After writing a recent T-Nation article on the use of multiple repetition ranges, one question from the comments afterwards stuck with me. If fatigue is essential for hypertrophy following training, why even bother with multiple repetition ranges? Couldn’t you train exclusively light, or heavy, as long as it was to failure (or fatigue) and still enjoy the same hypertrophic benefits regardless of load?
I offered up an answer, readdressing some of the points made in the article (conflicting research base, suitability of intensity ranges by specific exercises, high-load training optimal for strength development, training practices of experienced athletes, enhanced training variety). After thinking about it for a few weeks I feel that it’s possible that the issue has more to do with the interaction of load, fatigue, and the supposed preferential (or superior) hypertrophy of type II fibres, than the points in my initial answer to the question.
You dare question the almighty Type II fibre?
Type II fibres have long displayed greater hypertrophy following high intensity strength training (1-67), but that’s not the same thing as saying they have greater growth potential than the type I fibre. You see, the first statement is context specific, that they have higher growth potential with HIGH INTENSITY training, not necessarily this innate ability to outgrow type I fibres across all conditions. This relative relationship has gone unquestioned for decades; however, recent research suggests we’ve systematically underestimated our slow-twitch fibres, a consequence of studies that stack the deck in favour of the type II fibres. At this point, I’m willing to go as far as to say that the preferential growth of type II fibres is more an artifact of how we’ve studied them than a law of physiology to be etched in stone.
Type II fibre hypertrophy with high-intensity training
In a comprehensive review, Fry (1) collected a number of training studies, combined the hypertrophy data (by fibre-type) and performed a regression analysis, resulting in an expected percentage change in fibre size when trained at a given percentage of 1RM (adapted below).
These results demonstrate two main points critical to our current understanding of fibre-type specific hypertrophy:
- Type II Fibres (solid black line) have a higher peak percentage growth as compared to type I fibres (solid yellow line), and display greater growth at the majority of training intensities (>50%-1RM)
- At a given intensity however ( <50%-1RM), type I fibre hypertrophy can exceed that of the type II fibres
This indicates it’s not that type II fibres have a universal, superior growth potential, but that they display greater growth when trained on their own turf (high intensities). Give them home-field advantage, and more often than not they’ll win, but the same goes for the slow-twitch. Head over to the land of the light-weights, and we see that their growth can trump that of the type IIs. This collection of data makes a strong argument for the use of heavy weights in training for hypertrophy; greater growth of both fibre-types overall, but still demonstrates that fast-twitch fibres don’t have an innate ability to universally out-grow their type I brothers.
As it stands, we probably wouldn’t change much about our training, emphasizing the heaviest of weights (to 95%-1RM) seems to not only be best for the type II fibres, but also the type Is. However when you look at the characteristics of the studies used in Fry’s (1) analysis, you’ll see we did in fact stack the deck for type IIs, with the majority of studies using exclusively high intensities of training (8), and an under representation of studies using lighter intensities. Take this graph from Wernbom (8) who analyzed the increase in quadriceps cross-sectional area (CSA) across 46 studies (each point on the graph is a study). There are only 5 studies at or below 50%-1RM. When you look at the three studies between 20-30%-1RM, they more or less define the range of growth for all the higher intensities (shaded region) and this isn’t including the more recent study from Mitchell et al (9). While this is whole muscle CSA (not fibre-type specific), it’s still interesting how the hypertophy/intensity relationship for single fibre-types doesn’t necessarily pan out when looking at whole muscle CSA.
When you look at the breakdown of the individual studies by fibre-type specific hypertrophy from Fry (1), you see a similar pattern: many high-intensity studies and a relative dearth of low intensity training (8). There’s also another limitation to the regression analysis used by Fry (1); it’s difficult to put all the different training studies on equal footing. Despite the author’s best attempts, studies use different numbers of exercises, sets, durations of training, and often don’t account for whether sets were taken to failure or not (an important distinction). In this case, any investigation that measures fibre-type specific hypertrophy (type I vs type II) AND directly compares different training intensities (high vs low) is the gold standard, and while there are far fewer of these studies, there’s enough data to point us in the right direction.
