C0-HD-TOP.png C0-HD-BTM.png C H A P T E R 1 MUSCLES AND HOW THEY MOVE C0-HD-TOP.png Skeletal w Voluntary muscle; controlled consciously wOver 600 throughout the body Cardiac w Controls itself with assistance from the nervous and endocrine systems w Only in the heart Smooth w Involuntary muscle; controlled unconsciously wIn the walls of blood vessels and internal organs Types of Muscles C0-HD-TOP.png SKELETAL MUSCLE STRUCTURE 82959/e2862 00000002E2862 Wilmore PP B5AE00F7: C0-HD-TOP.png MUSCLE FIBER 82961/e2862 00000002E2862 Wilmore PP B5AE00F7: C0-HD-TOP.png MICROGRAPH OF MYOFIBRILS C0-HD-TOP.png ARRANGEMENT OF FILAMENTS 82963/e2862 00000002E2862 Wilmore PP B5AE00F7: C0-HD-TOP.png ARRANGEMENT OF FILAMENTS IN A SARCOMERE 82965/e2862 00000002E2862 Wilmore PP B5AE00F7: C0-HD-TOP.png ACTIN FILAMENT 82966/e2862 00000002E2862 Wilmore PP B5AE00F7: C0-HD-TOP.png MOTOR UNIT 82967/e2862 00000002E2862 Wilmore PP B5AE00F7: C0-HD-TOP.png w For a motor unit to be recruited into activity the motor nerve impulse must meet or exceed the threshold. All-Or-None-Response w More force is produced by activating more motor units. w When this occurs, all muscle fibers in the motor unit act maximally. w If the threshold is not met no fibers in that unit act. C0-HD-TOP.png 1. A motor neuron, with signals from the brain or spinal cord, releases the neurotransmitter acetylcholine (ACh) at the neuromuscular junction. 2. ACh crosses the junction and binds to receptors on the sarcolemma. 3. This initiates an action potential, providing sufficient ACh. Excitation/Contraction Coupling 4. The action potential travels along the sarcolemma and through the T tubules to the SR releasing Ca2+. 5. The Ca2+ binds to troponin on the actin filament, and the troponin pulls tropomyosin off the active sites, allowing myosin heads to attach to the actin filament. (continued) C0-HD-TOP.png 6. Once a strong binding state is established with actin, the myosin head tilts, pulling the actin filament (power stroke). 7. The myosin head binds to ATP, and ATPase found on the head splits ATP into ADP and Pi, releasing energy. 8. The new ATP binding releases the myosin head from the actin molecule. Excitation/Contraction Coupling 9. Muscle action ends when calcium is actively pumped out of the sarcoplasm back into the sarcoplasmic reticulum for storage. C0-HD-TOP.png EVENTS LEADING TO MUSCLE ACTION 82968/e2862 00000002E2862 Wilmore PP B5AE00F7: C0-HD-TOP.png • skenovat0010 C0-HD-TOP.png skenovat0010 C0-HD-TOP.png w When myosin cross-bridges are activated, they bind strongly with actin, resulting in a change in the cross-bridge. w The change in the cross-bridge causes the myosin head to tilt toward the arm of the cross-bridge and drag the actin and myosin filaments in opposite directions. w The tilt of the myosin head is known as a power stroke. Sliding Filament Theory w The pulling of the actin filament past the myosin results in muscle shortening and generation of muscle force. C0-HD-TOP.png CONTRACTING MUSCLE FIBER 82969a/e2862 000A4003 PROJECTS 1 B727F70A: 82969b/e2862 000A4003 PROJECTS 1 B727F70A: 82969c/e2862 000A4003 PROJECTS 1 B727F70A: C0-HD-TOP.png C0-HD-BTM.png https://www.youtube.com/watch?v=BVcgO4p88AA C0-HD-TOP.png Agonists—prime movers; responsible for the movement Functional Classification of Muscles Antagonists—oppose the agonists to prevent overstretching of them Synergists—assist the agonists and sometimes fine-tune the direction of movement C0-HD-TOP.png TYPES OF MUSCLE ACTION 82980/e2860 00000002E2862 Wilmore PP B5AE00F7: C0-HD-TOP.png w Number of motor units activated w Type of motor units activated (FT or ST) w Muscle size Factors Influencing Force Generation w Initial muscle length w Joint angle w Speed of muscle action (shortening or lengthening) C0-HD-TOP.png MUSCLE FIBRE TYPES C0-HD-TOP.png w High aerobic (oxidative) capacity and fatigue resistance w Low anaerobic (glycolytic) capacity and motor unit strength w Slow contractile speed (110 ms to reach peak tension) and myosin ATPase Slow-Twitch (ST; red) Muscle Fibers w 10–180 fibers per motor neuron w Low sarcoplasmic reticulum development C0-HD-TOP.png w Moderate aerobic (oxidative) capacity and fatigue resistance w High anaerobic (glycolytic) capacity and motor unit strength w