Muscle Series Part 3: The Sliding Filament Theory of Muscle Contraction
The Sliding Filament Theory was proposed 70 years ago in 1954 by Hugh Huxley and Jean Hanson and is still the best model that explains how muscles contract on a micro level
By Amirali Banani
During contraction, the thin actin filaments slide past the thick myosin filaments within muscle fibres, resulting in the overlapping of these filaments and thus the shortening of the sarcomere, the fundamental unit of a muscle. This process is initiated by the release of Calcium ions which bind to regulatory proteins on the actin filaments, enabling myosin heads to form cross-bridges with actin. ATP hydrolysis then powers the movement of these cross-bridges, causing the actin to slide along the myosin which thus results in a muscle contraction. This is The Sliding Filament Theory in a nutshell.
Before explaining the steps of this rather complex process in detail, it’s helpful to know a few terms outlined below.
Actin Filaments
The “thin filaments” that slide past myosin in muscle contraction
Myosin Filaments
The “thick filaments” that pull actin filaments by means of cross-bridges; are enzymatic and split ATP through hydrolysis
Troponin
Proteins found on tropomyosin that bind with calcium ions (forming the troponin-Ca2+ complex)
Tropomyosin
Protein strands found on actin filaments that cover myosin binding sites → move “out of the way” once calcium ions bind to troponin to enable the binding of actin and myosin
Calcium ions (Ca2+)
Needed for myosin to bind to actin by inducing a conformational change in the troponin complex
ATP (Adenosine Triphosphate)
Supplies the energy for muscle contraction
Sliding Filament Theory — Part 1
First, let’s review how muscle contraction is initiated by the activity of nerves:
Motor nerve fibres branch at their axon terminals end in axon bulbs which are in close proximity to the sarcolemma and are separated by a synaptic cleft. The entire region is known as the neuromuscular junction. The neurotransmitter acetylcholine (ACh) is released into the synaptic cleft. The acetylcholine binds to receptor sites on the sarcolemma which generates its own impulse. The impulse spreads over the entire sarcolemma and down the transverse tubules (T-tubules) to the sarcoplasmic reticulum. The sarcoplasmic reticulum then releases its stored calcium ions into the myofibrils (actin and myosin) within the muscle fibre.
Zooming into these myofibrils, we can see threads of tropomyosin that wind about an actin filament. Small, round proteins called troponin are found at intervals along these threads of tropomyosin; the calcium ions released from the sarcoplasmic reticulum bind to the troponin, forming the troponin-Ca2+ complex. This resulting complex causes the tropomyosin threads to change their shape, thus exposing the myosin binding sites.
Sliding Filament Theory — Part 2
The thick myosin filaments have globular heads with an ATP binding site. The heads also function as an ATPase enzyme capable of splitting ATP into ADP + P (adenosine diphosphate and phosphorus). The splitting of ATP also releases energy which causes the myosin to bind to the actin filament at the exposed binding sites forming an actin-myosin cross-bridge.
The ADP + P is now released, causing the myosin head to move and “sliding” the actin filament past the myosin filament.
Sliding Filament Theory — Part 3
Contraction continues (actin filaments sliding over myosin) until nerve impulse(s) stop. Once contraction stops, active transport proteins in the sarcoplasmic reticulum pump calcium ions back into the sarcoplasmic reticulum for storage until they are released again during the next nerve impulse.
Thank you for reading! This concludes my three-part series on muscles. Feel free to read parts 1 and 2 linked below:
