When training under certain variables, lifting weights can temporarily increase the concentrations of a variety of systemic anabolic hormones, such as testosterone and growth hormone.
Based on my assessment of the literature, it seems performing exercises that involve a large amount of muscle mass, using moderate loads and rap ranges with a good number of sets and short rest intervals evokes the greatest temporary increases in anabolic hormones.
As an example, one paper established that performing 10 sets of 10 repetitions with a 70% one-rep max load on the back squat (with the load adjusted on a set by set basis to ensure the achievement of 10 repetitions) generated significant temporary elevations in total testosterone, free testosterone, and growth hormone. On the whole, these spikes peak anywhere from immediately after to 60 minutes after the training session and thereafter fall.
Table of Contents
- The Hypothesis Behind Spikes in Anabolic Hormones and Hypertrophy
- How We Could Assess if Spikes in Anabolic Hormones Matter
- Correlation Between Anabolic Hormones Spikes and Hypertrophy
- Training Program Comparisons
- Attempting to Explain the Findings of the Literature
- Final Thoughts
The Hypothesis Behind Spikes in Anabolic Hormones and Hypertrophy
For quite a long time, there have been hypotheses that these temporary spikes in anabolic hormones triggered via lifting weights could be important for long-term muscle hypertrophy.
So much so that there have been a considerable number of studies only assessing the temporary anabolic hormonal responses to using a variety of training variables. The idea behind these studies is that by establishing which training variables and exercises best generate anabolic hormonal spikes, we would know what optimally builds muscle.
This isn’t entirely a ludicrous idea, spiking the concentrations of anabolic hormones via lifting weights could theoretically increase the likelihood they exert their anabolic effects.
Let me explain.
Testosterone and Hypertrophy
We know that circulating testosterone (more precisely free testosterone) can bind to what we call androgen receptors located within muscle fibers and thereafter prompt an increase in muscle protein synthesis (which in our case simply references an increase in the proteins that make muscles bigger).
Testosterone can also bind to a membrane-bound receptor to activate something called the PI3K/Akt/mTOR pathway, which is quite a well-known signaling pathway where a variety of specific proteins interact in a chain reaction fashion to generate an increase in muscle protein synthesis.
Considering these events, a spike in circulating testosterone evoked via lifting weights could theoretically increase the likelihood they occur, presumably amplifying muscle hypertrophy.
Growth Hormone, IGF-1, and Hypertrophy
Comparably, growth hormone is primarily believed to exert its anabolic effects via stimulating an increase in IGF-1 production from the liver, IGF-1 thereafter can activate the PI3K/Akt/mTOR pathway. Therefore, a spike in growth hormone concentrations evoked via lifting weights could theoretically increase the likelihood this event occurs.
Non-genomic Roles of Anabolic Hormones
Aside from these gene expression events, there are also nongenomic roles by which a spike in anabolic hormones could heighten long-term muscle hypertrophy.
Testosterone can increase the concentrations of calcium within muscle fibers. Calcium plays a fundamental role in force-producing events. Due to this, a spike in testosterone within a workout can boost calcium concentrations within muscle fibers, thereby enhancing force production which could enhance the degree of tension experienced by the muscle, ultimately leading to more muscle hypertrophy as mechanosensitive proteins within muscle fibers detect tension and thereafter convert tension into a signaling cascade that culminates in an increase in muscle protein synthesis.
How We Could Assess if Spikes in Anabolic Hormones Matter
All of the above hypotheses sound plausible and interesting. However, do they truly occur in reality?
In other words, should you be aiming to train in a way that maximally spikes the anabolic hormone response in order to optimally stimulate muscle hypertrophy?
From the current literature, I believe there are at least 2 ways we could evaluate this.
The first way is to evaluate the correlation between spikes in anabolic hormones and long-term muscle hypertrophy.
That is, do the individuals that experience the greatest spikes in anabolic hormones ultimately experience the greatest muscle hypertrophy. If so, we would have some evidence that temporary spikes in anabolic hormones evoked via lifting weights may be important for building muscle.
The second way is to compare a training program that generates greater temporary spikes in anabolic hormones to one that generates lesser (or even non-existent) spikes in anabolic hormones. If muscle hypertrophy is greater with a training program that generates greater spikes in anabolic hormones, we would have further potential evidence indicating temporary elevations in anabolic hormones is important.
Let us dive into the current literature, starting with the correlation data.
Correlation Between Anabolic Hormones Spikes and Hypertrophy
Studies Finding a Correlation
Intriguingly, two studies have indeed observed a correlation between the magnitude of spikes in anabolic hormones and long-term muscle hypertrophy.
