH) concentrations and blood lactate. Both protocols before the experimental training period (month 0) led to large acute increases (p < 0.05-0.001) in serum T, FT, C , and GH concentrations, as well as to large acute decreases (p < 0.05-0.001) in maximal isometric force and EMG activity. However, no significant differences were observed between the protocols. Significant increases of 7% in maximal isometric force, 16% in the right leg 1RM, and 4% in the muscle CSA of the quadriceps femoris were observed during the 6-month strength-training period. However, both 3-month training periods performed with either the longer or the shorter rest periods between the sets resulted in similar gains in muscle mass and strength. No statistically significant changes were observed in basal hormone concentrations or in the profiles of acute hormonal responses during the entire 6-month experimental training period. The present study indicated that, within typical hypertrophic strength-training protocols used in the present study, the length of the recovery times between the sets (2 vs. 5 minutes) did not have an influence on the magnitude of acute hormonal and neuromuscular responses or long-term training adaptations in muscle strength and mass in previously strength-trained men.

http://www.ncbi.nlm.nih.gov/pubmed/16095405

Will Brink
04-30-2010, 04:32 PM
Will,
Do you feel that short spikes of insulin have little effect on body comp too? Insulin seems to have had a profound affect on the physiques of todays champions.

Insulin is taken with T, other AAS, GH, etc, etc so can't really make a general statement like that. There's also long acting insulin that used, and it may be the effects it has on downstream issues, such as IGFBPs, IGF-1, etc. From a "real world" perspective, I consider it a moot issue whether it's acute, longer, or a combo of both.

JamesKrieger
05-06-2010, 12:26 PM
The studies you used for you a meta-analysis no? Multi set vs single set protocols have been compared since what, the early 90s? As you are the author, and did all the digging, I will refer to you feedback.

Hi, Will,

The problem is that many of these studies don't show significant differences in hypertrophy. A few do, but most do not. The main problem is that measures of hypertrophy are very insensitive and highly variable. Most resistance training studies lack the statistical power to detect differences between groups in hypertrophy when it comes to single versus multiple set training. And only one (Ostrowski) has attempted to look at dose response effects, but Ostrowski also had insufficient subject numbers.

ctmusc
08-31-2010, 09:04 AM
I'm curious how the author adjusted for kinesiology in this study. Its well know that your body learns to do something better with repetition. People doing 4 times as many sets would have a better ability to go to failure than people doing 1 set. Also, would a no rest, down the rack set (a variation of multiple sets) work better than just one set or multiple sets.

TPT
10-17-2010, 11:51 AM
This was a follow-up editorial by Kreiger regarding the previous highlighted study and summary of the literature with applications to the gym.



Strength & Conditioning Journal:
June 2010 - Volume 32 - Issue 3 - pp 30-32
doi: 10.1519/SSC.0b013e3181df16f4
Article

Determining Appropriate Set Volume for Resistance Exercise

Krieger, James MS

Abstract


DETERMINING THE APPROPRIATE NUMBER OF SETS PER EXERCISE IS AN IMPORTANT PART OF DESIGNING A RESISTANCE TRAINING PROGRAM. EVIDENCE FROM A RECENTLY PUBLISHED META-ANALYSIS INDICATES THAT 2-3 SETS PER EXERCISE PRODUCE 46% GREATER STRENGTH GAINS THAN A SINGLE SET. LITTLE BENEFIT IS OBSERVED FOR MORE THAN 3 SETS. FOR CLIENTS INTERESTED IN GENERAL FITNESS OR WHO LACK TIME, A SINGLE SET IS APPROPRIATE. THREE SETS PER EXERCISE IS AN APPROPRIATE STARTING POINT FOR CLIENTS LOOKING FOR MAXIMAL STRENGTH GAINS. ADJUSTMENTS CAN BE MADE FROM THESE STARTING POINTS BASED ON CLIENT RESPONSE.

