Structure and Function of the Muscular, Neuromuscular, Cardiovascular, and Respiratory Systems

1
Structure and Function of the Muscular,
Neuromuscular, Cardiovascular, and Respiratory
Systems
chapter 1
Structure and Function of the Muscular,
Neuromuscular, Cardiovascular, and Respiratory
Systems
Gary R. Hunter, PhD, CSCS, FACSMRobert T.
Harris, PhD
2
Chapter Objectives

• Describe the macrostructure and micro-structure
  of muscle.
• Describe the sliding-filament theory.
• Describe the characteristics of different muscle
  fiber types.
• Describe the characteristics of the
  cardio-vascular and respiratory systems.

3
Section Outline

• Muscular System
• Macrostructure and Microstructure
• Sliding-Filament Theory of Muscular Contraction
• Resting Phase
• Excitation-Contraction Coupling Phase
• Contraction Phase
• Recharge Phase
• Relaxation Phase

4
Muscular System

• Macrostructure and Microstructure
• Each skeletal muscle is an organ that contains
  muscle tissue, connective tissue, nerves, and
  blood vessels.
• Fibrous connective tissue, or epimysium, covers
  the body's more than 430 skeletal muscles.

5
Schematic Drawing of a Muscle

• Figure 1.1 (next slide)
• Schematic drawing of a muscle illustrating three
  types of connective tissue
• Epimysium (the outer layer)
• Perimysium (surrounding each fasciculus, or group
  of fibers)
• Endomysium (surrounding individual fibers)

6
Figure 1.1
7
Motor Unit

• Figure 1.2 (next slide)
• A motor unit consists of a motor neuron and the
  muscle fibers it innervates.
• There are typically several hundred muscle fibers
  in a single motor unit.

8
Figure 1.2
9
Muscle Fiber

• Figure 1.3 (next slide)
• Sectional view of a muscle fiber

10
Figure 1.3
11
Microstructure
Modified from Squire, pg. 66
12
Myosin and Actin

• Figure 1.4 (next slide)
• The slide shows a detailed view of the myosin and
  actin protein filaments in muscle.
• The arrangement of myosin (thick) and actin
  (thin) filaments gives skeletal muscle its
  striated appearance.

13
Figure 1.4
14
Sarcomere functional unit of striated muscle
Z line
Electron micrograph
15
(No Transcript)
16
Figure 5. Main Intermediate Filaments and
Cytoskeletal Proteins Linking the Extracellular
Matrix with the Structural Muscle Proteins
Associated with Mutations Causing Cardiac and
Skeletal Myopathy. In the mature cardiac and
skeletal muscle, the Z bands hold together the
actin filaments and have a fundamental role in
the transmission of tension throughout the
myofibril. The desmin filaments, consisting of
10-nm-wide intermediate filaments, encircle the Z
bands and are fastened to them and to one another
by plectin filaments.619 Desmin (from the Greek
noun desmos, meaning link or bond) mechanically
integrates the contractile actions of the muscle
fiber laterally by linking the individual
myofibrils at the Z-band level, as shown for
three adjacent myofibrils, and longitudinally by
linking the Z bands to the sarcolemma and nuclei
(along with other intermediate-filamentassociated
proteins).6 The heat-shock protein B-crystallin
protects, or chaperones, the desmin filaments
from stress-induced damage. Desmin, along with
B-crystallin and plectin, forms an organized
network at the Z-band level that protects the
structural integrity of the myofibrils during
mechanical stress.16 Mutations in desmin,
B-crystallin, and plectin1420 cause fragility of
the myofibrils and lead to their destruction
after repetitive mechanical stress. Mutations in
other cytoskeletal proteins, including
dystrophin, actin, the sarcoglycan complex,21 the
nuclear protein emerin, and the intermediate
nuclear filaments lamin A and C,22 are also
associated with cardiomyopathy and skeletal
myopathy. Dalakas et al. 342 (11) 770, Figure
5     March 16, 2000
cytoskeleton
17

• Figure 1. Functional Bypass of Genetic Defect by
  Enhanced Glycosylation.
• Under normal conditions, glycoproteins gain
  complex carbohydrate moieties during processing
  as they are transported to the cell membrane
  (Panel A). There, the carbohydrate components
  help bind to ligands in the extracellular milieu.
  In the case of skeletal muscle, the glycosylation
  of -dystroglycan is critical to its binding to
  laminin, agrin, and perlecan. Defects in
  glycosylation lead to truncated carbohydrate
  chains (Panel B). Abnormal glycosylation
  interferes with the interactions between normal
  -dystroglycan and matrix proteins and may be the
  reason for muscle cell degeneration in this group
  of muscular dystrophies. Barresi et al.2 showed
  that overexpression of a glycosyltransferase
  (LARGE) can hyperglycosylate -dystroglycan and
  thereby enhance its binding to matrix proteins,
  even though the pattern of glycosylation may be
  abnormal (Panel C). This restoration of function
  as a result of enhanced glycosylation may be an
  effective treatment for a variety of muscular
  dystrophies. Rando 351 (12) 1254, Figure
  1     September 16, 2004

