Muscle contraction is a very important activity that enables an organism perform various bodily movements and flexible actions, in response to nerve stimuli. Muscle fibers are multinucleated long cylindrical cells that have an outer membrane called sarcolemma, and are mainly composed of contractile elements called myofibrils (Dougherty, 2016). Myofibrils are made up of repeating units called sarcomeres. Sarcomeres in turn are composed of (thin) actin and (thick) myosin protein filaments called myofilaments (Dougherty, 2016). The muscle fiber structure and organization is shown in Fig 1.
Contraction Mechanism – Sliding Filament Theory
According to the sliding filament theory, during contraction myosin filaments remain constant in length, while the actin filaments (anchored to lateral ends of the sarcomere) slide past the myosin filaments (Krans, 2010). The tethering structures at the ends of sarcomere that enable creation of tension in actin filaments are called Z bands, and the stationary myosin segment is called the A band (Krans, 2010). Myosin protein has a globular region S1 hinged on a tail like S2 region that helps in sliding (Krans, 2010). During contraction myosin reaches forward with the S1-S2 cross bridge, binds to actin, contracts and releases actin, and the “power stroke” continues (Krans, 2010). This actin myosin interaction during contraction is shown in Fig 2.
Regulation of Muscle Contraction
Neural stimulation is essential for muscle contraction. The neuromuscular junction comprising of plasma membrane of the neuron’s axon terminal, the synaptic cleft and the sarcolemma portion with regulated Na+ and K+ ion channels (motor end plate), is the site of neural stimulation (Dougherty, 2016). The neuromuscular junction at which action potential is transferred from the neuron to the muscle fiber is depicted in Fig 3.
Contraction is an active process that requires energy in the form of ATP and Ca2+ influx. When contraction has to occur, ATP binds to myosin, hydrolyzes to ADP and inorganic phosphorus (Pi). The released energy is utilized for binding of myosin with actin. Muscle contraction is regulated by calcium ions. A protein called tropomyosin, which is attached to another regulatory protein called troponin, covers myosin binding sites in actin (Krans, 2010). The binding sites are revealed once Ca2+ ions bind to troponin, and tropomyosin is displaced (Krans, 2010). Thus, if sufficient ATP and Ca2+ ions are present muscle contraction occurs. Ca2+ ion influx is signaled by release of neurotransmitter acetylcholine (ACh) during the neuromuscular synapse. The neuron’s axon terminal passes its action potential to the muscle fiber through the release of ACh at the synaptic cleft (Dougherty, 2016). This process of regulation of muscle contraction is depicted in Fig 4.
ACh attaches to receptors on the sarcolemma, which initiates influx of Na+ ions, and leads to depolarization of the sarcolemma (Dougherty, 2016). Repolarization due to opening of K+ ion channels and efflux of K+ ions occurs at a lower rate (Dougherty, 2016). Due to depolarization, the sarcoplasmic reticulum releases stored Ca2+ ions, which interacts with troponin, and exposes myosin-binding sites on actin (Dougherty, 2016). Thus the action potential is transferred from neurons through synapse, to the sarcolemma, transverse (T) tubules, sarcoplasmic reticulum (SR) and to the myofibrils and myofilaments. Thus muscle contraction occurs is response to the nerve impulse.
References
Dougherty. (2016). Biology II: Human Anatomy & Physiology Chapter 9 Muscle Tissues.
Retrieved May 25, 2016, from http://www.rtmsd.org/page/1790
Florida Atlantic University. (2014). Chapter 14. Retrieved May 25, 2016, from
http://fau.pearlashes.com/anatomy/chapter 14/chapter 14.htm
Krans, J. L. (2010) The Sliding Filament Theory of Muscle Contraction. Nature
Education 3(9): 66. Retrieved May 25, 2016, from http://www.nature.com/
scitable/topicpage/the-sliding-filament-theory-of-muscle-contraction-14567666
