Muscle Physiology Midterm 1 Flashcards
1
Q
What are the 4 functions of muscles?
A
Generate force, fuel storage, temperature regulation, and force absorption.
2
Q
2 examples of isotonic contractions
A
concentric and eccentric
3
Q
Shortening contraction?
A
Concentric (fibres move closer to each other; up phase in a bicep curl)
4
Q
Lengthening contraction?
A
Eccentric (fibres move away from each other; lowering phase in bicep curl)
5
Q
Isometric contraction?
A
Muscle contracts, but muscle fibres are static/don’t move
6
Q
What type of isotonic contraction generates more force?
A
Eccentric contraction generate more force…can lower much more weight than we can curl or squat
7
Q
What type of muscle contraction causes the most damage?
A
Eccentric/lengthening…downhill running = muscles always shortening = painful
8
Q
Percentage muscle makes up of total body mass?
A
30-40%…sometimes closer to 50
9
Q
In order to maintain muscle mass, what must be equal?
A
The rate of protein synthesis and the rate of protein degradation
10
Q
During muscular hypertrophy what is occurring?
A
Less protein breakdown and more protein synthesis (extracting more AA from diet to build more muscle/protein) results in NET muscle growth
11
Q
What happens during muscular atrophy?
A
Protein degradation exceeds protein synthesis…AA used as a fuel source for other metabolic processes and to support other tissues
12
Q
3 fuels in muscle
A
proteins, glycogen, lipid droplets
13
Q
Why is it a good thing muscle protein is broken down for energy in times of need?
A
Muscles can still contract (just not with as much force) even at reduced protein levels, but my sacrificing itself, the muscle allows other systems/organs, like the kidney to continue working
14
Q
Shivering thermogenesis?
A
Get cold, muscles contract. Overal mechanical efficiency is on about 20% with the balance of energy given off as heat.
15
Q
Nonshivering thermogenesis?
A
UCP and SR Ca-ATPase
16
Q
How does uncoupling proteins generate heat?
A
Dissipate the protein gradient in the inner mitchondrial membrane created by food stuffs, by allowing the H ions to flow back into the matrix without going through the ATP-synthase molecules, releasing the energy as heat instead
17
Q
How do UCP increase BMR?
A
Food is being used to create gradient, but if no ATP is made from this gradient, more energy (food) must be used to create enough of a gradient to make ATP
18
Q
How do muscles work as force absorbers?
A
Protect the skeleton and internal organs
19
Q
What is muscle made of?
A
Approximately 20-30 thousand proteins
20
Q
Is muscle homogeneous?
A
NO…heterogeneous
21
Q
What makes a muscle heterogeneous?
A
Different proteins (pumps, channels, enzymes, etc), in different concentrations (more myosin than UCPs) and forms (different myosin isoforms,etc)
22
Q
What determiens the specialized function and characteristics of a muscle cell?
A
Amount and patterns of expressions of various Protein isoforms
23
Q
Are muscles homogeneous in structure/function?
A
YES! All have myosin, actin, Ca pumps, etc. Just in different amounts
24
Q
Is muscle adaptable?
A
YES. Depends on stress placed on muscle. Example, 12-18 hours after a limb is casted, already there is an increase in protein breakdown and wasting and concentrations of proteins are already changing, like mitochondrial proteins
25
Contractile proteins?
Actin and myosin
26
Bulk of sacroplasm in muscle is made up of ?
Actin and myosin (2/3 dry mass)
27
Actomyosin ATPase does what?
Allws for interaction between actin and myosin. Myosin is an ATPase that uses ATP to chanfe shape of myosin molecule and allot connection with actin
28
Regulatory proteins?
Troponin and tropopmyosin
29
Role of regulatory proteins?
Regulate actin/myosin interactions (blocking function), so control contraction/relaxation cyle
30
Why is Ca2+ regulated?
If it wasn't, contraction would be happening all the time.
31
Purpose of SR?
ER in other cells; storage, release and uptake of Ca2+; uses CA2+ ATPase to uptake CA into SR...used ATP because pumping Ca2+ against concentration gradient
32
What happens when calcium concentrations increase in the muscle fibre?
Ca binds to troponin, causing it to change shape and remove tropomyosin's blocking action, allowing for strong actin-myosin interaction (increase in force)
33
How is muscle an excitable tissue?
Innervated by a motoneuron, which releases Ach onto motor endplate, causing a depolarization.
34
Purpose of t-tubules?
Propagation of APs into muscle cell
35
5 cellular systems of muscle
1. Contractile system (myofibrils) 2. Ca2+ Regulation System 3. Excitation System--Electrical Potential 4. Metabolic/Energy System 5. Nucleus/multi-nucleation
36
The specific term used to refer to the ability of skeltal muscle to adapt to stress?
Plasticity
37
What is the function of SERCA?