The design of a resistance training program requires the appropriate manipulation of a variety of variables, all of which can affect the adaptations to a resistance training program. These variables include but are not limited to frequency, intensity, and volume. A primary way that training volume can be manipulated is through the number of sets performed per exercise and per muscle group. Thus, the number of sets can have a strong impact on the morphological and performance-based outcomes of a resistance training program. The response of the body to changes in set volume can be viewed as a dose-response relationship. For example, as the dose of a drug is increased, the body's response to that drug increases, until a plateau is reached. If the drug dose continues to increase, there is no further increase in the body's response to the drug, but an increase in side effects can occur. Similarly, as the number of sets of a resistance exercise increases, the body's response (the increase in strength and muscle mass) may increase. However, at some point, this response will plateau, and too many sets may increase the risk of injury.

The personal trainer should take an evidence-based approach when it comes to program design for a client. However, the evidence regarding the appropriate number of sets has not been straightforward. Review articles on this topic have come to different conclusions as to whether multiple sets can produce superior strength gains (1,3,4,23 (http://forums.rxmuscle.com/#P28)). Most studies published over the past decade have shown multiple sets to result in significantly greater strength gains than single sets (2,5-9,12-14,17,20,21 (http://forums.rxmuscle.com/#P29)). Some published meta-analyses indicate multiple sets to be superior (18,19,24 (http://forums.rxmuscle.com/#P45)); however, these articles have a number of methodological limitations, which has resulted in criticism of their conclusions (10,16 (http://forums.rxmuscle.com/#P37)). Also, the results of these articles have not been consistent. For example, Rhea et al. (19 (http://forums.rxmuscle.com/#P46)) reported multiple sets to be superior in both trained and untrained subjects, but Wolfe et al. (24 (http://forums.rxmuscle.com/#P51)) reported multiple sets to be superior in trained subjects only.

Another problem is that the majority of resistance training studies compare 1 set with 3 sets per exercise (1,4 (http://forums.rxmuscle.com/#P28)). However, there are many other variations in set volume that can be prescribed. There has been very little research done regarding the dose-response effects of the number of sets on strength gains. Ostrowski et al. (15 (http://forums.rxmuscle.com/#P42)) compared 1, 2, and 4 sets per exercise and reported no significant differences between groups. However, the variability of the responses and the small number of subjects per group limit the statistical power to detect differences between groups. Rhea et al. (19 (http://forums.rxmuscle.com/#P46)) looked at dose-response effects with a meta-analysis, reporting 4 sets per muscle group to be the optimal number for both trained and untrained subjects. However, as mentioned earlier, the limitations of the study design indicate that the results should be interpreted with caution. Also, since Rhea et al. reported the data as sets per muscle group, the sets-per-exercise problem is not adequately addressed. Given the lack of convincing scientific data regarding the dose-response effects of the number of sets, it can be difficult for the personal trainer to decide what number is appropriate for a client.

A recent meta-analysis was published in the Journal of Strength and Conditioning Research to try to shed more light on the dose-response effects of the number of sets per exercise (10 (http://forums.rxmuscle.com/#P37)). This meta-analysis had 2 purposes: to address the criticisms of previous meta-analyses in this area and to establish a dose-response relationship of set volume on strength. The main finding was that a single set per exercise resulted in strength gains, but multiple sets were superior. Specifically, 2-3 sets per exercise was associated with 46% greater strength gains than 1 set, and no further benefit was observed for more than 3 sets. These findings applied to both trained and untrained subjects, upper- and lower-body exercises, and a variety of training frequencies. These findings were also true whether or not multiple exercises were performed per muscle group.

The main limitation of this recent analysis is that there were only 2 studies included that incorporated 4 or more sets per exercise. This limits the statistical power to detect significant differences. It is still possible that 4 or more sets could result in greater strength gains than 2-3 sets, but more research in this area will be needed to answer this question. What is apparent is that there is a plateau in strength gains once you get to 4-6 sets per exercise; 2-3 sets resulted in 46% greater gains than 1 set, whereas 4-6 sets only resulted in 13% greater gains than 2-3 sets. The reason for this plateau is not currently known. It is known that mechanical loading stimulates protein synthesis in skeletal muscle (22 (http://forums.rxmuscle.com/#P49)), and increasing loads result in greater responses until a plateau is reached (11 (http://forums.rxmuscle.com/#P38)). It is likely that protein synthesis responds in a similar manner to the number of sets (i.e., an increasing response as the number of sets are increased, until a plateau is reached), although there is no research examining this.
The findings of this analysis allow for a number of practical applications that personal trainers can use in their program designs:

1. If a client is only interested in general fitness and does not need maximal gains in strength, then 1 set per exercise is a sufficient stimulus to improve strength. Also, clients who are lacking time can still experience strength gains by doing only 1 set to failure or near-failure per exercise.

