Training to Failure, or Just Training to Fail?

Training to failure

What you’re getting yourself into

~3300 words, 11-22 minute read time

Key Points

1. When comparing a WIDE array of training variables (number of reps, rest periods, rep speed, and loading), muscle growth is the same if sets are taken to failure.

2. Training to failure is likely safe.  Or, at the very least, there’s no direct evidence that it’s particularly dangerous.

3. Training to complete failure likely isn’t necessary to maximize growth – you can likely leave a couple reps in the tank.  Unfortunately, people aren’t very good at knowing how close to failure they actually are.  Taking a set to failure “idiot-proofs” it to make sure you maximized the stimulus.

4. The bottom line is that training to failure helps make sure you’re actually working hard enough for your muscles to grow, as far as we can tell it’s safe, but it’s neither necessary nor a magic bullet.


Note from Greg: Dan Ogborn’s isn’t a name too many people are familiar with, and that’s a crying shame.  He has a PhD in Medical Sciences specializing in the molecular effects of strength training in muscle, he’s worked as a post-doctoral fellow in muscle physiology, and he’s finishing up his course work to become a physical therapist.  Consequently, it’s not too surprising that he hasn’t had the time to write a ton and work on growing an audience, so he’s been flying under the radar.  I’m really honored that he found the time in his schedule to write this article for Strengtheory.  I’ve been a fan of Dan’s work since 2012, and this article is exactly what I’ve come to expect from him – well-researched but still very relatable and applicable.

A new perspective on training to failure for muscle hypertrophy

Failure: the proverbial “F” word of the training industry. Failure is heralded as the ticket to slabs of muscle by some, and to others, the unmanageable training stimulus sure to end in injury. We’re in the midst of the hypertrophy renaissance period, in which the strictly defined hypertrophy training parameters of days past are no more. It’s probably worth looking at the role that failure played in shaping these studies, and more importantly, revisiting the concept as a component of a hypertrophy training program.

Training to failure across the hypertrophy literature

Many in the training community have abandoned the practice of training to failure, while others still embrace it. It’s far from a forgotten concept, as many recent training studies used failure as a means to equate experimental conditions (1-3).

Much of the work demonstrating the comparable growth that occurs with both low and high-load training used failure as an endpoint (1,2,4), findings that we’ve recently replicated in trained individuals (3). We can’t be certain that concentric failure is entirely responsible for the observed response; however, comparisons of low-intensity training (30%-1RM) matched to high-intensity training (90%-1RM) to failure have shown a complete lack of an acute protein synthetic response for low-intensity training. When the low-intensity condition was taken to concentric failure, a comparable acute protein synthetic response was observed (5). The acute protein synthetic response may not predict the chronic adaptations to training (6), yet it’s still interesting that low-intensity training short of failure (work-matched to high-intensity training to failure) doesn’t seem to stimulate an acute protein synthetic response.

For tempo, my recent meta-analyses with Brad Schoenfeld and James Kreiger demonstrated that repetition durations between 0.5-10 seconds have comparable growth when considering only studies using concentric failure (7).

A comparable analysis doesn’t exist for rest intervals; however, a closer look at Menno Henselman’s and Brad Schoenfeld’s recent review yields similar findings (8). While lacking quantitative analysis, they came to a similar conclusion regarding the various rest intervals that can be used to promote growth. They didn’t group studies based on the use of failure as an end-point, but much of their narrative analyses on long-term hypertrophy was formulated from five studies (4, 9-12). Of those, the use of failure was either clearly indicated (4, 9), mentioned in the discussion (10), or wasn’t clearly stated at all (repetition maximum ranges) (11, 12). In all five of those cases, rest intervals from 1-5 minutes did not have a profound effect on the hypertrophic response to training (4, 9, 10), with the exception of Souza-Junior et al (12) favoring decreased rest intervals.

While existing evidence (1-4, 7-11) indicates a wide array of parameters that we can use in our training programs to promote growth when training to concentric failure, it doesn’t validate the assertion that training to failure is required, or enhances growth over other training conditions.

Failure means flexibility, but what about results?

