Download presentation
Presentation is loading. Please wait.
Published byAlexandrina Wilson Modified over 8 years ago
1
Fundamentals of Anatomy & Physiology Frederic H. Martini Unit 2 Support and Movement Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings PowerPoint ® Lecture Slides prepared by Professor Albia Dugger, Miami–Dade College, Miami, FL Professor Robert R. Speed, Ph.D., Wallace Community College, Dothan, AL 2/13/09 1
2
2
3
A primary tissue type, divided into: skeletal muscle cardiac muscle smooth muscle 2/13/09 3
4
4
5
Are attached to the skeletal system Allow us to move 2/13/09 5
6
Includes only skeletal muscles 2/13/09 6
7
Muscle tissue (muscle cells or fibers) Connective tissues Nerves Blood vessels 2/13/09 7
8
1. Produce skeletal movement 2. Maintain body position 3. Support soft tissues 4. Guard body openings 5. Maintain body temperature 2/13/09 8
9
9
10
10 Figure 10–1
11
Muscles have 3 layers of connective tissues: 1. epimysium 2. perimysium 3. endomysium 2/13/09 11
12
Exterior collagen layer Connected to deep fascia Separates muscle from surrounding tissues 2/13/09 12
13
Surrounds muscle fiber bundles (fascicles) Contains blood vessel and nerve supply to fascicles 2/13/09 13
14
Surrounds individual muscle cells (muscle fibers) Contains capillaries and nerve fibers contacting muscle cells Contains satellite cells (stem cells) that repair damage 2/13/09 14
15
Endomysium, perimysium, and epimysium come together: at ends of muscles to form connective tissue attachment to bone matrix i.e., tendon (bundle) or aponeurosis (sheet) 2/13/09 15
16
Skeletal muscles are voluntary muscles, controlled by nerves of the central nervous system 2/13/09 16
17
Muscles have extensive vascular systems that: supply large amounts of oxygen supply nutrients carry away wastes 2/13/09 17
18
2/13/09 18
19
Skeletal muscle cells are called fibers 2/13/09 19 Figure 10–2
20
Are very long Develop through fusion of mesodermal cells (myoblasts) Become very large Contain hundreds of nuclei 2/13/09 20
21
2/13/09 21 Figure 10–3
22
The cell membrane of a muscle cell Surrounds the sarcoplasm (cytoplasm of muscle fiber) A change in transmembrane potential begins contractions 2/13/09 22
23
Transmit action potential through cell Allow entire muscle fiber to contract simultaneously Have same properties as sarcolemma 2/13/09 23
24
Lengthwise subdivisions within muscle fiber Made up of bundles of protein filaments (myofilaments) Myofilaments are responsible for muscle contraction 2/13/09 24
25
Thin filaments: made of the protein actin Thick filaments: made of the protein myosin 2/13/09 25
26
A membranous structure surrounding each myofibril Helps transmit action potential to myofibril Similar in structure to smooth endoplasmic reticulum Forms chambers (terminal cisternae) attached to T tubules 2/13/09 26
27
Is formed by 1 T tubule and 2 terminal cisternae 2/13/09 27
28
Concentrate Ca 2+ (via ion pumps) Release Ca 2+ into sarcomeres to begin muscle contraction 2/13/09 28
29
2/13/09 29
30
2/13/09 30 Figure 10–4
31
The contractile units of muscle Structural units of myofibrils Form visible patterns within myofibrils 2/13/09 31
32
A striped or striated pattern within myofibrils: alternating dark, thick filaments (A bands) and light, thin filaments (I bands) 2/13/09 32
33
M line: the center of the A band at midline of sarcomere Z lines: the centers of the I bands at 2 ends of sarcomere 2/13/09 33
34
The densest, darkest area on a light micrograph Where thick and thin filaments overlap 2/13/09 34
35
The area around the M line Has thick filaments but no thin filaments 2/13/09 35
36
Are strands of protein Reach from tips of thick filaments to the Z line Stabilize the filaments 2/13/09 36
37
2/13/09 37 Figure 10–5
38
Transverse tubules encircle the sarcomere near zones of overlap Ca 2+ released by SR causes thin and thick filaments to interact 2/13/09 38
39
Figure 10–6 (1 of 5) 2/13/09 39
40
2/13/09 40 Figure 10–6 (2 of 5)
41
2/13/09 41 Figure 10–6 (3 of 5)
42