2. If a client is interested in maximal strength gains, then multiple sets per exercise are necessary. Because the majority of studies in this meta-analysis compared 1 set with 3 sets per exercise, than 3 sets per exercise is an appropriate starting point for a client. Because these numbers are based on averages, individual client responses may vary. Thus, set volume can be adjusted up or down from this starting point based on client response and tolerance.

3. The point of diminishing returns appears to be above 3 sets per exercise. In this meta-analysis, 4-6 sets per exercise was not significantly different from 2-3 sets. Thus, there is little additional benefit to doing more than 3 sets per exercise, although individual responses may vary.

4. There is no need to differentiate between trained and untrained subjects in regards to set volume; both are equally likely to benefit from multiple sets. However, for clients with little resistance training experience, it is probably prudent to keep initial volume to 1-2 sets per exercise to help prevent the delayed-onset muscle soreness that usually accompanies unaccustomed exercise. Set volume can then be progressed.

5. These set volumes are considered work sets and do not include warm-up sets.

There are still questions that science needs to answer regarding program design. For example, is it beneficial to incorporate multiple exercises targeting the same muscle group? The recent meta-analysis found no benefit to doing multiple exercises, although it was not specifically designed to answer this question. Also, more research is needed looking at dose-response relationships in regards to the number of sets; there are very few studies that use volumes of more than 3 sets per exercise (13,15 (http://forums.rxmuscle.com/#P40)). Another question that needs to be answered is the relationship between the number of sets and intensity. The studies in the recent meta-analysis involved an average of 7-10 repetition maximum (RM) per set. The optimal set volume for higher training intensities (1-5 RM) has not been adequately investigated.

Although scientists have more to investigate regarding other topics, the evidence in the single versus multiple set debate overwhelmingly favors multiple sets. It is also clear that there is a dose-response relationship in regards to set volume and strength, with an apparent plateau in the response beyond 3 sets per exercise. Clients who want maximal strength gains are best off doing 2-3 sets per exercise, whereas clients who just want to stay fit or lack time can achieve moderate strength improvements with a single set. It should also be noted that these conclusions are limited to general fitness and maximal strength and that the appropriate set volume may be different for other goals such as hypertrophy, power, and endurance. As always, a personal trainer should tailor a client's program to his/her individual needs, goals, and limitations.

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Keywords: volume; sets; strength; meta-analysis

sarcoplasm
11-30-2010, 11:12 AM
Mr Krieger
What role does exercise frequency have in all of this? Is 1 work set 3x's weekly equivalent to, 3 work sets once a week ect? Thank you

Nic Brunicardi
12-04-2010, 06:13 AM
A variable that I find most studies done on this subject doesn't include is the number of exercises done for that particular muscle group.
For example leg extensions are often used in the tests as the exercise performed either with a single set or multiple sets - but what if your workout includes multiple exercises (which most trainers and trainees prefer)?

I've found via trial and error (not scientific at all) that 2-3 exercises per muscle group done with maybe 1 or 2 warm-ups (going far from all out) and then 1 set going to failure creates the best results for me. And this is done with high frequency (each muscle group is trained 2-3 time per week). I also vary the rep ranges from time to time.

MikeS
12-05-2010, 10:48 AM
The original meta-analysis done in April looked at number of sets for 'hypertrophy'.....the paper just above seemingly following on from Aprils efforts talk about number of sets for 'strength'. Although hypertrophy can be a byproduct of getting stronger the two are different phenomenon and terms should not be used interchangeably...

Research needs to start looking at the effects of multiple sets&multiple exercises per bodypart...

BiggTexx
02-04-2011, 05:01 PM
just published for more chatter.


Single vs. Multiple Sets of Resistance Exercise for Muscle Hypertrophy: A Meta-Analysis (http://journals.lww.com/nsca-jscr/Fulltext/2010/04000/Single_vs__Multiple_Sets_of_Resistance_Exercise.36 .aspx)

Krieger, James W
The Journal of Strength & Conditioning Research. 24(4):1150-1159, April 2010.
doi: 10.1519/JSC.0b013e3181d4d436


Yet more evidence............

