Mobility in Sport: Beyond Flexibility and Into Function (Part 3: Static Stretching, Sarcomeres, Fascicles & Robustness)

Within this section of the blog, I want to (try!) explain the physical, architectural underpinnings of what enables a muscle-tendon unit (MTU) to be able to move through larger ranges, potentially resulting in larger joint ranges of motion in individuals. In doing so, I will critically examine some of the more commonly prescribed “mobility” interventions and unpack what they are actually changing—if anything! 

Before delving deeper into this section, you are probably wondering what the benefit is of bothering to understand the true ins and outs of muscle architecture. And my answer to that question lies in clarity. Having had the great privilege of sharing a room with Alex Wolf – one of my key takeaways (of many!) from a presentation of Alex’s recently was being able to clearly and accurately describe the ‘what’ (what is the quality you are changing) and the ‘why’ (your rationale behind why you are changing, i.e., how it will impact performance/health) behind exercise prescription and programme design. Once the ‘what’ and the ‘why’ have been clearly and accurately defined, the ‘how’ (the method) or specific conditions the coach needs to curate become obvious. If we lack the clarity in what quality we are trying to change and have no reason or rationale as to why we want to change that quality, the likelihood of a successful outcome will be minimal. As coaches, if we are unable to clearly and accurately outline what coordinative, structural or neural quality needs to change, then how will we be able to create the environment to drive the necessary adaptations? In my opinion, you won't!

Hill’s Elastic Mechanical Muscle Model (1938) 

To fully understand what actually limits or permits greater muscle extensibility within the structural makeup of the entire muscle-tendon unit (MTU), an appreciation of Hill’s Muscle Model is necessary to acknowledge which exact components are involved. However, before we go any further, we must understand what is meant by the term muscle extensibility. Weppler and Magnusson (2010) defined muscle extensibility as the ability of a muscle to lengthen to a predetermined end range – simply, the lengthening capacity of the entire MTU. In practical terms, it is the limit to which you can lengthen a muscle by moving a joint through a ROM before resistance within the muscle is met, preventing the joint from moving any further. 

Archibald Vivian Hill's (1938) Muscle Model

Hill’s model consists of the following: 

• Contractile Element (CE) – the active force-generating sarcomere (myosin-actin cross-bridges within fibres and fascicles) (TENSION & FORCE PRODUCER) 

• Series Elastic Component (SEC) – connective tissue on both sides of the muscle cell connecting to tendon, ligaments and bone (FORCE TRANSMITTER) 

• Parallel Elastic Component (PEC) – passive connective tissue surrounding the muscle (endomysium, perimysium, epimysium and fascia)

For simplicities sake (and your reading time!), I will only be focusing on what is going on in the contractile element (CE) within the MTU, more specifically discussing sarcomeres and muscle fascicles. This is because the length of muscle fascicles, which are described as a bundle of muscle fibres surrounded by a layer of connective tissue called perimysium (Lieber and Ward, 2011), plays a pivotal role in the ability to achieve greater muscle extensibility and consequently larger active joint ROMs within individuals. 

Structure of Skeletal Muscle

Now why should anyone be so concerned with increasing the length of their muscle fascicles to increase muscle extensibility? In another influential study by Richard Lieber and Samuel Ward (2011), they found that when a muscle had longer fascicles as a result of an increase in serial sarcomere number from the process of sarcomeregenesis, the muscle could lengthen (and shorten) over a greater distance, known as muscle excursion. This is because the excursions of each individual sarcomere are additive. Tim Caron explained this concept in his book Strength Deficit (2022) through the visualisation of a train pulling rail cars. The length of the entire train representing the muscle fascicle, and the engine car representing an individual sarcomere. By adding more engine cars (sarcomeres), the overall length of the train (fascicle) will increase. We can therefore deduce that muscles with a longer fascicle length have a greater potential for generating tension and force over a longer muscle fascicle, and if a muscle can lengthen further, then we have a greater potential to use our joints through wider, larger ranges of motion. This can be compared with how a larger muscle, or a muscle with a larger cross-sectional area (CSA), has the capacity to produce a greater amount of force. 

I will discuss sarcomeres and sarcomeregenesis shortly, so bear with me, but first, let's explore and unpack some of the literature out there which commonly gets people believing that statically stretching (i.e., holding a static pose for a prolonged period of time) is eliciting long-term, structural changes to the true length of muscle fascicles, in turn granting them access to larger joint ranges of motion. 

What Does Static Stretching Actually Do? 

