In recent years, the scientific literature is increasingly finding that achieving a stretch of a muscle during an exercise is powerful for building muscle.
However, some people have proposed that not every muscle will grow more when exposed to a stretch during an exercise. More precisely, they believe that the working sarcomere length of a muscle can inform us of whether that muscle will grow more when exposed to stretch.
The biceps is one examples of these muscles. Some people believe that the biceps’ working sarcomere length suggests this muscle shouldn’t grow more when exposed to stretch.
In this article, I’m going to share my views on whether the data on the bicep’s working sarcomere length is truly strong enough for us to believe this muscle shouldn’t grow more when exposed to a stretch during an exercise.
Firstly though, an understanding of the length-tension relationship is needed. Feel free to gloss over this part if you’re already well aware of it.
Understanding The Length-Tension Relationship
Within muscles are sarcomeres, and sarcomeres are the force generating units of muscles.
Sarcomeres have the ability to generate active tension and passive tension. Note, tension is analogous to force in this case.
Active tension occurs when the myosin head extends from the myosin filament and pulls the actin filament towards the M-line, shortening the length of the sarcomere.
This action produces force that is partly transmitted longitudinally, but mainly laterally to the extracellular matrix (surrounding muscle fibers). These forces end up pulling on the tendon, resulting in muscle contraction.
Passive tension is the force produced during stretch. Think of a rubber band, when you stretch a rubber band, it produces passive tension to try and resist that stretch. When you let go of the rubber band, that passive tension will snap it back into its original shape.
Titin is a protein within the sarcomere that produces passive tension when the sarcomere is stretched.
The Length-Tension Relationship
Now that we hopefully understand active and passive tension from the sarcomere, we can introduce the length-tension relationship.
In this relationship, the length of a sarcomere is on the x axis, while the amount of tension (analogous to force) produced by a sarcomere is on the y-axis.
We can see there are two components to it. Active tension is blue, and passive tension in green.
With passive tension, we can see it sharply increases at longer sarcomere lengths. This makes sense, since passive tenson is force from the stretch of titin, we’re going to want the sarcomere to be stretched for titin to be stretched.
Note, in all of the length tension relationship graphs shown in this article, passive tension begins to develop at a sarcomere length of 2.5μm. This would likely not be the case with all muscles. evidence indicates the passive tension curve is variable (much more so than the active tension curve), so keep this in mind.
With the active tension component of the length-tension relationship, there are generally 5 distinct components to it.
1) Excessively short sarcomere lengths result in little to no force production. At this length, the opposite actin filaments overlap with one another to some degree. This overlap prevents many of the myosin heads from extending and pulling on the correct actin filament. As a result, little force is produced.
2) Increasing the length of the sarcomere slightly removes some of the overlap between the opposite actin filaments, allowing some of the myosin heads to extend and pull on the correct actin filament. Therefore, the sarcomere can generate some force.
3) Increasing the sarcomere length slightly again removes any opposing actin filament overlap. Consequently, all the myosin heads can extend and pull the actin filament towards the M-line. This particular region of the length-tension relationship is known as the optimal length, as it is the length that allows the highest active tension. As a note, the optimal length isn’t one particular length, it is a region (2.6-2.8μm in humans), the small plateau region on the graph demonstrates this.
4) Further increasing the length of the sarcomere results in the actin filaments moving away from the myosin filament. This means that some myosin heads are not overlapping with the actin filament, meaning they cannot extend and pull the actin filament. Because fewer myosin heads can contribute to force here, active force production is less.
5) At this point, there is no overlap between the myosin heads and actin filaments, thus no myosin head can extend and pull the actin filament. Accordingly, no more active tension can be produced.
Passive Tension & Muscle Hypertrophy
It turns out within and around your muscle fibers are mechanosensors that are able to “detect” both active and passive tension, and convert this tension into a hypertrophy signal.
Therefore, to optimize the hypertrophy signal, it is favorable to have both active and passive tension being involved in an exercise.
