Anatomy & Physiology

Transcription

1 Anatomy & Physiology Unit 7 The Muscular System Paul Anderson 2012

2 Organs of the Muscular System The muscular system consists of all the skeletal muscle organs of the body together with their connections to bones (e.g. tendons). The muscle tendon is continuous with other muscle connective tissue sheaths binds muscles to the periosteum of a bone transmits the force of muscle contraction to the bone causing movement. Biceps brachii Rectus abdominis Tendons tendon of biceps brachii Martini & Bartholomew fig 1-2c

3 Origins & Insertions of Muscles The muscle that contracts to cause a movement is called a prime mover muscle. The biceps brachii is a prime mover for flexion (bending) of elbow. When the biceps brachii contracts its distal tendon pulls on the radius causing flexion of elbow. proximal end of muscle at origin of muscle The point of attachment of the prime mover muscle to its distal moveable bone is the insertion of the muscle. The opposite (proximal) end of a prime mover muscle is attached to a stationary bone at the origin of the muscle. tendon at origin of biceps brachii on scapula bone (stationary bone) biceps brachii flexion of elbow tendon at insertion of biceps brachii on radius bone (moveable bone) Tendon at insertion of muscle distal end of muscle 3

4 Muscular System: Major Functions - 1 The major homeostatic functions of the muscular system are to convert chemical energy to mechanical energy for -contraction and relaxation of muscles - generation of heat. Energy conversion by muscles is used for several specific functions of the muscular system. To power adaptive (homeostatic) movements, both voluntary and reflex ( behaviour ), breathing movements and facial expressions. Movements involve muscle contraction and relaxation Muscle contraction is the generation of a force by a muscle Muscle relaxation is the reverse process i.e. loss of force in a muscle Muscle contractions may be Isotonic: muscle shortens as the force of contraction exceeds the external resistance Isometric muscle does not shorten as the force of contraction is equal to or less than the external resistance. All movements involve both isotonic and isometric contraction

5 Muscular System: Major Functions - 2 Heat production: Muscles are a major source of body heat for body temperature control Cold stimulus shivering Muscle tone heat MUSCLE CONTRACTION CHEMICAL ENERGY MECHANICAL ENERGY (25%) + HEAT (75%) ATP ADP + Pi + ENERGY Muscle contraction glucose Glycogen Fatty acids Isotonic contraction Isometric contraction

6 Muscular System: Major Functions - 3 Posture and Balance: Posture is proper position or alignment of body parts against gravity. Maintaining an upright posture means positioning of body parts in opposition to gravity and is normally a function of anti - gravity muscles (extensors of legs, back & neck maintain upright posture). For Balance anti - gravity muscles put the center of gravity over the base of the body so that the body is stable. In walking, the center of gravity shifts first over one foot then over the other.

7 Muscular System: Major Functions - 4 Maintenance of muscle tone for: Stabilization of Joints by (especially for knee and shoulder joints): Support and Shape, (e.g. abdominal wall muscles) Protection of abdominal organs (via abdominal flexors, e.g. rectus abdominis). Voluntary Control of entrances and exits of digestive and urinary tracts. mouth esophagus anus (external anal sphincter muscle) urethra (external urethral sphincter muscle)

8 Tissues of Muscular System The two major tissues in the muscular system are skeletal (striated or voluntary) muscle and various collagenous dense connective tissues (e.g. tendons). These are organised into muscle organs e.g. biceps brachii muscle. Muscle tissue is specialised for the following properties: ability to generate an impulse when stimulated (excitability or irritability) ability to conduct the impulse to all parts of the cell (conductivity) ability to generate a force for movement (contractility) Muscle contraction = generation of a force Muscle tension = degree of force generated ability to stretch (extensibility) ability to return to original length after contracting or stretching (elasticity). 8

9 Properties of Skeletal Muscle Tissue Skeletal (striated or voluntary) muscle tissue differs from both smooth and cardiac muscle as follows: Cells are multinucleated, very long (stretching the length of a muscle organ), with obvious cross striations. striations Striated muscle x1000 nuclei Force of contraction is usually transmitted to bone and produces visible movements. Contraction always requires a nerve impulse so skeletal muscle is not autorhythmic. Controlled by the somatic branch of the peripheral nervous system and so is under voluntary control. Speed of contraction (<0.1sec.) is faster. Martini & Bartholomew Figure 7-2a Skeletal muscle contraction is subject to muscle fatigue. 9

10 Structure of Skeletal Muscle Organs Muscle organs are composed of various connective tissue sheaths which are of non - contractile, elastic, collagenous tissues. These connective tissue sheaths have the following functions: carry nerve fibers, blood & lymph vessels to muscle cells Bind cells together transmit the contractile force of the muscle cells to bones give shape to muscle organs contribute to muscle s extensibility & elasticity. 10