18
Figure 1. Components of Myocyte Cytoarchitecture
(Panel A) and Mutations Causing Dilated
Cardiomyopathy and Conduction-System Disease or
Autosomal Dominant EmeryDreifuss Muscular
Dystrophy (Panel B). Mutations in the rod domain
of the lamin A/C gene cause isolated dilated
cardiomyopathy and conduction-system disease,
presumably through perturbed interactions with
nuclear or cytoplasmic constituents (Panel A).
Other cytoskeletal molecules implicated in the
pathophysiology of human dilated cardiomyopathy
include actin, dystrophin, and the
dystrophin-associated glycoprotein
complex.12,23,24,25,26,27,28 Interactions between
lamins A and C and cytoskeletal or sarcomere
proteins are unknown. Conduction-system disease
is a common feature of EmeryDreifuss muscular
dystrophy caused by defects in the head or tail
domain of the lamin gene or by emerin mutations.
Mutations causing dilated cardiomyopathy and
conduction-system disease or autosomal dominant
EmeryDreifuss muscular dystrophy are distributed
in distinct domains of the lamin dimer (Panel B).
Lamins A and C have identical structures
throughout the amino-terminal head (NH3),
-helical rod domain, and proximal
carboxyl-terminal tail (COOH), but they differ in
their distal amino acids (lamin A is shown in
gray, and lamin C is shown in black). Mutations
in the rod domain (Arg60Gly, Leu85Arg, Asn195Lys,
and Glu203Gly) cause dilated cardiomyopathy and
conduction-system disease without skeletal
myopathy the mutation at the carboxyl terminal
(Arg571Ser) is associated with subclinical
skeletal-muscle disease. Mutations that cause
EmeryDreifuss muscular dystrophy (Gln6Stop,
Arg453Trp, Arg527Pro, and Leu530Pro) do not
affect the -helical rod domain. Fatkin et al.
341 (23) 1715, Figure 1     December 2, 1999
19
Hunter and Chien 341 (17) 1276, Figure
3     October 21, 1999
Figure 3. Primary Structural Components of the
Linkage between the Cytoskeleton and the
Extracellular Matrix, Including Actin, the
DystrophinGlycoprotein Complex, and Laminin-2
(Merosin). Genetic defects in these components
lead to dilated cardiomyopathy, with or without
associated skeletal myopathy. This complex is
physically associated with the Z-disk of cardiac
myocytes, the Z-disk components desmin
(associated with dilated cardiomyopathy in humans
and mice) and -actinin, and a muscle-specific
cytoskeletal protein (MLP) (associated with
dilated cardiomyopathy in mice).23 The question
mark indicates an unknown factor.
20
Muscular Dystrophy A frequently fatal disease of
muscle deterioration

• Muscular dystrophies have in the past been
  classified based on subjective and sometimes
• subtle differences in clinical presentation, such
  as age of onset, involvement of particular
• muscles, rate of progression of pathology, mode
  of inheritance.

• Since the discovery of dystrophin, numerous
  genetic disease loci have been linked to protein
• products and to cellular phenotypes, generating
  models for studying the pathogenesis of the
• dystrophies.

• Proteins localized in the nucleus, cytosol,
  cytoskeleton, sarcolemma, and ECM.

Cohn and Campbell (2000) Muscle Nerve
231459-1471.
21
Dystrophin function transmission of force to
extracellular matrix
DGC dystrophin dystroglycan (a and
b) sarcoglycans (a, b, g, d) syntrophins (a,
b1) dystrobrevins (a, b) sarcospan laminin-a2
(merosin)
(Some components of the dystrophin
glycoprotein complex are relatively recent
discoveries, so one cannot assume that all
players are yet known.)
Cohn and Campbell (2000) Muscle Nerve
231459-1471.
22
Key Point

• The discharge of an action potential from a motor
  nerve signals the release of calcium from the
  sarcoplasmic reticulum into the myofibril,
  causing tension development in muscle.

23
Muscular System

• Sliding-Filament Theory of Muscular Contraction
• The sliding-filament theory states that the actin
  filaments at each end of the sarcomere slide
  inward on myosin filaments, pulling the Z-lines
  toward the center of the sarcomere and thus
  shortening the muscle fiber.