2/13/09 42 Figure 10–6 (4 of 5)
43
2/13/09 43 Figure 10–6 (5 of 5)
44
Is caused by interactions of thick and thin filaments Structures of protein molecules determine interactions 2/13/09 44
45
2/13/09 45 Figure 10–7a
46
1. F actin: is 2 twisted rows of globular G actin the active sites on G actin strands bind to myosin 2/13/09 46
47
2. Nebulin: holds F actin strands together 2/13/09 47
48
3. Tropomyosin: is a double strand prevents actin–myosin interaction 2/13/09 48
49
4. Troponin: a globular protein binds tropomyosin to G actin controlled by Ca 2+ 2/13/09 49
50
2/13/09 50 Figure 10–7b
51
Ca 2+ binds to receptor on troponin molecule Troponin–tropomyosin complex changes Exposes active site of F actin 2/13/09 51
52
2/13/09 52 Figure 10–7c
53
Contain twisted myosin subunits Contain titin strands that recoil after stretching 2/13/09 53
54
2/13/09 54 Figure 10–7d
55
Tail: binds to other myosin molecules Head: made of 2 globular protein subunits reaches the nearest thin filament 2/13/09 55
56
During contraction, myosin heads: interact with actin filaments, forming cross- bridges pivot, producing motion 2/13/09 56
57
2/13/09 57 Figure 10–8
58
Sliding filament theory: thin filaments of sarcomere slide toward M line between thick filaments the width of A zone stays the same Z lines move closer together 2/13/09 58 InterActive Physiology: Sliding Filament Theory PLAY
59
2/13/09 59
60
2/13/09 60 Figure 10–9 (Navigator)
61
Neural stimulation of sarcolemma: causes excitation–contraction coupling Cisternae of SR release Ca 2+ : which triggers interaction of thick and thin filaments consuming ATP and producing tension 2/13/09 61
62
2/13/09 62 Figure 10–10a, b (Navigator)
63
2/13/09 63 Figure 10–10c
64
Is the location of neural stimulation Action potential (electrical signal): travels along nerve axon ends at synaptic terminal 2/13/09 64
65
Releases neurotransmitter (acetylcholine or ACh) Into the synaptic cleft (gap between synaptic terminal and motor end plate) 2/13/09 65
66
Acetylcholine or ACh: travels across the synaptic cleft binds to membrane receptors on sarcolemma (motor end plate) causes sodium–ion rush into sarcoplasm is quickly broken down by enzyme (acetylcholinesterase or AChE) 2/13/09 66
67
Generated by increase in sodium ions in sarcolemma Travels along the T tubules Leads to excitation–contraction coupling 2/13/09 67
68
Action potential reaches a triad: releasing Ca 2+ triggering contraction Requires myosin heads to be in “cocked” position: loaded by ATP energy 2/13/09 68
69
2/13/09 69
70
2/13/09 70 Figure 10–11
71
2/13/09 71 Figure 10–12 (1 of 4)
72
2/13/09 72 Figure 10–12 (2 of 4)
73
2/13/09 73 Figure 10–12 (3 of 4)
74
2/13/09 74 Figure 10–12 (Navigator) (4 of 4)
75
1. Exposure of active sites 2. Formation of cross-bridges 3. Pivoting of myosin heads 4. Detachment of cross-bridges 5. Reactivation of myosin 2/13/09 75
76
As sarcomeres shorten, muscle pulls together, producing tension 2/13/09 76 Figure 10–13
77
Depends on: duration of neural stimulus number of free calcium ions in sarcoplasm availability of ATP 2/13/09 77
78
Ca 2+ concentrations fall Ca 2+ detaches from troponin Active sites are recovered by tropomyosin Sarcomeres remain contracted 2/13/09 78
79
A fixed muscular contraction after death Caused when: ion pumps cease to function calcium builds up in the sarcoplasm 2/13/09 79
80
2/13/09 80 Table 10–1 (1 of 2)
81
2/13/09 81 Table 10–1 (2 of 2)
82
Skeletal muscle fibers shorten as thin filaments slide between thick filaments Free Ca 2+ in the sarcoplasm triggers contraction SR releases Ca 2+ when a motor neuron stimulates the muscle fiber 2/13/09 82
83
Contraction is an active process Relaxation and return to resting length is passive 2/13/09 83
84
2/13/09 84
85
The all–or–none principal: as a whole, a muscle fiber is either contracted or relaxed 2/13/09 85
86
Depends on: the number of pivoting cross-bridges the fiber’s resting length at the time of stimulation the frequency of stimulation 2/13/09 86
87
