In an isolation exercise, more or less all the load is distributed to the isolated muscle group, such as the triceps in a skull crusher.
Compound exercises, contrastingly, are more complex as two or more muscle groups are actively involved.
In a barbell bench press, the nervous system of one individual may distribute 40% of the total load to the pectoralis major, 40% to the triceps, and 20% to the anterior deltoid.
Of course, this is oversimplified for illustrative purposes. In reality, bones, tendons, synergetic and stabilization muscles also bear the load to varying degrees throughout an exercise.
Nevertheless, is it possible for an individual to change how their nervous system recruits the muscle groups involved in a compound exercise?
Using our oversimplified example, could the person alter their barbell bench press recruitment patterns, for example, such that the anterior deltoid now handles 40% of the load, the pectoralis major 20%, and the triceps 40%?
A fascinating study by Stronska et al. gives us potential insight. I will use the author’s terms and interpretations to describe the study. However, there are notable limitations and considerations with this study, so for those interested, please watch until the end to understand what I feel to be the best interpretation of the current evidence.
27 men with an average barbell bench press of 105.2kg were recruited, all subjects could bench at least 120% of their respective bodyweights.
During 2 4-second maximal isometric barbell bench press contractions (performed with the elbows flexed to 90 degrees and the upper arm perpendicular to the floor), and 3 reps with an 85% one-rep max load on the barbell bench press, surface EMG (which stands for electromyography) recorded muscle activation from the pectoralis major, anterior deltoid, and triceps.
For each subject, the researchers noted out of the pectoralis major, triceps, and anterior deltoid, which one displayed the lowest relative activation on the bench press tests.
Resultantly, three groups were formed: those with the lowest relative anterior deltoid activation (the anterior deltoid group), those with the lowest relative pectoralis major activation (the pectoralis major group), and those with the lowest relative triceps activation (the triceps group).
Then, subjects went on to perform targeted isolation training for their respective lowest activation muscle, performing 3 exercises per session, each for 4 sets of 10-15 repetitions to failure, 3x per week for 6 weeks.
The anterior deltoid group trained the upright row, lateral raise, and front raise.
The pectoralis major group trained dumbbell flyes, machine flyes, and cable chest flyes.
The triceps group trained barbell skullcrushers, cable overhead extensions, and incline skullcrushers.
Note, all three groups also performed 3 sets with a 4 rep-max load on the barbell bench press each week to ensure strength did not attenuate.
After the 6 training weeks, all three groups similarly increased bench press one-rep max strength.
Relevant to our discussion, all three groups re-measured their activation levels during the isometric and 85% one-rep max bench press tests. To keep things condensed, I’ll just present the results of the surface EMG recordings from the 3 reps on an 85% one-rep max bench press.
Focusing on the anterior deltoid group first, compared to before the study, they saw a significant increase in anterior deltoid relative activation with a concurrent significant decrease in pectoralis major and triceps relative activation.
The pectoralis major group, compared to before the study, saw a significant increase in relative pectoralis major activation, with a significant decrease in triceps and anterior deltoid relative activation.
Finally, the triceps group, compared to before the study, saw a significant increase in relative triceps activation, with a significant decrease in pectoralis major relative activation and a non-significant change in anterior deltoid relative activation.
Stated another way, this study indicates performing exclusive targeted isolation training for a certain muscle group ultimately increases its relative activation during a compound exercise, with a corresponding decrease or negligible change in the other involved muscle groups.
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Limitations of the Research
However, as alluded to, limitations and problems exist.
Noticed I’ve implied surface EMG measures a muscle’s activation. This is not actually accurate.
Instead, surface EMG approximately measures neuromuscular excitation, which is when neurons transmit electrical signals to the muscle fibers it innervates.
Muscle activation actually refers to when the contractile units are prepared to generate force. For those with some muscle physiology knowledge, it’s when calcium binds to troponin to enable subsequent cross-bridge cycling.
The problem here is intermediate steps between neuromuscular excitation and muscle activation exist, such that it’s not sensible to consider them in complete unison.
So, surface EMG approximates neuromuscular excitation. However, notice I’ve said approximates. I say this because research has found when actual neuromuscular excitation is kept constant, manipulating the length of a muscle, or joint angle produces different surface EMG recordings.
In other words, surface EMG still does not truly record neuromuscular excitation.
The second problem is how the researchers measured and interpreted their surface EMG recordings.
When presenting the results earlier, notice how the recordings of each muscle are expressed as a percentage of a maximum isometric contraction.
The researchers calculate this by first recording the surface EMG response to holding a maximum isometric contraction for each respective muscle group.
These respective values are then used to normalize the surface EMG response recorded during the 85% one-rep max barbell bench press.
Let’s use an example with the triceps to make this crystal clear.
Imagine during the a maximal isometric triceps contraction, 100 units were recorded from the triceps by surface EMG.
During an 85% one-rep max barbell bench press, we record 85 units from the triceps. As a result, we say the triceps produced 85% of its maximum isometric contraction.
The problem here is we’re basing the triceps relative contribution to an exercise on a random isometric contraction. It’s entirely possible if a different triceps isometric contraction was used to normalize our values, we would obtain a vastly different relative activation level.
For instance, if a different triceps isometric contraction generates 150 units from the triceps, our 85 units measured from the triceps during the barbell bench press would have only equated to a 57% maximum isometric contraction.
Based on all this information, you would see it’s not really sensible to compare maximum isometric contraction values between muscles.
Just because in a certain exercise, one muscle generates a higher percentage of a maximum isometric contraction compared to the percentage of maximum isometric contraction achieved by another muscle, we cannot definitively say that muscle is truly activated or involved more, simply because those percentages are based on arbitrary isometric contractions.
The thing is, the researchers did this. For example, we know those in the anterior deltoid group were the subjects that (before the study) experienced a lower percentage of the maximum isometric contraction of their anterior deltoid compared to the percentages of maximum isometric contractions of the pectoralis major or triceps during the bench press tests.
The researchers interpreted this as saying the anterior deltoid was the lowest relative activated muscle for these subjects. But the fact is (based on what we’ve described), the equipment and methods used were simply not adequate to truly say this.
Despite these notable limitations and problems, I still think this data holds value for two reasons.
Firstly, the consistency of the findings is noteworthy. After performing targeted isolation training for a muscle, that muscle saw increased EMG recordings during the bench press. The anterior deltoid group saw elevated anterior deltoid EMG recordings, the triceps group saw elevated triceps EMG recordings, and the pectoralis major group saw elevated pectoralis major EMG recordings.
Secondly, surface EMG recordings were compared within the same individual that performed the same exercise with the electrodes placed at roughly the same spot. This does likely attenuate potential limitations with muscle length, joint angle, and electrode positionings.
Combining these two reasons and I think this study by Stronska et al. potentially does suggest if an individual performs targeted isolation training for a muscle, its recruitment may be increased during a compound exercise.
Yet, several questions remain.
As some examples, the subjects performed quite high volume targeted isolation training. They executed 36 weekly sets for their targeted muscle. Could the same results be achieved with lower weekly set numbers?
We also know the subjects performed exclusive targeted isolation training for their specific muscle while ceasing training of all other muscle groups. Could the same results be obtained by continuing to train all your muscle groups, but increasing the volume with the muscle you want to recruit more during a compound exercise, and decreasing volume on the muscle or muscles you wish to remain similarly or less activated during that compound exercise?
Ultimately, higher quality data is unquestionably required to fully uncover the precise details and nuances.
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