Many studies, such as Gajdosik’s (1991) early work and Blazevich et al.’s (2014) more recent investigation into static stretching interventions, have shown that short-term (3-wk) stretching interventions can significantly increase joint ROM. At first glance, it seems obvious to assume that these ROM improvements must be due to the muscle physically lengthening, no? But let’s dive a little deeper here and not just assume that passive, static stretching for 3 weeks is your golden ticket to “unlocking” all your mobility gains, and you are suddenly going to be displaying Simone Biles’ level of mobility – spoiler alert, you won’t! This assumption was directly challenged by the widely cited work by Magnusson and colleagues (1996) almost 30 years ago, who quickly debunked this idea, stating that “the increased range of motion achieved from training [static stretching protocols] is a consequence of increased stretch tolerance on the part of the subject rather than a change in the mechanical or viscoelastic properties of the muscle.” Put simply, neither the muscle nor the fascicles are structurally lengthening — the nervous system is merely allowing a greater stretch by altering sensation and threat perception. Joint ROM increases, but no structural change has occurred. Immediate ROM changes can be commonly demonstrated with proprioceptive neuromuscular facilitation (PNF) stretching, where increases in joint ROM largely reflect neural adaptations, not true structural changes to the fascicles.

Naturally this leads to the next obvious question, which is how long do these neural effects of static stretching last? For example, could I perform a bout of static stretching the day before a game of tennis and expect to carry over those improvements in ROM a day later? The work of Hatano et al. (2019) and Matsuo et al. (2023) explored this exact question. Both concluded that these neural, stretch-tolerance–driven gains in ROM are very short-lived acutely, often returning towards baseline within approximately 30 minutes after a single static stretching bout. In other words, immediately after stretching, a joint can be moved through a larger ROM due to altered sensation, but without evidence of sustained muscle architectural change. 

It should be acknowledged that 3 of these studies were carried out on the hamstrings and the other on the triceps surae muscle group, and other muscles or muscle groups may show different adaptation profiles. Nonetheless, the vast number of studies evaluating static stretching protocols over the last 30 years primarily modify neural factors (stretch tolerance and perception) and produce little to no lasting change in the mechanical properties of the fascicles that would meaningfully increase mobility through improvements in true muscle extensibility. 

Now, if you thought I was going to leave the static-stretching lovers with nothing to show for, you would be wrong! A systematic review with meta analysis by Panidi et al. published in 2023 actually found that if you performed static stretches hard enough and for long enough, you can actually increase muscle fascicle length. In other words, static stretching can induce mechanical, structural changes to the contractile element of the muscle that many studies before stated did not do. However, you now may be wondering what does “hard and long enough” actually mean? Although the paper does not allude to the exact interventions it does provide guidelines to the how “hard and long enough” question. “High volume” means a total of 4,725seconds/week of static stretching - on average this is over 11 minutes of stretching every day! On the other hand, “high intensity” is described as at the “point of discomfort” or “maximum tolerable after the onset of pain”. To me both phrases are fairly vague and subjective, but in each quote “discomfort” and “pain” are mentioned, so one can only assume this is not your puppy yoga class type of stretching. So, to get this straight, you have to stretch one specific muscle for over 11 minutes every day for 12 weeks to elicit any form of mechanical change to the muscle. But what happens if the physio has told that your pain is because you’re “very tight” (whatever that means!) because you can’t touch your toes, you spend too much time sat at a desk and so you need to stretch your hamstrings, hip flexors and pecs. Well, that would equate to a grand total 14,175seconds/week of stretching time - a total of 33 minutes/day, what fun!! To rub further salt into the wounds, the fascicle length improvements are very minimal and primarily attributed to length increases, specifically within the sarcomere, and not due to the addition of sarcomeres in series (sarcomeregenesis). Therefore, I would argue that this newly acquired sarcomere length may not meaningful translate to useable, muscle extensibility or mobility improvements. 

Sarcomeres & Eccentric Training 

If static stretching alone does not reliably produce long-term structural change, the next logical question is: what intervention does? The answer lies in eccentric strength training. A substantial body of research has demonstrated that eccentric loading leads to increases in muscle fascicle length (Blazevich et al., 2007), providing the structural capacity for muscles to operate through greater excursions and, in turn, enabling joint ranges of motion. 

To understand how and why muscle fascicles lengthen in response to eccentric training, we need to revisit a concept introduced earlier this blog - sarcomeregenesis. Sarcomeregenesis refers to the addition of sarcomeres in series (end-to-end) within a myofibril. Unlike temporary increases in stretch tolerance, this represents true architectural adaption to the muscle. Crucially, the number of sarcomeres in arranged in series directly determines the optimal operating length of a muscle fibre, and by extension, the overall length of the muscle belly itself. As Kruse and colleagues (2021) succinctly state, “the number of sarcomeres in series determines optimum muscle fiber length, which together determines muscle belly length.” 