2/13/09 87 Figure 10–14
88
Number of pivoting cross-bridges depends on: amount of overlap between thick and thin fibers Optimum overlap produces greatest amount of tension: too much or too little reduces efficiency 2/13/09 88
89
Normal resting sarcomere length: is 75% to 130% of optimal length 2/13/09 89
90
A single neural stimulation produces: a single contraction or twitch which lasts about 7–100 msec Sustained muscular contractions: require many repeated stimuli 2/13/09 90
91
Figure 10–15a (Navigator) Length of twitch depends on type of muscle 2/13/09 91
92
A graph of twitch tension development 2/13/09 92 Figure 10–15b (Navigator)
93
1. Latent period before contraction: the action potential moves through sarcolemma causing Ca 2+ release 2/13/09 93
94
2. Contraction phase: calcium ions bind tension builds to peak 2/13/09 94
95
3. Relaxation phase: Ca 2+ levels fall active sites are covered tension falls to resting levels 2/13/09 95
96
A stair-step increase in twitch tension 2/13/09 96 Figure 10–16a
97
Repeated stimulations immediately after relaxation phase: stimulus frequency < 50/second Causes a series of contractions with increasing tension 2/13/09 97
98
Increasing tension or summation of twitches 2/13/09 98 Figure 10–16b
99
Repeated stimulations before the end of relaxation phase: stimulus frequency > 50/second Causes increasing tension or summation of twitches 2/13/09 99
100
Twitches reach maximum tension 2/13/09 100 Figure 10–16c
101
If rapid stimulation continues and muscle is not allowed to relax, twitches reach maximum level of tension 2/13/09 101
102
102 Figure 10–16d
103
If stimulation frequency is high enough, muscle never begins to relax, and is in continuous contraction 2/13/09 103
104
104
105
InterActive Physiology: Contraction of Whole Muscle PLAY Depends on: internal tension produced by muscle fibers external tension exerted by muscle fibers on elastic extracellular fibers total number of muscle fibers stimulated 2/13/09 105
106
106 Figure 10–17
107
Contain hundreds of muscle fibers That contract at the same time Controlled by a single motor neuron 2/13/09 107 InterActive Physiology: Contraction of Motor Units PLAY
108
In a whole muscle or group of muscles, smooth motion and increasing tension is produced by slowly increasing size or number of motor units stimulated 2/13/09 108
109
Achieved when all motor units reach tetanus Can be sustained only a very short time 2/13/09 109
110
Less than maximum tension Allows motor units to rest in rotation 2/13/09 110
111
Voluntary muscle contractions involve sustained, tetanic contractions of skeletal muscle fibers Force is increased by increasing the number of stimulated motor units (recruitment) 2/13/09 111
112
The normal tension and firmness of a muscle at rest Muscle units actively maintain body position, without motion Increasing muscle tone increases metabolic energy used, even at rest 2/13/09 112
113
113
114
1. Isotonic contraction 2. Isometric contraction 2/13/09 114
115
115 Figure 10–18a, b
116
Skeletal muscle changes length: resulting in motion If muscle tension > resistance: muscle shortens (concentric contraction) If muscle tension < resistance: muscle lengthens (eccentric contraction) 2/13/09 116
117
117 Figure 10–18c, d
118
Skeletal muscle develops tension, but is prevented from changing length Note: Iso = same, metric = measure 2/13/09 118
119
119 Figure 10–19
120
Are inversely related The heavier the resistance on a muscle: the longer it takes for shortening to begin and the less the muscle will shorten 2/13/09 120
121
After contraction, a muscle fiber returns to resting length by: elastic forces opposing muscle contractions gravity 2/13/09 121
122
The pull of elastic elements (tendons and ligaments) Expands the sarcomeres to resting length 2/13/09 122
123
Reverse the direction of the original motion Are the work of opposing skeletal muscle pairs 2/13/09 123
124
Can take the place of opposing muscle contraction to return a muscle to its resting state 2/13/09 124
125