Nicholas A Burd, Andrew M Holwerda, Keegan C Selby, Daniel WD West, Aaron W Staples, Nathan E Cain, Joshua G Cashaback, James R Potvin, Steven K Bakerand Stuart M Phillips. Resistance exercise volume affects myofibrillar protein synthesis and anabolic signalling molecule phosphorylation in young men. J Physiol. 2010 Jun 25. [Epub ahead of print].

Abstract

We aimed to determine if any mechanistic differences exist between a single (1SET)- versus multiple-sets (i.e., 3 sets; 3SET) of resistance exercise by utilizing a primed constant infusion of [ring-13C6] phenylalanine to determine myofibrillar protein synthesis (MPS) and Western blot analysis to examine anabolic signalling molecule phosphorylation following an acute bout of resistance exercise. Eight resistance-trained men (24±5 years, BMI= 25±4 kg·m-2) were randomly assigned to perform unilateral leg extension exercise at 70% concentric 1 repetition maximum (1RM) until volitional fatigue for 1SET or 3SET. Biopsies from the vastus lateralis were taken at rest, 5 h Fed, 24 h Fast, 29 h Fed post-exercise in the fasted- and fed- (20g of whey protein isolate) states. Fed-state MPS was transiently elevated above rest at 5 h for 1SET (2.3-fold) and returned to resting levels by 29 h post-exercise. However, the exercise induced increase in MPS following 3SET was superior in amplitude and duration as compared to 1SET at both 5 h (3.1-fold above rest) and 29 h post-exercise (2.3-fold above rest). Phosphorylation p70S6K demonstrated a coordinated increase with MPS at 5 h and 29 h post-exercise such that the extent of p70S6K phosphorylation was related to the MPS response (r=0.338, P=0.033). Phosphorylation of p90RSK and rps6 was similar for 1SET and 3SET at 24 h Fast and 29 h Fed, respectively. However, 3SET induced a greater activation of eIF2Bå and rpS6 at 5 h Fed. These data suggest that 3SET of resistance exercise are more anabolic than 1SET and may lead to greater increases in myofibrillar protein accretion over time.

In this study 8 experienced weightlifters (~1.5 years) were assigned 1/2 to do leg extensions 1 set until failure and 1/2 to do 3 sets at 70%. After the training all subjects were given a 20g whey protein shake.

Myofibrillar protein fractional synthesis rate was determined by taking muscle biopsy samples from the subjects before exercise and 5 and 29 hours PWO. This data was used to determine the protein increases in teh subjects.

As shown in the data below the myofibrillar protein fractional synthesis rate was significantly higher with 3 sets that 1 set to failure at the 5th and 29th hour.


http://ergo-log.com/plaatjes/1or3sets.gif

In the tissue samples, the researchers measured the activity of signal proteins which tell the muscle cells to make more contracting muscle proteins. If this signal protein is active, it called phosphorylated which means it has a phosphorus group attached to it. The researchers observed some pretty interesting things going on with the signal protein p70S6K. The more active it became, the faster the cells grew. So what does this mean? Simple, it mean you grow muscle much faster. As shown in the graph below.

http://ergo-log.com/plaatjes/1or3sets3.gif
The graph below shows the activity of p70S6K at 5, 24 and 29 hours after the training session. The measurement done 24 hours after the training session took place before the subjects had eaten. You’ll notice that on the day after a 3-set training session, a meal [high protein of course] activates the anabolic machinery in the muscle cells again. This is a very important boost in growth over 1 set to failure.

http://ergo-log.com/plaatjes/1or3sets2.gif

BiggTexx
02-04-2011, 05:10 PM
But there are question marks as to whether damage is necessary to increase muscle size, or even desirable. In fact, there is some research showing superior results for hypertrophy with concentric-only training (which does little tissue damage) compared to eccentric-only training (which is damaging to tissue), although data is not consistent in this area.



Recent research has shown that the acute anabolic hormonal response to a training session plays no role in the hypertrophy process.