A relaxed (top) versus contracted (bottom) sarcomere

From a structural perspective, skeletal muscle is a highly organised, hierarchal structure. Whole muscles are composed of multiple muscle fascicles, which consist of bundles of individual muscle fibres. Each muscle fibre contains numerous myofibrils, and within these myofibrils lie the fundamental contractile units known as sarcomeres, arranged in series along their length (Lieber, 2002). Within each sarcomere, force (or tension) is generated through the sliding filament mechanism (Huxley & Hanson, 1954; Huxley & Niedergerke, 1954), whereby contractile proteins of myosin and actin form cross-bridges by sliding past one another. A crucial insight from this foundational work was that each sarcomere has an optimal length at which force production is maximised. When a sarcomere operates in an excessively shortened or lengthened state, actin-myosin overlap is reduced, resulting in diminished force production. Consequently, the addition of sarcomeres in series allows a muscle operating at a given joint position or overall length to distribute strain across more contractile units, enabling each individual sarcomere to function closer to its optimal force-producing length. 

With the anatomical foundations now established, we can now turn our attention to some particularly interesting research that further attempts to answer several key questions. First, how long does it take for sarcomeregenesis to occur within muscle fascicles? Second, what frequency of eccentric training is required to promote this adaption? And finally, perhaps most importantly, what level of intensity is necessary to elicit meaningful adaptations upon sarcomeres? 

A recent study by Andrews and colleagues (2025) provides valuable insight into these questions. The authors investigated the effects of a 9-week eccentric nordic hamstring curl intervention on muscle fascicle length. While research in this area is growing, it is worth noting that the majority of studies to date have focused predominantly on lower limb musculature, specifically hamstrings. There remains a notable lack of equivalent research examining upper-body eccentric interventions and their effects on fascicle length - an area that clearly warrants further investigation (and perhaps a future dissertation topic!). 

A nordic hamstring curl.

The 9-week intervention involved performing Nordic hamstring curls three times per week, with training volume progressively increasing across the programme. Participants began with 4 sets of 6 repetitions and finished the final weeks performing 5 sets of 8 repetitions, highlighting the relatively high frequency and volume required to elicit meaningful architectural adaptations. The study demonstrated that after just 3 weeks of training, muscle fascicle length had already increased; however, this early increase was not the result of sarcomerogenesis (the addition of sarcomeres in series), but rather due to elongation of existing sarcomeres — an adaptation that would not confer the same long-term functional benefits. It was only after the full 9-week intervention that true sarcomerogenesis was observed as the long-head bicep femoris fascicles had increased in length. In terms of intensity, participants “continued lowering their bodies until they could no longer hold themselves up or their hands touched the floor. Catching themselves upon reaching the floor, participants used their arms to assist as they returned to the initial position to minimize concentric load as they prepared for the next repetition.” From this, it can be deduced that the exercise was performed at a supramaximal intensity, with participants unable to complete the concentric (upward) phase and instead focusing exclusively on the eccentric lowering. Finally, it is worth noting that following just 3 weeks of detraining, fascicle length had almost returned to baseline values recorded at week 0, highlighting the transient nature of these adaptations in the absence of continued loading.

These results were mirrored by another study by Bizet and colleagues (2025) which found that early (3-week) increases in fascicle length was again attributed to existing sarcomere elongation, rather than sarcomeregenesis. What is worth mentioning from this study in particular, is that while maximal voluntary torque (strength) improved in groups performing short and long-muscle length calf raises, only the long-muscle-length training group exhibited increased fascicle length, indicating an expanded capacity to express force at longer muscle lengths. Appreciating this detail may seem obvious, but is crucial if increasing mobility and access to end-range joint positions is the goal of the training programme.

Screenshot from Bizet et al. (2025).

Fascicle Length and Implications on Injury Risk 

Alongside the benefits of accessing greater joint excursions and improvements in overall mobility, increased muscle fascicle length also carries important implications for injury risk. Continuing with the hamstring theme, research has shown that shorter biceps femoris long-head fascicles are associated with a 4.1 times greater risk of sustaining a hamstring strain injury (Timmins et al., 2016). 

Further supporting this idea, Gabbe and colleagues (2005) identified rectus femoris length as a risk factor for hamstring injury. Shortened hip flexors can bias the pelvis into an anterior pelvic tilt, thereby increasing the length demand and strain placed on the hamstrings. Mendiguchia and colleagues (2024) quantified this relationship, reporting that for every additional 5° of anterior pelvic tilt, approximately 1cm of elongation occurs in the hamstring at their proximal (pelvic) attachment. 

From this perspective, increasing muscle fascicle length within muscles such as the rectus femoris becomes crucial. Doing so may reduce excessive length demands placed on hamstrings, ensuring they are not forced to operate at muscle lengths where they lack the architectural capacity to tolerate strain or produce force effectively. No doubt there are plenty of other examples in the body where fascicle length can alter kinematics, placing certain tissues under more stress, leading to

In the final part of this blog series, the discussion will shift towards the dynamic relationship between mobility and stability, questioning whether one can truly exist without the other. Concepts such as the joint-by-joint approach, an appreciation of sport-specific adaptations to the length–tension relationship, and the ability to control and produce force through range will be explored to challenge the notion that “more mobility is always better”. The discussion will then briefly address the dreaded “T” word before concluding with practical applications surrounding what to do both pre and post-exercise.