Direct comparisons of Training Intensity and Fibre-Type Hypertrophy
Looking at the direct comparison of various training intensities on fibre-type specific hypertrophy, we see that the Type II fibre is not the superior grower that we thought. In a recent, now infamous study, Mitchell et al (9) compared low-load training (3 sets @ 30%-1RM) to failure against two higher-intensity conditions (3 sets @ 80%-1RM, 1 set @ 80%-1RM). At the end of the 10 weeks, whole muscle hypertrophy was similar across the groups (although half for the one set condition), and when looking at the specific fibre types, we see that the type I fibres more than kept up with the type IIs (see Table 1 from the original paper, adapted below). The robust increase in type I CSA while training at 30%-1RM seems supportive of the home-field advantage assertion, although no statistical differences by intensity or fibre type are stated.
|Training Condition||Type I||Type II|
|80%-1RM 1 set||16±7%||20±5|
|80%-1RM 3 sets||17±4%||16±4%|
|30%-1RM 3 sets||30±12%||18±8%|
Up until Mitchell et al’s (9) study, Campos et al (3) had the definitive investigation of training intensities, that more or less agreed with the relationship in the graph above (1), higher-training intensities (4×3-5RM, 3 min rest or 3×9-11RM, 2 min rest) produced greater growth in both type I and II fibres than lower intensity (2×20-28RM, 1 min rest). I’ve adapted their data to percent change based on their averages (excluded deviations) to fit with Mitchell et al (2012), and preserved the indicated statistical significance from the original data (bolded).
|Training Condition||Type I||Type IIA||Type IIb|
These results are more or less in direct conflict with Mitchell et al (9), however in a recent attempt to reproduce these results, albeit NOT at the fibre-type level (whole muscle hypertrophy), a subsequent study (10) demonstrated no difference under the exact same training program (3). This agrees with the Mitchell et al (9) whole muscle data, and combined in the context of the fibre-type discrepancy makes a strong case for using multiple training intensities in your training and that we’ve systematically neglected, or at least underestimated our type I fibres. The one caveat however is a recent study from Schuenke et al (7), where high intensity training (Traditional Strength; 3×6-10RM @ 80-85%-1RM,) resulted in superior hypertrophy of type I, IIa, and Iix fibres, with no change following 6 weeks of low-intensity training (Traditional Endurance; 3×20-30RM @ 40-60%-1RM).
|Training Condition||Type I||Type IIA||Type IIX|
Evidence from the real world
Bodybuilders (11), powerlifters (12), and strongman (13) all use multiple repetition ranges to develop superior levels of muscle mass, the premise of my T-Nation article with JC Deen, however the amount of work devoted to different rep ranges varies between the groups. Powerlifters emphasize load (intensity) while bodybuilders emphasize volume; however, both pay respect to each others domains, borrowing principles as necessary to maximize results. The result of these focused efforts is fibre-type changes respective of these intensity domains. Powerlifters (and olympic weightlifters) have larger type II fibres than their bodybuilding brethren, but bodybuilders display a greater balance between the type I and IIs. This is best summarized in a figure from Fry (1), that combines multiple studies to show the relationship between fibre-type area (type I fibres yellow, type II fibres black) by sport (olympic weightlifters, powerlifters, and bodybuilders).
This data alone doesn’t indicate the responsiveness of the type I fibre for growth as it could certainly be possible that people with large type I fibres tend to gravitate towards bodybuilding as compared to their fast-twitch counterparts who prefer powerlifting and the olympic lifts. When combined with the fibre-type hypertrophy data from the training studies above however, we start to see those that train with heavy weights (or somewhat lighter weights with maximal speed) tend to end up with larger fast-twitch fibres, and those who have a tendency to emphasize volume or fatigue show a greater balance between the fibre types, and large type I fibres. This suggests that the supposed enhanced growth of the type II fibres may be more a consequence of training intensity (and how we study them) than an intrinsic ability of the fibre-type itself.
How could high intensity training limit Type I fibre hypertrophy?