Goldberg AL, Etlinger JD, Goldspink DF, Jablecki C. Mechanism of work-induced hypertrophy of skeletal muscle. Med Sci Sports, 1975 Fall;7(3):185-98.
Abstract

Skeletal muscle can undergo rapid growth in response to a sudden increase in work load. For example, the rat soleus muscle increases in weight by 40% within six days after the tendon of the synergistic gas' ocnemius is sectioned. Such growth of the overworked muscle involves an enlargement of muscle fibers and occasional longitudinal splitting. Hypertrophy leads to greater maximal tension development, although decreased contraction time and reduced contractility have also been reported. Unlike normal developmental growth, work-induced hypertrophy can be induced in hypophysectomized or diabetic animals. This process thus appears independent of growth hormone and insulin as well as testosterone and thyroid hormones. Hypertrophy of the soleus can also be induced in fasting animals, in which there is a generalized muscle wasting. Thus muscular activity takes precedence 'over endocrine influences on muscle size. The increase in muscle weight reflects an increase in protein, especially sarcoplasmic protein, and results from greater protein synthesis and reduced protein breakdown. Within several hours after operation, the hypertrophying soleus shows more rapid uptake of certain amino acids and synthesis of phosphatidyl-inositol. By 8 hours, protein synthesis is enhanced. RNA synthesis also increases, and hypertrophy can be prevented with actinomycin D. Nuclear DNA synthesis also increases on the second day after operation and leads to a greater DNA content. The significance of the increased RNA and DNA synthesis is not clear, since most of it occurs in interstitial and satellite cells. The proliferation of the non-muscle cells seems linked to the growth of the muscle fibers; in addition, factors causing muscle atrophy (e.g. denervation) decrease DNA synthesis by such cells. In order to define more precisely the early events in hypertrophy, the effects of contractile activity were studied in rat muscles in vitro. Electrical stimulation enhanced active transport of certain amino acids within an hour, and the magnitude of this effect depended on the amount of contractile activity. Stimulation or passive stretch of the soleus or diaphragm also retarded protein degradation. Presumably these effects of mechanical activity contribute to the changes occuring during hypertrophy in vivo. However, under the same conditions, or even after more prolonged stimulation, no change in rates of protein synthesis was detected. These findings with passive tension in vitro are particularly interesting, since passive stretch has been reported to retard atrophy or to induce hypertrophy of denervated muscle in vivo. It is suggested that in; creased tension development (either passive or active) is the critical event in initiating compensatory growth.

Increases in muscle size have largely been attributed to two factors: the mechanical load (tension on muscle) and the growth factor environment that the muscle experiences (external hormones such as testosterone and GH). However, in this study done in 1975, Goldberg, realized that if you took a rat and induced tension overload by putting a muscle on stretch (eccentric contractions) it woud not stop muscle growth from occurring. He further experimented byremoved their pituitary so they could not produce GH or IGF-1, castrated them so they could not produce testosterone, removed their thyroid, or just didn't feed them. Despite all of this, the rats still had increases in muscle hypertrophy in their legs. Goldberg suggested that mechanical overload increases muscle hypertrophy independent of testosterone. Goldberg further noted in a review of his research on muscle hypertrophy, "Maximal tension development leads to increases in muscle hypertrophy. The hypertrophy process thus appears independent of growth hormone and insulin as well as testosterone and thyroid hormones. Hypertrophy can also be induced in fasting animals, in which there is a generalized muscle wasting. Thus, muscular activity takes precedence over endocrine influences on muscle size."


Two other studies of interest and both are related to "intramuscular growth factors" that are independent of peripheral levels of hormones such as IGF-1.



