Hypertrophy of muscle is characterized by expression of genes in the DNA primarily coding for the contractile elements of muscle fibers. That is, the DNA, which codes for the mRNA, which codes for the amino acid sequence, which eventually gets folded into a usable contractile protein and incorporated in the macro-structure of the muscle cell, is unpacked and unzipped, starting the process of growing new muscle componentry. Over time, this process leads to increases in muscle size and strength. Muscle activation, on the other hand, is characterized by signaling within motor neurons, which synapse on the motor end plate of muscle cell membranes, causing ions to cross the muscle cell membrane in such a rapid fashion that an electrical event called depolarization occurs within the muscle cell. This depolarization, and subsequent repolarization of the muscle cell, is what is responsible for allowing the molecular machinery within the cell to do what it was designed to do: produce contractile force. While hypertrophy is measured usually by changes in cross sectional area of a muscle or by changes in size of muscle fibers, muscle activation is measured by electrical current registered using sensors like inserted wires or a pair of surface electrodes. This process of reading electrical activity within a muscle is called electromyography (EMG).
It is quite common, especially in non-scientific forums, that increased muscle activation is assumed, or even marketed, to be causative of increased hypertrophy. That is, if an exercise is identified to create higher muscle activation levels (higher EMG, for short) than another exercise targeting the same muscle or muscle group, the exercise with the higher EMG is often purported to be better for building muscle. In this article I’ll examine if that’s the case, and when specifically, it may or may not be.
The prime movers (the muscles that do most of the work) for most compound, heavily loaded barbell and dumbbell movements like presses, pulls, squats, and pulls from the floor, undergo the greatest amount of hypertrophy AND experience the highest levels of muscle activation within those movements. In these cases, muscle hypertrophy over time is correlated at some level to the EMG seen within the muscle while performing the exercise. Specifically, in the high bar squat, the quadriceps exhibit very high EMG and a high degree of hypertrophy. Likewise, in the bench press, the anterior deltoids, pectoralis major, and triceps brachii undergo both high EMG and have the propensity for high levels of hypertrophy at high training volumes. This correlation between the magnitude of EMG and the magnitude of hypertrophy might lead some to believe that it was the EMG that was causative of the hypertrophy. It is indeed correlated. And, as far as time-order is concerned, the EMG does come before the hypertrophy, so that constraint is fulfilled. However, we have yet to establish if the EMG is both necessary and sufficient for hypertrophy to occur. We may see in the next few examples that EMG is neither completely necessary, nor completely sufficient to cause hypertrophy.
Imagine a scenario where you are instructed to seat yourself on a chair with your lower legs pointing straight out in front of you, unsupported from below, and with knees locked out in a straight position. You are then asked to contract (tense or “flex”) your quads as hard as you can. This activation of your quadricep muscles creates very high muscle activation (EMG readings) even though the mechanical load on your lower leg is only the weight of your leg itself. The reason for this phenomenon is that muscle activation tends to trend higher, for a given external torque, at the shortest muscle lengths. That is, muscles “work harder,” needing more electrical input, to create the same amount of tension when they are in extremely shortened positions. A similar example might be in the top half of a standing or seated bicep curl (NOT preacher curl). As the forearm passes the horizontal position the weight of the bar or dumbbell moves closer to the elbow joint center which serves as the fulcrum. As the DB moves closer to the fulcrum, the need for force generation within the bicep musculature is reduced dramatically, and yet, as you may have felt during execution of the bicep curl in training, it takes a substantial amount of effort to hold the weight in the top position of the bicep curl movement (as long as you don’t move your elbows forward, underneath the load). That effort is reflected in high EMG activity, relative to the magnitude of force created. If you were asked to hold the weight in this very shortened muscle position for any length of time you would find that the external load would soon overcome your over shortened muscles activation ability and its ability to generate force. Unfortunately, in neither of these examples (quad flexing, and weighted top-end bicep contraction) would there by significant hypertrophic stimulus. It is well-demonstrated in the literature that the magnitude of mechanical work performed is very well correlated to the magnitude of hypertrophy. In both situations, the mechanical work performed is nearly zero.