UPTAKE of Ca2+
38
3 energy systems in muscle
PCr/High Energy Phosphate transfer system, Glycolytic system in cytosol of 11 reactions to form ATP from carbs, Oxidative Phosphorylation in mitochondria to make ATP from carbs, fats, AA
39
Broad term for enzymes that split ATP into ADP and Pi?
ATPase
40
Why are muscles multi-nucleated?
Need LOTS of proteins and also helps allow the cells to be elongated, which is better than many single nucleated cells working independently
41
Can muscle fibres regenerate?
NO, but can gain more nuclei, which allows for more proteins to be synthesized
42
% of ATP Actomyosin ATPase uses for crossbridge cycling?
70-80%
43
% ATP Ca2+ ATPase uses to pump calcium unto the SR?
20-30%
44
% ATP sarcolemma ATPase uses to maintain Na+/K+ gradient?
less then 10%
45
Purpose of t-tubules?
Allow AP to go into the muscle fibre, not just along the sarcolemma
46
Triad of the reticulum consists of?
2 terminal cisternae and tranverse tubule
47
2 types of mitchondria in muscle
SS mitochondria near the sarcolemma and IMF mitochondria between fibres
48
Purpose of triad of the reticulum?
Where AP is linked to calcium release...where electrical event is turned into chemical event
49
Does the sarcolemma cover the nuclei?
YES...want genetic information inside the cell
50
Skeletal muscle is composed of?
Connective tissues, muscle fasicles, blood vessels, nerves
51
Muscle fasicles are composed of?
individual muscle fibres/cells
52
Muscle fibres are composed of?
Sarcolemms, t-tubules, sarcoplasm, and multiple nuclei
53
Sarcoplasm consists of?
SR, myofibrils, mitochondria, gylcogen granules
54
Myofibrils are composed of?
Troponin, actin, tropomyosin, myosin, titin, nebulin
55
Thin filaments are composed of?
Actin, tropomyosin, troponin
56
Thick filaments are made of?
Myosin
57
Thin and thick filaments are organized into?
Sarcomeres
58
Cytoskeleton proteins?
Titin and nebulin
59
Purpose of cytoskeleton proteins?
Provide structure
60
What is the smallest function unit (can see length change) unit of a muscle?
Sarcomere...about 2.5 micrometres, but can change by stretching/shortening of sarcomeres
61
What is the most abundant molecule in skeletal muscle?
Myosin
62
Why is myosin considered a motor protein?
Converts chemical energy in ARP into the mechanical energy of movement
63
What does a certain myosin isoform determine?
Contractile speed (Vmax)
64
How many heavy chains does a myosin molecule have?
2 HC that intertwine to form a long coiled tail and a pair of heads that bind actin, forming cross bridges
65
How many reactive sites does myosin have and for what?
1 for actin and 1 for nucleotide (ATP) binding site
66
How many light chains are associated with the heavy change of each myosin head?
2...phoshphorylatable light chain and alkali light chain
67
Isoforms of the alkali light chain?
2 isoforms (LC1 and LC3)
68
Purpose of the alkali light chain?
Provides structural stability to cross bridge and regulates myosin ATPase activity (dependent on if it is LC1 or LC3)
69
Alkali light train is also known as?
The ESSENTIAL light chain
70
Phosphorylatable light chain is also known as?
The REGULATORY light chain (LC2)
71
Purpose of phosphorylatable light chain?
As Ca2+ is released during muscle activation, some of the Ca2+ can activate myosin light chain kinase, resulting in the phosphorylation of the P light chain, which can increase force and rate of force development
72
How many myosin molecule makes up a thick filament?
250 molecules, each thick filament arranged so bipolar myosin heads clustered at the ends and contral region is a bundle of myosin tails (H zone)
73
2nd most abundant protein in muscle
actin
74
Actin is composed of?
Small globular units (G action) that form long strands of fibrous actin (F actin)
75
Actin filament is formed by?
2 strands of F actin in coiled coil
76
How many active sites and for what does a G actin molecule have?
2 active site to which myosin heads will bind during contraction
77
Shape of tropomyosin?
long, rod-shaped, double-stranded, helical protein that is wrapped about the long axis of the actin backbone
78
Purpsoe of tropomyosin?
Serves to block the active site on actin, thereby inhibiting action and myosin from binding under resting conditions (Steric Blocking Model)...muscle contraction cannot occur
79
Troponin is a complex of how many polypeptides/subunits?
3
80
3 types of troponin?
Tropomyosin binding (T), inhibitory binding (I), and calcium-binding (C)
81
Job of T troponin?
Positions the 3 subunit complex of troponin on thin filament
82
Job of troponin I>
Binds to actin and inhibits interaction of actin and myosin
83
Job of troponin C?