The Working Sarcomere Lengths of the Biceps
It may be logical to assume that when the whole muscle is fully shortened (like at the top of a biceps curl), all the sarcomeres within the biceps are fully shortened. Likewise, when the muscle is stretched (like at the bottom of a biceps curl), all the sarcomeres within the biceps are stretched.
Although this is a very reasonable assumption, it isn’t actually always the case.
Different muscles have their sarcomeres organized in different ways that directly impact the length their sarcomeres can work through during any movement.
With the biceps, this study by Murrary et al. indicates when the elbow is flexed to 120 degrees (near the biceps being fully shortened), the sarcomeres of the biceps short and long head are at the very start of the length tension-relationship. However, when the elbow is more straightened out to 20 degrees of elbow flexion (when the biceps are stretched to a degree), the sarcomeres of the biceps short and long head are at the middle area of the length-tension relationship (near the plateau region of the active tension component).
In other words, despite the biceps being stretched to a degree when the elbows are flexed to 20 degrees, its sarcomeres are not stretched fully.
Therefore, some people have used this data to suggest since the sarcomeres are not stretched (presumably to the point where signficant passive tension can occur from titin), this means the biceps should not grow more when exposed to stretch during an exercise.
However, I think there are some important limitations people are missing if they make this conclusion.
Limitations with the Working Sarcomere Length Data
- It’s Important to know that the research measuring the working sarcomere length of the biceps did so during isometric contractions (static contractions). This is a notable point because people commonly train the biceps with dynamic exercises that involve eccentric contractions (when the muscle is lengthening while producing force), and it seems that during eccentric contractions, titin is might actually be capable of producing passive tension earlier and to a greater magnitude. Additionally, recall how I noted earlier the precise sarcomere length at which passive tension is generated is variable between muscles. What this implies is we can’t rule out the possibilty that although the sarcomeres of the biceps may only reach the middle portion of the length-tension relationship, titin may still be generating some decent passive tension during biceps exercises.
- This working sarcomere length data also ignores the potential interaction at other joints. Remember it only looked at the sarcomere length of the biceps during elbow flexion (isometrically) at 120 and 20 degrees of elbow flexion. However, we know that the biceps originate from the scapula, and will actually be stretched more when the shoulders are extended. What this means is that if we lengthen the biceps with simultaneous shoulder extension (such as done during an incline curl or cable face away curl), perhaps the sarcomeres reach an even greater length, permitting passive tension from titin.
- Perhaps most importantly (in my view), the research evaluating the working sarcomere length of the biceps only look at a small proportion of sarcomeres relative to the overall muscle. This is problematic as it’s likely not all the sarcomeres within a single muscle go through identical lengths during a movement . In other words, when a whole muscle is stretched, it’s possible for some of its sarcomeres to be stretched quite a bit and other sarcomeres to not be stretched as much. This is termed sarcomere non-uniformity. Therefore, it is very possible (if not almost certainly the case) that if we looked at all the sarcomeres within the biceps, we’d discover various sarcomeres do indeed get signficantly stretched.
- It’s also worth pointing out that titin isn’t the only source of passive tension. Although it’s possible titin is the predominant source of passive tension in the human body, the extracellular matrix surrounding muscle fibers is also capable of generating passive tension, and this extracellular matrix generated passive tension may also be capable of signaling hypertrophy too.
- Finally, we still do not know everything about muscle hypertrophy. It is very possible that there are other reasons as to why stretch during an exercise could be beneficial for muscle hypertrophy.
Due to these range of very strong limitations, I simply do not believe we can use the current research on the working sarcomere lengths of the biceps to definitively conclude this muscle should not grow more when exposed to a stretch during an exercise.
Hi Dhimant Indrayan, It is great to have someone on YouTube that likes to go so in depth. It is greatly appreciated! I do like to discuss this article and your latest video on biceps. Chris Beardsley just released some content (podcast on stretch mediated hypertrophy) which illustrates some of my point I would like to bring up. You might have listened to it already. I curious about your perspective on it.
