1. Muscle tissue accounts for around half of the body's weight.
2. Muscle tissue shows contractility, extensibility, and elasticity.
3. The major types of muscle tissue are skeletal (striated voluntary), cardiac (striated involuntary), and smooth (nonstriated, involuntary).
4. The functions of muscle tissue include locomotion, maintaining posture and balance, supporting soft tissues, guarding entrances and exits, movement along internal passageways, regulating blood flow, and maintaining body temperature.
SKELETAL MUSCLE TISSUE
Gross Anatomy and Organization
1. Each skeletal muscle cell is surrounded by an epimysium, a perimysium, and an endomysium.The collagen fibers of these layers are interwoven and continuous with those of the attached tendon.
2. A process from a neuron, the synaptic knob, contacts each muscle cell midway along its length at the neuromuscular (myoneural) junction.
1. Because they are long and slender, muscle cells are often called muscle fibers.
2. A muscle cell has a sarcolemma, sarcoplasm, and a
3. Each multinucleate skeletal muscle cell contains myofibrils, and each myofibril contains myofilaments organized into sarcomeres.
4. A sarcomere contains the protein myofilaments actin (thin filaments) and myosin (thick filaments) in an organized array.
5. Within the zone of overlap thick and thin filaments can interact to produce a contraction.
6. Each sarcomere is surrounded by branches of the sarcoplasmic reticulum and a T tubule continuous with the sarcolemma.
The Sliding Filament Theory of Contraction
1. Active sites are found along the actin filament. At rest these are covered by troponin and tropomyosin.
2. Myosin molecules have cross-bridges that extend outward from the surface of the thick filament. During a contraction the cross- bridges attach, pivot, and detach, sliding the thin filaments towards the center of the sarcomere.
3. Relaxation is a passive process.
Skeletal Muscle Physiology
1. A change in the transmembrane potential begins the chain of events leading to a contraction.
The Transmembrane Potential
1. The extracellular fluid contains sodium (Na+) and chlorideions (Cl-), whereas the sarcoplasm contains potassium ions (K+) and proteins (Pr-).
2. The active and passive properties of cell membranes enable
living cells to maintain these concentration differences.
3. Sodium channels do not allow sodium ions into the cell as fast as the potassium channels permit the departure of potassium ions. Proteins cannot cross the membrane at all, but chloride ions can diffuse into the cell.
4. Living cells normally have an excess of negative ions inside of their cell membranes, and an excess of positive ions outside. This represents the transmembrane potential.
5. The resting potential is the transmembrane potential of an undisturbed cell. The actual value depends on the type of cell considered. For skeletal muscle cells the transmembrane potential averages about -85 mV; for neurons the average is about -70 mV.
6. The resting potential remains stable because when the transmembrane potential is at that level the sodium/potassium exchange pumps can keep pace with the rates of sodium entry andpotassium loss.
7. Many stimuli alter the resting potential by changing the membrane permeability to sodium or potassium. The changes may result in hyperpolarization or depolarization of the membrane.
8. Graded changes in the transmembrane potential are local events, and only affect the regions in contact with the stimulus.
9. The membranes of skeletal muscle cells and neurons show excitability. When stimulated a conducted change occurs in the transmembrane potential. An action potential begins at the contact point but spread to affect the entire surface of the cell.
10. To initiate an action potential the transmembrane potential must depolarize to threshold. A liminal stimulus accomplishes this, and a subliminal stimulus does not.
11. At threshold the sodium channels open, and sodium enters the cell in a rush. In a skeletal muscle cell the transmembrane potential in that portion of the membrane then changes from -65 mV to +30 mV.
12. The sodium channels then close, and the potassium channels open. Potassium leaves the cell, and repolarization begins. The ion exchange pumps restore the normal distribution of sodium and potassium ions, and the resting potential reappears.
13. During the refractory period the cell will not respond to stimuli normally. The refractory period ends when repolarization has been completed.
