The Key To Success?

I always have to smile a bit, when I hear people say that "desire" and "passion" are all you need to be successful. I doubt that, because I have seen too many people being successful without showing any passion or desire for what they are doing. Instead, what they all had in common is: Persistence. Maybe passion and desire are driving forces behind it, however what really clears the way to achieve something are your continuous actions and behaviour towards it. Over and over again, because the things that seem attractive to us usually don't come easy (and according to Psychologists this is actually among the main reasons WHY they seem attractive to us).

Therefore we all have to keep in mind, that having romantic feelings or dreaming about something alone is not enough - we have to DO something to get closer.

We all know how Nike breaks this down to: "Just do it" and I believe in the end it's really as simple as that:

When in doubt, consider...

Bulletproof Muscle Growth Through Science

Science can certainly make you grow: Normal vs. Myostatin -Knockout Mice

As an exercise physiologist, my main interest is understanding the mechanisms behind an adaptation of the human body to training, which enables us to give practical advice of how to stimulate those pathways for optimizing individual performance. That being said, let's take a look at those fancy scientific backgrounds that are responsible for one of the main adaptation that is interesting for us strength athletes: Hypertrophy!
  
IGF-1, AKT, m-TORC1 and why they may or may not be interesting for us

Earlier, the IGF-1 and AKT pathway was thought to be the main signaling cascade to induce muscle growth (1,2). In the last couple of years it was shown though, that after developmental growth hypertrophy occurs even without functional IGF-1 receptors and therefore it's unlikely that this pathway plays a big role for muscle growth in adults (3). Meanwhile, one of the downstream targets of IGF-1 and AKT began to draw more attention: It is now well established, that activating the Mammalian Target of Rapamycin (m-TORC1) is one main target that has to be turned on in order for muscle hypertrophy to occur, and it does that by increasing protein synthesis (4). In general, m-TORC1 is activated through loading and its activity is proportional to the load across the muscle (5). The most efficient way to maximize loading on the muscle are eccentric contractions as they allow by far for the heaviest weights. Since this eccentric training was oftentimes accompanied by DOMS (Delayed On Muscle Soreness), many people concluded that traumatizing the muscle tissues is neccessary for activating the gene expressions that initiate hypertrophy and one should therefore aim for maximal destruction of the filaments during training as a bodybuilder and strength athlete. However, recent studies in the last years have shown that hypertrophy occurs even without damage of muscle tissues (6), so DOMS is really more a side effect and rather correlating with hypertrophy than causing it.

What is critical for hypertrophy then and what is not?

There are a couple of parameters in training that we can manipulate, e.g. volume, frequency and intensity. The question for us is and always was, how to do that appropriately in order to get the best of the bargain. Although all of those parameters have been shown to play a role in hypertrophy, none of them is the exclusive single predictor of the Muscle Protein Synthesis (MPS) following Resistance Exercise (RE).

Progressively overloading the muscle through RE including manipulation of those parameters above provides growth through increasing MPS as we know for decades. But how to manipulate them? Usually it is recommended to achieve hypertrophy by using more than 70% of your 1RM for 1-3 sets, but as we recently learned, even that approach has been disproved as not neccessarily critical (7,8). So again, how do we overload the muscle efficiently and how do we keep up that stimulus consistently? It suggests itself as the simplest way to still do that via load, as it is basically possible to increase it indefintely, while the other two parameters mentioned are somewhat limited by time. But we all know that it's practically impossible to put on a new weight in every session, so how do we ensure that hypertrophy was still stimulated? We do that by 'Maximum-Activation' of the muscle!

A little excursus of why this should be the critical goal in RE and how it is reached: We know that the large motor units and fast twitch fibers yield the biggest potential for significant hypertrophy as they usually account for the biggest part of the CSA in skeletal muscle (9). To activate them you need to either do a very fast and explosive movement, to work with a very high intensity, or to exhaust your smaller fibers till the bigger ones are forced to join the party to still get the demanded work done (Henneman's Size Principle). Let's take a quick look back: Heavy loads do activate big motor units as they're naturally a high intensity. Since they do that from the first repetition on, going till failure seems not as essential as it is for low intensities: Light loads do not make all the big motor units neccessary to move the weight – at least not from the first repetition on. So that is where failure becomes absolutely inevitable: In order to still stimulate remarkable growth of the bigger fibers, you have to overload them, which is not going to happen if you don't even activate them. So independently from heavy or light loads, going till failure always ensures appropriate recruitment of all the big fibers, as they are the last ones to get involved when the muscle continuously contracts.