Despite the fact that training to failure has been a prominent and unsettled debate in the training industry for decades, there’s remarkably few direct comparisons to determine its relevance to training adaptations (13, 14). What’s surprising is that there is a particular lack of literature on hypertrophy, and most of what exists focuses on strength (15-18). As far as hypertrophy is concerned, much is focused on fluctuations in hormone levels (18-21), used as a proxy for growth down the road. Given that recent work demonstrates that acute fluctuations in certain hormones don’t actually correlate with the long-term growth response, using arguments on hormonal fluctuations that occur when training to failure may not be a sound idea (22, 23).

Recent evidence suggests that failure may not be necessary as far as hypertrophy is concerned (14). Sampson et al (14) blocked-randomized 28 males following a four-week training familiarization period (50-80% 1RM, 2:2) to one of three conditions: 1) rapid shortening (RS), 2) stretch shortening cycle (SSC), and 3) controls. All groups trained unilateral elbow flexion at 85%-1RM for four sets with three minutes rest between sets. The control group completed a tempo of 2:2, the RS accelerated the weight maximally during flexion and two-second eccentric, and the SSC group completed maximal speed flexion and extension. Only the control group completed repetitions to failure (6 repetitions per set), whereas the RS and SSC groups completed four repetitions per set.

Following 12 weeks of training, the control group (who trained to failure) ended up completing more repetitions per set, training volume, time under tension, and rated higher levels of exertion than those in the RS and SSC groups. Despite this, actual adaptations between the groups were comparable. One-repetition maximum strength increased 30.5%, along with isometric maximal voluntary contraction of the elbow flexors (13.3%) over the 12 weeks, with no differences between the groups. Similarly, alterations in elbow flexor cross-sectional area were not different between groups. To make a long story short, training to failure meant completing more work for a comparable amount of growth.

The fact that failure wasn’t entirely necessary for hypertrophy isn’t surprising in the context of previous data.  Much of the “magic” of training to failure across various training parameters is that it can alter motor unit recruitment, and this is best understood when comparing training intensities (24). The force demands of high versus low load intensity require, for a similar muscle, differing numbers of motor units. Under high load conditions, greater numbers of motor units will be needed as compared to training with light loads at the start of a set. When training to failure, low-load training is associated with longer sets, greater time under tension, and mechanical work completed (5). Throughout this, as fatigue sets in, some motor units keep working, others drop in and out, and others may reduce their force output over time (25). Motor units that may not have been necessary based on the initial load during low-load training will be progressively recruited as other motor units drop out or reduce their force output. While both conditions start with differing motor unit requirements, over the course of a set to failure, comparable motor unit numbers and types may end up being recruited regardless of training parameters (i.e.: intensity).

It would be premature to suggest that concentric failure is required to “equate” motor unit demands across varying training parameters. While EMG data isn’t necessarily directly reflective of motor unit recruitment, Sundstrup et al (26) demonstrated that normalized EMG signals plateaued approximately 3-5 repetitions before the onset of concentric failure. This indicates that training to failure may not be necessary to “equate” motor unit activity across training conditions. Let’s not forget that motor unit recruitment isn’t a passive process either (27-29), set by load and/or fatigue. They’re your motor units, you chose to use them (27).

This isn’t an open and shut case. Giessing et al (13) had participants train twice a week for 10 weeks in one of three, single-set conditions: 1) training to their self-determined repetition maximum (short of failure), 2) training to concentric failure, and 3) training performing repetitions to self-determined repetition maximum using the rest pause technique. Following training, the group that trained to failure demonstrated larger effects for various body composition changes (moderate to large effects) as compared to the rest pause group (small to moderate effects). Those who trained to their self-predicted repetition maximum failed to increase muscle mass. These suggest that we may not be that great at identifying where our true repetition maximum is, and that training to failure and using rest-pause techniques may be important for the adaptations to strength training to ensure we’re actually pushing as hard as we think we are.

So while it seemed that training to failure equates growth across many training parameters (1, 3, 7, 8, 30), the results of Sampson et al (14) suggest that comparable training adaptations can be achieved with less work training short of failure, and Giessing et al (13), just the opposite.  As it stands, the evidence suggests that training to failure makes program design easier, but completing that program may be harder than necessary.