14. The action potential develops at a single site, but the membrane events there set up a local current that depolarizes adjacent portions of the membrane to threshold. In this way the action potential, or impulse, moves across the surface of the sarcolemma.
The Physiological Basis for Muscular Contraction
1. When an action potential sweeps over the sarcolemma it travels along the T tubules. The properties of the sarcoplasmic reticulum change in the first few milliseconds after the passage of an action potential.
2. The membrane of the sarcoplasmic reticulum normally removes calcium ions from the sarcoplasm and stores them in the cisternae.
3. Following the passage of a single action potential along anadjacent T tubule, the sarcoplasmic reticulum becomes very permeable to calcium ions.
4. Calcium ions interact with the troponin and tropomyosin along the thin filaments, uncovering the active sites.
5. Calcium ions give the cross-bridges the ability to split ATP and release the energy needed for contraction.
6. Once started, the contraction proceeds until the concentration of calcium ions is reduced by the activities of thesarcoplasmic reticulum.
The Control of Skeletal Muscle Activity
1. A motor neuron provides the stimulus for action potential generation in a skeletal muscle cell. All of the muscle cells controlled by a single motor neuron represents a motor unit.
2. Acetylcholine released by the synaptic knob diffuses across the synaptic cleft to reach the opposing surface of the sarcolemma.
3. Depolarization of the sarcolemma at the neuromuscular junction then leads to the generation of a single action potential in the sarcolemma
4. Further action potentials do not occur because the enzyme cholinesterase (acetylcholinesterase/AChE) breaks down the ACh molecules and allows the repolarization of the membrane surface.
1. During an isotonic contraction the tension within the muscle remains constant, and the length of the muscle decreases.
2. During an isometric contraction the tension rises to a peak, but the length of the muscle does not change.
3. A twitch is a single contraction/relaxation event. It consists of a latent period, a contraction phase, and a relaxation phase.
4. The amount of pull a muscle can exert depends upon the degree of overlap between the thick and thin filaments. Tension production is most efficient over a relatively narrow range of resting lengths.
5. Muscular performance therefore varies depending on theposition of the skeleton and the length of the muscle.
The Effects of Repeated Stimulation
1. Repeated stimulations following the completion ofrelaxation phase produces treppe, a gradual increase in peak tension.
2. Repeated stimulations before the completion of the relaxation period may produce summation of twitches (wave summation), incomplete tetanus, or complete tetanus, depending on thefrequency of stimulation.
3. Tension production peaks in a muscle when the maximum possible number of motor units are in complete tetanus.
1. A entire muscle shows a resting muscle tone due to the continual background activity of motor units.
2. Muscle spindles are innervated by sensory nerves. They monitor the state of contraction in the surrounding muscle tissue.
The Energetics of Muscular Activity
ATP and Creatine Phosphate
1. ATP is the direct energy source for muscular contaction. Creatine phosphate can give up its stored energy to convert ADP to ATP.
2. At rest a skeletal muscle cell has about six times as much creatine phosphate as ATP available in the sarcoplasm.
ATP and Glycogen Reserves
1. A resting skeletal muscle cell obtains energy primarily through the mitochondrial catabolism of fatty acids. The energy gained is used to build ATP, CP, and glycogen reserves.
2. When the muscle starts contracting, glycolysis becomes themajor method of energy production. Aerobic glycolysis works
efficiently but is oxygen limited. Anaerobic glycolysis provides
ATP when the demand for energy exceeds the capabilities of the
3. At peak levels of activity the muscle relies on anaerobic glycolysis for roughly 2/3 of the ATP required for contraction.
4. The muscle becomes fatigued when it runs out of ATP or the pH falls outside of normal limits.
5. If all of the ATP disappears, the cross-bridges cannot detach, and the sarcoplasmic reticulum cannot remove calcium ions from the sarcoplasm. A painful cramp may then develop.
6. After death, lysosomal enzymes break down the sarcoplasmic reticulum and free the calcium ions. This produces the muscular contractions of rigor mortis.