11 Structure of Skeletal Muscle Organs-2 The epimysium covers the surface of a muscle and shapes the muscle. The perimysium covers the fasciculi (fascicles) -bundles of microscopic muscle fibers and also contains stretch receptors. The thin endomysium surrounds each muscle fiber or cell. Muscle Organs are divided internally into Fascicles Martini & Bartholomew Figure

12 Structure of Skeletal Muscle Organs - 3 Striated muscle fiber (cell) endomysium perimysium Fascicles are divided internally into Muscle Fibers or Muscle Cells fascicles perimysium epimysium Muscle organ 12

13 Structure of Skeletal Muscle Organs - 4 Myofibrils within muscle cell Striated muscle x1000 bands dark light bands dark light nuclei sarcolemma Striated muscle fiber (cell) endomysium perimysium Muscle Fibers are divided internally into Myofibrils 13

14 Structure of Skeletal Muscle Cells with protein myosin I band H zone in center of A band H zone Z Z line in center of I band dark band light band A band with protein actin Myofibrils within muscle cell Myofibrils contain Myofilaments 14

15 Structure of a Sarcomere The muscle fiber is tightly packed with parallel cylindrical units called myofibrils. The myofibril has the same striated (or striped) appearance as the muscle fiber with alternating light (I) bands and dark (A) bands (light-dark). The striations are caused by cylindrical proteins in each myofibril called myofilaments; these interact to cause muscle contraction. A band myofibril Martini & Bartholomew Figure 7-2b I band Thick filament myofilaments Thin filament 15

16 Structure of a Sarcomere- 2 The light (I) bands consist of thin myofilaments containing actin. In the center of the I band is a line called the Z line (or Z disk) containing another protein connecting the thin actin myofilaments together. The dark (A) bands consist of thick myofilaments containing the protein myosin together with overlapping thin (actin) myofilaments. In the center of the A band is a lighter zone (the H zone; this represents the region containing only thick myosin myofilaments (no actin myofilaments). Z line A band Z line myofibril Martini & Bartholomew Figure 7-2b I band Thick myosin filament H zone Zone of overlap Thin actin 16 filament

17 Structure of a Sarcomere- 3 In the center of the H zone is another line (the M line) containing proteins that bind the myosin myofilaments together. The region of a myofibril between successive Z lines is called a sarcomere and is the functional unit of a muscle cell. sarcomere Z line A band Z line myofibril Martini & Bartholomew Figure 7-2b I band Thick filament M line H zone Zone of overlap Thin filament 17

18 Structure of a Sarcomere - Summary Z line in center of I band H zone (thick filaments only) Thick filament with myosin I band (thin filaments only) Z line Z line Thin filament with actin M line in center of H zone sarcomere A band (thick & thin filaments

19 Sliding Filament Theory of Muscle Contraction The sliding filament theory of muscle contraction states that when a muscle contracts the myofilaments do not shorten but instead slide past each other. The thin actin filaments are pulled towards the H zone by the thick myosin filaments which therefore approach the Z line. Z line H zone Z Z H zone Z MUSCLE ANIMATION\MUSCLE.htm Thick filaments now near Z line 19

20 Sliding Filament Theory of Muscle Contraction - 2 The Sliding Filament Theory is borne out by the following observed changes when a muscle contracts: the H zone gets smaller and disappears, as the thin actin filaments on each side approach each other the I band gets smaller and disappears as the thick myosin filaments approach the Z line I band H zone Relaxed Sarcomere Z Z H zone now smaller Contracted Sarcomere Z Z I band now smaller 20

21 Sliding Filament Theory of Muscle Contraction - 3 the A bands get closer together but do not change their length since this is equal in length to the thick myosin filaments the sarcomere gets shorter since adjacent Z lines are pulled together H A band Relaxed Sarcomere Z Z Z Sarcomere H A band same length I band Contracted Sarcomere Z Z Z Sarcomere now smaller I band now smaller 21

22 Function of Myosin in Muscle Cell Contraction The thick filaments contain many myosin molecules each with two globular heads oriented towards the Z line. Therefore on either side of the H zone the myosin molecules are oriented in opposite directions. In the presence of Ca +2 the myosin heads bind to the adjacent actin molecules of the thin filament forming cross bridges and pull these towards the center of the sarcomere (the H zone) by flexing. This happens during muscle contraction. Z H Z In presence of Ca +2 myosin heads flex & pull thin actin filaments to center of A band 22 Martini & Bartholomew fig 7-2e

