Transcript bio 342 human physiology

S1
Characteristics: Location, cell shape, nuclei per cell, innervation,
connections to adjacent myofibers, arrangement of actin and myosin,
regulation of cross bridges, sources of Ca++, response to injury, twitch
duration, etc.
Different types of muscles for different tasks!
S2
Synonyms:
NMJ = neuromuscular junction
Myoneural junction
Motor end plate
S3
1Fig.AP
in motor axon releases sufficient
09.15
ACh for 1 AP in skeletal muscle.
Nicotinic
EPP
Myasthenia gravis and loss of nAChRs
S4
Terms: Myofiber, myofibril, myofilament
Fig. 09.11b
Thick myofilament = myosin
Thin myofilament = actin
S5
Fig. 09.12
High fAP leads
to accumulation
of Ca++ in
sarcoplasm
because Ca++
ATPase doesn’t
return all Ca++
to SR quickly
enough.
The concentration of free calcium is directly related to force
of contraction in skeletal muscle
Thus we need to understand the cellular mechanism of
contraction… cell biology flashbacks…
S6
YouTube Videos
Role of ATP in muscle
Creepy Muscle demo
Sarcomere contraction
Powerstoke in muscle I
S7
Fig. 09.08
Two roles of ATP:
1) Energy for
powerstroke &
2) Necessary for
detaching myosin
from actin
Crossbridge
cycling continues
as long as ATP
and Ca++ present.
S8
Classes of Myofibers based on Twitch Duration
Each skeletal muscle fiber express only one of
two different myosins isozymes:
• Fast twitch = rapid hydrolysis of ATP means
crossbridges cycle faster
• Slow twitch = slower hydrolysis, isozyme
catalyzes the reaction slower
Isozymes not modified by athletic training!
Contraction velocity also affected by load!
S9
Fig. 09.02
dArk band = aligned myosin filaments
lIght band = absence of myosin filaments
Myofilaments
S 10
S 11
Fig. 09.03
S 12
Fig. 09.04
S 13
Fig. 09.05a
S 14
Fig. 09.05b
Contracted
S 15
Fig. 09.05a
Image if the sarcomeres were stretched? How would the
number of cross bridges capable of binding to actin be
affected? How would the overlap affect the tension produced?
1QQ # 13 Answer one.
1. Suppose there was a mutation that rendered
troponin incapable of binding Ca++. Would
that embryo survive? Why or why not?
2. What would happen if you injected Ca++ into
a skeletal myofiber?
3. For our twitch recordings in lab, what events
(in the proper sequence) were occurring
during the latent period?
4. Why is peak tetanic tension 3-5 times greater
than peak twitch tension? How is Ca++
involved?
S 16
Fig. 09.16
S 17
Length-tension Relationship
So….. Tension produced by a
single myofiber varies
depending on
sarcomere length.
S 18
Muscle kinetics
Link to cytosolic calcium
concentration, release, and
reuptake?
S 19
Fig. 09.20
Why does this plateau?
So….. Tension produced by a single myofiber varies depending on frequency of Action Potentials.
Why is peak TETANIC tension so much greater than peak TWITCH tension?
S 20
Muscle Metabolism
• Classification of Myofiber types
– Speed of myosin ATPase
– Metabolic sources of ATP
– Fatigability
S 21
Classes of Myofibers based on Twitch Duration
Each muscle fiber express only one of two
different myosins isozymes:
• Fast twitch = rapid hydrolysis of ATP means
crossbridges cycle faster
• Slow twitch = slower hydrolysis, isozyme
catalyzes the reaction slower
Myosin isozymes not modified by athletic training!
S 22
Classes of Myofibers based on
Metabolic and Enzyme profiles
• Oxidative: at peak activity rely on full aerobic
cellular respiration
– many mitochondria, enzymes for oxidative
phosphorylation, numerous capillaries, lots of
myoglobin (red)
• Glycolytic: at peak activity rely on glycolysis
– few mitochondria, many glycolytic enzymes, large
store of glycogen, fewer capillaries, little
myoglobin (white)
Metabolic and Enzyme profiles CAN BE modified by athletic training!