K. M. Heinemeier, J. L. Olesen, P. Schjerling, F. Haddad, H. Langberg, K. M. Baldwin, and M. Kjaer. Short-term strength training and the expression of myostatin and IGF-I isoforms in rat muscle and tendon: differential effects of specific contraction types. J Appl Physiol, Feb 2007; 102: 573 - 581.
Abstract

In skeletal muscle, an increased expression of insulin like growth factor-I isoforms IGF-IEa and mechano-growth factor (MGF) combined with downregulation of myostatin is thought to be essential for training-induced hypertrophy. However, the specific effects of different contraction types on regulation of these factors in muscle are still unclear, and in tendon the functions of myostatin, IGF-IEa, and MGF in relation to training are unknown. Female Sprague-Dawley rats were subjected to 4 days of concentric, eccentric, or isometric training (n = 7–9 per group) of the medial gastrocnemius, by stimulation of the sciatic nerve during general anesthesia. mRNA levels for myostatin, IGF-IEa, and MGF in muscle and Achilles' tendon were measured by real-time RT-PCR. Muscle myostatin mRNA decreased in response to all types of training (2- to 8-fold) (P < 0.05), but the effect of eccentric training was greater than concentric and isometric training (P < 0.05). In tendon, myostatin mRNA was detected, but no changes were seen after exercise. IGF-IEa and MGF increased in muscle (up to 15-fold) and tendon (up to 4-fold) in response to training (P < 0.01). In tendon no difference was seen between training types, but in muscle the effect of eccentric training was greater than concentric training for both IGF-IEa and MGF (P < 0.05), and for IGF-IEa isometric training had greater effect than concentric (P < 0.05). The results indicate a possible role for IGF-IEa and MGF in adaptation of tendon to training, and the combined changes in myostatin and IGF-IEa/MGF expression could explain the important effect of eccentric actions for muscle hypertrophy.
In a Heinemeier et.al. (2007) study researchers able to distinguish between the effects of the mechanical load and the peripheral growth factors such as IGF-1. As a result using transgenic mice researchers found they could directly determine the contribution of mechanical loading independently of systemic and external growth factors. Since growth factors play an important role in developmental growth, the muscles of the transgenic mice were not responsive to IGF-1 as expected and had smaller muscle size than normal mice. The surprise comes when the muscles of the IGF-1-deficient mice were challenged with an increased muscle overload. Whereas the prevailing hypothesis would predict a diminished ability to grow, the muscles of the transgenic IGF-1-deficient mice grew in response to overload and activated mTOR in muscle to the same extent as controls. The implication is that the activation of mTOR and muscle growth is entirely dictated by the mechanical load the muscle experiences. So according to these finding if two bodybuilders have similar IGF-1 levels, the bodybuilder who trains with more muscle tension is going to grow more. Muscle tension in this case in not time-under-tension but instead the amount of load applied to the muscle. In other words. The regardless of the amount of IGF-1 those of us who train with heavier weight will grow more.

McKoy G, Ashley W, Mander J, Yang SY, Williams N, Russell B, Goldspink G. Expression of insulin growth factor-1 splice variants and structural genes in rabbit skeletal muscle induced by stretch and stimulation.
J Physiol. 1999 Apr 15;516 ( Pt 2):583-92.
Abstract

Skeletal muscle is a major source of circulating insulin growth factor-1 (IGF-1), particularly during exercise. It expresses two main isoforms. One of the muscle IGF-1 isoforms (muscle L.IGF-1) is similar to the main liver IGF-1 and presumably has an endocrine action. The other muscle isoform as a result of alternative splicing has a different 3' exon sequence and is apparently designed for an autocrine/paracrine action (mechano-growth factor, MGF). Using RNase protection assays with a probe that distinguishes these differently spliced forms of IGF-1, their expression and also the expression of two structural genes was measured in rabbit extensor digitorum longus muscles subjected to different mechanical signals. 2. Within 4 days, stretch using plaster cast immobilization with the limb in the plantar flexed position resulted in marked upregulation of both forms of IGF-1 mRNA. Electrical stimulation at 10 Hz combined with stretch (overload) resulted in an even greater increase of both types of IGF-1 transcript, whereas electrical stimulation alone, i.e. without stretch, resulted in no significant increase over muscle from sham-operated controls. Previously, it was shown that stretch combined with electrical stimulation of the dorsiflexor muscles in the adult rabbit results in a marked increase in muscle mass involving increases in both length and girth, within a few days. The expression of both systemic and autocrine IGF-1 growth factors provides a link between the mechanical signal and the marked increase in the structural gene expression involved in tissue remodelling and repair. 3. The expression of the beta actin gene was seen to be markedly upregulated in the stretched and stretched/stimulated muscles. It was concluded that the increased expression of this cytoskeletal protein gene is an indication that the production of IGF-1 may initially be a response to local damage. 4. Switches in muscle fibre phenotype were studied using a specific gene probe for the 2X myosin heavy chain gene. Type 2X expression was found to decrease markedly with stimulation alone and when electrical stimulation was combined with stretch. Unlike the induction of IGF-1 and beta actin, the decreased expression of the 2X myosin mRNA was less marked in the 'stretch only' muscles. This indicates that the interconversion of fibre type 2X to 2A may in some situations be commensurate with, but not under the control of IGF-1.