1. Neuromechanical matching: This is the effect of different muscles or muscle regions having a biomechanical advantage across different joint angles/range of motion. In the case of the elbow flexors different elbow flexors potentially have an optimal leverage at different elbow angles. A big limitation in the research exploring the effect of stretch mediated hypertrophy is that they only analysis CSA/ circumference at the upper arm. This not only means there is a lack of data for all potential muscle regions, but it is also fully excludes the growth of the brachioradialis. The question then would be: Would we still see a net positive effect of long muscle length biased training on the elbow flexors when we analysis all muscle regions and elbow flexors?
2. Eccentric-only training and passive tension: When you look at the research exploring eccentric-only training (think of nordic hamstring curls for example) we see that hypertrophy mostly occurs do to inline sarcomere additions (sarcomerogenesis), shown by measuring fascicle length. You can also see a decrease in muscle fiber recruitment compared to concentric-only training, probably because of an increased demand of coordination. Indeed, the research I have read about titin shows eccentric loading allows a stretching of the titin molecule more so compared to conpared to concentric loading, which means eccentric-only training is accompanied by much more passive tension compared to concentric-only training. This would mean that stretch mediated hypertrophy and eccentric-only training have a large overlap in the type of addaptation. It also means that fascicle length measurements are much better indication of stretch mediated hypertrophy than other measurements. Indeed, tricep studies don’t show an increase in fascicle length when looking at long vs short muscle length, making stretch mediated hypertrophy questionable in this case.
3. Sarcomerogenesis and long term adaptations: Again eccentric-only and overload training show an earlier plateau in adaptations. This makes sense, considering the amount of sarcomeres in line also influences the length tension relationship as well as the amount of tension experienced per titin molecule. This would assume the effects of stretch mediated hypertrophy has a limited value long term. We also have to take in account the increased calcium influx accompanied with passive tension, highly influencing fatigue dynamics. So yes, in some cases we see a better hypertrophic effect of stretch mediated hypertrophy by a set to set bases. However, the picture could potentially be totally different when we take into considerations stimulus to fatigue ratios, making concentric-only and short muscle length training to maybe really shine in higher weekly volume scenarios.
Curious to hear more from you about this.
Hey! Thank you for the kind words!
1) If I understand the point correctly, some people speculate that the brachioradialis has proportionally greater leverage at higher elbow flexion angles relative to the biceps, meaning that partial range of motions at a short position bias the brachioradialis over the biceps. I do actually believe this is a really solid point. However, I’m skepetical this is the only explanation for the results of studies on the biceps. Interestingly, both the studies on the biceps showed considerably more hypertrophy (thickness in this case) at the 70% region of the elbow flexors (biceps and brachialis). This seems to be a phenomenon associated with stretched mediated hypertrophy, the distal parts of the muscle seem to grow considerably more, leading me to speculate stretch mediated hypertrophy was occuring in the studies.
2) I certainly think an increase in fascicle length could be involved in stretch mediated hypertrophy, but I really think it’s premature to definitively say this is the only thing happening. I don’t think we truly have strong data to prove this is the only thing going on, and strong enough to rule out other mechanisms. I will note we did have a study finding greater long head triceps gains with overhead extensions versus pushdowns: https://pubmed.ncbi.nlm.nih.gov/35819335/ – I know some people think the results are odd since the combined medial and lateral heads also grew more with overhead extensions, but I think this just shows there’s things we fully don’t understand about hypertrophy yet.
3) This is assuming the only mechanism behind stretch mediated hypertrophy is fascicle length gains, which again I don’t believe is a conclusion we can confidently say for the time being.
Thanks for your view on this topic. Have you read the research from Walter Herzog and Kiisa Nishikawa on titin? I can definitely recommend it:
– The multiple roles of titin in muscle contraction and force production [review], 2018
– Titin: A Tunable Spring in Active Muscle, 2020
A thing that really improved my understanding about titin recently is knowing that it is not bound to the thick filament (myosin). In schematic pictures it always seems this way, but now I understand this is because it runs parallel the thick filament. it connects the z-line and the m-line. Therefor it looks like titin is actually compressed during muscle shortening.
Have a nice day,
Sytse Roos (Netherlands)