Mangine et al. had 33 men with an average of 5.7 years of training experience perform a range of exercises 4 times per week for 8 weeks.
Every session, subjects trained each exercise for 4 sets with 3-12 repetitions with 70-90% one-rep max load, using 1 to 3 minutes of rest between sets.
Blood samples taken at various time points during training sessions on the first and last week successfully demonstrated training immediately temporarily spiked testosterone, IGF-1, and growth hormone.
Moreover, by the end of the 8th week, thickness and cross-sectional area of the rectus femoris and vastus lateralis (measured at approximately 50% of the thigh bone length) increased.
Most relevant to our discussion, a thorough analysis of the data indicates there was a relationship between the temporary spikes in testosterone and muscle hypertrophy. In other words, it appears the subjects that experienced the greatest temporary increases in testosterone concentrations as a result of training ultimately experienced the highest increases in thickness and cross-sectional area of the rectus femoris and vastus lateralis. The temporary spikes of other hormones, including growth hormone, did not seem predictive of muscle hypertrophy.
However, another study by Mccall et al. somewhat conflicts with this data.
11 men with prior resistance training experience performed a range of exercises each for 3 sets with a 10 rep-max load, using 1 minute of rest between sets, three times per week for 12 weeks.
Blood samples taken at various time points during training sessions in the 4th and 8th week demonstrated that training successfully temporarily elevated growth hormone concentrations, but had little impact on testosterone and IGF-1 concentrations.
Measurements taken before and after the 8 training weeks revealed training increased whole biceps cross-sectional area and cross-sectional area of slow and fast-twitch fibers obtained from the biceps.
Relevant to our discussion, the temporary spikes in growth hormone correlated with increases in slow-twitch as well as fast-twitch fiber cross-sectional area gains. In other words, those that experienced the highest temporary elevations in growth hormone evoked via training tended to experience the most growth of the fast and slow-twitch fibers of the biceps.
There were no other correlations, implying contrary to the Mangine study, there was no association between testosterone spikes and hypertrophy. However, recall testosterone concentrations were virtually unaffected via training, and so this may explain this finding.
Overall, the results of this Mcall et al. study are a little difficult to wrap our heads around. Although a correlation between growth hormone spikes and slow and fast-twitch fiber growth was noted, there was no correlation between growth hormones spikes and increases in whole biceps cross-sectional area, which is difficult to reconcile.
What’s also difficult to reconcile is IGF-1 concentrations were virtually unimpacted via training, and as we noted earlier, it’s thought growth hormone primarily exerts its anabolic effects via stimulating an increase in IGF-1 production from the liver.
Nonetheless, these two studies by Mangine and Mcall, despite conflicting to some degree and having some inconsistencies, broadly indicate some relationship between temporary hormones spikes generated via lifting weights and long-term muscle hypertrophy.
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Studies Finding No Correlation
However, 4 other studies find very weak or non-existent associations between temporary spikes in anabolic hormones and long-term muscle hypertrophy.
West and Phillips found that after 56 men (untrained at least in the last 8 months before the study) trained a variety of exercises each for 2-4 sets of 6-12 reps 5 times per week for 12 weeks, there was no correlation between temporary spikes in free testosterone and growth of slow and fast-twitch fibers from the vastus lateralis, nor was there a correlation between temporary spikes in IGF-1 and growth of slow and fast-twitch fibers from the vastus lateralis.
However, there was a weak correlation between temporary spikes in growth hormone and slow and fast-twitch fiber growth, but again these relationships were very weak. There was also a weak correlation between cortisol temporary spikes and fast-twitch fiber growth, but not slow-twitch fiber growth.
It’s worth mentioning cortisol is actually catabolic, it increases muscle protein breakdown and as such, is considered counteractive to hypertrophy, so this relationship (again, which was weak) between cortisol spikes and fast-twitch fiber growth does not readily make much sense, and perhaps may be best interpreted as a coincidence.
Another study by Fink et al. found after 20 men (untrained at least in the last 2 years leading up to the study) trained a variety of arm exercises each for 3 sets with 8-20 repetitions and between 30 seconds and 3 minutes of rest between sets, there was no correlation between temporary spikes in growth hormone (measured during a training session in the second week) and increases in arm cross-sectional area. No other hormones were assessed in this study.
Thirdly, Mitchell et al. found after 23 men (untrained at least in the year leading up to the study) trained a range of exercises each for 2-4 sets with 6-12 reps, using 60-120 seconds of rest between sets for four times per week for 16 weeks, there was no relationship between any temporary spikes in the main anabolic hormones evoked via an acute training loading protocol (which occurred during the first and last weeks of training) and growth of slow and fast-twitch muscle fibers from the vastus lateralis.
