The podcast discusses stretch mediated hypertrophy, its definition, and misconceptions surrounding it. They delve into studies on muscle fiber length, sarcomere stretching, and the role of Titan. The importance of reaching maximum range of motion is explored, along with the effects of Nordic leg curls. They address the differences between stretch-mediated hypertrophy and strength training, and the use of EMG in studying muscle activation. The concept of neuro-mechanical matching, triceps study findings, and inconsistencies in calf muscle growth are discussed. The hosts challenge alternative models and emphasize the need for evidence-based explanations.
Stretch-mediated hypertrophy refers specifically to the increase in size of single muscle fibers stimulated by stretching them.
Sarcomereogenesis, the addition of sarcomeres in a series within a muscle fiber, occurs rapidly when muscles are stretched to longer lengths.
Static stretching studies in animals consistently show increases in sarcomere length and sarcomeregenesis.
Reaching the end range of physiological joint motion is crucial for creating the necessary tension and facilitating stretch-mediated adaptations.
Static stretching and eccentric training both stimulate stretch-mediated hypertrophy through the lengthening of muscle fascicles.
The idea that stretch can overcome a lack of leverage in muscle activation is not supported by evidence and neuro-mechanical principles.
Deep dives
Stretch-mediated hypertrophy defined and misunderstood
In this episode, the hosts discuss the concept of stretch-mediated hypertrophy and the confusion surrounding its definition. They acknowledge that there is currently a lack of consensus on what exactly constitutes stretch-mediated hypertrophy and how it differs from contraction-mediated hypertrophy. The hosts propose that stretch-mediated hypertrophy should refer specifically to the increase in size of single muscle fibers stimulated by stretching them, rather than the overall muscle mass increase that occurs after training with a stretch position exercise.
The significance of sarcomereogenesis
The hosts highlight the importance of sarcomereogenesis in stretch-mediated hypertrophy. Sarcomereogenesis refers to the addition of sarcomeres in a series within a muscle fiber, leading to an increase in fiber length. They explain that animal studies have consistently shown that sarcomereogenesis occurs rapidly when muscles are stretched to longer lengths for extended periods of time. The adaptation tapers off after approximately two weeks if the range of motion is not further increased. However, if the range of motion is continually expanded, sarcomereogenesis continues to occur.
Static stretching as a valuable source of information
The hosts argue that static stretching studies are a valuable source of information for understanding stretch-mediated hypertrophy. These studies specifically focus on the stretch stimulus that produces stretch-mediated adaptations, without the simultaneous involvement of contraction-mediated adaptations. They explain that static stretching studies in animals consistently show increases in sarcomere length and sarcomeregenesis, providing insights into the specific adaptations associated with stretch-mediated hypertrophy.
The role of Titan and sarcomere length
The hosts delve into the role of Titan, a protein within the sarcomere, in stretch-mediated hypertrophy. They explain that as the sarcomere is stretched, Titan provides the resistance and determines the passive tension stimulus. Initially, stretching the sarcomere primarily stretches the compliant part of Titan, but once the sarcomere breaches a critical length threshold, the stiffer segment of Titan is stretched, leading to force production and sarcomeregenesis. They emphasize that reaching the end range of physiological joint motion is crucial for creating the necessary tension and facilitating stretch-mediated adaptations.
Static stretching exercises, which involve reaching the maximum muscle length close to the body's physiological range of motion, stimulate stretch-mediated hypertrophy. During static stretching, sarcomeres within the activated muscle fibers experience passive tension from tightness, leading to sarcomerogenesis, the formation of new sarcomeres. This stretch stimulus does not require muscle activation and produces hypertrophy primarily through the lengthening of muscle fascicles. Studies have shown that static stretching results in increased muscle fascicle length and changes in the angle of peak torque. These adaptations occur predominantly at longer muscle lengths, reflecting an alteration in the length-tension relationship. The passive tension created by tightness in the muscle fibers triggers the increase in muscle fascicle length and subsequent strength gains at longer muscle lengths.
Eccentric training induces sarcomerogenesis and passive tension
Eccentric training, whether performed as the eccentric phase in dynamic contractions or in isolation with super maximal loads, also induces sarcomerogenesis and passive tension in the muscle fibers. During eccentric training, the activated muscle fibers experience passive tension from titin, a vital protein in muscle contraction. The compliance segment of the muscle fibers does not stretch, but instead, the stiffer segment, which starts at a shorter muscle length, stretches due to tightness and passive tension. This mechanism occurs only in active muscle fibers, which are the ones being recruited in the eccentric phase. Eccentric training has shown to produce greater increases in fascicle length and changes in the angle of peak torque compared to static stretching. The greater number of active muscle fibers being exposed to the stretch stimulus in eccentric training contributes to its effectiveness in inducing sarcomerogenesis and muscle hypertrophy.
Leverage (internal moment arms) and muscle activation
Muscle activation and leverage, specifically internal moment arms, are closely related in neuro-mechanical matching. Leverage refers to the efficiency of muscle force production in relation to joint angles. Muscles with better leverage typically exhibit higher muscle activation levels, as the central nervous system allocates motor unit recruitment to muscles that can generate movement with minimal muscle activation. The idea that stretch can overcome a lack of leverage is not supported by evidence and defies neuro-mechanical principles. Muscle fibers without leverage do not receive significant motor unit recruitment, as the focus is on muscles that can generate movement efficiently. Therefore, the argument that stretch can compensate for poor leverage is flawed.
Importance of study design and statistical power
When evaluating studies, it is important to consider the study design and statistical power. The number of participants in a study should be determined based on the specific research question and effect size expected. For investigations targeting specific outcomes like fast-skilling measurements, pinnation angle increase, or cross-sectional area, a smaller number of participants may be sufficient to detect meaningful results within a given timeframe. The quality of a study does not solely depend on the number of participants, but on the rigor of the methodology and the ability to detect statistically significant findings. Therefore, it is essential to avoid dismissing a study simply based on the number of participants without performing a reverse power calculation.
Main Idea 1
Stretch-mediated hypertrophy is the result of stretching a muscle fiber, while contraction-mediated hypertrophy is caused by actin-myosin cross-bridge formations during force production.
Main Idea 2
Muscle fascicle length is the primary indicator of stretch-mediated hypertrophy, with an increase in fascicle length indicating stretch-mediated adaptations.
Main Idea 3
The length-tension relationship and leverage play a significant role in stretch-mediated hypertrophy, especially in muscles like the quads, hamstrings, and pecs.
Main Idea 4
There is ongoing debate about the role of stretch-mediated hypertrophy in the calves, as the literature presents conflicting results and challenges our understanding of the mechanisms involved.
Chis and I cover this topic yet again because of the fact that "lengthened partials" has become so popular yet the "hivemind" that talk about it, don't even understand what stretch mediated hypertrophy is, or how to measure it.
