Matt Perryman Matt Perryman

Intensity & Training to Failure [Muscle Gain]

Heavy is always better, right? That’s the going mantra. Lift heavy things and you’ll grow and get stronger. I push this position myself, because I think it’s mostly right. If you want to reap gains from a strength training workout, you focus on the basics. Anything involving a barbell, picking it up, putting it overhead, or squatting it — or any combination thereof. Low reps, as few as one and as many as six, allow you to use challenging weights.

That’s the time-tested recipe, whether you’re trying to get big, build muscle, or get strong. I don’t think that ever changes. If you’re after strength or big muscles, the bulk of your training should revolve around that foundation of heavy, simple lifts. This is proven by the practices of strength athletes and by scientific research.

Lifting heavy weights teaches you how to lift heavy weights. The training is as much neurological as muscular; indeed, most of the adaptations to heavy lifting happen in the nervous system. When you load up enough weight and lift it, you produce very high tension in the working muscles, which in turn activates all your available fibers. High tension, which is usually cited as roughly 80-85% of the maximum voluntary contraction, is sufficient to bring all the motor units into the movement.

The heavy lifting mindset suggests that heavy, slow, and strenuous is enough to build a great physique. And I largely agree. Lifters following the minimalist approach inevitably build impressive bodies. The evidence is all there.

Bodies are built with heavy weights. Science validates the idea. You’d think there’s no reason to do higher reps if you’re concerned with maximizing the growth stimulus.

Those tidbits of information aside, bodybuilders all do it. Bodybuilders train with higher volume, if you measure total tonnage and muscular work done in a workout, and on average use higher reps, and more diversity in their rep ranges, than strength-focused athletes. Bodybuilders may focus their attention on work sets from single reps to 20 (or even more), with 10 being the unspoken average.

While I’m not one to accept anecdotes that contradict solid evidence, there are two points to consider. We don’t understand the process of muscle growth, in scientific terms, with the degree of fine grain we’d need to make the argument against bodybuilding methods. We can say there is a component of both work and strain or tension on muscle fibers that is required to trigger growth, and we can observe the practices of strength training subjects, but generalizing beyond that using purely academic sources isn’t possible.

Bodybuilders have converged towards higher-rep, higher-volume training for a reason. Science aside, the process of trial-and-error has a way of figuring things out. If large groups of people are training using common methods and common approaches, then there’s something worth investigating. My desire has never been to promote any one method or any single approach to ‘working out’. I think there are useful elements to take away from bodybuilding, if you have physique-inspired goals, but I don’t want to endorse some of the less-informed viewpoints that are often bundled with traditional bodybuilding culture.

I’m looking for themes, not specifics. The question, given the above information, is why higher reps can work, given all the commonly repeated benefits of training heavy.

Bringing the argument back to science for a moment, the research is far from equivocal on What Works. While there is much evidence backing the Heavy approach, there’s another angle to consider. The idea of vascular occlusion has been making waves over the last decade, thanks to the efforts of the Kaatsu researchers in Japan. I’ve written about this in another post, so I’m not going to rehash the topic here.

Work from Stu Phillip’s team at McMaster University has produced this gem of a paper which, along with the Kaatsu/occlusion research, leads to interesting possibilities. You can read it for yourself thanks to PLoS One being a decent journal. The introduction tells you this is going to be interesting, if you come from the Lift Heavy school of thought.

As opposed to the requirement for high intensity contractions we posited that the total volume of contractions, independent of intensity, would result in full motor unit activation and muscle fibre recruitment and would be of equal or greater importance as intensity to the acute stimulation of muscle protein synthesis. Specifically, the same degree of muscle fibre activation and presumably a similar stimulation of myofibrillar (MYO) protein synthesis, would occur regardless of intensity provided that the exercise was performed until volitional fatigue (failure) in line with observations from occlusion training.