The only situation that comes to mind where hypertrophy stimulus is high, and mechanical work performed low, leads me to my next breakdown in the EMG-causes-hypertrophy misinterpretation of scientific literature. There are some cases where EMG is very low, and yet hypertrophic stimulus quite high. One of note has been well-demonstrated in birds, though you’d be hard pressed to find human volunteers for this one. If you strap a bird on its back on a bird-sized bench, and hang weights from its wings so that the pectoral muscles are under prolonged and intense stretch, there will be significant muscle hypertrophy of the pectoral muscles without any muscle activation. This has carryover to our own training. Tension within the muscle is a major driver of hypertrophy. We can create tension through stretch and through muscle contraction, and we can do both, at the same time. It turns out that some of the most hypertrophic exercises for our muscles do just that. The reason stiff legged deadlifts are so effective for hamstring hypertrophy is because the great degree of active force generated in the hamstrings and because of the passive force generated in the hamstrings when they are stretched under load. The same can be said for properly executed pull ups and the latissimus dorsi muscle, and for the pectoralis major and bench flyes. Interestingly EMG may not be the highest at the moment of highest magnitude of stretch in these movements, and certainly isn’t during the eccentric phase. And yet, if we were to shorten the range of motion of these movements and remove that end range stretch, we would likely find a reduced hypertrophic effect if all other things were kept equal (load, volume etc.).
What so many Instagram coaches do wrong is to forget that tension, and the total mechanical work done under tension is the primary driver of hypertrophy. Just because a muscle is working hard, putting out loads of EMG (usually when you’re exhibiting higher EMG, you’ll report that it feels “more difficult”), does not mean that the actual force generated by that muscle is high, nor that the total mechanical work being performed by that muscle is great. Only that it’s working hard to do what little it’s doing. To appropriately interpret if EMG might be well-correlated with hypertrophy in a specific movement we should also have information presented on the intra-muscular tension that is developed, and assess the movement for it’s range of motion. If the range of motion is low (i.e. The muscle doesn’t move through more than at least half of the ROM, it’s capable of) then the stimulus for hypertrophy is probably limited. If the tension developed within the muscle is low throughout the movement, OR low for most of the movement’s ROM then, even if the EMG readings are high, the hypertrophy stimulus is probably still quite low. To identify intramuscular tension, you’ll either need a very strong handle on physics or biomechanics AND anatomy here, or actual data on intramuscular tension from scientific research on the movement in question. Without these three pieces, the assessment of hypertrophic stimulus magnitude is fatally flawed.
The glute bridge is my personal favorite misapplication of this. In the glute bridge, the gluteus maximus muscle is placed into a nearly maximally shortened position by the top of the exercise. The reason such large loads can be lifted is because of the mechanical advantage from the weight being directly over the hip joint center. While the loads lifted might imply high forces within the gluteus maximus muscles and the high EMG might corroborate that, the intramuscular tension and mechanical work performed by the glutes is substantially less that it appears externally. So, why on earth do all those Instagram models and coaches get such great glute results promoting their EMG-based programming? If you spent 1/3 of all your training programming on one muscle group, you’d probably be disproportionately large in that one muscle group too. It’s not the EMG driving the hypertrophy, but the volume load on the specific muscle group that drives the hypertrophy.
Recommendations for your own training:
- Your muscles should probably be active during lifting. Good luck lifting without that happening on your own! This is a no-brainer.
- Don’t obsess about some report of an EMG reading of one muscle group or another.
- When comparing exercises for effectiveness of hypertrophy examine the intra-muscular forces, and ranges of motion through which those forces are present. More force, and longer range of motion is better, even if peak or average EMG readings are lower than some other lower-intramuscular-force exercise or lower-ROM exercise that has higher EMG.
- If you’re excited about growing a specific body part (say… your glutes) allocate more volume load to that muscle group saving some of your training recovery and adaptation energy reserves by limiting some of your other training volume on other muscle groups.