Evidence for Muscle Cell-Based Mechanisms of Enhanced Performance in Stretch-Shortening Cycle in Skeletal Muscle
Abstract
The stretch-shortening cycle (SSC) enhances force during concentric contraction following eccentric contraction in skeletal muscle. This review explores mechanisms beyond stretch-reflex activation and tendon energy storage, focusing on pre-activation, cross-bridge kinetics, and residual force enhancement (RFE). Experimental evidence suggests these mechanisms contribute to SSC effects under specific contractile conditions.
Introduction
SSC involves active muscle stretching before shortening, enhancing performance in movements like jumping. Traditional mechanisms, such as stretch-reflex activation and energy storage in tendons, are insufficient to explain SSC effects observed in single muscle fibers. This review discusses alternative mechanisms like pre-activation, cross-bridge kinetics, and RFE.
Pre-Activation
In SSCs, muscles are pre-activated during the stretch phase, leading to higher force at the onset of shortening. This is due to the muscle being already activated, unlike in pure concentric contractions. Pre-activation contributes to SSC effects but does not fully explain the observed differences.
Cross-Bridge Kinetics
Active stretching enhances force by elongating attached cross-bridges, storing elastic energy that can be released during subsequent shortening. Introducing pauses between stretch and shortening phases diminishes the SSC effect, supporting the role of cross-bridge kinetics
Residual Force Enhancement (RFE)
RFE, characterized by increased isometric force after stretching, is linked to the protein titin. Titin's engagement during active stretching leads to increased force, contributing to SSC effects. RFE persists even with pauses between stretch and shortening, indicating its significant role.
Factors Modulating SSC Effects
SSC effects vary with shortening velocity, stretching velocity, and muscle fiber type. Slow-twitch fibers show greater SSC effects due to slower cross-bridge kinetics. Understanding these factors helps in optimizing performance and training regimens.
Applicability and Limitations
Laboratory findings on isolated muscles may not fully translate to natural human movements. More research is needed under physiological conditions to better understand SSC mechanisms in vivo.
Conclusion
SSC effects are not solely due to traditional mechanisms. Protein-based mechanisms, particularly involving titin, play a significant role. Future research should focus on elucidating these molecular mechanisms to enhance understanding and application of SSCs.
KEY TERMINOLOGY
Stretch-Shortening Cycle (SSC): A muscle action involving a pre-stretch (eccentric contraction) followed by a shortening (concentric contraction), enhancing performance.
Pre-Activation: The activation of muscles during the stretching phase of SSC, leading to higher force at the onset of shortening.
Cross-Bridge Kinetics: The interaction between myosin heads and actin filaments in muscle fibers, contributing to force production during SSC.
Residual Force Enhancement (RFE): Increased steady-state isometric force following active stretching of a muscle.
Titin: A giant protein that contributes to muscle elasticity and force production, particularly during RFE.
Stretch-Reflex Activation: A reflexive muscle contraction in response to stretching, traditionally considered a mechanism for SSC effects.
Elastic Energy Storage: The storage and release of energy in tendons during muscle stretching and shortening.
Eccentric Contraction: Muscle action where the muscle lengthens under tension.
Concentric Contraction: Muscle action where the muscle shortens under tension.
Isometric Contraction: Muscle action where the muscle length remains constant under tension.
Series Elastic Components: Tendinous structures in muscles that store elastic energy during stretching.
Force-Velocity Relationship: The inverse relationship between the force a muscle generates and the velocity of muscle shortening.