7. Recovery from a period of anaerobic activity may take an hour or more. During this period the muscle cells consume excess oxygen as they metabolize lactic acid. The ATP is used to synthesize glucose and rebuild glycogen reserves.
8. After the period of exercise has ended, lactic acid molecules in the blood are reconverted to glucose within the liver. The glucose is then released into the circulation for use by skeletal muscles.
9. The amount of oxygen needed to support the conversion of lactic acid to glucose and the rebuilding of glycogen reserves represents the oxygen debt of the activity.
Specialized Skeletal Muscle Cells
1. Skeletal muscle fibers may be classified as fast muscle or slow muscle.
2. Fast muscle fibers account for 98 percent of the skeletalmuscle cells in the body. They respond quickly and develop more power, but they are subject to fatigue.
3. Slow muscles can continue contracting for extended periods because they have more mitochondria, a better circulatory supply, and abundant oxygen reserves.
4.Muscles dominated by fast fibers appear relatively pale (white muscles); those dominated by slow fibers are known as red muscles. Most of our muscles contain a mixture of the two fiber types.
Muscular Performance and Endurance
1. Muscular performance can be considered in terms of power or endurance. Physical conditioning affects both aspects of muscular
2. Energy requiring bursts of intense muscular activity require anaerobic endurance.
3. Athletes training for such events attempt to produce muscular hypertrophy by stimulating muscles to produce near maximal tension.
4. Muscle cells increase their mass when exposed to the male sex hormone, testosterone.
5. Aerobic endurance is the time period over which a muscle can continue to contract while supported by aerobic metabolism.
6. Prolonged aerobic activity is supported by nutrients absorbed from the blood.
7. Extending aerobic endurance involves improving the performance of the cardiovascular and respiratory systems, and keeping muscular demands for oxygen below the anaerobic threshold.
8. The composition of fast and slow fibers in a particular muscle is genetically determined, but the capabilities of the existing muscles can be altered by training because muscle cells respond to changes in the patterns of neural stimulation.
9. Inadequate stimulation leads to a flaccid muscle that may later undergo atrophy.Shortening of the muscle cells may produce a contracture.
Skeletal Muscles and Thermoregulation
1. Living cells capture less than half of the energy released by catabolic reactions. The lost energy heats the surrounding tissues.
2. Active skeletal muscles operate at even lower efficiency, so heat production increases dramatically during exercise.
3. If muscle temperatures get too high, rigor appears.
4. Initial heat is generated by the muscular activity itself; the recovery heat is produced during the repayment of the oxygen debt.
5. Shivering represents an effective mechanism for raising body temperature.
CARDIAC AND SMOOTH MUSCLE TISSUES
1. Cardiocytes are relatively small striated muscle cells with single nuclei.Adjacent cardiocytes are interconnected at intercalated discs.
2. Action potentials can pass from membrane to membrane across an intercalated disc. Because the myofibrils are attached to the
complex, the cells contract in a coordinated fashion.
3. Cardiocytes are not under the control of motor neurons, and special pacemaker cells determine the basic heart rate. Neural or hormonal stimuli can change the pace or strength of cardiac contractions.
4. Because cardiac muscle cells have an extended refractory period, they cannot be stimulated to produce partial or complete tetanus. A tetanic contraction of the heart would lead to death due to the interruption of circulation to the brain.
1. Smooth muscle tissue is found in sheets, bundles, or sheaths as a component of almost every organ.
2. Smooth muscle cells are small and spindle-shaped, with a single nucleus.
3. Smooth muscle cells lack sarcomeres, and they can contract over a much wider range of lengths. This plasticity allows them to function in the walls of organs that undergo great changes in size.
4. Multiunit smooth muscle fibers are innervated in motor units, although several motor neurons may contact each muscle cell.
5. Many visceral smooth muscle fibers lack direct connections to motor neurons.Junctional complexes and common environmental stimuli may coordinate their contractions.