The molecular argument against training to failure

Others have suggested that the fatiguing nature of training to failure could impair growth. During fatiguing contractions, an increase in adenosine monophosphate (AMP) occurs as a consequence of increased flux through adenylate kinase, ultimately working to, at least partially, restore ATP concentrations. Gorostiaga et al (31) demonstrated that ATP:AMP ratio was reduced to a greater extent when participants completed 5 sets of 10 repetitions of leg press to failure as opposed to 10 sets of 5 repetitions (non-failure condition). Changes in the ratio of AMP:ATP can activate AMPK kinase (AMPK)(32), which has been shown to act as an inhibitor of a key signaling protein involved in protein synthesis known as the mammalian target of rapamycin (mTOR) (33,34).

While this certainly seems like sound reasoning, I suspect we’ve put the cart before the horse. It’s tempting to associate certain signaling proteins with one training condition or another, and AMPK has been associated with endurance exercise (35), playing a key role in the mitochondrial adaptations required to support the prolonged, repetitive demands of endurance exercise {Hardie:2011fx}. In reality, proteins like AMPK are sensitive to fluctuations in metabolites within the cell, and alterations in the ratio of ATP:AMP can occur irrespective of mode of exercise (36, 37).

Dreyer et al (36) demonstrated that protein synthesis is impaired during a strength training session along with a corresponding increase in AMPK. Inhibiting the metabolically expensive protein synthetic response within cells undergoing the metabolic demands of exercise makes sense. But an AMPK response has also been observed outside of the training session. Others have shown an immediate post-exercise AMPK response when sets were taken to concentric failure (37), and activation of p70s6k still occurred, often used as a proxy of subsequent protein synthesis.

Recent work has also shown that activation of AMPK in a concurrent training program had no detrimental effect on mTOR signaling in recovery from a strength training session (38). Coupled with the fact that we’ve already reviewed the existing literature on our outcome of interest that also fails to demonstrate any detriment despite the greater change in the ratio of ATP:AMP when training to failure suggests that we shouldn’t put more weight on the molecular argument over what we know at the “functional,” or hypertrophic level.

I love studying signaling proteins as much as the next guy, but if we have data on the actual primary outcome of interest, in this case hypertrophy, this trumps any arguments constructed on the highly complicated interactions of signaling proteins alone.

More options, not more growth

While it’s entirely plausible that training to failure isn’t necessary for growth (14), it does afford us greater flexibility in the training parameters we can use for hypertrophy training.

But that increased flexibility may come at price. Many critics often cite increased injury risk and the potential for overtraining (19, 39), but these are merely theoretical arguments, with no hard data to support them. Stone et al (39) have suggested risks to consistently training to failure include overtraining syndrome, and that repetitive micro traumas may result in overuse injuries. Nimmons et al (40) has been cited to support impaired adaptations in strength and power (39), but their data, while lacking the precision measurements used in modern studies, shows no disadvantage from a hypertrophic perspective.  Others suggest that blunted hormonal responses will compromise subsequent adaptations to training (18,41), but reliance on acute hormonal fluctuations to anticipate changes in muscle size isn’t a strong argument (22,23). Such arguments fall short by over-emphasizing the role of failure in training without consideration of the role, and proper programming of other training parameters. Is there really no combination of training parameters (frequency, intensity, etc…) that can be created to use failure successfully in a training program?

If anything, the frequent use of concentric failure in research studies is evidence of feasibility (1-4,7,8,13,14), although adverse event and adherence reporting in many of these trials leaves much to be desired.

In the end, training to failure may increase the program design options you have that can promote growth, but may result in the completion of more work than is necessary for a given training adaptation (14). In my opinion, given the purely theoretical basis for injury risk, and the documented, successful use of this training method in much of the literature, it is possible to safely integrate failure into your hypertrophy program, but don’t expect more gains than you trained for.

Take-Home Points

  • Recent studies have demonstrated comparable hypertrophy when training across varying intensities (30-80%-1RM), tempos (0.5-10s), and rest intervals when training to concentric failure.
  • There are relatively few direct comparisons on the effects of training to failure on muscle growth. Data regarding the superiority of training to failure is mixed, with some studies showing increased benefit, while others show equivalence to training short of failure.
  • Arguments against training to failure center on the potential for elevated risk of injury, altered hormonal responses to training, and the creation of a metabolic environment inhibitory to growth. These arguments are largely theoretical in nature lacking objective data on the outcomes of interest.
  • The use of concentric failure in a training program may not enhance the rate of growth consequent to training, but it does provide greater flexibility in the combinations of training parameters that produce growth.

