- Muscles convert chemical energy into mechanical energy.
(striated (striped) w/ multiple nuclei; many, long, cylindrical cells bundled together; several bundles enclosed in tough connective tissue sheath to form "a muscle"; responsible for voluntary movement)
(not striated, single nucleus; cells tapered at both ends, held together by tight junctions; located in walls of "hollow organs" s.a. blood vessels, stomach, bladder, other internal organs; 'involuntary' movement s.a. peritalsis)
(striated w/ multiple nuclei/cell; cells branched, connected end-to-end by junctions (fused cell membranes) that allow electrical current flow; located only in heart wall)
1. Muscles are attached to bones by dense connective tissue = tendons.
2. Pairs of muscles often arranged to work in opposition (example: triceps and biceps). Other muscles may be arranged to perform together in groups to promote same movement.
3. Contraction causes movement of bones around joints (mechanical adavantage provided by different lever systems)
1. One muscle cell (= single muscle fiber) contains many myofibrils.
2. Each myofibril is made up of many sarcomeres = basic units of contraction
3. Sarcomeres contain thick and thin filaments. Thick filaments are made of many myosin molecules bundled together with their heads facing out. Actin filaments are made up of beaded strands (two) twisted together.
- Each bead is an actin molecule and each has a binding site for myosin heads.
- Each myosin head contains an ATPase.
4. A given muscle fiber (one cell) contracts when all of its sarcomeres shorten simultaneously. Each sarcomere shortens by a little, but all of them acting together can develop a considerable force. When one fiber contracts in all-or-none fashion, it is called a twitch.
1. Arrangement of thick and thin filaments: In each sarcomere two sets of actin filaments extend partway toward the center. The myosin filaments are arranged such that they partially overlap the actin filaments. Myosin heads on each side point away from the center of the sarcomere.
2. During contraction, the interaction of myosin heads with the actin filaments pulls the thin filaments toward the center of the sarcomere. The actin and myosin filaments slide past each other.
3. Cross-bridges = attachement betwn myosin heads and binding sites on actin filaments.
4. When a muscle cell is stimulated, myosin heads are energized by ATP. They attach to adjacent actin filaments, and tilt in a short "power stroke" toward the center of the sarcomere. Each power sroke requires an ATP. With many power strokes in rapid succession, the actin filaments are made to slide past the myosin filaments.
[Why does the sarcomere get shorter?]
Note: ATP molecules cause cross-bridges to release from actin. The myosin ATPase the splits the ATP into ADP and Pi and energizes the myosin. When the head reattaches to actin, the ADP and Pi are released during the power stroke. A new ATP molecule is then needed to break the myosin-actin bond.
[What happens when the muscle runs out of ATP? Myosin forms permanent cross bridges = rigor mortis.] )
1. Motor neuron control.
Every muscle cell is contacted by a motor nerve axon or a branch of a motor nerve axon [cf. Figs. 34.8 and 38.17]
action pot. in axon --> release of ACh from axon terminal --> stimulation of muscle fiber.
2. Muscle action potential --> invades SR
The membrane of the muscle fiber is electrically excitable just like a nerve cell axon. ACh causes the muscle fiber to depolarize and this triggers an all-or-none MAP which is conducted along the full length of the muscle fiber and which invades the membranes of the sarcoplasmic retiulum.
3. Calcium released into cytoplasm, complexes with troponin --> tropomyosin changes shape
4. Tropomyosin moves, uncovers binding site on actin --> cross-bridges form, filaments slide. [Fig. 38.18]
5. Calcium removed --> fiber relaxes
The SR membrane has an active pump that pulls Ca back into the chambers of the SR. This lowers the intracellular Ca ion concentration, troponin again binds tightly to tropomyosin, tropomyosin again covers binding sites on actin filaments. Cross bridges can no longer form and muscle relaxes (sarcomeres return to rest length)
(Muscle contraction uses up a lot of ATP.)
1. Creatine phosphate dephosphorylation = Fast regeneration of ATP from ADP and Pi
2. Glycogen --> glucose. Aerobic respiration provides most of the ATP needed during moderate exercise.
3. Blood glucose and fatty acids --> Fuel for aerobic respiration when muscle glycogen exhausted.
4. Fermentation (anaerobic metabolism) --> When respiratory and circulatory systems cannot deliver enough oxygen to sustain muscle contraction during vigorous exercise, glycolysis supplies ATP and produces lactic acid (lactate) from the breakdown of glucose. Recall that the net yield is 2 ATP per glucose molecule instead of 34-36. Lactic acid rapidly builds up in cell.
1. Muscle tension = total force developed
by cross-bridge activation. Isometric contraction occurs when the muscle is
stimulated but not allowed to shorten (constant length). [Does isometric contraction
use up ATP?]
2. Strength of contraction
(depends on muscle size, how many muscle cells in the muscle are contracting (# of motor units active), how rapidly the nervous system is stimulating them; motor unit = single motor neuron and all the muscle fibers (cells) that it forms juctions with. Recruitment of more motor units results in greater tension devlopment.)
3. Muscle twitch, tetanus
(whole muscle stimulated by brief electrical shock --> record isometric tension, relaxation over time. Repeated shocks cause "staircase" tension development. Tetanus = large contraction due to rapid, repeated stimulation so that twitches run together.)
(maintained tetanic contraction leads to eventual decline in tension = fatigue. Some muscles fatigue rapidly, but also recover rapidly. Other muscles fatigue more slowly, but take much longer to recover. Regular exercise can make muscles more resistant to fatigue by increasing blood supply and number of mitochondria.)