Skeletal muscle has the remarkable ability to remodel and adapt, such as the increase in serial sarcomere number (SSN) or fascicle length (FL) observed after overstretching a muscle. This type of remodelling is termed longitudinal muscle fascicle growth, and its impact on biomechanical function has been of interest since the 1960s due to its clinical applications in muscle strain injury, muscle spasticity, and sarcopenia. Despite simplified hypotheses on how longitudinal muscle fascicle growth might influence mechanical function, existing literature presents conflicting results partly due to a breadth of methodologies. The purpose of this review is to outline what is currently known about the influence of longitudinal muscle fascicle growth on mechanical function and suggest future directions to address current knowledge gaps and methodological limitations. Various interventions indicate longitudinal muscle fascicle growth can increase the optimal muscle length for active force, but whether the whole force-length relationship widens has been less investigated. Future research should also explore the ability for longitudinal fascicle growth to broaden the torque-angle relationship's plateau region, and the relation to increased force during shortening. Without a concurrent increase in intramuscular collagen, longitudinal muscle fascicle growth also reduces passive tension at long muscle lengths; further research is required to understand whether this translates to increased joint range of motion. Lastly, some evidence suggests longitudinal fascicle growth can increase maximum shortening velocity and peak isotonic power, however, there has yet to be direct assessment of these measures in a neurologically intact model of longitudinal muscle fascicle growth.

Eight weeks of isometric training at a long or short muscle-tendon unit length increased and did not change fascicle length, respectively. The “width” of the torque-angle relationship plateau became broader following isometric training at the long length. Despite marked differences in muscle architecture and functional adaptations between the groups, there was only a small-magnitude improvement in neuromuscular fatigue resistance, which was surprisingly negatively related to increased fascicle length in the long length-training group.

Increased serial sarcomere number (SSN) has been observed in rats following downhill running training due to the emphasis on active lengthening contractions; however, little is known about the influence on dynamic contractile function. Therefore, we employed 4 weeks of weighted downhill running training in rats, then assessed soleus SSN and work loop performance. We hypothesised trained rats would produce greater net work output during work loops due to a greater SSN. Thirty-one Sprague-Dawley rats were assigned to a training or sedentary control group. Weight was added during downhill running via a custom-made vest, progressing from 5–15% body mass. Following sacrifice, the soleus was dissected, and a force-length relationship was constructed. Work loops (cyclic muscle length changes) were then performed about optimal muscle length (LO) at 1.5–3-Hz cycle frequencies and 1–7-mm length changes. Muscles were then fixed in formalin at LO. Fascicle lengths and sarcomere lengths were measured to calculate SSN. Intramuscular collagen content and crosslinking were quantified via a hydroxyproline content and pepsin-solubility assay. Trained rats had longer fascicle lengths (+13%), greater SSN (+8%), and a less steep passive force-length curve than controls (P<0.05). There were no differences in collagen parameters (P>0.05). Net work output was greater (+78–209%) in trained than control rats for the 1.5-Hz work loops at 1 and 3-mm length changes (P<0.05), however, net work output was more related to maximum specific force (R2=0.17-0.48, P<0.05) than SSN (R2=0.03-0.07, P=0.17-0.86). Therefore, contrary to our hypothesis, training-induced sarcomerogenesis likely contributed little to the improvements in work loop performance. This article has an associated First Person interview with the first author of the paper.

The purpose of this study was to investigate the relationship between fatigue‐induced reductions in isometric torque and isotonic power and to quantify the extent to which the decreases in angular velocity and dynamic torque can explain the power loss immediately following an isotonic fatiguing task and throughout recovery in seven young males and six young females. All measurements were performed with both legs. For dorsiflexion, fatigue‐related time‐course changes in isometric maximal voluntary contraction (MVC) torque, angular velocity, dynamic torque, and power production following repeated maximal isotonic contractions (load: 20% MVC) were investigated before, immediately after, and 1, 2, 5 and 10 min after a fatiguing task. There were no relationships between the fatigue‐related reductions in isometric MVC torque and peak power at any timepoint, suggesting that fatigue‐induced reductions in isometric MVC torque does not entirely reflect fatigue‐induced changes in dynamic performance. The relative contribution of fatigue‐related reduction in dynamic torque on power loss was greater immediately following the task, and lower throughout recovery than the corresponding decrease in angular velocity. Thus, power loss immediately following the task was more strongly related to the decline in dynamic torque; however, this relationship shifted throughout recovery to a greater dependence on slowing of angular velocity for power loss.

Active muscle shortening and lengthening are prevalent in all sports, and when these motions precede an isometric (ie, constant muscle-tendon unit length) contraction, they influence force production. Specifically, the amount of force produced in an isometric steady-state is less following active shortening (residual force depression; rFD) and more following active lengthening (residual force enhancement; rFE) than a purely isometric contraction at the same muscle length and level of activation. Together, rFD and rFE encompass the intrinsic property of muscle known as the history dependence of force. 1 Since the initial discovery of the history dependence of force by Abbott and Aubert in 1952, 1 rFD and rFE have been observed in single sarcomeres, 2 single human muscle fibers, 3 and humans in vivo during submaximal and maximal contraction intensities. 4-6 The modifiability of the history dependence of force through training has recently become an area of interest: if rFD can be decreased and rFE increased, there is potential to optimize sport performance. 7-10 However, no definitive conclusions have been