Addendum August 2017

(from Greg)

A recent study by Martorelli et. al further investigated the effects of training to failure on hypertrophy and strength.

Over 10 weeks, 89 untrained young women did biceps curls using one of three programs:

  1. 3 sets to failure with 70% of 1RM
  2. 4 sets stopping shy of failure with 70% of 1RM, with volume matched to that of the failure group (4 sets of 7 reps)
  3. 3 sets of 7 reps with 70% of 1RM

All three groups experienced very similar increases in strength (which should be expected, since relative loading was matched), but the group training to failure experienced the most hypertrophy – a 17.5% increase in biceps thickness, vs. an 8.5% increase in the volume-matched group, and only a 2.1% increase in the group doing 3 sets of 7 reps.

From Martorelli et. al (2017)

However, there are a couple reasons to be skeptical of this finding.

  1. We’re not even entirely sure there was a significant difference between groups.  The stats in this paper were weird, and didn’t report whether or not there were between-group differences for some key measures.
  2. Method of load progression wasn’t specified, though it seems load only increased after retesting 1RMs on week 5.  If that’s the case, the group training to failure was training hard every week, whereas weeks 2-5 and 7-10 would have gotten progressively easier for the two non-failure groups as their strength increased (i.e. their sets may have only been 2 reps shy of failure on weeks 1 and 6, but 4-5 reps from failure on weeks 5 and 10).

It’s also worth nothing that this finding contrasts with that of Sampson and colleagues (14).

With all of that in mind, this study adds another piece to the puzzle, and muddies the waters a bit.  It’s still clear that training to failure isn’t necessary for hypertrophy, but this study provides some evidence that training to failure may help increase the rate of hypertrophy (though again, that’s not a unanimous finding).

For a more in-depth discussion of this study, subscribe to Monthly Applications in Strength Sport (MASS) and check out the August 2017 issue.  My colleague Mike Zourdos broke it down in much more detail.

Addendum November 2017

A recent study (reviewed in more depth in MASS) was the first to test the impact of training to failure on recovery.  It included three groups.  One group did three sets of squats and bench to failure, one group did three sets of squats and bench halfway to failure (determined by bar velocity), and one group did six sets of squats and bench halfway to failure.  With this design, the first and third groups performed the same training volume, but only the first group took their sets to failure.

The group training to failure had larger, longer-lasting decrements in performance (bar speed with various loads) than the groups not training to failure, including the group with matched volume.

This is a snippet of a larger graphic from the November 2017 issue of MASS. Dotted line is training to failure, dashed line is volume-matched non-failure, and solid line is half-volume non-failure.

Now, a drawback of this study is that the non-failure groups stayed a long way from failure.  The story may be different if the non-failure groups trained at something closer to an 8-9RPE.  However, it does provide us with evidence that training to failure may cause a disproportionate amount of fatigue, which could negatively impact training frequency.