24
Contraction of a Myofibril

• Figure 1.5 (next slide)
• (a) In stretched muscle the I-bands and H-zone
  are elongated, and there is low force potential
  due to reduced cross-bridgeactin alignment.
• (b) When muscle contracts (here partially), the
  I-bands and H-zone are shortened.
• (c) With completely contracted muscle, there is
  low force potential due to reduced
  cross-bridgeactin alignment.

25
Figure 1.5
26
Myosin is a molecular motor
Myosin is a hexamer 2 myosin heavy chains 4
myosin light chains
27
Shortening velocity dependent on ATPase
activity Different myosin heavy chains (MHCs)
have different ATPase activities. There are at
least 7 separate skeletal muscle MHC
genesarranged in series on chromosome 17. Two
cardiac MHC genes located in tandem on chromosome
14. The slow b cardiac MHC is the predominant
gene expressed in slow fibers of mammals.
Goldspink (1999) J Anat 194323-334.
28
http//health.howstuffworks.com/muscle2.htm
29
Muscular System

• Sliding-Filament Theory of Muscular Contraction
• Resting Phase
• Excitation-Contraction Coupling Phase
• Contraction Phase
• Recharge Phase
• Relaxation Phase

30
Section Outline

• Neuromuscular System
• Activation of Muscles
• Muscle Fiber Types
• Motor Unit Recruitment Patterns During Exercise
• Preloading
• Proprioception
• Muscle Spindles
• Golgi Tendon Organs
• Older Muscle

31
Neuromuscular System

• Activation of Muscles
• Arrival of the action potential at the nerve
  terminal causes the release of acetylcholine.
  Once a sufficient amount of acetylcholine is
  released, an action potential is generated across
  the sarco-lemma, and the fiber contracts.
• The extent of control of a muscle depends on the
  number of muscle fibers within each motor unit.
• Muscles that function with great precision may
  have as few as one muscle fiber per motor
  neuron.
• Muscles that require less precision may have
  several hundred fibers served by one motor
  neuron.

32
Key Term

• all-or-none principle All of the muscle fibers
  in the motor unit contract and develop force at
  the same time. There is no such thing as a motor
  neuron stimulus that causes only some of the
  fibers to contract. Similarly, a stronger action
  potential cannot produce a stronger contraction.

33
Stimulated Motor Unit

• Figure 1.6 (next slide)
• Twitch, twitch summation, and tetanus of a motor
  unit
• a single twitch
• b force resulting from summation of two
  twitches
• c unfused tetanus
• d fused tetanus

34
Figure 1.6
35
Neuromuscular System

• Muscle Fiber Types
• Type I (slow-twitch)
• Type IIa (fast-twitch)
• Type IIab (fast-twitch) now named as Type IIax
• Type IIb (fast-twitch) now named as Type IIx

36
Table 1.1
37
Key Point

• Motor units are composed of muscle fibers with
  specific morphological and physio-logical
  characteristics that determine their functional
  capacity.

38
Neuromuscular System

• Motor Unit Recruitment Patterns During Exercise
• The force output of a muscle can be varied
  through change in the frequency of activation of
  individual motor units or change in the number of
  activated motor units.

39
Table 1.2
40
Neuromuscular System

• Preloading
• Occurs when a load is lifted, since sufficient
  force must be developed to overcome the inertia
  of the load
• Proprioception
• Information concerning kinesthetic sense, or
  conscious appreciation of the position of body
  parts with respect to gravity
• Processed at subconscious levels

41
Key Point

• Proprioceptors are specialized sensory receptors
  that provide the central nervous system with
  information needed to maintain muscle tone and
  perform complex coordi-nated movements.

42
Neuromuscular System

• How Can Athletes Improve Force Production?
• Recruit large muscles or muscle groups during an
  activity.
• Increase the cross-sectional area of muscles
  involved in the desired activity.
• Preload a muscle just before a concentric action
  to enhance force production during the subsequent
  muscle action.
• Use preloading during training to develop
  strength early in the range of motion.

43
Force Production Influencing Factors

• Motor Unit Recruitment
• Rate of stimulation of the motor unit (rate
  coding)
• Type of motor units activated (FT or ST)
• Preloading
• Cross-sectional area (Muscle size)
• Velocity of shortening
• Angle of pennation (acute or joint angle and
  fixed or inherent)
• Sarcomere and muscle length
• Initial muscle length
• Speed of muscle action
• Shortening or lengthening contractions

44
Neuromuscular System

• Proprioception
• Muscle Spindles
• Muscle spindles are proprioceptors that consist
  of several modified muscle fibers enclosed in a
  sheath of connective tissue.