Binds up to 4 Ca2+ and with Ca2+ bound, relieves inhibition of myosin binding to action by sliding troponin I out of the way, what moves tropomyosin and frees up the active site to allow strong cross bridges between actin and myosin
84
How many troponin complexes for every actin monomer?
7 troponin complexes for every 7 actin monomers
85
How many thin filaments surround each thick filament?
6
86
How many thick filaments surround each thin filament?
3
87
I-band consists of?
Thin filaments only
88
A band consists of?
Thin and thick filaments
89
H-zone consists of?
Tails of myosin/thick filaments only
90
Purpose of M line?
Keeps thick filaments in position and proper spacing. Also holds them in a regular hexagonal lattice
91
Purpose of A disk?
Keeps thin filaments in position
92
Purpose of alpha actinin?
Actin cross-linking protein in Z-disk region that anchors thin (actin) filaments, 2 isoforms
93
Purpose of desmin?
Conect 2 sarcomeres from adjacent myofibrils
94
Purpose of nebulin?
An ineleastic (rigid) giant protein that lies alongside think filaments and attaches to Z-dosk...helps align the actin filaments of the sarcomere, which stops them from being "floppy"
95
Purpose of titin?
Huge elastic molecule that stretched from 1 Z-disk to next M-line (1/2 a sarcomere), stabilizes position of contractile filaments (keeps thick filaments in middle between 2 z-lines for optimal length to generate force), and its elasticity returns stretched muscles to resting length
96
3rd most abundant protein in muscle?
TITIN
97
Major protein damaged during eccentric loading?
TITIN...actually breaks, which causes some sarcomeres not to return to optimal resting spot, so not optimum amount of myosin.actin interaction, so not enough force
98
Proteins at the M-line?
M protein and myomesin
99
Purpose of dystrophin?
Flexible, elongated actin-binding protein that anchors superficial myofibrils to sarcolemms, which allows for even distribution of force across the sarcolemms to avoid tearing of the membrane
100
Largest protein in body?
TITIN
101
Largest gene in the body codes for?
Dystrophin
102
Scientist that discovered sliding filament theory?
Huxley inn 1954
103
Basis of sliding filament theory?
Overlapping muscle filaments of fized lengths (thick and thin filaments slide past each other in an energy-requiring process, resulting in muscle contraction
104
During muscle contraction what shortens in the sarcomere?
H-zone nad I-band shorten, as z disks come closer together
105
What remains constant during muscle contraction?
A band
106
A band represents the length of?
Thick filaments (250 myosin molecules put together)
107
Myosin molecule consists of?
2 heavy chains intertwined to form a long coiled tail and a pair of heads that bind actin, forming cross bridges. Each head has 2 binding sites and 2 light chains associated with it.
108
2 thin filaments consist of?
2 strands of F-actin molecules in a coil with troponin subunits every 7 actin and tropomyosin wrapped about the long axis of the actin backbone
109
Excitation-Contraction coupling?
The sequence of events by which an action potential at the sarcolemms (an electrical event) initiates the sliding of the myofilaments, resulting in contraction (a mechanical event)
110
Steps on excitation-contraction coupling?
AP generated in MN, which releases ACh at NMJ, starting depolrization of sarcolemms. AP conducted along sarcolemma and into t-tubules. AP triggers Ca2+ release from the SR. Ca2+ binds to Troponin C, relieving troponin C, allowing tropomyosin to move from the actin active site. Strong cross bridges between actin and myosin. The power stroke of myosin moves actin filaments past it and the muscle contraction
111
Relaxation in muscle?
Excitation (neural input) stops and Ca2+ is pumped back into SR by SERCA. Decrease in cystolic Ca2+ causes Troponin ! to go back to original spot, placing tropomyosin back to covering actin binding site. Binding site is blcoked so the actin and myosin dissociate and the muscle relaxes
112
Can a muscle contract without an AP?
Yes, just needs calcium
113
The Steric Blocking Model?
States that the regulatory protein, tropomyosin, exerts a blocking function between actin and myosin effectively preventing their interaction. Essentially, there's NO actin-myosin interaction possible at low Ca2+ levels and role of calcium is simply to control the movement of TM in and out of blocking position
114
Kinetic studies show what contradictory evidence against the Steric Blocking Model>
Myosin can bind actin in 2 steps...an initial weak bound state (even at low Ca2+) and a strongly bond or rigor-like state in the presence of high Ca2+
115
TM movement into grovve of teh F-actin helix results in?
An increase in the number of myosin heads attached to actin
116
Calcium regulates both what and what?
Both the attachment of myosin ot actin and the transition from weak to strong binding states
117
The Kinetic Model?