Bamman MM, Shipp JR, Jiang J, Gower BA, Hunter GR, Goodman A, McLafferty CL Jr, Urban RJ. Mechanical load increases muscle IGF-1 and androgen receptor mRNA concentrations in humans. Am J Physiol Endocrinol Metab, 2001 Mar;280(3):E383-90.
Abstract
The mechanism(s) of load-induced muscle hypertrophy is as yet unclear, but increasing evidence suggests a role for locally expressed insulin-like growth factor I (IGF-I). We investigated the effects of concentric (CON) vs. eccentric (ECC) loading on muscle IGF-I mRNA concentration. We hypothesized a greater IGF-I response after ECC compared with CON. Ten healthy subjects (24.4 ± 0.7 yr, 174.5 ± 2.6 cm, 70.9 ± 4.3 kg) completed eight sets of eight CON or ECC squats separated by 6-10 days. IGF-I, IGF binding protein-4 (IGFBP-4), and androgen receptor (AR) mRNA concentrations were determined in vastus lateralis muscle by RT-PCR before and 48 h after ECC and CON. Serum total testosterone (TT) and IGF-I were measured serially across 48 h, and serum creatine kinase activity (CK), isometric maximum voluntary contraction (MVC), and soreness were determined at 48 h. IGF-I mRNA concentration increased 62% and IGFBP-4 mRNA concentration decreased 57% after ECC (P < 0.05). Changes after CON were similar but not significant (P = 0.06-0.12). AR mRNA concentration increased (P < 0.05) after ECC (63%) and CON (102%). Serum TT and IGF-I showed little change. MVC fell 10% and CK rose 183% after ECC (P < 0.05). Perceived soreness was higher (P < 0.01) after ECC compared with CON. Results indicate that a single bout of mechanical loading in humans alters activity of the muscle IGF-I system, and the enhanced response to ECC suggests that IGF-I may somehow modulate tissue regeneration after mechanical damage.

Researchers are now finding out that the signaling pathway by which contracting muscle and intramuscular growth factors such as IGF-1 leads to changes in satellite cells and muscle DNA content. In this study, 10 healthy men completed 8 sets of maximal eccentric squats. The intramuscular IGF-1 mRNA concentration increased 62 percent, but serum testosterone showed little change. This means changes in muscle overload are occurring in the absence of changes in testosterone.


Wilkinson SB, Tarnopolsky MA, Grant EJ, Correia CE, Phillips SM. Hypertrophy with unilateral resistance exercise occurs without increases in endogenous anabolic hormone concentration. Eur J Appl Physiol, Volume 98, Number 6, 546-555. (2006).