23 Storage & Release of Calcium Ions in Muscle Cells The cell membrane (sarcolemma) of a muscle cell has invaginations that form tubules (T tubules) running around each myofibril at the junction of A & I bands. The cytoplasm of a muscle cell (sarcoplasm) has an extensive SER (sarcoplasmic reticulum or SR) which stores Ca +2 in its lateral sacs. Each T tubule passes between two adjacent lateral sacs of the SR forming a triad. When an impulse from T tubules reaches the triad it causes release of Ca+2 from the lateral sacs of the SR. This triggers muscle contraction. T tubule + 2 lateral sacs forms a TRIAD store Ca +2 Muscle cell(fiber) Impulse in T tubule causes Ca release here

24 Microscopic Anatomy of a Skeletal Muscle Fiber Each Myofibril in a muscle fiber is surrounded by the SR. lateral sac of SR TRIAD T tubule lateral sac of SR TRIAD =T tubule + 2 lateral sacs Martini & Bartholomew fig 7-2a, Martini, fig

25 Storage of Calcium in Resting Muscle Cell In the resting muscle cell Ca +2 is actively transported into the SR, the function of which is to store Ca +2 until needed. Therefore there is a low ICF [Ca+2] in the resting cell, insufficient to trigger contraction. Z T tubule sarcomere Calcium ions stored in lateral sacs of SR in resting muscle cell sarcolemma 25

26 Calcium Release Triggers Muscle Cell Contraction Muscle cell contraction is triggered by the release of Ca +2 from the SR into the ICF. Ca +2 release from the sacs of the SR is triggered by an impulse (action potential) which arrives at the triad from the sarcolemma via the T tubules. The triggering of muscle contraction by an impulse is called excitation contraction coupling. Z Z Release of Calcium ions from lateral sacs of SR triggers muscle cell contraction Impulse in sarcolemma enters T tubules causing release of Ca+2 from lateral sacs of SR 26

27 Removal of Calcium Causes Muscle Cell Relaxation In the absence of impulses Ca +2 is pumped back into the sacs of the SR. Removal of Ca +2 from the muscle cell ICF causes relaxation of muscle cells. Z Z Calcium ions pumped back into lateral sacs of SR in relaxing muscle cell 27

28 Three Roles of ATP in Muscle Contraction ATP plays three roles when it powers muscle contraction. 1.Energy from ATP hydrolysis activates myosin molecules so they can pull on actin molecules causing muscle contraction. Myosin heads have an enzyme (ATPase) to split ATP and release energy that activates the myosin heads. 2.When the energy from ATP hydrolysis is spent, a new ATP molecule binds to myosin. Binding of ATP to myosin causes the detachment of myosin from actin allowing a new contraction cycle to begin. 3.Energy from ATP hydrolysis is used to pump Ca +2 into the SR after contraction. 28

29 Two Proteins Block Contraction in a Resting Muscle In the resting muscle binding of activated myosin is prevented by two proteins in the thin filament (troponin and tropomyosin). These are attached to actin molecules and protect their binding sites. All myosin heads are in extended position. Ca +2 concentration is low. Myosin heads previously activated by ATP hydrolysis ADP P Actin molecules in thin filament active sites of actin blocked by Tropomyosin Troponin ADP P thick filament with Myosin Resting Sarcomere Martini & Bartholomew fig

30 Release of Ca +2 Unblocks Binding Sites on Actin Release of Ca +2 from the sacs of the SR causes a shape change in troponin. Troponin pulls tropomyosin away from the actin binding site. This allows myosin to bind to actin and muscle contraction to occur. Ca +2 binds to troponin & unblocks active sites on actin ADP P Ca +2 Tropomyosin moves away active sites of actin now exposed ADP P thick filament with Myosin Active Site Exposure 30 Ca +2 Martini & Bartholomew fig 7-5 STEP 1

31 Myosin Binds to Actin:Cross Bridge Formation If Ca +2 is present the activated myosin heads bind to actin forming cross bridges and flexing. Actin is pulled towards the center of the sarcomere (center of H zone). This releases ADP and Pi from myosin which allows another ATP to bind to myosin. ADP P Myosin heads bind to actin & forms cross bridge Ca +2 ADP P Ca +2 Ca +2 ADP P Myosin head flexes & pulls actin toward H zone Martini & Bartholomew fig 7-5 STEP 3 ADP & P released from myosin head Ca +2 ADP P thick filament with Myosin Martini & Bartholomew fig 7-5 STEP 2 Cross Bridge Formation Pivoting ( flexing ) of myosin heads 31

32 ATP Causes Detachment of Myosin Heads ATP binds to myosin heads. The binding of ATP to the myosin head causes it to detach from actin. ATP Ca +2 Ca +2 ATP Martini & Bartholomew fig 7-5 STEP 4 Detachment of myosin heads 32