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  1. Mitchell CJ, Churchward-Venne TA, West DWD, Burd NA, Breen L, Baker SK, et al. Resistance exercise load does not determine training-mediated hypertrophic gains in young men. J Appl Physiol. 2012 Jul;113(1):71–7.
  2. Ogasawara R, Loenneke JP, Thiebaud RS, Abe T. Low-load bench press training to fatigue results in muscle hypertrophy similar to high-load bench press training. International Journal of Clinical Medicine. 2013 Feb;4:114–21.
  3. Schoenfeld BJ, Peterson MD, Ogborn D, Contreras B, Sonmez GT. Effects of Low- Versus High-Load Resistance Training on Muscle Strength and Hypertrophy in Well-Trained Men. J Strength Cond Res. 2015 Apr 3;:1.
  4. Schoenfeld BJ, Ratamess NA, Peterson MD, Contreras B, Sonmez GT, Alvar BA. Effects of different volume-equated resistance training loading strategies on muscular adaptations in well-trained men. J Strength Cond Res. 2014 Oct;28(10):2909–18.
  5. Burd NA, West DWD, Staples AW, Atherton PJ, Baker JM, Moore DR, et al. Low-load high volume resistance exercise stimulates muscle protein synthesis more than high-load low volume resistance exercise in young men. PLoS ONE. 2010;5(8):e12033.
  6. Acute post-exercise myofibrillar protein synthesis is not correlated with resistance training-induced muscle hypertrophy in young men. 2014;9(2):e89431.
  7. Schoenfeld BJ, Ogborn DI, Krieger JW. Effect of repetition duration during resistance training on muscle hypertrophy: a systematic review and meta-analysis. Sports Med. 2015 Apr;45(4):577–85.
  8. Henselmans M, Schoenfeld BJ. The effect of inter-set rest intervals on resistance exercise-induced muscle hypertrophy. Sports Med. 2014 Dec;44(12):1635–43.
  9. Buresh R, Berg K, French J. The effect of resistive exercise rest interval on hormonal response, strength, and hypertrophy with training. J Strength Cond Res. 2009 Jan;23(1):62–71.
  10. Ahtiainen JP, Pakarinen A, Alen M, Kraemer WJ, Hakkinen K. Short vs. long rest period between the sets in hypertrophic resistance training: influence on muscle strength, size, and hormonal adaptations in trained men. J Strength Cond Res. 2005 Aug;19(3):572–82.
  11. de Souza TP, Fleck SJ, Simão R, Dubas JP, Pereira B, de Brito Pacheco EM, et al. Comparison between constant and decreasing rest intervals: influence on maximal strength and hypertrophy. J Strength Cond Res. 2010 Jul;24(7):1843–50.
  12. Souza-Junior TP, Willardson JM, Bloomer R, Leite RD, Fleck SJ, Oliveira PR, et al. Strength and hypertrophy responses to constant and decreasing rest intervals in trained men using creatine supplementation. J Int Soc Sports Nutr. BioMed Central Ltd; 2011 Oct 27;8(1):17.
  13. Giessing J, Fisher J, Steele J, Rothe F, Raubold K, Eichmann B. The effects of low volume resistance training with and without advanced techniques in trained participants. J Sports Med Phys Fitness. 2014 Oct 10.
  14. Sampson JA, Groeller H. Is repetition failure critical for the development of muscle hypertrophy and strength? Scand J Med Sci Sports. 2015 Mar 24;:1–9.
  15. Drinkwater EJ, Lawton TW, Lindsell RP, Pyne DB, Hunt PH, McKenna MJ. Training leading to repetition failure enhances bench press strength gains in elite junior athletes. J Strength Cond Res. 2005 May;19(2):382–8.
  16. Folland JP, Irish CS, Roberts JC, Tarr JE, Jones DA. Fatigue is not a necessary stimulus for strength gains during resistance training. Br J Sports Med. 2002 Oct;36(5):370–3–discussion374.
  17. Rooney KJ, Herbert RD, Balnave RJ. Fatigue contributes to the strength training stimulus. Med Sci Sports Exerc. 1994 Sep;26(9):1160–4.
  18. Izquierdo M, Ibañez J, González-Badillo JJ, Hakkinen K, Ratamess NA, Kraemer WJ, et al. Differential effects of strength training leading to failure versus not to failure on hormonal responses, strength, and muscle power gains. J Appl Physiol. American Physiological Society. American Physiological Society; 2006;100(5):1647–56.
  19. Willardson JM. The application of training to failure in periodized multiple-set resistance exercise programs. J Strength Cond Res. 2007 May;21(2):628–31.
  20. Willardson JM, norton L, wilson G. Training to Failure and Beyond in Mainstream Resistance Exercise. Strength And Conditioning Journal. 2010 May 24;32(3):21–9.