They’re suggesting it’s the volume of work done (number of sets and reps), rather than the intensity, which leads to fiber recruitment (they use the term activation, but they’re synonymous) and stimulation of myofibrillar protein synthesis — as long as the exercise is done to failure. They cite previous work suggesting that protein synthesis is maximally stimulated at 60% of 1RM, with no further increases at higher loads in the 75-90% range. The authors clarify that low-load training, even at 20% intensity, has been observed to stimulate mixed protein synthesis* — which is to say, we’re not simply seeing ‘sarcoplasmic hypertrophy’.

* Protein synthesis in muscle fibers churns various protein fractions, which is where you get the distinction between sarcoplasmic and myofibrillar growth. Increased MPS rates could mean synthesis of mitochondrial proteins or it could mean new myofibrils, which is what we want for hypertrophy. In this case, ‘mixed’ means that both are happening.

This study tested two different exercise loads and volumes, as they affected various signals of anabolism, gene expression, and protein synthesis. There were three groups: 90% 1RM to failure (90FAIL), 30% 1RM which matched the external work to the 90FAIL group (30WM), and 30% 1RM to failure (30FAIL). The authors hypothesized that the anabolic response would be similar between the two FAIL groups (that make anyone else laugh? No?) because of maximal fiber activation, but that the intensity would be important to maximize the response between the work-matched groups.

There were fifteen recreationally-active male subjects with an exercise background: “Participants reported engaging in lower body exercise such as resistance exercise alone or in combination with cycling more than 3 times weekly for the prior 6 months.” Subjects fasted from 10pm the previous night, and were fed a standardized liquid-meal drink 2 hours before the trial.

I have to say, this is one reason I really like any paper with Stu Phillips’ name on it — he’s one of the researchers who takes pains to control for ‘real life’ factors in his research. Obviously you can only get so close due to the limitations of science, but it seems like every paper I see from his team has taken pains to control for exercise history, diet, and even quasi-realistic testing protocols.

Speaking of the protocol, it was pretty standard stuff. Testing was done on a leg extension machine with a unilateral protocol — that is, one leg did one thing, and the other fell into another group in order to expand the comparisons between the groups. The to-failure groups “were given verbal encouragement until concentric failure”, where failure was inability to complete the range of motion. The work-matched group didn’t get anywhere near failure, which you’d expect. All three groups did four sets with three minutes rest between. Tempo was set to a 50 bpm metronome, which worked out to be 1s concentric, no pause, and 1s eccentric.

As you’d expect, the number of reps, volume load (sets * reps), and time under tension were all highest in the 30FAIL group. At 4 hours post-exercise, mixed MPS and myofibrillar MPS was elevated in all three groups, and highest in the 90FAIL and 30FAIL groups. Nothing unusual about any of that.

But here’s the kicker: “At 24 h post-exercise, MYO protein synthesis remained elevated (P < 0.05) above rest only in the 30FAIL condition (~2.9 fold).” What about sarcoplasmic MPS? That jumped by ~1.7 fold in the 90FAIL group, but was gone at 24 hours post. The 30FAIL group, however, “induced a significant increase in SARC protein synthesis above rest at 4 h (,1.4-fold) and 24 h (,1.5-fold greater than rest) post-exercise.” To recap, of the three groups, 30FAIL could statistically match 90FAIL at 4 hours post-exercise in all measure of MPS, and beat 90FAIL in all three at 24 hours post-exercise. Growth factors mostly matched up with this trend, including our friends p70s6k and mTOR (if you don’t know what those mean, don’t worry. The groupies will know.) Summarized by the authors,

We report for the first time that low-load high volume resistance exercise (30FAIL) is more effective at increasing muscle protein synthesis than high-load low volume resistance exercise (90FAIL). Specifically, the 30FAIL protocol induced similar increases in MYO protein synthesis to that induced by the 90FAIL protocol at 4 h post-exercise but this response was sustained at 24 h only in 30FAIL.

Why’s this happening? The Heavy approach says that motor units are recruited with heavy weights. This result seems contradictory. No need to panic; this is easily explained. As I find myself saying when this discussion comes up, recruiting a motor unit isn’t the same as training it. Recruitment of the motor unit causes the attached fibers to contract, bringing them into the movement. Recruitment generates tension and creates strain on the working muscle fibers.

