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How Do Growth Factors and Lactate Build Muscle?

Coach, I believe you said (and I could have misunderstood) that there are five pathways to building muscle:

  1. mechanical tension (breaking muscle down)
  2. mTor
  3. cumulative fatigue (taking a set to failure or fatigue built up during the session)
  4. growth factors
  5. lactate

Numbers 1, 2, and 3 would all result in increased protein synthesis post workout, correct? Your body has 36 hours to first repair the muscle protein breakdown and then the rest of the time to build new tissue.

How does this same process work for growth factors and lactate muscle growth?

There are four pathways:

  1. Muscle damage: damaging muscle fibers through high mechanical tension by resisting moderate to heavy loads. Mechanical tension by itself is not a growth pathway, it activates growth pathways based on the load that you’re using and the total time under tension. You can also produce mechanical tension with low loads. High mechanical tension and slow eccentric contractions with moderate to heavy loads produce microtears (aka muscle damage) in the muscle fibers because the myosin heads are trying to hold on to the actin filaments while there are being stretched against resistance. The physiological effect is an increase in intracellular production of phosphatidic acid inside the muscle fibers. PA activates mTORC1 & mTORC2 and thus contributes to muscle protein synthesis.

  2. Muscle fiber fatigue: fatiguing the fast twitch muscle fibers via low to heavy loads. Low and moderate loads need more volume or time under tension to recruit and fatigue the fast twitch muscle fibers (a low volume approach with every set taken to failure is also effective for muscle fiber fatigue) whereas heavier loads need less volume but still enough sets to produce enough fatigue for hypertrophy. Typical high volume, bodybuilding workouts or moderate volume strength focused workouts (with constant loading instead of step loading to accumulate volume) are usually the trigger for muscle fiber fatigue. The increased blood flow to the muscles worked increases local oxygen, glucose and amino acid concentrations. Oxygen levels and usually carbohydrates (fats work to some extent as well) provide the energy. Amino acids are necessary to downregulate or upregulate the mechanisms that stop AMPK/ activate mTORC1 and provide the building blocks to initiate muscle protein synthesis.

  3. mTor activation: all muscle growth pathways activate mTOR via different mechanisms but eccentric contractions with fairly heavy weights and contracting a muscle under load in the stretched position activate mTOR the most. PA, muscle fiber fatigue and local growth factors contribute to mTOR activation. Examples of emphasizing this growth pathway in a training session are either using pauses in the stretched position of an exercise: incline db chest press with 3210 tempo. Or you can use loaded stretching which means you use an isolation exercise for a muscle in which you hold and contract against resistance in the stretched position for 45-60 seconds per set. The total amount of time to shoot for is 2-3 minutes. Or you can combine normal execution and loaded stretching in an exercise to get a similar effect. Do incline db presses 1-2 reps shy of failure, then hold the stretched position for as long as you can (shoot for 20-30 seconds). This will provide a massive trigger for mTor activation.

  4. Lactate/local growth factors: lactate facilitates the release of IGF-1 in the liver and local growth factors inside the muscle. Low to moderate loads with a long time under tension (40-80 seconds) produce a lot of metabolic stress and deprive the muscle fibers of oxygen. The result is an accumulation of lactate inside the muscle that stimulates the production of growth hormone and IGF-1 in the liver and local muscle growth factors (mechano growth factor or MGF) via interaction with the cell nuclei. MGF are a local variant of IGF-1 with similar characteristics. Testosterone, when it binds to its androgen receptors, also faciliates IGF-1 and growth hormone production. By binding to their designated cell receptors, growth hormone, testosterone and growth factors facilitate the upwards signalling of cell proteins (mostly enzymes/kinases) that encourage the translocation of mTORC1 to the lysosome where it gets activated and initiates muscle protein synthesis. If you want a more in depth explanation of the regulatory cellular mechanisms that contribute to mTORC1 activation and MPS, I suggest you do a bit of research. Otherwise it might be too complex/confusing. NCBI and researchgate are two excellent sources that have numerous studies on all the mechanisms behind mTOR (functions, inhibition, activation, interaction with phospholipids/hormones/growth factors etc). If you would like to have a visual presentation of mTOR signalling, mTOR regulation and its impact on gene expression, I recommend the images from Mathieu Laplante and David M. Sabatini. They are titled “mTOR signalling at a glance” and “regulation of mTORC1 and its impact on gene expression”. Both images were published in the journal of cell science.

Keep in mind though that all these growth pathways are activated too some degree in a training session (although you can prevent lactate production by keeping your time under tension short). BUT you can emphasize one growth pathway over the others by adjusting your training variables.

How long it takes to repair muscle breakdown and stimulate muscle growth in time before the next training session comes down to the individual. There are general guidelines yes, but epigenetics, biofeedback and external factors are way more specific to how fast you can repair and build muscle tissue.

That’s why it is so important to customize training programs to the individual because workouts that focus on the lactate/growth factor pathway are easier to recover from than workouts that produce a lot of muscle damage. If your client is older, has more stress or a weaker immune system, then the first pathway would be a better approach to stimulate muscle growth. If your client is young, very confident and naturally strong, muscle damage can be the better strategy.

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By virtue of the fact metabolic stress leads to a transient rise in growth hormone which, in turn, is known to trigger increased production of IGF-1.

What strength training research is less clear about is whether these changes are enough to stimulate muscle growth in their own right or whether this would happen anyway as a result of the mechanical tension from the loading. I’ve heard folks like Menno Henselmans stating hypertrophy is down to the latter. That said, blood flow restriction training experiments have also demonstrated muscle hypertrophy without significant damage to fibers so it would appear there is some merit in targeting that pathway.

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This is the most thorough answer ever!