33 Myosin is Reactivated by ATP Hydrolysis ATP hydrolysis reactivates the myosin head. If Ca +2 is reabsorbed into the SR the contraction cycle ends here. If Ca +2 is not reabsorbed into the SR the contraction sequence repeats. ATP ADP P Ca +2 ATP Ca +2 ADP P Martini & Bartholomew fig 7-5 STEP 5 Myosin Reactivation 33

34 Arrival of Impulse at Neuromuscular Junction A nerve impulse (action potential) arrives at the axon terminals of a motor neuron to a skeletal muscle. The junction of the two cells is called a neuromuscular junction. myofibril Martini Figure 10.10a, 34

35 Excitation of Muscle Cell at the Motor End Plate The axon terminal ends in a swelling which fits into a depression in the sarcolemma called the motor end plate. Release of neurotransmitter acetylcholine from the synaptic terminal causes excitation of the motor end plate impulse motor end plate Martini & Bartholomew Fig 7-4b: Martini Figure 10.10a, 35

36 Release of Acetylcholine at the Neuromuscular Junction The motor impulse causes release of the neurotransmitter acetylcholine (Ach) by exocytosis. Ach activates membrane receptors in the motor end plate triggering an impulse in the sarcolemma of the muscle cell. MOTOR MPULSE SYNAPTIC CLEFT SYNAPTIC VESICLES Acetylcholine (Ach) in synaptic vesicles is released by exocytosis into the synaptic cleft SARCOLEMMA OF MOTOR END PLATE Ach MEMBRANE RECEPTOR An enzyme acetylcholinesterase (AchE) in the synaptic cleft later destroys Ach by hydrolysis Martini & Bartholomew Fig 7-4c STEP 2: Martini Figure 10.10c,

37 Excitation of Muscle Cell The binding of ACh to the membrane receptors at the motor end plate increases the membrane permeability to Na +. Na + rapidly flows into the sarcoplasm from the ECF by net diffusion. Na + inflow depolarises the motor end plate, triggering an impulse in the sarcolemma. IMPULSE IN MUSCLE CELL Na + Na + enters sarcoplasm, depolarising muscle cell & causing an impulse in the sarcolemma of muscle cell. Ach binds to membrane receptor Na + Na + 37 Martini & Bartholomew Fig 7-4c STEP 3: Martini Figure 10.10c,

38 Excitation of Muscle Cell The impulse spreads over the surface of the muscle cell and enters the T tubules where it is conducted to the triad. Arrival of the impulse causes Ca +2 release from the lateral sacs of the SR. Ca +2 release triggers muscle cell contraction. IMPULSE ENTERS MUSCLE CELL Impulse causes Ca +2 release from lateral sacs of SR, triggering muscle cell contraction AchE breaks down Ach in the synaptic cleft 38 Martini & Bartholomew Fig 7c STEP 4: Martini Figure 10.10c

39 Summary of Contraction Steps in a Muscle Impulse No Impulse 39 Martini & Bartholomew Table 7-1

40 Contraction Cycle of a Muscle Cell Impulse Contraction No Impulse Martini, Figure Relaxation 40

41 RIGOR MORTIS In the complete absence of ATP (following cellular death): Ca +2 cannot be actively transported into the SR. Therefore ICF Ca +2 levels will be high so actin sites are exposed and myosin can bind to actin. Myosin molecules are unable to detach from actin since this requires ATP. Therefore the muscle remains stiffly contracted, a condition called rigor mortis. 41

42 Contraction and Relaxation of Muscle Organs MUSCLE CONTRACTION is the process of generating a force in a muscle organ. The net force produced by a muscle organ is called muscle tension. MUSCLE RELAXATION is loss of force in a muscle and so is the opposite of muscle contraction. Muscle contractions may be Isotonic: muscle usually shortens as the force of contraction exceeds the external resistance Isometric muscle does not shorten as the force of contraction is equal to or less than the external resistance. 42

43 Isotonic Muscle Contraction ISOTONIC CONTRACTION occurs whenever a muscle changes its length (usually shortening) while contracting. Part of the energy of contraction performs mechanical work (= resistance x distance moved). Resistance is the load or force opposing the action Any movement involves Isotonic Contraction. Muscle contracts In Isotonic Contraction Muscle changes its length In Concentric Contraction Muscle shortens Martini Fig kg 2 kg Resistance here is load due to gravity 43

44 Concentric Muscle Contraction There are two types of Isotonic Contraction Concentric Eccentric CONCENTRIC CONTRACTION occurs whenever a muscle shortens while contracting isotonically. Here the tension generated by the muscle exceeds the load (resistance, or force opposing the muscle). 2 kg 44