45
Muscle Spindle

• Figure 1.7 (next slide)
• When a muscle is stretched, deformation of the
  muscle spindle activates the sensory neuron,
  which sends an impulse to the spinal cord, where
  it synapses with a motor neuron, causing the
  muscleto contract.

46
Figure 1.7
47
Neuromuscular System

• Proprioception
• Golgi Tendon Organs (GTO)
• Golgi tendon organs are proprioceptors located in
  tendons near the myotendinous junction.
• They occur in series (i.e., attached end to end)
  with extrafusal muscle fibers.

48
Golgi Tendon Organ

• Figure 1.8 (next slide)
• When an extremely heavy load is placed on the
  muscle, discharge of the GTO occurs.
• The sensory neuron of the GTO activates an
  inhibitory interneuron in the spinal cord, which
  in turn synapses with and inhibits a motor neuron
  serving the same muscle.

49
Figure 1.8
50
Neuromuscular System

• Older Muscle
• Muscle function is reduced in older adults.
• Reductions in muscle size and strength are
  amplified in weight-bearing extensor muscles.
• Muscle atrophy with aging results from losses in
  both number and size of muscle fibers, especially
  Type II muscle fibers.
• Inactivity plays a major role but cannot account
  for all of the age-related loss of muscle and
  function.

51
Section Outline

• Cardiovascular System
• Heart
• Valves
• Conduction System
• Electrocardiogram
• Blood Vessels
• Arteries
• Capillaries
• Veins
• Blood

52
Cardiovascular System

• Heart
• The heart is a muscular organ made up of two
  interconnected but separate pumps.
• The right ventricle pumps blood to the lungs.
• The left ventricle pumps blood to the rest of the
  body.

53
Heart and Blood Flow

• Figure 1.9 (next slide)
• Structure of the human heart and course of blood
  flow through its chambers

54
Figure 1.9
55
Cardiovascular System

• Heart
• Valves
• Tricuspid valve and mitral (bicuspid) valve
• Aortic valve and pulmonary valve
• Valves open and close passively, depending on the
  pressure gradient
• Conduction System
• Controls the mechanical contraction of the heart

56
Electrical Conduction System

• Figure 1.10 (next slide)
• The electrical conduction system of the heart

57
Figure 1.10
58
Cardiac Impulse

• Figure 1.11 (next slide)
• Transmission of the cardiac impulse through the
  heart, showing the time of appearance (in
  fractionsof a second) of the impulse in
  different parts of the heart

59
Figure 1.11
60
Cardiovascular System

• Heart
• Electrocardiogram
• Recorded at the surface of the body
• A graphic representation of the electrical
  activity of the heart

61
Electrocardiogram

• Figure 1.12 (next slide)
• Normal electrocardiogram

62
Figure 1.12
63
Cardiovascular System

• Blood Vessels
• Blood vessels operate in a closed-circuit system.
  
• The arterial system carries blood away from the
  heart.
• The venous system returns blood toward the heart.

64
Distribution of Blood

• Figure 1.13 (next slide)
• The slide shows the arterial (right) and venous
  (left) components of the circulatory system.
• The percent values indicate the distribution of
  blood volume throughout the circulatory system at
  rest.

65
Figure 1.13
66
Cardiovascular System

• Blood Vessels
• Arteries
• Capillaries
• Veins

67
Cardiovascular System

• Blood
• Hemoglobin transports oxygen and serves as an
  acidbase buffer.
• Red blood cells facilitate carbon dioxide removal.

68
Key Point

• The cardiovascular system transports nutrients
  and removes waste products while helping to
  maintain the environment for all the bodys
  functions. The blood transports oxygen from the
  lungs to the tissues for use in cellular
  metabolism, and it transports carbon dioxide from
  the tissues to the lungs, where it is removed
  from the body.

69
Section Outline

• Respiratory System
• Exchange of Air
• Exchange of Respiratory Gases

70
Respiratory System

• Figure 1.14 (next slide)
• Gross anatomy of the human respiratory system

71
Figure 1.14
72
Respiratory System

• Exchange of Air
• The amount and movement of air and expired gases
  in and out of the lungs are controlled by
  expansion and recoil of the lungs.

73
Expiration and Inspiration

• Figure 1.15 (next slide)
• The slide shows contraction and expansion of the
  thoracic cage during expiration and inspiration,
  illustrating diaphragmatic contraction, elevation
  of the rib cage, and function of the
  intercostals.
• The vertical and anteroposterior diameters
  increase during inspiration.

74
Figure 1.15
75
Respiratory System

• Exchange of Respiratory Gases
• The primary function of the respiratory system is
  the basic exchange of oxygen and carbon dioxide.