Fast contractile speed (50 ms to reach peak tension) and myosin ATPase Fast-Twitch (FTa; white) Muscle Fibers w 300–800 fibers per motor neuron w High sarcoplasmic reticulum development C0-HD-TOP.png w Low aerobic (oxidative) capacity and fatigue resistance w Highest anaerobic (glycolytic) capacity and motor unit strength w Fast contractile speed (50 ms to reach peak tension) and myosin ATPase Fast-Twitch (FTb; white) Muscle Fibers w 300–800 fibers per motor neuron w High sarcoplasmic reticulum development C0-HD-TOP.png Main characteristics of muscle fibre types Slow-twitch (ST) Fast-twitch (FTa) Fast-twitch (FTb) Contraction speed low high high Contraction power low medium high Fatigue resistance high medium low Glycogen volume low high high Diameter low medium high Mitochondrial density high high low Capillary density high high low ATPase activity low high high Glycolytic capacity low high high C0-HD-TOP.png PEAK POWER GENERATED BY FIBERS 82978/e2862 00000002E2862 Wilmore PP B5AE00F7: C0-HD-TOP.png w Genetics determine which type of motor neurons innervate our individual muscle fibers. w Muscle fibers become specialized according to the type of neuron that stimulates them. w Endurance training, strength training, and muscular inactivity may result in small changes (less than 10%) in the percentage of FT and ST fibers. What Determines Fiber Type? w Aging may result in changes in the percentage of FT and ST fibers. w Endurance training has been shown to reduce the percentage of FTb fibers, while increasing the fraction of FTa fibers. C0-HD-TOP.png C0-HD-BTM.png C H A P T E R 2 NEUROLOGICAL CONTROL OF MOVEMENT C0-HD-TOP.png ORGANIZATION OF THE NERVOUS SYSTEM 82982/e2862 000002BBE2862 Wilmore PP B5AE00F7: C0-HD-TOP.png STRUCTURE OF A NEURON 82983/e2862 000002BBE2862 Wilmore PP B5AE00F7: C0-HD-TOP.png An electrical charge that passes from one neuron to the next and finally to an end organ, such as a group of muscle fibers. Nerve Impulse C0-HD-TOP.png w Difference between the electrical charges inside and outside a cell, caused by separation of charges across a membrane w High concentration of K+ inside the neuron and Na+ outside the neuron w K+ ions can move freely, even outside the cell to help maintain imbalance Resting Membrane Potential (RMP) w Sodium-potassium pump actively transports K+ and Na+ ions to maintain imbalance w The constant imbalance keeps the RMP at –70 mV C0-HD-TOP.png RESTING STATE C0-HD-TOP.png Depolarization—inside of cell becomes less negative relative to outside (> –70 mV) Hyperpolarization—inside of cell becomes more negative relative to outside (< –70 mV) Graded potentials—localized changes in membrane potential (either depolarization or hyperpolarization) Changes in Membrane Potential Action potentials—rapid, substantial depolarization of the membrane (–70 mV to +30 mV to –70 mV all in 1 ms) C0-HD-TOP.png w Starts as a graded potential w Requires depolarization greater than the threshold value of 15 mV to 20 mV (e.g., –50 to –55 mV) w Once threshold is met or exceeded, the all-or-none principle applies What Is an Action Potential? C0-HD-TOP.png ACTION POTENTIAL C0-HD-TOP.png 1. The resting state 2. Depolarization 3. Propagation of an action potential Events During an Action Potential 4. Repolarization 5. Return to the resting state with the help of the sodium- potassium pump C0-HD-TOP.png Myelinated fibers w Saltatory conduction—action potential travels quickly from one break in myelin to the next. w Action potential is 5 to 150 times faster in myelinated compared to unmyelinated axons. Velocity of an Action Potential Diameter of the neuron w Larger diameter neurons conduct nerve impulses faster. w Larger diameter neurons present less resistance to current flow (remember FT muscle fibers!). C0-HD-TOP.png w A synapse is the site of an impulse transmission between two neurons. w An impulse travels to a presynaptic axon terminal where it causes synaptic vesicles on the terminal to release chemicals (neurotransmitters) into the synaptic cleft. w The neurotransmitters bind to postsynaptic receptors on an adjacent neuron usually on the dendrites (80–95%). Synapse w Neural impulses can only be transmitted from the dendrite or cell body through the axon to the adjacent neuron since the