Abstract
We aimed to gain insight into the role that the transitory increases in anabolic hormones play in muscle hypertrophy with unilateral resistance training. Ten healthy young male subjects (21.8 ± 0.4 years, 1.78 ± 0.04 m, 75.6 ± 2.9 kg; mean ± SE) engaged in unilateral resistance training for 8 week (3 days/week). Exercises were knee extension and leg press performed at 80–90% of the subject’s single repetition maximum (1RM). Blood samples were collected in the acute period before and after the first training bout and following the last training bout and analyzed for total testosterone, free-testosterone, luteinizing hormone, sex hormone binding globulin, growth hormone, cortisol, and insulin-like growth factor-1. Thigh muscle cross sectional area (CSA) and muscle fibre CSA by biopsy (vastus lateralis) were measured pre- and post-training. Acutely, no changes in systemic hormone concentrations were observed in the 90 min period following exercise and there was no influence of training on these results. Training-induced increases were observed in type IIx and IIa muscle fibre CSA of 22 ± 3 and 13 ± 2% (both P < 0.001). No changes were observed in fibre CSA in the untrained leg (all P > 0.5). Whole muscle CSA increased by 5.4 ± 0.9% in the trained leg (P < 0.001) and remained unchanged in the untrained leg (P = 0.76). Isotonic 1RM increased in the trained leg for leg press and for knee extension (P < 0.001). No changes were seen in the untrained leg. In conclusion, unilateral training induced local muscle hypertrophy only in the exercised limb, which occurred in the absence of changes in systemic hormones that ostensibly play a role in muscle hypertrophy.
In this study 10 healthy young male subjects performed unilateral resistance training for eight weeks (three days/week). Unilateral resistance exercise is basically when you train one arm or in this case leg, while the other arm or leg is used as a control or untrained muscle. Exercises performed in the study were knee extensions and leg presses performed at 80 percent-90 percent of the subject's 1 RM. Blood samples were collected before, immediately after, 30, 60, 90 and 120 minutes post-exercise. Subjects were analyzed after the first training bout and following the last training bout for total testosterone, free testosterone, GH and IGF-1, along with other hormones. Thigh muscle cross-sectional area of the vastus lateralis were measured pre- and post-training. Acutely, no changes in GH, testosterone or IGF-1 concentrations were observed in the 90-minute period following exercise and there was no influence of training on the anabolic hormones measured. GH did show a moderate increase 30 minutes post-exercise, but returned to baseline values by 90 minutes. Training-induced increases in muscle hypertrophy were observed in type 2 b (beta) and 2 a (alpha) muscle fiber. No changes were observed in muscle size in the untrained leg. In conclusion, unilateral training induced local muscle hypertrophy only in the exercised limb, which occurred in the absence of testosterone, GH, or IGF-1 circulating levels.


In other words.... researchers found that muscle hypertrophy took place without acute increases in anabolic hormone concentrations. How many years have we been told that for optimal growth we heed to lift intensely and take short rest periods (<1)? Apparently the below study which lead us to believe this back in the 90's tis now obsolete.

KRAEMER WJ, L MARCHITELLI, SE GORDON, E HARMAN, JE DZIADOS, R MELLO, P FRYKMAN, D MCCURRY AND SJ FLECK. Hormonal and growth factor responses to heavy resistance exercise protocols. J Appl Physiol, 69:1442–1450. 1990.

To examine endogenous anabolic hormone and growth factor responses to various heavy resistance exercise protocols (HREPs), nine male subjects performed each of six randomly assigned HREPs, which consisted of identically ordered exercises carefully designed to control for load [5 vs. 10 repetitions maximum (RM)], rest period length (1 vs. 3 min), and total work effects. Serum human growth hormone (hGH), testosterone (T), somatomedin-C (SM-C), glucose, and whole blood lactate (HLa) concentrations were determined preexercise, midexercise (i.e., after 4 of 8 exercises), and at 0, 5, 15, 30, 60, 90, and 120 min postexercise. All HREPs produced significant (P less than 0.05) temporal increases in serum T concentrations, although the magnitude and time point of occurrence above resting values varied across HREPs. No differences were observed for T when integrated areas under the curve (AUCs) were compared. Although not all HREPs produced increases in serum hGH, the highest responses were observed consequent to the H10/1 exercise protocol (high total work, 1 min rest, 10-RM load) for both temporal and time integrated (AUC) responses. The pattern of SM-C increases varied among HREPs and did not consistently follow hGH changes. Whereas temporal changes were observed, no integrated time (AUC) differences between exercise protocols occurred. These data indicate that the release patterns (temporal or time integrated) observed are complex functions of the type of HREPs utilized and the physiological mechanisms involved with determining peripheral circulatory concentrations (e.g., clearance rates, transport, receptor binding). All HREPs may not affect muscle and connective tissue growth in the same manner because of possible differences in hormonal and growth factor release.

BiggTexx
02-04-2011, 05:32 PM
So in spite of all the purple crap that some how got on my posting, it seems that applying optimal mechanical stress may be the key to growth. I have found research that determined that 4-11 reps may be optimal, 3-6 sets, with 3 minute or greater rest periods. From what Goldgerg has theorized mechanical stress put in the muscle causes damage which in turn release Mechano Growth Factor.