If you’re after strength gains, this is what you need to happen. Being able to voluntarily switch on your muscle fibers, learning to strain and grind through heavy and slow exercises, is largely neurological. Motor learning is sensitive to conditions. Squatting at 70% might as well be an entirely different movement from squatting at 95%, for all the brain is concerned. Levers change, mechanics of the lift change, and the patterns of neurological activity change.

Stress on the muscle, however, is different. Hypertrophy is work-induced. Work, contrary to common belief, is not merely a function of weight lifted or force applied or tension created. Work is done when that force is used to move things. Maximum work doesn’t mean maximum weight — it means using a heavy-enough weight and moving it around a lot.

What we’re seeing in this paper is about more than simple recruitment of motor fibers with heavy weights and high tension. These results demonstrate a role for both volume and fatigue, which is usually glossed over in the rush to pile more weight on the bar. The authors make the same suggestion.

In contrast to recommendations, that heavy loads (i.e., high intensity) are necessary to optimally stimulate MYO protein synthesis, it is now apparent that the extent of MYO protein synthesis after resistance exercise is not entirely load dependent, but appears to be related to exercise volume and, we speculate, to muscle fibre activation and most likely to the extent of type II fibre recruitment.

This is not news per se but it does require a reevaluation of our context and, more importantly, questioning our own dogma.

[T]he duration of the MYO response may be determined by exercise volume at extended time points beyond the exercise bout. It is worth highlighting, however, the early amplitude of MYO protein synthesis is dependent on contraction intensity as indicated by a greater response of muscle protein synthesis in the 90FAIL and 30WM conditions. This suggests that the volume of exercise, which we view as being related to the degree of fibre activation affects the duration and intensity affects the acute amplitude of the MYO response.

High-intensity contraction gives you a higher kick to MPS immediately post-exercise, but it’s the higher volume which sustains it over time. The difference between ‘simply stimulating’ increased MPS, and carrying it out over time in order to realize a bigger muscle, is a factor not often mentioned.

We propose that this finding provides support for the idea that 30FAIL exercise mode may function as an exercise mode to increase proteins from all fractions in muscle including mitochondrial and myofibrillar proteins leading to both enhanced oxidative capacity and hypertrophy.

This ability to stimulate mixed protein fractions (both sarcoplasmic and myofibrillar) and to sustain that elevation over time may be one explanation for the observation that bodybuilders have ‘bigger, rounder, fuller-looking’ muscles compared to those focused on purely heavy weights. The volume of work done (regardless of load or rep range) may be the link.

This isn’t the first paper to suggest such a thing. There’s plenty of evidence that training muscle fibers for maximum growth requires (or at least benefits from) a fatigue component. Call it training to failure, call it a high RPE, call it training for the burn — the name doesn’t matter. What’s important is that you’re pushing the set to a substantial fraction of your capability.

The HIT crowd calls this momentary muscular ability, and they’ve long assumed that fatigue and discomfort are goals in themselves. I don’t buy that premise. The HIT school and its current derivatives have come to fetishize training to failure, refusing to recognize any form of effort-grading (such as using RPE scores) or periodization as basic as cycling.

That said, there’s plenty of reason that effort, combined with volume, contributes to the total growth response. Yes, heavy poundages build muscle, and yes, big weights do good things for the body, but this is not something to ignore if you’re into any form of body-sculpting activity. This acute fatigue, the fatigue that happens when you take a hard set very close to the limit, does contribute to hypertrophy.

This concept goes as far back as the energetics hypothesis laid out by Zatsiorsky in Science and Practice of Strength Training, Second Edition. The cell lacks the energy reserves to keep its house in order, so the whole thing falls to pieces. Current research backs this up. During fatiguing contractions, sarcomere units can’t return to their unattached resting state and calcium ions flood the place, tearing up even more delicate biochemistry. In response, we see a dramatic increase not only in the myogenic regulatory factors that govern protein synthesis, but in various markers of inflammation and regeneration — including the oft-mentioned satellite cells.

