Steric blocking mechanism explains stretch activation in insect flight muscle

Over 60 y have elapsed since John Pringle (1) described a remarkable property of insect flight muscles: If you stretch them, after short a delay, they exert more force. This explains how insects beat their wings. The flight muscles are organized in antagonistic pairs coupled to the wing. The system is a free-running oscillator: Each time one muscle contracts, it stretches the opposing muscle, which then contracts. How does this come about? Muscle works by myosin cross-bridges interacting with actin to move the actin filaments past the myosin filaments (reviewed in 2). Muscle movement is inhibited if the myosin cross-bridges cannot bind to the actin filaments. In skeletal muscle, the release of Ca2+ under nervous control results in the movement of tropomyosin molecules across the surface of the actin filaments to uncover the myosin-binding sites on actin (3–5)—the steric blocking model. Flight muscles are switched on by release of Ca2+ into the sarcoplasm; however, in insect flight muscles, Ca2+ alone is not enough to free up the myosin-binding sites—you need stretch as well. The paper in PNAS by Perz-Edwards et al. (6) shows that the stretch activation of insect flight muscle uses the same steric blocking model for controlling the actin-myosin interaction that was found in skeletal muscle. In the case of insect flight muscles, stretching the muscle causes the tropomyosin to move across the surface of actin to free up the myosin-binding sites.