Finally, Morton et al. found after 49 men (with at least 2 years of training experience) trained a range of exercises for 3 sets of 8-25 reps to failure 4 times per week for 12 weeks, there was no relationship between all temporary spikes in the anabolic hormones evoked via an acute training loading protocol (which occurred before and after the training period) and growth of slow and fast-twitch muscle fibers from the vastus lateralis.
So in total, the majority of the current literature fails to find a correlation between temporary spikes evoked via training and long-term muscle hypertrophy.
Training Program Comparisons
Now, this is above data is only correlational data, and it still does not necessarily inform us how a training with a program that generates significant temporary spikes in anabolic hormones compares to a program that generates lesser (if any) spikes in anabolic hormones for direct muscle hypertrophy.
The best way to assess this is to directly analyze the current literature that has looked at this.
Quite interestingly, one study by Ronnestad et al. indicates long-term muscle hypertrophy may be enhanced with a program that generates high temporary spikes in anabolic hormones.
11 previously untrained men had one arm assigned to a low hormone condition and their other arm assigned to a high hormone condition.
Both arms were trained twice per week for 12 weeks.
Each session, the low hormone arm trained the biceps curl, hammer curl, and reverse curl each for 2 sets with a 6-10 rep-max load. This training session, due to involving low amounts of muscle mass, failed to evoke any significant temporary spikes in testosterone or growth hormone.
The high hormone arm, each session, performed exactly what the low hormone arm did, but before doing so, performed the leg press, leg extension, and leg curl each for 3 sets with a 10 rep-max load using 60-90 seconds of rest between sets. Due to these additional leg exercises which involve large amounts of muscle mass, as well as the short rest intervals between sets of them, this lower-body training generated significant spikes in testosterone and growth hormone during the subsequent biceps exercises, with the growth hormone spike remaining further elevated after the completion of the biceps exercises.
By the end of the study, increases in cross-sectional area of the elbow flexors at two proximal sites were similar between both conditions, but at two distal sites, increases were greater for the high hormone arm.
Therefore, this data suggests preceding biceps exercises with lower body training that evokes spikes in testosterone and growth hormone may ultimately enhance overall biceps hypertrophy.
This is quite fascinating, however, a different study by West et al. somewhat conflicts with these findings.
12 previously untrained men had one arm assigned to a low hormone condition and their other arm assigned to a high hormone condition.
Both arms were trained one to two times per week for 15 weeks.
Each session, the low hormone arm performed an arm curl (they weren’t specific on which arm curl) for 3-4 sets of 8-12 repetitions with a 95% 10 rep-max load. Due to the low amounts of muscle mass trained, this exercise failed to temporarily spike free testosterone, growth hormone, or IGF-1.
The high hormone arm, each session, performed exactly what the low hormone arm did, but thereafter performed 5 sets of 10 repetitions on the leg press and 3 sets of 10 repetitions on a leg extension/leg curl superset, both were performed with a 95% 10 rep-max load. Due to these lower body exercises performed after, this session successfully provoked spikes in testosterone, growth hormone, and IGF-1.
Despite this, by the end of the study, increases in cross-sectional area of the elbow flexors at all measured regions were similar between both conditions. Moreover, increases in slow-twitch and fast-twitch fiber cross-sectional area from the elbow flexors were also similar between both conditions.
What could explain the conflicting findings between the West and Ronnestad studies?
The West study had the high hormone condition perform the lower body exercises that evoked spikes in anabolic hormones after the biceps exercise, whereas the Ronnestad study had the high hormone condition perform the lower body exercises before the biceps exercises.
Perhaps performing the lower body exercises that generate spikes in anabolic hormones prior to the biceps exercises, due to resulting in you performing the biceps exercises under elevated anabolic hormone concentrations, somehow potentiates long-term biceps hypertrophy via some mechanism.
One such mechanism might relate to enhanced testosterone and androgen receptor content.
More precisely, creating an elevated anabolic environment via performing lower body exercises prior to biceps training may not only elevate circulating testosterone concentrations but also androgen receptor content within the biceps itself. Such events would presumably enhance the likelihood testosterone can bind to androgen receptors to thereafter provoke an increase in muscle protein synthesis.
I speculate this because one study by Spiering et al. found that performing a range of compound upper body exercises each for 4 sets with a 10 rep-max load (which temporarily spiked testosterone) before performing 5 sets with a 5 rep-max load on a knee extension and flexion dynamometer increased androgen receptor content within the vastus lateralis 180 minutes after exercise. This was in contrast to only performing 5 sets with a 5 rep-max load on the knee extension and flexion dynamometer, which failed to spike testosterone and androgen receptor content within the vastus lateralis.