References / Sources:

Alex Wolf – Co-Founder of Strength and Conditioning Acdemy & Ex-Head of S&C and Learning at the English Institue of Sport

Andrews, M. H., Pai, A., Gurchiek, R. D., Pincheira, P. A., Chaudhari, A. S., Hodges, P. W., ... & Delp, S. L. (2025). Multiscale hamstring muscle adaptations following 9 weeks of eccentric training. Journal of sport and health science, 14, 100996.

Bizet, B., Nordez, A., Tallio, T., Lacourpaille, L., Cattagni, T., Colard, J., ... & Andrade, R. J. (2025). Eight weeks of eccentric training at long-muscle length increases fascicle length independently of adaptations in passive mechanical properties. Journal of Applied Physiology, 138(4), 939-949.

Blazevich, A. J., Cannavan, D., Coleman, D. R., & Horne, S. (2007). Influence of concentric and eccentric resistance training on architectural adaptation in human quadriceps muscles. Journal of applied physiology.

Blazevich, A. J., Cannavan, D., Waugh, C. M., Miller, S. C., Thorlund, J. B., Aagaard, P., & Kay, A. D. (2014). Range of motion, neuromechanical, and architectural adaptations to plantar flexor stretch training in humans. Journal of applied physiology.

Caron, T. (2022). Strength Deficit.

Gabbe, B. J., Finch, C. F., Bennell, K. L., & Wajswelner, H. (2005). Risk factors for hamstring injuries in community level Australian football. British journal of sports medicine, 39(2), 106-110.

Gajdosik, R. L. (1991). Effects of static stretching on the maximal length and resistance to passive stretch of short hamstring muscles. Journal of orthopaedic & sports physical therapy, 14(6), 250-255.

Hatano, G., Suzuki, S., Matsuo, S., Kataura, S., Yokoi, K., Fukaya, T., ... & Iwata, M. (2019). Hamstring stiffness returns more rapidly after static stretching than range of motion, stretch tolerance, and isometric peak torque. Journal of sport rehabilitation, 28(4), 325-331.

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Huxley, A. F., & Niedergerke, R. (1954). Structural changes in muscle during contraction: interference microscopy of living muscle fibres. Nature, 173(4412), 971-973.

Huxley, H., & Hanson, J. (1954). Changes in the cross-striations of muscle during contraction and stretch and their structural interpretation. Nature, 173(4412), 973-976.

Kruse, A., Rivares, C., Weide, G., Tilp, M., & Jaspers, R. T. (2021). Stimuli for adaptations in muscle length and the length range of active force exertion—a narrative review. Frontiers in Physiology, 12, 742034.

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Lieber, R. L., & Ward, S. R. (2011). Skeletal muscle design to meet functional demands. Philosophical Transactions of the Royal Society B: Biological Sciences, 366(1570), 1466-1476.

Magnusson, S. P., Simonsen, E. B., Aagaard, P., Sørensen, H., & Kjaer, M. (1996). A mechanism for altered flexibility in human skeletal muscle. The Journal of physiology, 497(1), 291-298.

Matsuo, S., Iwata, M., Miyazaki, M., Fukaya, T., Yamanaka, E., Nagata, K., ... & Suzuki, S. (2023). Acute and prolonged effects of 300 sec of static, dynamic, and combined stretching on flexibility and muscle force. Journal of Sports Science & Medicine, 22(4), 626.

Mendiguchia, J., Garrues, M. A., Schilders, E., Myer, G. D., & Dalmau‐Pastor, M. (2024). Anterior pelvic tilt increases hamstring strain and is a key factor to target for injury prevention and rehabilitation. Knee Surgery, Sports Traumatology, Arthroscopy, 32(3), 573-582.

Panidi, I., Donti, O., Konrad, A., Dinas, P. C., Terzis, G., Mouratidis, A., ... & Bogdanis, G. C. (2023). Muscle architecture adaptations to static stretching training: a systematic review with meta-analysis. Sports medicine-open, 9(1), 47.

Timmins, R. G., Bourne, M. N., Shield, A. J., Williams, M. D., Lorenzen, C., & Opar, D. A. (2016). Short biceps femoris fascicles and eccentric knee flexor weakness increase the risk of hamstring injury in elite football (soccer): a prospective cohort study. British journal of sports medicine, 50(24), 1524–1535.

Weppler, C. H., & Magnusson, S. P. (2010). Increasing muscle extensibility: a matter of increasing length or modifying sensation?. Physical therapy, 90(3), 438-449.