neurotransmitters are released only from the terminal end of the axon. C0-HD-TOP.png CHEMICAL SYNAPSE 82984/e2862 000002BBE2862 Wilmore PP B5AE00F7: C0-HD-TOP.png w The junction is a site where a motor neuron communicates with a muscle fiber. w Motor axon terminal releases neurotransmitters (such as acetylcholine or norepinephrine) which travel across a synaptic cleft and bind to receptors on a muscle fiber. w This binding causes depolarization, thus possibly causing an action potential. Neuromuscular Junction w The action potential spreads across the sarcolemma into the T tubules causing the muscle fiber to contract. C0-HD-TOP.png NEUROMUSCULAR JUNCTION 82985/e2862 000002BBE2862 Wilmore PP B5AE00F7: C0-HD-TOP.png w Period of repolarization. w The refractory period limits a motor unit's firing frequency. Refractory Period w The muscle fiber is unable to respond to any further stimulation. C0-HD-TOP.png Spinal cord Central Nervous System Brain w Cerebrum—Site of the mind and intellect. w Diencephalon—Site of sensory integration and regulation of homeostasis. w Cerebellum—Plays crucial role in coordinating movement. w Brain stem—Connects brain to spinal cord; coordinates skeletal muscle function and maintains muscle tone; contains regulators of respiratory and cardiovascular systems. C0-HD-TOP.png REGIONS OF THE BRAIN 82986/e2862 000002BBE2862 Wilmore PP B5AE00F7: C0-HD-TOP.png Peripheral Nervous System w 12 pairs of cranial nerves connected with the brain. w 31 pairs of spinal nerves connected with the spinal cord. w Sensory division—carries sensory information from the body via afferent fibers to the CNS. w Motor division—transmits information from CNS via efferent fibers to target organs. w Autonomic nervous system—controls involuntary internal functions. C0-HD-TOP.png Sympathetic Nervous System Fight-or-flight—prepares you for acute stress or physical activity Facilitates your motor response with increases in w Heart rate and strength of heart contraction w Blood supply to the heart and active muscles w Metabolic rate and release of glucose by the liver w Blood pressure w Rate of gas exchange between lungs and blood w Mental activity and quickness of response C0-HD-TOP.png Parasympathetic Nervous System Housekeeping (rest-or-digest)—digestion, urination, glandular secretion, and energy conservation Actions oppose those of the sympathetic system w Decreases heart rate w Constricts coronary vessels wConstricts tissues in the lungs w wStimulates sexual functions w wDigestion C0-HD-TOP.png Motor Control w Sensory impulses evoke a response through a motor neuron. w The closer to the brain the impulse stops, the more complex the motor reaction. w A motor reflex is a preprogrammed response that is integrated by the spinal cord without conscious thought. C0-HD-TOP.png SENSORY-MOTOR INTEGRATION 82987/e2862 000002BBE2862 Wilmore PP B5AE00F7: C0-HD-TOP.png Types of Sensory Receptors Mechanoreceptors—respond to mechanical forces such as pressure, touch, vibration, or stretch. Thermoreceptors—respond to changes in temperature. Nociceptors—respond to painful stimuli. Photoreceptors—respond to light to allow vision. Chemoreceptors—respond to chemical stimuli from foods, odors, and changes in blood concentrations of gases and substances. C0-HD-TOP.png Muscle and Joint Nerve Endings w Joint kinesthetic receptors in joint capsules sense the position and movement of joints. w Muscle spindles sense how much a muscle is stretched. w Golgi tendon organs detect the tension of a muscle on its tendon, providing information about the strength of muscle contraction. C0-HD-TOP.png Muscle Spindles w A group of 4 to 20 small muscle fibers (intrafusal) with sensory and motor nerve endings, covered by a connective tissue sheath, and connected to extrafusal (or regular) muscle fibers. w The middle of the spindle can stretch but cannot contract as it contains little or no actin and myosin. w When extrafusal fibers attached to the spindle are stretched, sensory neurons on the spindle transmit information to the CNS about the muscle’s length. w Reflexive muscle contraction is triggered through the alpha motor neuron to resist further stretching. w Gamma motor neurons activate intrafusal fibers, causing the middle of the spindle to