125
126
Sustained muscle contraction uses a lot of ATP energy Muscles store enough energy to start contraction Muscle fibers must manufacture more ATP as needed 2/13/09 126
127
Adenosine triphosphate (ATP): the active energy molecule Creatine phosphate (CP): the storage molecule for excess ATP energy in resting muscle 2/13/09 127
128
Energy recharges ADP to ATP: using the enzyme creatine phosphokinase (CPK) When CP is used up, other mechanisms generate ATP 2/13/09 128
129
129 Table 10–2
130
Cells produce ATP in 2 ways: aerobic metabolism of fatty acids in the mitochondria anaerobic glycolysis in the cytoplasm 2/13/09 130
131
Is the primary energy source of resting muscles Breaks down fatty acids Produces 34 ATP molecules per glucose molecule 2/13/09 131
132
Is the primary energy source for peak muscular activity Produces 2 ATP molecules per molecule of glucose Breaks down glucose from glycogen stored in skeletal muscles 2/13/09 132
133
At peak exertion: muscles lack oxygen to support mitochondria muscles rely on glycolysis for ATP pyruvic acid builds up, is converted to lactic acid 2/13/09 133
134
134 InterActive Physiology: Muscle Metabolism PLAY Figure 10–20a
135
2/13/09 135 Figure 10–20b
136
2/13/09 136 Figure 10–20c
137
2/13/09 137 Figure 10–20 (Navigator)
138
2/13/09 138
139
When muscles can no longer perform a required activity, they are fatigued 2/13/09 139
140
1. Depletion of metabolic reserves 2. Damage to sarcolemma and sarcoplasmic reticulum 3. Low pH (lactic acid) 4. Muscle exhaustion and pain 2/13/09 140
141
The time required after exertion for muscles to return to normal Oxygen becomes available Mitochondrial activity resumes 2/13/09 141
142
The removal and recycling of lactic acid by the liver Liver converts lactic acid to pyruvic acid Glucose is released to recharge muscle glycogen reserves 2/13/09 142
143
After exercise: the body needs more oxygen than usual to normalize metabolic activities resulting in heavy breathing 2/13/09 143
144
Skeletal muscles at rest metabolize fatty acids and store glycogen During light activity, muscles generate ATP through anaerobic breakdown of carbohydrates, lipids or amino acids At peak activity, energy is provided by anaerobic reactions that generate lactic acid as a byproduct 2/13/09 144
145
Active muscles produce heat Up to 70% of muscle energy can be lost as heat, raising body temperature 2/13/09 145
146
Growth hormone Testosterone Thyroid hormones Epinephrine 2/13/09 146
147
147
148
Power: the maximum amount of tension produced Endurance: the amount of time an activity can be sustained Power and endurance depend on: the types of muscle fibers physical conditioning 2/13/09 148
149
1. Fast fibers 2. Slow fibers 3. Intermediate fibers 2/13/09 149
150
Contract very quickly Have large diameter, large glycogen reserves, few mitochondria Have strong contractions, fatigue quickly 2/13/09 150
151
Are slow to contract, slow to fatigue Have small diameter, more mitochondria Have high oxygen supply Contain myoglobin (red pigment, binds oxygen) 2/13/09 151
152
Are mid-sized Have low myoglobin Have more capillaries than fast fiber, slower to fatigue 2/13/09 152
153
153 Figure 10–21
154
2/13/09 154 Table 10–3
155
White muscle: mostly fast fibers pale (e.g., chicken breast) Red muscle: mostly slow fibers dark (e.g., chicken legs) Most human muscles: mixed fibers pink 2/13/09 155
156
Muscle growth from heavy training: increases diameter of muscle fibers increases number of myofibrils increases mitochondria, glycogen reserves 2/13/09 156
157
Lack of muscle activity: reduces muscle size, tone, and power 2/13/09 157
158
158
159
Improves both power and endurance 2/13/09 159
160
Anaerobic activities (e.g., 50-meter dash, weightlifting): use fast fibers fatigue quickly with strenuous activity Improved by: frequent, brief, intensive workouts hypertrophy 2/13/09 160
161
Aerobic activities (prolonged activity): supported by mitochondria require oxygen and nutrients Improved by: repetitive training (neural responses) cardiovascular training 2/13/09 161