45 Eccentric Muscle Contraction Sometimes an antagonistic muscle lengthens while contracting isotonically e.g. the quadriceps femoris (knee extensors) while sitting down, or the biceps brachii (elbow flexor) while lowering a weight in the hand). Here the load exceeds the tension. This is referred to as ECCENTRIC CONTRACTION (or paradoxical action) and the muscle performs negative work. The function of the contracting muscle in this case is to slow the rate of descent of the body part to protect the body from injury. Note that in eccentric contraction the prime mover for the movement may be relaxed as gravity is causing the movement. Here the triceps muscle, (elbow extensor) is relaxed while lowering a weight Biceps muscle contracts eccentrically when lowering a weight 2 kg 45

46 Isometric Muscle Contraction ISOMETRIC CONTRACTION occurs when the tension exerted by a muscle does not exceed the load (resistance) opposing the muscle and the muscle organ does not change its length. Here all the energy escapes as heat and no mechanical work is done. Examples: standing still (extensors of leg), pushing against a closed door (extensors of arm), holding a weight in a stationary position. Biceps muscle contracts isometrically while holding a weight 2 kg No movement Martini Fig Isometric Contraction Muscle does not change length 46

47 All Movements Involve Isotonic and Isometric Phases Normal functioning of the skeleto-muscular system depends on a combination of isotonic and isometric contractions. In walking and running isometric contractions keep the legs stiff when the feet touch the ground. All movements begin with a brief isometric phase when the tension is increasing but is still less than the load. Force (F) Resistance (R) Muscle contraction Isotonic contraction Isometric contraction F > R muscle shortens Concentric contraction F < R muscle lengthens Eccentric contraction F < or = R muscle length unchanged Movement No Movement 47 2 kg

48 Muscle Twitch vs Graded Responses of Muscle Organs A single impulse to a muscle produces a single brief all- or -none contraction and relaxation response called a muscle twitch. However, muscle responses are normally smooth and vary in intensity according to needs. Martini & Bartholomew Fig 7-6 Martini Fig Muscle Twitch Such GRADED RESPONSES of muscles depend on temporal and spatial summation of individual contractions (twitches). Summation of twitches temporal spatial smoothness intensity 48

49 Temporal (Wave) Summation A TEMPORAL (OR WAVE) SUMMATION occurs when motor impulses arrive in such rapid succession (i.e. at a high frequency) that each contraction adds onto the previous one. Eventually a fusion of twitches occurs, forming a smooth sustained stronger contraction, called tetanus. Most normal movements involve tetanus. stimulus Higher frequency stronger smoother contraction Maximum frequency strongest smooth contraction tension Temporal summation of muscle twitches Stronger contraction Incomplete Tetanus incomplete fusion of twitches Complete tetanus complete fusion of twitches time Martini & Bartholomew Fig 7-7 Martini Fig

50 Causes of Temporal (Wave) Summation TEMPORAL (OR WAVE) SUMMATION is caused by Increased availability of Ca +2. Each impulse releases more Ca +2 Sustained stretching of non- contractile tissues ( series elastic elements ) such as tendons in the muscle (i.e. these are not allowed to recoil as in a twitch). Repeated impulses cause Increased [Ca +2 ] Greater Increase in [Ca +2 ] Martini & Bartholomew Fig 7-7 Martini Fig Maximum increase in [Ca +2 ] 50

51 Spatial Summation of Muscle Twitches (Recruitment of Motor Units) SPATIAL SUMMATION refers to the RECRUITMENT of increasing numbers of motor units in a muscle. A motor unit consists of all the muscle cells controlled by a single motor neuron. A motor unit is the smallest unit of contraction for a muscle, i.e. represents the minimum response of a muscle. Each muscle cell contracts as part of a motor unit. Both muscle cells and motor units obey the all or none law. Spatial summation (by multiple motor unit summation or recruitment) is therefore largely responsible for increasing the force of contraction of the muscle. Recruitment occurs when the brain activates more axons in each motor nerve to a muscle. 51

52 Recruitment of Motor Units Motor Unit Muscle cells controlled by one axon minimum response unit of muscle obeys all or none law Constant tension in muscle due to: Rotation of motor units Asynchronous motor unit summation Fascicle: does not obey all or none law Martini & Bartholomew Fig 7-8 Martini Fig

53 Innervation Ratio of a Muscle The Innervation Ratio is the ratio between the number of axons in a motor nerve to a muscle and the number of muscle cells in the muscle. It is used to calculate the average motor unit size for a muscle. Muscles controlling precision movements requiring many fine gradations of movement have small motor units - flexors of the fingers, 1 axon: 10 muscle fibers - extrinsic eye muscles, 1: 3. Muscles controlling gross movements requiring little variation have large motor units, e.g. extensors of the thighs 1:

54 Innervation Ratio of a Muscle 20 3 Innervation Ratio Average motor unit size 3 axons: 20 muscle cells = 1 axon: 7 muscle cells This is a precision muscle with small IR Martini & Bartholomew Fig 7-8 Martini Fig

