The maintenance of skeletal muscle mass plays a critical role in health and quality of life. One of the most potent regulators of skeletal muscle mass is mechanical loading, and numerous studies have led to a reasonably clear understanding of the macroscopic and microscopic changes that occur when the mechanical environment is altered. For instance, an increase in mechanical loading induces a growth response that is mediated, at least in part, by an increase in the cross-sectional area of the myofibers (i.e., myofiber hypertrophy). However, very little is known about the ultrastructural adaptations that drive this response. Even the most basic questions, such as whether mechanical load-induced myofiber hypertrophy is mediated by an increase in the size of the pre-existing myofibrils and/or an increase in the number myofibrils, have not been resolved. In this review, we thoroughly summarize what is currently known about the macroscopic, microscopic and ultrastructural changes that drive mechanical load-induced growth and highlight the critical gaps in knowledge that need to be filled.

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This study describes a mouse model of progressive resistance exercise that utilizes a full-body/multi-joint exercise (weight pulling) along with a training protocol that mimics a traditional human paradigm (three training sessions per week, ~8–12 repetitions per set, 2 min of rest between sets, around two maximal-intensity sets per session, last set taken to failure, and a progressive increase in loading that is based on the individual’s performance). We demonstrate that weight pulling can induce an increase in the mass of numerous muscles throughout the body. The relative increase in muscle mass is similar to what has been observed in human studies, and is associated with the same type of long-term adaptations that occur in humans (e.g., fiber hypertrophy, myonuclear accretion, and, in some instances, a fast-to-slow transition in Type II fiber composition). Moreover, we demonstrate that weight pulling can induce the same type of acute responses that are thought to drive these long-term adaptations (e.g., the activation of signaling through mTORC1 and the induction of protein synthesis at 1 h post-exercise). Collectively, the results of this study indicate that weight pulling can serve as a highly translatable mouse model of progressive resistance exercise.

This study describes a mouse model of human progressive resistance exercise that utilizes a full-body/multi-joint exercise (weight pulling) along with a training protocol that mimics a traditional human paradigm (3 training sessions per week, ~8-12 repetitions per set, 2 minutes of rest between sets, ~2 maximal-intensity sets per session, last set taken to failure, and a progressive increase in loading that is based on the individual's performance). We demonstrate that weight pulling can induce an increase in the mass of numerous muscles throughout the body. The magnitude of increase in muscle mass is similar to what has been observed in human studies, and it is associated with the same type of long-term adaptations that occur in humans (e.g., fiber hypertrophy, myonuclear accretion, and in some instances a fast-to-slow transition in Type II fiber composition). Moreover, we demonstrate that weight pulling can induce the same type of acute responses that are thought to drive these long-term adaptations (e.g., the activation of signaling through mTORC1 and the induction of protein synthesis at 1 hr post-exercise). Collectively, the results of this study indicate that weight pulling can serve as a highly translatable mouse model of human progressive resistance exercise.

The actin cytoskeleton in neurons plays critical roles in axonal growth and synaptic organization. Until recently, most studies on axonal actin were limited to terminal growth cones or synapses, whereas the organization of actin along the shaft of the axon was relatively ignored. However, experiments using super-resolution microscopy and live imaging have revealed previously unknown actin structures along the axonal shaft, such as periodic 'actin rings' circumferentially wrapping underneath the plasma membrane and dynamic actin pools deeper within the axon shaft (termed actin 'hotspots' and 'trails'). In this short review, we highlight some open questions that have surfaced as a direct result of these discoveries.

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