The size principle of motor unit recruitment dictates that motor units are recruited on the basis of their size where small, slow motor units (slow twitch fibres) are recruited first, followed by progressively larger units (eventually fast-twitch fibres) until the required force for the task at hand is met (15,16). This principle is the basis for high-load strength training. Heavy weights maximize muscle recruitment from the get-go via the size principle and allow you to tap the growth potential of the type IIs (conscious manipulation of activation independent of load is a confounding factor here).
|I (Slow Oxidative)||IIA (Fast Oxidative Glycolytic)||IIB (Fast Glycolytic)|
In a high-load set to failure, just like the size principle dictated the order the motor units are recruited, it also dictates how they drop out when they fatigue. Under fatiguing conditions, the principle operates in reverse. Those strong, fast motor units that were late to the party, after the slow units started doing their thing, also leave early. The fast motor units fatigue first, dropping out and leaving all the force-generating duties to their weaker, type I counterparts.
As fast motor units are larger and produce more force than the slow units (16-17), when they drop out under high load, you create a situation where the load on the bar is too great for the remaining active fibres to lift, even though they haven’t been fatigued (to the same extent as the high-threshold, fast motor units). So our fast-twitch motor units are worked to fatigue, but our slow motor units still have a ways to go. In this case, the insufficient force production results in concentric failure and the set stops with ideal, fatiguing stimulation of the fast motor units and the slow units left unsatisfied. This explains why the majority of our studies on the intensity/hypertrophy relationship favour type II hypertrophy, since they tend to use higher training intensities (>60%-1RM) that may fail to sufficiently fatigue specific motor unit/fibre types, and ultimately stimulate hypertrophy in the type I fibres.
Conversely with low-load training, as fatigue is induced, higher-threshold motor units are progressively recruited, in the order dictated by the size principle (18). As fatigue increases motor units eventually drop out (fail to produce force) or remain active with compromised force production. The size principle is still preserved, and while the fast units may influence when failure ultimately occurs (19), the slow motor units will have been active for a longer duration within the set regardless. In this case, with a lower-load even if drop out of the fast-twitch units ultimately limit when the set ends (failure) the slow-twitch fibres have been active for a greater amount of time, receiving greater stimulation than under the high-load condition. This potential recruitment strategy can explain recent data finding equivalent hypertrophy with low-load training (9), and that the existing literature base (1) using exclusively high-intensity training may have under-estimated our slow-twitch fibres.
The case for fatigue in hypertrophy, reconciling the differences between studies
The argument that we have chronically under stimulated, and ultimately under-estimated our type I fibres hinges on the fact that a certain minimal threshold of time-under-tension is required, and that this is higher for type I fibres than type IIs and for lower intensity training in general. Up until now, we’ve seen data in support of both arguments, and when you look at direct comparison of fibre-type specific hypertrophy by training intensity, the data is split. But considering the neural mechanisms, the specific recruitment strategy behind both high and low intensity, we can explain the equivocal nature of the existing literature.
These divergent results are easily explained in how each study addresses the differential in exercise volume that occurs when training at each end of the RM continuum. In fact, studies that show equivalent results between training intensities make no attempt at matching work or volume (9,20), while studies that show the relative superiority of higher training intensities do (3,21), (with the one exception being Schuenke et al (7)). This is the oft repeated mantra of any periodization course (inverse relationship between volume and intensity), and as I’ve stated previously, time-under-tension can compensate for reduced intensity when hypertrophy is the desired outcome in training.
Looking at the acute protein synthesis data from Burd et al (20), we can see that attempting to work-match low-load training impairs the protein synthetic response. The authors tested three conditions (90%-1RM to failure, 30%-1RM to failure and 30%-1RM work-matched to the 90%-1RM condition) using a leg extension and four sets per exercise, three minutes rest between sets. I’ve discussed this study previously on this site, so I don’t want to belabour the point, but the 30%-1RM work matched condition failed to augment mixed muscle fractional synthetic rate as well as myofibrillar and sarcoplasmic protein synthesis whereas the 90%-1RM and 30%-1RM conditions did (albeit with slightly different time-courses).