In practice, this makes it as 'easy' as this: The needed gene transcription/translation in your muscle for enhancing the protein synthesis is induced by ordinarily activating the tissues maximally. This is achievable through different ways and now we are coming back to the three main parameters:

Intensity: The mentioned load-phenomenons from above (light or heavy eventually doesn't really matter regarding hypertrophy [7,8]) explain why muscle growth can still be stimulated, indepently from which of the parameters we are focussing on. For example more advanced lifters often claim to be able to stimulate gains with relatively light weights by focussing on „feeling“ the muscle: They simply contract and activate there muscles to the maximum, using techniques such as going till failure, forced repetitions, drop sets etc. Seems to me, like solid science once again delivered an explanation for an, up to the present, rather gnostic gym-myth: It's not only the intensity of the load that determines the quality of your set, it's how close to your limit you can get with that load.

Volume: More of this gene expression that enhances hypertrophy comes by contracting your muscles more often while you are loading them with high intensities and/or going till failure. This means, doing more than one effecient repetition and doing it for multiple sets is providing better growth – more is indeed better. However, like it often seems to be the case in science, the positive effect of this follows some kind of a  logarithmical function and plateaus really quick. Therefore, doing more than one set is hardly neccessary and certainly not time-efficient, as the difference to a single set is insignificant (8).

Frequency: We know about intensity and volume now, but what about the number of sessions that one should shoot for during a week? Wait for it, I'll give it a whole new passage and on that occasion introduce you a new term of growing interest in exercise physiology.

Changes in your genome: Epigenetics!

Epigenetics describe modifications of the genome without changes in nucleotide sequences. This may include for example, the folding and unfolding of different Proteins, DNA and RNA. As the activity of those proteins and the amount of sequences of DNA and RNA that gets transcribed and translated depends on how 'open' they are, the efficiency of how the MPS gets activated to make us grow bigger and stronger is determined by their folding, too. Simply put, an unfolded protein or gene is activated and open, as well as DNA/RNA that is unfolded is open and therefore readily available for transcription or translation initiation. We can influence that through the frequency by which we induce those processes and that, in turn, is of course controlled by our training frequency. As this still may sound cryptic to somebody who's not accustomed to those terms, let's break it down to this: The more often you train, the more open and ready for MPS your genes will stay and the faster and more continuously you will grow.


Turning the nerd stuff into practical advices for meatheads:

Now finally, let's make sure you get the most out of your training with the upcoming hints:

- Consciously activate the muscle as much as possible at every single exercise, set and rep.

- Limit momentum. This is not so much for preventing injury (although this is true, too), but for saving you from making your training less efficient: A lot of jerk in your movements increases the involvement of the stretch-shortening-cycle, which simply means more reliance and stress on your tendons and less stress (and therefore less stimulus) for your muscles.

-Ditch too many pure eccentric, tissue destroying contractions with supraphysiological loads (weights you couldn't possibly move concentric), in order to reach a higher trainingfrequence (being less injured on a microcellular level allows for an earlier, next training-session).

-Choose high intensities (>70% 1RM), go till failure (regardless the % of your 1RM) or be explosive in your movements. Theoretically you could use all at the same time, just make sure to be clear about risks and benefits (extremely heavy, supraphysiological loads and explosive movements may alter the likelihood of injuries like mentioned above). Despite the fact that they are more 'dangerous', in contrast to light intensity loads, high intensity loads also yield the advantage of making you stronger, which in turn allows for more load progression and hence an efficient way to increasingly stimulate hypertrophy. This is most likely due to a combination of motor learning effects (intra- and intermuscular coordination) and connective tissue stiffening.

-If you are going super heavy in order to save time, get stronger and maximize the recruitment of the Type II Fibers from the first rep on, use RPS or Clustering to reach at least a fair amount of volume and thereby accumulate a decent amount of reps that were close to failure (or beyond). Every repetition that is done shortly before or after failure is an absolute quality rep for inducing growth! Don't forget that the more often you stimulate the expression of the involved genes, the more MPS. But again: This effect becomes less promiment very fast. So don't sacrifice frequency (which allows for constantly keeping the stimulus for the MPS up high) for volume.

