6.4: Muscle Contraction - Biology

Arm Wrestling

A sport like arm-wrestling depends on muscle contractions. Arm wrestlers must contract muscles in their hands and arms and keep them contracted to resist their opponent's opposing force. The wrestler whose muscles can contract with greater force wins the match.

Muscle Contraction

How a Skeletal Muscle Contraction Begins

Excluding reflexes, all skeletal muscle contractions occur as a result of conscious effort originating in the brain. The brain sends electrochemical signals through the somatic nervous system to motor neurons that innervate muscle fibers (to review how the brain and neurons function, see the chapter Nervous System). A single motor neuron with multiple axon terminals can innervate multiple muscle fibers, thereby causing them to contract at the same time. The connection between a motor neuron axon terminal and a muscle fiber occurs at a neuromuscular junction site. This is a chemical synapse where a motor neuron transmits a signal to muscle fiber to initiate a muscle contraction.

The process by which a signal is transmitted at a neuromuscular junction is illustrated in Figure (PageIndex{2}). The sequence of events begins when an action potential is initiated in the cell body of a motor neuron, and the action potential is propagated along the neuron’s axon to the neuromuscular junction. Once the action potential reaches the end of the axon terminal, it causes the neurotransmitter acetylcholine (ACh) from synaptic vesicles in the axon terminal. The ACh molecules diffuse across the synaptic cleft and bind to the muscle fiber receptors, thereby initiating a muscle contraction. Muscle contraction is initiated with the depolarization of the sarcolemma caused by the sodium ions' entrance through the sodium channels associated with the ACh receptors.

Things happen very quickly in the world of excitable membranes (think about how quickly you can snap your fingers as soon as you decide to do it). Immediately following depolarization of the membrane, it repolarizes, re-establishing the negative membrane potential. Meanwhile, the ACh in the synaptic cleft is degraded by the enzyme acetylcholinesterase (AChE). The ACh cannot rebind to a receptor and reopen its channel, which would cause unwanted extended muscle excitation and contraction.

Propagation of an action potential along the sarcolemma enters the T-tubules. For the action potential to reach the membrane of the SR, there are periodic invaginations in the sarcolemma, called T-tubules (“T” stands for “transverse”). The arrangement of a T-tubule with the membranes of SR on either side is called a triad (Figure (PageIndex{3})). The triad surrounds the cylindrical structure called a myofibril, which contains actin and myosin. The T-tubules carry the action potential into the interior of the cell, which triggers the opening of calcium channels in the membrane of the adjacent SR, causing ( ext{Ca}^{++}) to diffuse out of the SR and into the sarcoplasm. It is the arrival of ( ext{Ca}^{++}) in the sarcoplasm that initiates contraction of the muscle fiber by its contractile units, or sarcomeres.

Excitation-contraction coupling

Although the term excitation-contraction coupling confuses or scares some students, it comes down to this: for a skeletal muscle fiber to contract, its membrane must first be “excited”—in other words, it must be stimulated to fire an action potential. The muscle fiber action potential, which sweeps along the sarcolemma as a wave, is “coupled” to the actual contraction through the release of calcium ions (( ext{Ca}^{++})) from the SR. Once released, the ( ext{Ca}^{++}) interacts with the shielding proteins, troponin and tropomyosin complex, forcing them to move aside so that the actin-binding sites are available for attachment by myosin heads. The myosin then pulls the actin filaments toward the center, shortening the muscle fiber.

In skeletal muscle, this sequence begins with signals from the somatic motor division of the nervous system. In other words, the “excitation” step in skeletal muscles is always triggered by signaling from the nervous system.

Sliding Filament Theory of Muscle Contraction

Once the muscle fiber is stimulated by the motor neuron, actin, and myosin protein filaments within the skeletal muscle fiber slide past each other to produce a contraction. The sliding filament theory is the most widely accepted explanation for how this occurs. According to this theory, muscle contraction is a cycle of molecular events in which thick myosin filaments repeatedly attach to and pull on thin actin filaments, so they slide over one another. The actin filaments are attached to Z discs, each of which marks the end of a sarcomere. The sliding of the filaments pulls the Z discs of a sarcomere closer together, thus shortening the sarcomere. As this occurs, the muscle contracts.

Crossbridge Cycling

Crossbridge cycling is a sequence of molecular events that underlies the sliding filament theory. There are many projections from the thick myosin filaments, each of which consists of two myosin heads (you can see the projections and heads in Figures (PageIndex{5}) and (PageIndex{3})). Each myosin head has binding sites for ATP (or ATP hydrolysis products: ADP and Pi) and actin. The thin actin filaments also have binding sites for the myosin heads—a cross-bridge forms when a myosin head binds with an actin filament.