  21. Linnamo V, Pakarinen A, Komi PV, Kraemer WJ, Hakkinen K. Acute hormonal responses to submaximal and maximal heavy resistance and explosive exercises in men and women. J Strength Cond Res. 2005 Aug;19(3):566–71.
  22. Mitchell CJ, Churchward-Venne TA, Bellamy L, Parise G, Baker SK, Phillips SM. Muscular and Systemic Correlates of Resistance Training-Induced Muscle Hypertrophy. PLoS ONE. 2013;8(10):e78636.
  23. West DWD, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. 2012 Jul;112(7):2693–702.
  24. Burd NA, Mitchell CJ, Churchward-Venne TA, Phillips SM. Bigger weights may not beget bigger muscles: evidence from acute muscle protein synthetic responses after resistance exercise. Appl Physiol Nutr Metab. 2012 Jun;37(3):551–4.
  25. De Luca CJ, LeFever RS, McCue MP, Xenakis AP. Behaviour of human motor units in different muscles during linearly varying contractions. J Physiol (Lond). 1982 Aug;329:113–28.
  26. Sundstrup E, Jakobsen MD, Andersen CH, Zebis MK, Mortensen OS, Andersen LL. Muscle Activation Strategies During Strength Training With Heavy Loading vs. Repetitions to Failure. J Strength Cond Res. 2012 Jul;26(7):1897–903.
  27. Carpinelli RN. The size principle and a critical analysis of the unsubstantiated heavier-is-better recommendation for resistance training. J Exerc Sci fit. 2008 Jun 18;6(2):67–86.
  28. Henneman E, Somjen G, Carpenter DO. Excitability and inhibitability of motoneurons of different sizes. J Neurophysiol. 1965 May;28(3):599–620.
  29. Henneman E, Somjen G, Carpenter DO. FUNCTIONAL SIGNIFICANCE OF CELL SIZE IN SPINAL MOTONEURONS. J Neurophysiol. 1965 May;28:560–80.
  30. Ogasawara R, Yasuda T, Ishii N, Abe T. Comparison of muscle hypertrophy following 6-month of continuous and periodic strength training. 2013 Apr;113(4):975–85.
  31. Gorostiaga EM, Navarro-Amézqueta I, Calbet JAL, Hellsten Y, Cusso R, Guerrero M, et al. Energy metabolism during repeated sets of leg press exercise leading to failure or not. PLoS ONE. 2012;7(7):e40621.
  32. Hardie DG. AMP-activated protein kinase: an energy sensor that regulates all aspects of cell function. Genes & Development. Cold Spring Harbor Lab; 2011 Sep 15;25(18):1895–908.
  33. Bolster DR, Crozier SJ, Kimball SR, Jefferson LS. AMP-activated protein kinase suppresses protein synthesis in rat skeletal muscle through down-regulated mammalian target of rapamycin (mTOR) signaling. J Biol Chem. American Society for Biochemistry and Molecular Biology; 2002 Jul 5;277(27):23977–80.
  34. Pruznak AM, Kazi AA, Frost RA, Vary TC, Lang CH. Activation of AMP-activated protein kinase by 5-aminoimidazole-4-carboxamide-1-beta-D-ribonucleoside prevents leucine-stimulated protein synthesis in rat skeletal muscle. J Nutr. 2008 Oct;138(10):1887–94.
  35. Atherton PJ, Babraj J, Smith K, Singh J, Rennie MJ, Wackerhage H. Selective activation of AMPK-PGC-1alpha or PKB-TSC2-mTOR signaling can explain specific adaptive responses to endurance or resistance training-like electrical muscle stimulation. FASEB J. 2005 May;19(7):786–8.
  36. Dreyer HC, Fujita S, Cadenas JG, Chinkes DL, Volpi E, Rasmussen BB. Resistance exercise increases AMPK activity and reduces 4E-BP1 phosphorylation and protein synthesis in human skeletal muscle. J Physiol (Lond). 2006 Oct 15;576(Pt 2):613–24.
  37. Koopman R, Zorenc AHG, Gransier RJJ, Cameron-Smith D, van Loon LJC. Increase in S6K1 phosphorylation in human skeletal muscle following resistance exercise occurs mainly in type II muscle fibers. Am J Physiol Endocrinol Metab. 2006 Jun;290(6):E1245–52.
  38. Apró W, Moberg M, Hamilton DL, Ekblom B, van Hall G, Holmberg H-C, et al. Resistance exercise-induced S6K1 kinase activity is not inhibited in human skeletal muscle despite prior activation of AMPK by high-intensity interval cycling. AJP: Endocrinology and Metabolism. 2015 Mar 15;308(6):E470–81.
  39. Stone MH, Chandler J, Conley M, Kramer JB, Stone ME. Training to muscular failure: is it necessary. Strength And Conditioning Journal. 1996 Jun 1;18(3):44–8.
  40. Nimmons MJ, Marsit JL, Stone MH. Physiological and Performance Effects of Two Commercially Marketed Supplement Systems. Strength & Conditioning. 1995;17(4):52–8.
  41. Schoenfeld BJ. The Mechanisms of Muscle Hypertrophy and Their Application to Resistance Training. J Strength Cond Res. 2010 Oct;24(10):2857–72.
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