-Train as often as possible. If neccessary, reduce the volume in order to achieve a high frequence. Each muscle group once per day seems to be sufficient in order to allow for the epigenetical effects, a continuously high MPS and the recovery that nevertheless especially the passive elements and connective tissues of the body still need. This might mean, that you have to train multiple times per day, as stimulating each group efficiently in a single session is extremely taxing for the CNS and could lead to overreaching soon. Splitting it into two or more short sessions with proper nutrition between each training is far less strenuous. You will still have to go through a couple of "dark weeks", train through soreness, but eventually your body will adapt to it.

-Again a reminder: The lighter you go, the greater the need for failure is (7): Not until the last, hard reps you are making sure your muscle is fully activated and growth stimulated. Go at least till concentric failure, use (I mention this again, because it's a remarkably good method) RPS, use forced reps, drop- and super sets. Everything that fully activates the muscle is legitimate. Funny, many people concluded that the papers of Stuart Phillips, Nicholas Burd and Cameron Mitchell would mean that it's "easier to stimulate growth now, since we can use lighter loads". Yeah, right: Ever did a set of squats with your 30%1RM till failure? I'd be glad to receive a quick feedback about the easiness of this feat, when you woke up after you passed out between your 38th and 39th rep.

-Finally understand, what really counts is that you are training 'hard'. Meaning with heavy weights and/or close to failure. There is no such thing as 'easy' in strength training. Keep that in mind before you do your next set and then be ready to go all in. Lacking this mindset that enables you to push yourself to the very maxmimum for a short duration means, that you might want to give it a second thought if you weren't better off with longer durations and training on the treadmill instead of the weightroom, where as little as 30% of your VO2max are already enough to cause central adaptations of the endurance phenotype (10).


1.Ka-Man V. Lai, Michael Gonzalez, William T. Poueymirou, William O. Kline et al. (2004): Conditional Activation of Akt in Adult Skeletal Muscle Induces Rapid Hypertrophy. Mol. Cell. Biol. November 2004 vol. 24 no. 21 9295-9304.

2.Stefano Schiaffin and Cristina Mammucari (2011): Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models.Skeletal Muscle 2011, 1:4. doi:10.1186/2044-5040-1-4

3. Espen E Spangenburg, Derek Le Roith, Chris W Ward, and Sue C Bodine (2008): A functional insulin-like growth factor receptor is not necessary for load-induced skeletal muscle hypertrophy. J Physiol. 2008 January 1; 586(Pt 1): 283–291.

4.Baar, K., Esser, K. (1999): Phosphorylation of p70 (S6k) Correlates with Increased Skeletal Mass Following Resistance Exercise, Am. J. Physiology, 276: C120-C127, 1999.

5.Terzis G, Georgiadis G, Stratakos G, Vogiatzis I, Kavouras S, Manta P, et al.. 2008. Resistance exercise-induced increase in muscle mass correlates with p70S6 kinase phosphorylation in human subjects. Eur. J. Appl. Physiol. 102: 145-152.

6.Paul LaStayo; Paul McDonagh; Dani Lipovic; Phyllis Napoles; Amelia Bartholomew; Karyn Esser; Stan Lindstedt (2007): Elderly patients and high force resistance exercise--a descriptive report: can an anabolic, muscle growth response occur without muscle damage or inflammation?Journal of Geriatric Physical Therapy: December 2007 - Volume 30 - Issue 3 - p 128–134.

7.Burd NA, West DWD, Staples AW, Atherton PJ, Baker JM, 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. doi:10.1371/journal.pone.0012033

8.Cameron J. Mitchell, Tyler A. Churchward-Venne, Daniel D.W. West, Nicholas A. Burd, Leigh Breen, Steven K. Baker, and Stuart M. Phillips (2012): Resistance exercise load does not determine training-mediated hypertrophic gains in young men. J Appl Physiol April 19, 2012, doi: 10.1152/japplphysiol.00307.2012

9.D'Antona G, Lanfranconi F, Pellegrino MA, Brocca L, Adami R, Rossi R, Moro G, Miotti D, Canepari M, Bottinelli R (2006): Skeletal muscle hypertrophy and structure and function of skeletal muscle fibres in male body builders. Journal of Physiology (Oxford) 2006, 570(3):611-627. 

10.Stepien Rl, Hinchcliff Kw, Constable Pd, Olson J (1998): Effect of endurance training on cardiac morphology in Alaskan sled dogs. J Appl Physiol 85: 1368-1375, 1998.