3.1.1: Competing Theories for Regional Hypertrophy: SMH vs. NMM
The tension-based model of hypertrophy established in Chapters 1 and 2 leaves an important question unanswered: given that a muscle is being subjected to high mechanical tension, where along its length will the growth occur? Two distinct hypotheses attempt to answer this.
The table below is one of the more science-heavy sections in this book. You do not need to fully understand every row to apply the practical takeaway that follows in 3.1.2. If the terminology feels dense, skip to the Bottom Line for the Lifter in the next section and come back to this table later as your understanding deepens.
| Dimension | Stretch-Mediated Hypertrophy (SMH) | Neuromechanical Matching (NMM) |
|---|---|---|
| Core premise | Regional growth is driven by the magnitude of passive mechanical tension a region experiences when the muscle is elongated under load. Regions placed under greater stretch receive a larger stimulus [1]. | Regional growth is driven by which motor units are recruited. The nervous system activates muscle regions in proportion to their leverage—their internal moment arm—at a given joint angle [2,3]. |
| Primary mechanism | Passive tension transmitted through titin and the Z-disc, activating mechanosensitive signaling pathways (including mTORC1) independently of neural activation [4,5]. | Differential motor unit recruitment based on regional leverage. Fibers that are not activated cannot grow, regardless of how much passive stretch the region experiences [6]. |
| Type of growth predicted | Increases in fascicle length via sarcomerogenesis in series—the addition of new sarcomeres (the smallest contractile units of the muscle) end-to-end, making fibers physically longer [1,7]. This biases growth toward longitudinal hypertrophy rather than cross-sectional area. | Standard myofibrillar hypertrophy (increases in cross-sectional area and diameter) in whichever region has the greatest leverage for the exercise [3,8]. |
| Role of activation | Passive tension can stimulate some growth even without muscle activation, as demonstrated in denervated muscle stretching studies in animals [5]. However, combining passive tension with activation (as in loaded eccentrics) amplifies the effect [1]. | Activation is mandatory. A muscle fiber must be recruited via its motor neuron to experience active tension and trigger the full mechanotransduction cascade [6]. |
| Primary evidence base | Animal stretching studies (e.g., denervated muscle growth), lengthened partial ROM human trials (Maeo et al. 2021; Pedrosa et al. 2022), static stretching hypertrophy studies [9,10,11]. | Animal and human studies on differential motor unit activation based on moment arm (established in respiratory muscles), regional EMG patterns correlating with internal moment arm length, and computational modeling [2,12,13]. |
| Key advocate(s) | Broad consensus in the sports science community, with varied definitions. Both Beardsley (emphasizing pure passive tension) and researchers like Schoenfeld, Henselmans, and Nuckols (emphasizing lengthened-position dynamic training) have contributed to the concept [14]. | Primarily developed and championed by Chris Beardsley as a framework for exercise selection [3,8]. |
| Respiratory muscle precedent | Not applicable in the same way. | Well-established: the diaphragm and intercostal muscles display clear NMM, with neural drive distributed to regions with the most favorable mechanical advantage during different breathing tasks [12,13]. |