162
What you don’t use, you loose Muscle tone indicates base activity in motor units of skeletal muscles Muscles become flaccid when inactive for days or weeks 2/13/09 162
163
Muscle fibers break down proteins, become smaller and weaker With prolonged inactivity, fibrous tissue may replace muscle fibers 2/13/09 163
164
164
165
Cardiac muscle is striated, found only in the heart 2/13/09 165 Figure 10–22
166
Unlike skeletal muscle, cardiac muscle cells (cardiocytes): are small have a single nucleus have short, wide T tubules 2/13/09 166
167
have no triads have SR with no terminal cisternae are aerobic (high in myoglobin, mitochondria) have intercalated discs 2/13/09 167
168
Are specialized contact points between cardiocytes Join cell membranes of adjacent cardiocytes (gap junctions, desmosomes) 2/13/09 168
169
Maintain structure Enhance molecular and electrical connections Conduct action potentials 2/13/09 169
170
Because intercalated discs link heart cells mechanically, chemically, and electrically, the heart functions like a single, fused mass of cells 2/13/09 170
171
1. Automaticity: contraction without neural stimulation controlled by pacemaker cells 2. Variable contraction tension: controlled by nervous system 2/13/09 171
172
3. Extended contraction time 4. Prevention of wave summation and tetanic contractions by cell membranes 2/13/09 172
173
173
174
Forms around other tissues In blood vessels: regulates blood pressure and flow In reproductive and glandular systems: produces movements 2/13/09 174
175
In digestive and urinary systems: forms sphincters produces contractions In integumentary system: arrector pili muscles cause goose bumps 2/13/09 175
176
176
177
Nonstriated tissue 2/13/09 177 Figure 10–23
178
Different internal organization of actin and myosin Different functional characteristics 2/13/09 178
179
1. Long, slender, and spindle shaped 2. Have a single, central nucleus 3. Have no T tubules, myofibrils, or sarcomeres 4. Have no tendons or aponeuroses 2/13/09 179
180
5. Have scattered myosin fibers 6. Myosin fibers have more heads per thick filament 7. Have thin filaments attached to dense bodies 8. Dense bodies transmit contractions from cell to cell 2/13/09 180
181
1. Excitation–contraction coupling 2. Length–tension relationships 3. Control of contractions 4. Smooth muscle tone 2/13/09 181
182
Free Ca 2+ in cytoplasm triggers contraction Ca 2+ binds with calmodulin: in the sarcoplasm activates myosin light chain kinase Enzyme breaks down ATP, initiates contraction 2/13/09 182
183
Thick and thin filaments are scattered Resting length not related to tension development Functions over a wide range of lengths (plasticity) 2/13/09 183
184
Subdivisions: multiunit smooth muscle cells: connected to motor neurons visceral smooth muscle cells: not connected to motor neurons rhythmic cycles of activity controlled by pacesetter cells 2/13/09 184
185
Maintains normal levels of activity Modified by neural, hormonal, or chemical factors 2/13/09 185
186
186 Table 10–4
187
3 types of muscle tissue: skeletal cardiac smooth Functions of skeletal muscles 2/13/09 187
188
Structure of skeletal muscle cells: endomysium perimysium epimysium Functional anatomy of skeletal muscle fiber: actin and myosin 2/13/09 188
189
Nervous control of skeletal muscle fibers: neuromuscular junctions action potentials Tension production in skeletal muscle fibers: twitch, treppe, tetanus 2/13/09 189
190
Tension production by skeletal muscles: motor units and contractions Skeletal muscle activity and energy: ATP and CP aerobic and anaerobic energy 2/13/09 190
191
Skeletal muscle fatigue and recovery 3 types of skeletal muscle fibers: fast, slow, and intermediate Skeletal muscle performance: white and red muscles physical conditioning 2/13/09 191
192
Structures and functions of: cardiac muscle tissue smooth muscle tissue 2/13/09 192
Similar presentations
© 2024 SlidePlayer.com Inc.
All rights reserved.