55 Muscle Tone and the Stretch Reflex MUSCLE TONE is the continual partial contraction of a resting muscle and is maintained by the stretch reflex. Tone is most important for "anti- gravity" muscles. The STRETCH REFLEX is initiated by stretching of a muscle: in response the same muscle shortens. Stretching of extensor muscles of the trunk and legs ("anti - gravity" muscles) by gravity causes a reflex contraction of the same muscles which therefore stiffen and oppose gravity. Quadriceps femoris anti - gravity knee extensors contract via stretch reflex when gravity causes knees to buckle Martini & Bartholomew 55 fig 1-2c

56 The Stretch Reflex The nerve pathway mediating the stretch reflex involves muscle receptors called muscle spindles, a sensory nerve fiber, a motor nerve fiber and a synapse in the spinal cord. gravity causes synapse anti - gravity extensor muscle 56

57 Stretching of muscle tendon stimulates muscle spindles Stretch Example of Stretch Reflex: The Knee Jerk Muscle spindle (stretch receptor) REFLEX ARC Spinal cord Contraction Activation of motor neuron produces reflex muscle contraction Martini & Bartholomew Figure 8-29

58 Importance of Muscle Tone for Health Muscle tone is important for muscle health, rapidity of response, for stabilizing joints and for posture. Muscle tone is present during waking hours and is dependent on - the stretch reflex and on - descending motor pathways from the brain. Tone is reduced during sleep and in flaccid paralysis. 58

59 Muscle Paralysis Muscle Paralysis means loss of voluntary control over muscles. Spastic paralysis is characterised by hypertonia (spasticity) and exaggerated reflexes. Spasticity is caused by the stretch reflex which is overactive. The usual cause is a stroke (cerebrovascular accident) which damages upper motor neurons. Flaccid paralysis is characterised by hypotonia (flaccidity) and the absence of reflexes. Flaccidity is caused by muscle denervation, i.e. damage to lower motor neurons (e. g. with poliomyelitis). 59

60 Damage to Motor Neurons Causes Paralysis Loss of voluntary control LMNs overactive (exaggerated reflexes) Spastic paralysis Loss of inhibitory control over LMNs Excitatory synapses Upper motor neuron (UMN) in brain damaged by stroke (CVA) - Inhibitory synapse + + X lower motor neuron (LMN) to muscle damaged e.g. by polio Loss of voluntary & reflex control LMNs inactive Flaccid 60 paralysis

61 Muscle Atrophy & Hypertrophy Flaccid paralysis causes muscle atrophy or shrinking of the muscle caused by shrinking of cells and/or reduction in cell number. Types of Muscle Atrophy. There are two types of muscle atrophy depending on the cause: Atrophy of Denervation is caused by the cutting of the nerve supply (innervation) to the muscle i.e. denervation (e.g. in poliomyelitis); unless the muscle is renervated (or electrically stimulated) within four months the atrophy is irreversible. Atrophy of Disuse occurs when a muscle is not used for an extended period (e.g. limb in a cast, bedridden person; since the muscle is not stretched muscle tone is reduced (hypotonia). This type of atrophy is reversible if the muscle is reused. Muscle Hypertrophy refers to an increase in size of the muscle by an increase in the size of individual cells (more myofibrils) without increase in cell number. This is caused by increased use of muscles with or without the use of anabolic steroids. 61

62 Roles of Muscles in Movements During any movement muscles may function as Prime Movers (or agonists) which directly cause a movement by their contraction e.g. biceps brachii is a prime mover for flexion of the elbow. Antagonists which oppose a given movement when they contract e.g. the triceps brachii is an antagonist for flexion of the elbow. Synergists which are muscles which also contract during a movement but do not directly cause the movement but help the prime mover to work efficiently. Fixators are synergists which steady the movement by stabilising (or fixing ) a joint e.g. the pectoralis major and deltoid muscles steady the humerus bone during flexion of the elbow and so are fixators. 62

63 Reciprocal Inhibition of Antagonists during Movements Muscles in the body are grouped into antagonistic pairs. The two members of the antagonistic pair are prime movers for opposing movements and occur on opposite sides of the limb or trunk (e.g. biceps brachii and triceps brachii are on opposite sides of the upper arm. During any movement the antagonist must relax while the prime mover contracts. Relaxation of the antagonist during a movement involves inhibiting the motor nerve fibers going to the muscle, thus preventing the stretch reflex (which would otherwise cause contraction of the antagonist). The reflex inhibition of motor fibers to an antagonist during a movement with the simultaneous excitation of motor fibers to the prime mover is called reciprocal inhibition. 63