stretch, making the spindle sensitive to small degrees of stretch. C0-HD-TOP.png Golgi Tendon Organs (GTOs) w Encapsulated sensory organs through which muscle tendon fibers pass w Located close to the tendon's attachment to the muscle w Sense small changes in tension w Inhibit contracting (agonist) muscles and excite antagonist muscles to prevent injury C0-HD-TOP.png MUSCLE BODY, MUSCLE SPINDLE, AND GTO 82991/e2862 000002BBE2862 Wilmore PP B5AE00F7: C0-HD-TOP.png Conscious Control of Movement w Neurons in the primary motor cortex control voluntary muscle movement. w Clusters of nerve cells in the basal ganglia initiate sustained and repetitive movements—walking, running, maintaining posture, and muscle tone. w The cerebellum controls fast and complex muscular activity. C0-HD-TOP.png Did You Know…? Muscles controlling fine movements, such as those controlling the eyes, have a small number of muscle fibers per motor neuron (about 1 neuron for every 15 muscle fibers). Muscles with more general function, such as those controlling the calf muscle in the leg, have many fibers per motor neuron (about 1 neuron for every 2,000 muscle fibers). C0-HD-TOP.png C0-HD-BTM.png C H A P T E R 3 NEUROMUSCULAR ADAPTATIONS TO RESISTANCE TRAINING C0-HD-TOP.png Defining Muscular Performance Strength—the maximal force a muscle or muscle group can generate (dynamometer). Power—the product of strength and the speed of movement. Muscular endurance—the capacity to sustain repeated muscle actions. C0-HD-TOP.png Mechanisms of Gains in Muscle Strength Neural Adaptations w Synchronization and recruitment of additional motor units wAutogenic inhibition w Coactivation of agonist and antagonist muscles w Rate coding—the firing frequency of motor units Muscle Hypertrophy w Fiber hypertrophy w Fiber hyperplasia C0-HD-TOP.png Neural Activation and Fiber Hypertrophy w Early gains in strength appear to be more influenced by neural factors. w Long-term strength increases are largely the result of muscle fiber hypertrophy. C0-HD-TOP.png Muscle Size w Hypertrophy refers to increases in muscle size. w Atrophy refers to decreases in muscle size. w Muscle strength involves more than just muscle size. C0-HD-TOP.png Muscle Hypertrophy Transient—pumping up of muscle during a single exercise bout due to fluid accumulation from the blood plasma into the interstitial spaces of the muscle. Chronic—increase of muscle size after long-term resistance training due to changes in muscle fiber number (fiber hyperplasia) or muscle fiber size (fiber hypertrophy). C0-HD-TOP.png Fiber Hypertrophy w The numbers of myofibrils and actin and myosin filaments increase, resulting in more cross-bridges; sarcoplasm and connective tissue increase. w Muscle protein synthesis increases during the postexercise period. w Testosterone plays a role in promoting muscle growth. w Training at higher intensities appears to cause greater fiber hypertrophy than training at lower intensities. C0-HD-TOP.png FIBER HYPERTROPHY AFTER TRAINING C0-HD-TOP.png Fiber Hyperplasia w It has been proposed that muscle fibers can split in half with intense weight training. w Each half then increases to the size of the parent fiber. w Satellite cells may also be involved in skeletal muscle fiber generation. w It has been clearly shown to occur in animal models; only a few studies indirectly suggest this occurs in humans too. C0-HD-TOP.png SPLITTING MUSCLE FIBER 83000/e2862 000002BBE2862 Wilmore PP B5AE00F7: C0-HD-TOP.png Results of Resistance Training w Increased muscle size (hypertrophy). w Alterations of neural control of trained muscle. w Studies show strength gains can be achieved without changes in muscle size, but not without neural adaptations. C0-HD-TOP.png Acute Muscle Soreness w Results from an accumulation of the end products of exercise in the muscles w Usually disappears within minutes or hours after exercise C0-HD-TOP.png Delayed-Onset Muscle Soreness (DOMS) w Results primarily from eccentric action w Is associated with damage or injury within muscle w May be caused by inflammatory reaction inside damaged muscles w May be due to edema (accumulation of fluid) inside muscle compartment w Is felt 12 to 48 hours after a strenuous bout of exercise C0-HD-TOP.png MUSCLE FIBERS AFTER A MARATHON