The process of cross-bridge cycling is shown in Figure (PageIndex{6}). A cross-bridge cycle begins when the myosin head binds to an actin filament. ADP and Pi are also bound to the myosin head at this stage. Next, a power stroke moves the actin filament inward toward the sarcomere center, thereby shortening the sarcomere. At the end of the power stroke, ADP and Pi are released from the myosin head, leaving the myosin head attached to the thin filament until another ATP binds to the myosin head. When ATP binds to the myosin head, it causes the myosin head to detach from the actin filament. ATP is again split into ADP and Pi and the energy released is used to move the myosin head into a "cocked" position. Once in this position, the myosin head can bind to the actin filament again, and another cross-bridge cycle begins.

Feature: Human Biology in the News

Interesting and hopeful basic research on muscle contraction is often in the news because muscle contractions are involved in so many different body processes and disorders, including heart failure and stroke.

  • Heart failure is a chronic condition in which cardiac muscle cells cannot contract forcefully enough to keep body cells adequately supplied with oxygen. In 2016, researchers at the University of Texas Southwestern Medical Center identified a potential new target for developing drugs to increase the strength of cardiac muscle contractions in patients with heart failure. The UT researchers found a previously unidentified protein involved in muscle contraction. The minimal protein turns off the “brake” on the heart, so it pumps blood more vigorously. At the molecular level, the protein affects the calcium-ion pump that controls muscle contraction. This result is likely to lead to searches for additional such proteins.
  • A stroke occurs when a blood clot lodges in an artery in the brain and cuts off blood flow to part of the brain. Damage from the clot would be reduced if the smooth muscles lining brain arteries relaxed following a stroke because the arteries would dilate and allow greater blood flow to the brain. In a recent study undertaken at the Yale University School of Medicine, researchers determined that the muscles lining blood vessels in the brain actually contract after a stroke. This constricts the vessels, reduces blood flow to the brain, and appears to contribute to permanent brain damage. The hopeful takeaway of this finding is that it suggests a new target for stroke therapy.


  1. What is skeletal muscle contraction?
  2. Distinguish between isometric and isotonic contractions of skeletal muscle.
  3. How does a motor neuron stimulate a skeletal muscle contraction?
  4. What is the sliding filament theory?
  5. Describe cross-bridge cycling.
  6. Where does the ATP needed for a muscle contraction come from?
  7. Explain why an action potential in a single motor neuron can cause multiple muscle fibers to contract.
  8. The name of the synapse between a motor neuron and a muscle fiber is the _______________ _________.
  9. If a drug blocks the acetylcholine receptors on muscle fibers, what do you think this would do to muscle contraction? Explain your answer.
  10. True or False: According to the sliding filament theory, actin filaments actively attach to and pull on myosin filaments.
  11. True or False: When a motor neuron produces an action potential, the sarcomeres in the muscle fiber that it innervates become shorter as a result.
  12. Explain how cross-bridge cycling and sliding filament theory are related to each other.
  13. When does anaerobic respiration typically occur in human muscle cells?
  14. If there were no ATP available in a muscle, how would this affect cross-bridge cycling? What would this do to muscle contraction?

6.4: Muscle Contraction - Biology

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6.4: Muscle Contraction - Biology

In order to answer this question we must first examine what tells a muscle to contract. Let’s say that I am sitting here writing and want to pick up a cup of coffee. In order to do so I must send a command to the muscles in my arm. The command comes from a thought generated in my nervous system. The command travels from my brain to my spinal cord to a nerve that attaches to a muscle in my arm. The command tells my muscle to contract and my arm dutifully responds by moving closer to the coffee. Muscles are made of protein. If we were to examine a skeletal muscle under a microscope we would see that it is composed of tiny protein fibers or filaments. When a muscle receives a command from the nervous system to contract the protein filaments slide past each other. In fact one of the filaments connects to the other and drags it along. Think of thousands of overlapping filaments sliding past each other as the muscle contracts. The command to contract must somehow get from the outside of the muscle to the inside. Tiny messengers called neurotransmitters bring the message from the nerve to the muscle. Other chemical messengers that tell the protein filaments to contract then pass on the message. Muscles need energy to contract. Muscles must have some sort of power source in order to power the sliding filaments. The energy comes from ATP. ATP connects to one type of filament and extracts the energy so that it can pull the other filament along.

Matrix Metalloproteinases and Tissue Remodeling in Health and Disease: Target Tissues and Therapy

9 Dysregulation of Uterine MMPs During Preterm Labor

Myometrium activity is tightly regulated during pregnancy. At the first- and mid-trimester, myometrium relaxation is needed to accommodate fetal growth. As fetal growth nears its completion during late pregnancy, the uterine activity is first stabilized then starts to increase in preparation for delivery. We have demonstrated a relationship between uterine stretch, MMPs expression, and uterine relaxation during gestation. We have also shown a role of sex hormones in promoting the effects of uterine stretch on MMPs expression and uterine relaxation. MMP-1, MMP-2, MMP-3, MMP-7, and MMP-9 are found in the amniotic fluid and fetal membranes during normal pregnancy. MMP-2 and MMP-3 are expressed constitutively, while MMP-9 is barely detectable until labor. At labor, MMP-9 is the major MMP responsible for gelatinolytic activity in the membranes, while MMP-2 is dominant in the decidua. These findings may have clinical relevance as a disturbance in the balance of MMPs or TIMPs could disturb uterine activity and lead to premature labor. The MMP/TIMP imbalance may be further aggravated by changes in the sex hormone levels or their uterine receptors.