64 Reciprocal Inhibition of Antagonists during Movements The withdrawal reflex involves reflex inhibition of nerve fibers to ipsilateral (same side) limb extensors. In the crossed - extensor reflex flexion of one limb is accompanied by reflex inhibition of flexors of the opposite (contralateral) limb so that this limb can extend and support the body s weight. Crossed extensor reflex of right leg Withdrawal reflex of left leg Left Leg Excitation of flexors Inhibition of extensors Painful Right Leg stimulus to Excitation of extensors left foot 64 Inhibition of flexors Right Leg extends Left Leg flexes

65 Flexor & Crossed Extensor Reflexes Painful stimulus to right foot withdrawal reflex of right leg Crossed extensor reflex of left leg Painful stimulus to right foot withdrawal reflex of right leg Martini & Bartholomew Figure Martini Figure 13.22

66 Muscles provide Force for Levers The skeleto - muscular system is a system of levers (devices for performing work). A Lever is a rigid bar (in the body, a bone) that turns about an axis of rotation or a fulcrum (in the body, a joint) the insertion point of a muscle is the power point (P) of the lever the fulcrum (F) of the lever is the moveable joint at which movement occur the resistance (R) is the weight of the part being moved Resistance (R) = Weight of body part moved R F P Fulcrum(F) = Joint Power point (P) = Insertion of muscle 66

67 The Action of the Biceps Brachii in Elbow Flexion The most common type of lever in the body is type III (R - P - F) as in biceps brachii flexing the elbow. Resistance (R) = Weight of lower arm Power point (P) = Insertion of muscle on radial tuberosity animation P R Type III lever F Fulcrum( F) = elbow Joint Biceps brachii muscle 67

68 Mechanical Advantage of Levers A lever may offer a mechanical advantage (less muscle power required to move a given weight). The PF/RF ratio determines the mechanical advantage of a lever. If the PF/RF ratio of a lever is >1 the lever works at a mechanical advantage i.e. the power used can be less than the load (resistance). If the PF/RF ratio of a lever is <1 the lever works at a mechanical disadvantage, i.e. the power used must be much greater than the load (resistance). Therefore Type 3 levers always have a mechanical disadvantage P R RF PF/RF ratio <1 PF F 68

69 Mechanical Advantage vs Mobility of Levers Many levers in the body sacrifice mechanical advantage (i.e. power) for increased speed and range of movement by having a smaller PF/RF ratio. For the biceps brachii PF/RF may equal 1/6 or 0.17, a mechanical disadvantage. Thus to lift a 10kg wt. the biceps must generate a force of 10/0.17 = 60 kg (or 6 x10kg). However, the speed of hand movement is increased by an equivalent factor of 6 giving increased mobility of the hand. If the biceps moves 1cm in 1 sec the hand moves 6cm. R 6 P 1 F 1cm 6cm 69

70 How the Insertion of a Muscle Affects Mobility & Power The MOBILITY (degree of movement), SPEED & Power of a muscle depends partly on the INSERTION POINT of the muscle tendon on the bone. - The closer the insertion point is to the fulcrum of the lever the greater is the muscle s mobility. This is because a small degree of movement near the fulcrum causes a large degree of moment of the other end of the bone. - The further the insertion point is from the fulcrum of the lever the greater is the mechanical advantage and so the greater the muscle s power. Long insertion reduced hand mobility Greater muscle power Short insertion Greater hand mobility Reduced muscle power 70

71 How the Tendon -Fiber Angle of a Muscle Affects Mobility The smaller the tendon - fiber angle the greater the mobility and speed. Maximum mobility and speed occurs when the tendon - fiber angle is zero (i.e. they are parallel) where the muscle fibers are pulling the tendon in the direction of the movement. This also means that fewer fasciculi are possible so the muscle power is relatively weak e.g. rectus abdominis, sartorius, sternohyoid, superior rectus, gracilis muscles. Muscle with parallel tendons & muscle fibers Great mobility Fewer fasciculi so often weaker muscles Biceps brachii achieves power by its fusiform shape- bulky in center Parallel muscle 71

72 How the Number of Fasciculi of a Muscle Affects Power The STRENGTH (POWER) of a muscle depends partly on the NUMBER OF FASCICULI (bundles of fibers). The greater the number of fasciculi the stronger the muscle. This is achieved by having the muscle fibers pulling at an angle to the tendon. By increasing the tendon - muscle fiber angle more fasciculi can be packed into the same muscle diameter which increases power but reduces mobility. Unipennate muscle have muscle fibers pulling the tendon on one side only Bipennate muscle (with even more fasciculi) have fibers on two sides of the tendon The more fasciculi the stronger the muscle. Unipennate Vastus muscle Bipennate Rectus femoris muscle muscle fibers pull at an angle to the tendon. 72