S 23
3 Sources of ATP in muscle
Powerstroking &
Disconnecting crossbridges
Creatine phosphate, then oxidative phosphorylation (OP) from
glycogen, then OP from blood glucose, then blood fatty acids. If
intense, switch to glycolysis… then take a breather… oxygen debt
S 24
S 25
Type I
Type II A
Fig. 09.03
Type II B
S 26
S 27
Type I
What are the causes of
fatigue?
Type IIA
Depends on the type of
activity…
Type IIB
S 28
Causes of fatigue
• High intensity, short duration exercise
– Conduction failure in t-tubules
– Lactic acid accumulation
– Accumulation of ADP and inorganic phosphate
• Low intensity, long duration exercise
–
–
–
–
As above, and
Depletion of muscle glycogen
Low plasma glucose (hypoglycemia)
Dehydration
• Control pathways: “willpower”
– Common in couch potatoes
S 29
So what are the ways a muscle
(consisting of many myofibers)
increases tension?
S 30
Fig. 09.13
Motor unit = a single somatic motor neuron
and all the muscle fibers in innervates
S 31
But each motor unit
has myofibers of the
same type: I or IIA or
IIB.
S 33
Fig. 09.26
Relationship between
recruitment and
motor unit type
The Size Principle
Size of somatic
motoneuron cell
body
S 32
Increasing tension in a whole muscle
• Frequency of stimulation of motor neuron
• Activate larger motor units
• Recruitment: activate more motor units
• These factors also influence actual tension
– Fiber length (length-tension) relationship
– Fiber diameter
– Level of fatigue (state of activity)
Types of
Contractions
S 34
Isotonic =
Same tension
Isometric =
Same length
Aka Lengthening contraction
S 35
Response to training
• Resistance training
Type II change enzyme profiles: II A to II B
Type II add more actin and myosin
Type II increase cross-sectional area (hypertrophy)
• Endurance training
– Type I increases vascularity
– Type I increase number of mitochondria
S 36
Read section of
King et al., 1999
that deals with
analysis of muscle
biopsy material in
subjects taking
Andro or placebo
while resistance
training.
What changes
were expected?
What changes
were observed?
Fig. 09.24b
S 37
Consider blood flow to skeletal muscles during isometric contractions.
Consider blood pressure during isometric contractions.
S 38
The benefits of using trekking poles?
S 39
Chapter 9 B Properties of
Smooth Muscle
How does smooth muscle differ from skeletal muscle?
(innervation, membrane potentials, excitation-contraction coupling, twitch
duration, fatigue, etc. (Table 9-6 p.287)
What are the features of membrane potential of smooth muscle?
(pacemakers and slow waves)
What are the differences between single-unit and multi-unit smooth muscle?
(location, spread of excitation)
Who cares about smooth muscles?
S 40
Excitation-contraction coupling in Smooth Muscles
Figure 9.34
from SR and influx during Action Potential or graded potential
Ca++
Graded potentials
result in graded
contractions
Slow twitch of SM
due to slow action
of myosin ATPase.
Lack troponin
Special situation:
Dephosphorylation &
latch bridge
S 41
Comparison of Twitch Duration
Latchbridge =latch state
Thankful for latch state!
Crucial for long-term tension of
sphincters.
S 42
Comparison of Single-Unit and
Multi-Unit Smooth Muscles
Slow waves and pacemaker potentials
Intestinal tract, uterus, small diameter blood vessels
Large airways of lungs, large arteries, ciliary muscle
Often with pacemaker cells
Control of membrane potential by neurotransmitters, hormones, local factors
for some smooth muscles (02, NO, pH, stretch, vasodilators ….)
S 43
Cardiac
Myofibers
Intercalated Discs: mechanical attachments of cardiac myofibers to
each other, with gap junctions (electrical synapses) to conduct AP
Analogy: Falling dominoes
S 44
Plateau phase
S 45
Why no tetanic contractions of cardiac muscle?
S 46
Figure 12.17
ExcitationContraction
Coupling
Calcium-induced calcium release
What ends the twitch?
Ca++ channels blockers:
•How and where do they work?
•When are they used?
S 47
this table p. 287
Fig.Know
09.06