This explanation is part of a wider discussion. For the direct explanation CLICK HERE.
Discussion: explaining why desirable, highly scalable BMR elevation via muscle anabolism through training is only possible with BRIEF, INTENSE exercise.
“Brief, intense training leads to the most mechanical tension, consequently the most stimulus relative to fatigue, and therefore the most growth, which in turn leads to higher maintenance.”
Ok, this was my response to your claim: “More than active. Cmon bro, be honest: that’s a lot of vigorous physical activity per day” in response to someone saying 3000kcals was maintenance for active 180cm+ individuals.
Now, I didn’t say anything about running a 10K w/ 7min miles. I didn’t mention cardio at all. My point was that your claim that a lot of vigorous physical activity per day to have a maintenance of over 3,000 was wrong; I said: “A “lot” of physical activity every day isn’t a requirement. Don’t conflate volume with intensity.”
Why? Because the sort of training that gets your maintenance caloric requirements that high, if we’re doing that by elevating your BMR that high, is going to be predominantly anabolic. Sure, you can burn those calories with lots of vigorous physical activity every day — my point is that’s not the only way to get such a high maintenance.
In fact, pretty much the main way to get your maintenance that high without lots of volume every day is to increase your BMR. This is done by inducing muscle anabolism (mainly by hypertrophy) because, as we know, more mass requires more energy to maintain, especially muscle mass.
I’m no Greg Kovacs; however, my maintenance is significantly above 3,000 kcals a day, even when mostly sedentary.
The best way to induce hypertrophy is with brief, intense training. This is simply because of the way hypertrophy works (I recommend following my account @VMHypertrophy for more information or getting a membership at enhancedbb.com to ask any questions).
Why does muscle grow, and why is this the sort of training that causes it to grow the most?
When muscle fibres controlled by the high threshold motor units (remember when I mentioned MUR) experience an adequately high level of mechanical tension as a result of slowing contraction velocities (look at force-velocity relationship image: credit to Chris Beardsley from S&C Research), we have what we will call “stimulating reps.”
Quickly explaining the importance of high threshold motor units: they are largely composed of type II (fast-twitch) muscle fibres, which have the higher intrinsic capacity/potential for force production and hypertrophy. As the name explains, they are only recruited at high force demands, during ONLY brief, intense training; they have a greater density of contractile proteins and more potential for MPS compared to type I fibres. Motor units are recruited from smallest to largest (lowest threshold to highest threshold) based on force required; low to moderate intensities recruit the low threshold units (type I and endurance based); consequently, ONLY brief, intense exercise recruits high threshold motor units.
Now, these reps occur at approximately 90% (roughly equivalent to 5RM loads) of maximal unfatigued isometric force production (so you can see how repetitions of cardio are not going to be stimulating in a way which is scalably anabolic — have to be specific here because of untrained -> beginner cardio is slightly anabolic but in a way which isn’t sufficiently scalable due to novel stimulus and more MUR than before).
As those who strength train or bodybuild (or engage in similar resistance training) are already familiar with, such rep ranges when taken to “failure” (hence, INTENSE) result in an INVOLUNTARY SLOWING OF CONTRACTILE VELOCITY — meaning as we approach the end of the set, the rep gets slower and harder, and we can’t do anything about it.
Next, I’m going to explain why high threshold motor units experiencing high mechanical tension is what’s required for adequate training stimulus to cause sufficient anabolic adaptations to increase BMR in a scalable way via muscle growth:
Mechanical tension is determined by the force-velocity relationship as applied to a single muscle fibre. Under quick shortening, the fibre produces a small force (few myosins attach to actin), however, under slow shortening (REMEMBER what I say about INVOLUNTARY SLOWING CONTRACTILE VELOCITY and how this is achieved only with INTENSE training, meaning high effort per repetition of which approximately the last 5 are meaningful or more precisely that 90% of max force production figure? Well, you’re not going to generate such forces with ultra-high-rep exercise or cardio, because you will be too fatigued to be able to produce 90% of your maximal unfatigued isometric force with the loads which allow you to perform that many reps in such a fashion) a large force is produced (more myosins attach to actin).
Now, when contraction velocity is significantly slowed (remember that ONLY BRIEF INTENSE TRAINING allows for this because if the training is not brief then you are fatigued by the point that you get to these reps and therefore cannot produce sufficient force for your high threshold motor units to experience adequate mechanical tension), the dwell time (the time where the myosin heads remain attached to actin) increases ∴ increasing the duty ratio which is the fraction of the contraction cycle during which a cross-bridge — connection between myosin and actin — is active.
Btw, the contraction cycle is a repeating series of the following molecular events:
Attachment: myosin head binds to actin filament, forming cross-bridge
Power Stroke: myosin head pivots; pulls actin filament; generates force
Detachment: ATP binds to myosin head ∴ causes it to detach from actin
Reactivation: myosin hydrolyses ATP; preparing for another cycle
Now, the higher proportion of time in this cycle that myosin remains bound to actin (actively generating force) indicates more myosin-actin interactions occur during a given time period, meaning greater overall force production by the muscle fibre
Simply, by slowing down the contraction, you allow more myosin-actin interactions to occur ∴ increasing the overall force produced by the muscle fibre.
So, to summarise, the higher proportion of time myosin is bound to actin, the higher number of active cross-bridges during each contraction cycle, which amplifies the mechanical tension within that fibre).
Now, this concentration of mechanical tension is the key to the activation of various mechanosensitive signalling complexes (via protein detection), e.g. integrin-associated focal adhesion kinase (FAK) — enzyme converting mechanical tension into biochemical signal; kinase domain of titin (large protein with role in muscle elasticity, however, more relevantly here, it also acts as a sensor), etc…
Once these are activated, they trigger signalling cascades intracellularly e.g. mTORC1 (cell growth and protein synthesis regulator) — I think at this point, most gymbros or familiar readers will have gotten the point and the “lightbulb moment” and understand the picture of what I’m saying because most have now had all their familiar terms interact with each other via these steps and now have a holistic picture; however, I will conclude anyway. These pathways are then responsible for initiating the processes which lead to MPS, hypertrophy, etc.