This work does not necessarily implicate failure as a required end-point, it’s possible that there may be a ‘sweet-spot’ between the point of fatigue, a noticeable decrement in a performance variable (i.e. bar speed) and concentric failure. It does support that, when lower intensity training is used, training volume has to be higher to support hypertrophic adaptations similar to that of high intensity training. We can’t discount the ability of failure to maximize fatigue-induced motor unit recruitment and maximize metabolic stress that may be important for hypertrophic adaptations to training (22,23).
Forming evidence-based hypertrophy guidelines
Given the possibility that we’ve underestimated type I fibre hypertrophy an approach that varies training loads, over-time (periodization), within the session (different intensities by exercise type), and even within the set (rest-pause, dropsets) represents the best of both worlds. Using multiple intensity ranges acknowledges the existing literature base (3,7,21), summarized best in Fry’s (1) regression analysis (high intensity means more growth for both fibre-types), while also taking recent literature into account emphasizing the pivotal role of fatigue/failure (and relative independence of load) (9,20,24,25).
- Fry, AC (2004). The role of resistance exercise intensity on muscle fibre adaptations. Sports Medicine, 34(10), 663–679.
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- Campos, GER et al. (2002). Muscular adaptations in response to three different resistance-training regimens: specificity of repetition maximum training zones. European Journal of Applied Physiology, 88(1-2), 50–60.
- Harber, MP et al (2004). Skeletal muscle and hormonal adaptations to circuit weight training in untrained men. Scandinavian Journal of Medicine & Science in Sports, 14(3), 176–185.
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- Kosek, DJ et al (2006). Efficacy of 3 days/wk resistance training on myofiber hypertrophy and myogenic mechanisms in young vs. older adults. Journal of Applied Physiology (Bethesda, Md : 1985), 101(2), 531–544.
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- Wernbom, M et al (2007). The influence of frequency, intensity, volume and mode of strength training on whole muscle cross-sectional area in humans. Sports Medicine (Auckland, NZ), 37(3), 225–264.
- Mitchell, CJ et al (2012). Resistance exercise load does not determine training-mediated hypertrophic gains in young men. Journal of Applied Physiology (Bethesda, Md : 1985), 113(1), 71–77.
- Léger, B et al. (2006). Akt signalling through GSK-3beta, mTOR and Foxo1 is involved in human skeletal muscle hypertrophy and atrophy. The Journal of Physiology, 576(Pt 3), 923–933.
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- Burke, RE et al (1971). Mammalian motor units: physiological-histochemical correlation in three types in cat gastrocnemius. Science (New York, NY), 174(4010), 709–712.
- Burke, RE et al (1973). Physiological types and histochemical profiles in motor units of the cat gastrocnemius. The Journal of Physiology, 234(3), 723–748.
- Adam, A et al (2003). Recruitment order of motor units in human vastus lateralis muscle is maintained during fatiguing contractions. Journal of Neurophysiology, 90(5), 2919–2927.
- Carpentier, A et al (2001). Motor unit behaviour and contractile changes during fatigue in the human first dorsal interosseus. The Journal of Physiology, 534(Pt 3), 903–912.
- Burd, NA et al. (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), e12033.
- Holm, L et al. (2008). Changes in muscle size and MHC composition in response to resistance exercise with heavy and light loading intensity. Journal of Applied Physiology (Bethesda, Md : 1985), 105(5), 1454–1461.
- Schoenfeld, BJ (2010). The Mechanisms of Muscle Hypertrophy and Their Application to Resistance Training. Journal of Strength and Conditioning Research / National Strength & Conditioning Association, 24(10), 2857–2872
- Schoenfeld, BJ (2013). Potential Mechanisms for a Role of Metabolic Stress in Hypertrophic Adaptations to Resistance Training. Sports Medicine ePUB Retrieved online Jan 22, 2013
- Burd, NA et al (2012). Bigger weights may not beget bigger muscles: evidence from acute muscle protein synthetic responses after resistance exercise. Applied Physiology, Nutrition, and Metabolism, 37(3), 551–554.
- Burd, NA et al (2013). Big claims for big weights but with little evidence. European Journal of Applied Physiology, 113(1), 267–268.