73 Strongest Muscles have Greatest Numbers of Fasciculi The following muscles have fibers pulling on several sides of the tendon, have the greatest numbers of fasciculi and so are the strongest muscles. - Multipennate muscles (e.g. deltoid) - Convergent muscles (e.g. pectoralis major) and - Circumpennate muscles (e.g. tibialis anterior) Mutiipennate deltoid Martini Figure 11-1 Convergent pectoralis major Circumpennate tibialis anterior 73

74 Muscle Activity & Muscle Strength The STRENGTH (POWER) of a muscle depends on three factors: NUMBER OF FASCICULI INSERTION POINT of the muscle DEGREE OF ACTIVITY OF THE MUSCLE. Fixed by muscle anatomy -If a muscle is used forcefully (especially isometrically) on a regular (daily) basis there will be an increase in muscle cell diameter, number of contractile units and strength of connective tissue components. -The muscle will therefore show hypertrophy and increased strength.

75 Sources of Energy for Muscle Contraction Muscle contraction depends directly on energy from ATP hydrolysis. ATP is replenished in exercising muscle cells from two sources, - hydrolysis of creatine phosphate (CP) - cell respiration of glucose and other organic molecules. Blood sugar Muscle glycogen Aerobic cell respiration energy energy energy energy 75

76 Hydrolysis & Synthesis of ATP high energy bond stores energy in ATP Muscle contraction 76

77 Creatine Phosphate Transfers Energy to ATP for Muscle Contraction Creatine phosphate (CP) is a second high energy molecule in muscle cells. During rest CP is formed from ATP During exercise as ATP is being depleted CP is the most direct and so is the first source for regenerating ATP. Creatine Phosphate high energy bond stores energy in CP Creatine + ATP rest exercise CP + ADP 77

78 During Rest Creatine Phosphate & Glycogen Reserves are built up using ATP Glycogen energy During rest Energy from ATP hydrolysis is used to make CP & Glycogen from glucose energy Fatty acids are major source of energy for ATP in resting muscles By using fatty acids during rest glucose in muscle cells is available to form glycogen. 78

79 Metabolism of Resting Muscle Cell During rest Energy from ATP hydrolysis is used to make CP & Glycogen from glucose 79 Martini & BartholomewFigure 7-9(a)

80 Anaerobic Respiration in Muscle Cells supplies little ATP & forms Lactic Acid During intense exercise blood supply cannot keep up with oxygen demands of muscles and muscles respire anaerobically. Anaerobic respiration (anaerobic glycolysis) oxidises glucose incompletely to lactic acid and forms only 2 ATP per glucose. Anaerobically muscles therefore fatigue easily due to -a shortage of ATP - buildup of lactic acid (which lowers the ph of muscle cells). C 6 H 12 O 6 2ATP INTENSE EXERCISE 2 lactic acid 2ADP + 2Pi + ENERGY After anaerobic exercise an oxygen debt must be paid to reoxidise excess lactic acid to CO 2 and H 2 O and to replenish ATP and CP 80 reserves from aerobic respiration: therefore hyperventilation occurs.

81 Anaerobic Metabolism of Contracting Muscle Cell LIVER Lactic Acid Cycle: Liver converts lactic acid to glucose for use by muscles GLUCOSE Absence of oxygen 81 Martini & BartholomewFigure 7-9(c)

82 Aerobic Respiration in Muscle Cells forms Maximum ATP During moderate exercise ATP is replenished by aerobic respiration of glucose or fatty acids. Glucose is first obtained from glycogen reserves and then from the blood sugar. Aerobic respiration of glucose forms ATP per glucose molecule and completely oxidises glucose to CO 2 and H 2 O. Muscle fatigue occurs more slowly since more ATP is available and lactic acid is not formed. C 6 H 12 O 6 + 6O 2 38 ATP AEROBIC RESPIRATION 6CO 2 + 6H 2 O + ENERGY 38ADP + 38Pi Provides energy for Muscle contraction 82

83 Summary of Respiration in Muscle Cells Occurs in cytosol Provides some ATP anaerobically ATP Some is converted to glucose by liver & sent back to muscles Occurs in mitochondrion Main source of ATP when oxygen available 83

84 Aerobic Metabolism of Contracting Muscle Cell 84 Martini & BartholomewFigure 7-9(b)

85 Oxidative (Red) Muscle Fibers vs Glycolytic (White) Muscle fibers Muscle cells which specialize for aerobic respiration are called oxidative fibers or slow fibers. Slow fibers have many mitochondria and contain much myoglobin for O 2 storage so are also called red fibers. Muscle cells which specialize for anaerobic respiration (anaerobic glycolysis) are called glycolytic fibers or fast fibers. Fast fibers have few mitochondria and little myoglobin so are also called white fibers. Fast fibers are adapted for rapid bursts of intense exercise and fatigue easily