It’s important to realize that an event which stimulates growth factors and signal pathways associated with protein synthesis don’t always mean protein synthesis actually increases, or that the increase will be sustained long enough to create the best size increases. Likewise, simple recruitment of muscle fibers doesn’t mean those fibers are trained to their fullest.

As far as current speculation goes, the effect of low-load constant-tension training winds up looking very much like the effects of real occlusion training like the Kaatsu method.

Finally, while it appears that low load paradigms utilizing blood flow restriction during exercise, induced via a pressure cuff are effective at inducing an anabolic response in both young and older subjects, the low-load high volume training employed in the current study may provide a more practical alternative for inducing hypertrophy and/or attenuating sarcopenia.

And you may not even have to use dynamic, full-ROM movements to make it happen, which I’ve suggested in my older article. Using low-load high-volume training, combined with the heavy stuff, is your best bet for size and overall development.

Our results support previous findings that demonstrated after 16 weeks of isometric training at 30% maximal voluntary contraction that significant increases in fibre area can be achieved. Although, the contraction type employed in the current study (i.e., dynamic) differed from Alway and colleagues (i.e., isometic), our data provides further support that low-load contractions performed with numerous repetitions or high-load contractions performed for fewer repetitions will result in similar training induced gains in muscle hypertrophy as previously suggested, or even superior gains, as results from the current study would predict. This premise is further supported by data which demonstrates that short-term changes in muscle protein synthesis are predictive of training induced gains in muscle mass.

I find it almost funny that popular bodybuilding training, emphasizing volume and post-fatigue methods, has taken a beating for so long — only to find that most likely, they were right. The idea of maximizing volume for a muscle group over the course of 4-8 sets, using both heavy and light loads, while training to failure (or near it) is the essence of bodybuilding. No magic, no steroid-user volume or Hardgainer infrequency required.

Hypertrophy is as much a function of volume and the area under the force-time curve as it is pure load. It is true that strength must increase for growth to occur over a career. That said, there’s nothing to say that this requires rapid, or even constant, strength gains over short periods of time. Bodybuilders and anyone else trying to add bulk can be lazy and gradual with their strength increases; I’m not convinced there’s any rush as long as the attempt to increase working poundages is made over some span of time.

The nervous system is what adapts quickly, not the muscles. Any variety in the program, which includes periodization strategies, would have to take that into account. The good news is that damn near anything can work. Train heavy, train light, and rotate through them.

In Conclusion

  • There’s a volume component to hypertrophy. Mechanical work, as determined by volume load (load * reps), is the trigger for growth. Intensity is only a permissive factor; you need your weights to be ‘heavy enough’ but you also need to do enough reps with those weights.
  • The fatigue element is important, perhaps more than the actual weight used (as long as the weight is above a minimum threshold). Using various rep ranges is likely useful to avoid staleness, and can be productive as long as effort is high and you train to a high percentage of your maximum ability. If you’re using RPE scores, train to a point where you only have 1-2 reps left, and occasionally go all-out for maximum reps.
  • Higher reps make it easier to rack up volume. Lower reps are better at building strength. Using a combination of low and high reps can attack the problem from different directions, and rotating between the two helps avoid staleness.
  • You don’t have to limit yourself to dynamic contractions. This method of constant-tension, peak-contraction training appears to work with isometrics and partial movements as well as anything.

Burd NA, West DW, Staples AW, Atherton PJ, Baker JM, Moore DR, Holwerda AM, Parise G, Rennie MJ, Baker SK, & Phillips SM (2010). Low-load high volume resistance exercise stimulates muscle protein synthesis more than high-load low volume resistance exercise in young men. PloS one, 5 (8) PMID: 20711498

Goldspink G, & Howells KF (1974). Work-induced hypertrophy in exercised normal muscles of different ages and the reversibility of hypertrophy after cessation of exercise. The Journal of physiology, 239 (1), 179-93 PMID: 4855427

Goldberg AL, Etlinger JD, Goldspink DF, & Jablecki C (1975). Mechanism of work-induced hypertrophy of skeletal muscle. Medicine and science in sports, 7 (3), 185-98 PMID: 128681