Preterm labor complicates 10%–15% of all pregnancies and is a leading cause of perinatal morbidity and death 14 however, the mechanisms involved are not fully understood. MMP-2 and MMP-9 exhibit cell-specific expression in the human placenta. Studies have suggested that an increase in MMP-9 expression may contribute to degradation of ECM in the fetal membranes and placenta, thereby facilitating fetal membrane rupture and placental detachment from the maternal uterus at labor, both term and preterm. 408 Also, studies on samples of amniochorion and amniotic fluid collected from women undergoing cesarean delivery before term, with either premature rupture of membranes or with preterm labor with no rupture of membranes, demonstrated an increased mRNA expression of MMP-2, MMP-9, and MT1-MMP and a decreased expression of TIMP-2 in prematurely ruptured membranes compared with preterm labor membranes. ELISA showed increases in the amniotic fluid concentrations of immunoreactive and bioactive MMP-2 and MMP-9 and immunoreactive MMP-3 and a decreased TIMP-2 concentration in fluids obtained from the premature rupture of membranes group compared with the preterm labor group. 14 In contrast, in a study of 25 patients at preterm or term, MMP-2 protein and MMP-2 and MMP-9 proenzyme activities in the amnion markedly increased with labor at term and were much higher than at preterm labor. There were no changes in chorion MMPs under any condition. These observations support a role of MMP-2 and MMP-9 in regulation of membrane rupture and other labor-associated mechanisms at term vs preterm parturition. 409 Cervicovaginal and/or intrauterine infection may be associated with preterm premature rupture of membranes (PPROM) and spontaneous preterm birth, likely due to the triggered inflammatory response. Microbial invasion of the amniotic cavity is associated with marked reduction in the levels of active MMP-2. 408,410 A decrease in uterine MMP-2 and MMP-9 in preeclampsia, intrauterine infection, and other pregnancy-related risk conditions is expected to hinder uterine expansion and cause IUGR and premature birth ( Fig. 3 ). 8,93 Other MMPs may also be involved in the regulation of membrane rupture and uterine contraction in term and preterm labor. Studies have suggested that inflammation could induce myometrial activator protein-1 (AP-1) which could in turn drive the production of stromelysins MMP-3 and MMP-10 and result in preterm labor in mice. 411 Also, a cross-sectional study in 275 women examined whether parturition (either term or preterm), premature rupture of the membranes, and microbial invasion of the amniotic cavity are associated with changes in the levels of matrilysin MMP-7 in the amniotic fluid. MMP-7 was detected in 97.4% (268/275) of the samples and showed an increase with advancing gestational age. Parturition at term and premature rupture of membranes without microbial invasion of the amniotic cavity (either term or preterm) was not associated with a change in MMP-7. On the other hand, preterm parturition in the absence of microbial invasion of the amniotic cavity and intraamniotic infection in both patients with preterm labor and patients with PPROM were associated with marked increase in MMP-7. It was concluded that MMP-7 is a physiologic constituent of amniotic fluid, and its levels increase with advancing gestational age, and markedly increase during microbial invasion of the amniotic cavity in preterm gestations, and the changes in MMP-7 may represent a maternal regulatory mechanism during infection and preterm labor. 412 Studies have also shown that plasma progesterone levels are lower in some preterm delivery patients compared to normal term pregnancies. For example, progesterone concentration was

30% lower at 28–34 weeks gestation in women who delivered prematurely than in women who delivered at term. 413 Studies have suggested that progestin supplementation may prevent initiation of preterm labor or treat it once it is already established. 414 Whether changes in MMPs and sex hormones could interfere with uterine relaxation and trigger uterus contraction and preterm delivery needs to be further examined. Also, whether the potential beneficial effects of progesterone in preterm labor are mediated via modulation of MMP expression/activity warrant further investigation.

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can someone explain the isometric contraction

Isometric contraction is defined as a contraction that is not associated with any movement. . Assessment of the nature of isometric contraction in terms of its causative force is difficult because no displacement occurs except within the muscle itself and at a microscopic level.

Posted by Felicia Paniagua on 2/23/2021 8:40:44 PM Reply

Isometric contraction is defined as a contraction that is not associated with any movement. . Assessment of the nature of isometric contraction in terms of its causative force is difficult because no displacement occurs except within the muscle itself and at a microscopic level.


Posted by mingyang zu on 6/4/2009 12:00:00 AM Reply

Excellent! This animation really helped me see how it all works--its difficult to comprehend the workings of something so tiny, this really helped make it clear! Thanks!

Posted by Jenny Midbrod on 2/2/2009 12:00:00 AM Reply

Creative Commons Attribution-NonCommercial 4.0 International License.

Watch the video: Explain mechanism of ventilation (December 2021).