Stated another way, performing exercises that spike anabolic hormones before training a certain muscle may ultimately increase the androgen receptor content within that certain muscle.
Having said all of this, some data challenges these aforementioned ideas and results.
There exist studies finding that despite a training protocol evoking temporary spikes in testosterone, androgen receptor content actually downregulates in the hours after (that is, it decreases).
Additionally, if spiking anabolic hormones prior to training a muscle enhanced its hypertrophy long-term, we would expect training compound exercises, due to spiking anabolic hormones as they involve large amounts of muscle mass, prior to single-joint biceps and triceps exercises to enhance biceps and triceps hypertrophy.
However, this does not appear to be the case.
Three studies (one, two, and three) have found biceps and/or triceps hypertrophy was similar regardless of if compound or biceps and triceps isolation exercises were performed first in a session. If anything, the results of these studies might favor performing the biceps and triceps isolation exercises first, therefore conflicting with the Ronnestad study.
On the basis of this data, I believe we cannot be certain the results of the Ronnestad study can be truly confirmed, the results might just be random and related to the small sample size of the study.
Moving forward, two further areas of the literature indicate a program that evokes higher spikes in anabolic hormones does not confer additional hypertrophy.
Firstly, Schwanbeck et al. found in men, performing free weight squats and bench presses temporarily spiked free testosterone more than smith machines squats and bench presses. Yet, after an 8 week training period, a free weight program (including the free weight squat and bench press) produced similar increases in quadriceps and biceps thickness to an exclusive machine program (that included the smith machine squat and bench press).
Secondly, as we noted much earlier in this article, using shorter rest intervals between sets (90 seconds or less) tends to evoke greater spikes in anabolic hormones (particularly growth hormone) compared to training with longer rest intervals (2.5 minutes or more). However, as we’ve thoroughly described in our complete guide to rest intervals article, it seems with compound exercises and all other training variables equivalent, resting for 2.5 minutes or more generates more muscle hypertrophy than resting for 90 seconds or less.
Therefore, this free weight vs machine literature, as well as the rest interval literature, together further support the idea that programs that evoke higher temporary spikes in anabolic hormones do not necessarily produce greater long-term hypertrophy.
Attempting to Explain the Findings of the Literature
Combining all of the current evidence assessed thus far, and its apparent training in a way designed to maximally spike anabolic hormones is unnecessary.
Not only are there weak (virtually non-existent) correlations between the magnitude of temporary spikes in anabolic hormones and muscle hypertrophy, but programs that generate higher temporary spikes in anabolic hormones do not appear to enhance muscle hypertrophy.
Why might this be?
The earlier mechanisms we outlined, that spikes in anabolic hormones could increase the likelihood of hormone-receptor interactions that culminate in increased muscle protein synthesis, seemed pretty logical. But evidently, this seems to not be occurring in reality.
There are a few reasons I can think of that could potentially resolve this.
Firstly, receptor content could just downregulate (that is, decrease in number) despite spikes in anabolic hormones, thereby counteracting the increase in anabolic hormones and making it no more likely hormone receptor interactions would be enhanced. Supporting this, and as I noted earlier already, there’s evidence despite training evoking a spike in testosterone, androgen receptor content decreased.
Secondly, it’s important to recognize these temporary spikes in anabolic hormones are typically not very substantial, and it’s quite possible these transient elevations are just too insignificant to influence muscle hypertrophy. Of course, we know that chronic supraphysiological elevations of anabolic hormones (achieved via exogenous administration, that is, you use steroids), very powerfully enhance muscle hypertrophy. Yet, the very transient elevations achieved via training naturally generally do not reach supraphysiological levels.
Thirdly, it’s quite plausible the temporary spikes in anabolic hormones may just simply be a response to the build of metabolites (like lactate) within a muscle and/or be more so oriented towards mobilizing fuel for muscle contraction, rather than promoting an increase in muscle protein synthesis post-exercise.
At this time, I don’t believe we have enough evidence to comment on which of these three reasons (if any) explains the current observations of the literature.
Nonetheless, at the end of the day, I think everything outlined in this article more or less indirectly demonstrates that for natural individuals that are within the normal physiological anabolic hormones ranges, local factors within the muscle are more important for muscle hypertrophy than any systemic factors.
What I mean by this is training sufficiently to stimulate the full spectrum of muscle fibers (which would enable mechanosensitive proteins within the fibers to detect tension and subsequently initiate a signaling cascade the results in an increase in muscle protein synthesis), and then fuelling your muscles correctly via sufficient caloric and protein intake (depending of course on your goals) is far more important for muscle hypertrophy than any transient spike in systemic anabolic hormone concentrations.
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