Why stretching a muscle beyond its optimal length reduce ability to contract?
When stretching muscle beyond its optimal length, its passive tension increases. This leads to several factors that collectively hinder the muscle's ability to contract.
1. Reduced Overlap:
When a muscle is stretched to a point where the actin and myosin filaments overly less, the chances of attachment between them decrease. With fewer binding sites for the myosin head, the overall contractile force generated during contraction is reduced.
2. Increased Internal Resistance:
Excessive muscle stretching can lead to increased internal resistance within them muscle fibers. This higher internal resistance inhibits smooth sliding of myosin heads along the actin filaments, causing a decrease in contractile efficiency and force production.
3. Damage to Muscle Structure:
Overstretching may cause damage to muscle's internal structure, such as the myofilaments, causing a decrease in contractile force. This damage impairs the muscle's ability to develop and maintain normal contractile tension, leading to reduced contractile capacity.
4. Disruption of Muscle Innervation:
Excessive muscle stretching can also affect the muscle's nerve supply, leading to problems in signal transmission between the nervous system and muscle fibers. This diminished neural drive to the muscle can disrupt the muscle's ability to contract effectively.
5. Pain and Reflexive Inhibition:
Overstretching can cause pain, leading to protective reflex mechanisms that inhibit excessive muscle contraction. This reflex response limits the muscle's capacity to contract due to the activation of pain-induced inhibitory signals.
It important to note that while muscle can regain most of their functionality after mild to moderate stretching, excessive and repeated overstretching can result in persistent muscular weakness and reduced contractile capacity. Hence, it is essential to approach muscle stretching with caution and not exceed the optimal limits of what the muscles are designed to handle.