Is based on the observation that actin-myosin can combine in weak binding at low Ca2+, and therefore the steric blocking mod is not entirely valid, although, there can still be some steric blocking. Rather, a KINETIC STEP in actin-myosin is involved, working through ATPase activity but results in transition from weak to strong binding
118
In An intact muscle, the initial event that is needed to begin contraction (not force generation) is?
Generation of an AP
119
What is responsible for the transition from weak to strong binding?
Increase in cystolic Ca2+ results In Myosin releasing Pi, allowing for strong attachment betwee actin and myosin because tropomyosin is out of blocking position
120
Steps on the Kinetic Model?
Myosin can bind to TN-TM-Actin both in the presence and absence of activating calcium levels, but activating calcium levels enhance interaction. Binding of Ca2+ to TN-C overcomes the inhibition of TN-I. TM filament moves. Activation of TN-TM-Actin (open binding site on actin). M-ADP-Pi binding to TN-TM-Actin* overcomes the rate limiting step of myosin ATP hydrolysis with release of Pi molecule. M-ADP binds the thin filament with a higher affinity and muscle contraction proceeds
121
What is the cross-bridging cycle?
The cyclic events that are necessary for the generation of force within the myosin heads during muscle contraction
122
Event responsible for the power stroke?
Release of ADP
123
Cross bridge cycling biochemical events?
Ca2+ activates Thin Filament, which alters ATPase to release Pi. Release of Pi is responsible for transition from weak to strong binding. Release of ADP responsible for power stroke,. ATP binding results in detachment from actin and/or weak binding
124
Sarcolemma?
Outer surface of plasma membrane that surrounds the entire cell
125
T-tubules?
Invaginations of the sarcolemma into the fibers interior along a line vertical to the fibre axis. Lumen of the t-tubule system is continuous with the extracellular space
126
Where are t-tubules located in sarcomere?
Near border of A-I junction in sarcomere and connects with Z-line of the myofibrils via intermediate filaments called desmin
127
Composition of sarcolemma and t-tubules?
Phospholipid bilayer with a variety of specialized proteins (channels, pumps, transporters, receptors, etc)
128
How is Ca2+ released from SR?
AP travels down t-tubules trips off DHPR, which is physically connected to RyR on the SR, causing them to open ad release Ca2+ into cytosol
129
What is resting membrane potential difference?
An electrical gradient between the extracellular fluid and the intracellular fluid
130
For sarcolemms and the T-tubules' membrane potentials are determined essentially by what 3 ions?
Na+, K+, and Cl-
131
What 2 factors contribute to the net membrane potential?
Concentration gradient across the membrane (how many ions are where) and membrane permeability (more permeable to some ions than others, can change permeability by opening/closing ion channels)
132
Extracellular, intracellular concentrations of Na+?
150 Extracellular mM and 15 Intracellular mM
133
What is the extracellular and intracellular concentrations of K+?
5 mM Extracellular and 150 mM intracellular
134
What is the extracellular and intracellular concentrations of Cl-?
123 mM Extracellularly and 4.2 mM Intracellularly
135
What is equilibrium potential?
The embrane potential difference that exactly opposes the concentration gradient of the ion
136
What is the equilibrium of K+?
-90 mV
137
Equilibrium potential of Na+?
+60 mV
138
What is the RESTING membrane potential of muscle?
-70 mV
139
Why is the resting MP of muscle -70 mV?
Muscle cells are about 40x more permeable to K+ that to Na+, and as a result, a cells resting MP is closer to the Ek of -90 mV than to the ENa of +60 mV
140
What determines membrane permeability to a particular ion?
Opening and closing of ion channels
141
What causes changes in MP (i.e. the AP)?
Changes in membrane permeability to Na+ and K+ (i.e. opening of Na+ or K+ channels)
142
Steps in an AP
1. Resting MP -70 mV 2. Depolarizing stimulus (ACh onto motor end plate) 3. Membrane depolarizes to threshold. Voltage-gated Na+ channels open and Na+ enters cell. Voltage-gated K+ channels begin to open slowly 4. Rapid Na+ entry depolarizes cell 5. Na+ channels close and sower K+ channels open 6. K+ moves from cell to ECF 7. K+ channels remain open and additional K+ leaves cell, hyperpolarizing it 8. Voltage-gated K+ channels close, some K+ enters cell through leaky channels 9. Cell returns to resting ion permeability and resting MP
143
What does the Na+ - K+ - ATPase do?
Carries 3 Na+ out of the cell at the same time as 2 K+ are moved into the cell. This action requires 1 ATP for every 3 Na+ and 2K+ pumped across.
144
Why is the ratio of Na+ pumped out of the cell and K+ pumped into the cell in a 3:2 ratio?
Want to have more positive charges leaving than coming in, in order to maintain negative MP
145
Function of Na+-K+-ATPase?
Insure the primary control of cell volume and maintenance of Na+ and K+ gradients across the cell membrane
146
Structure of the Na+-K+-ATPase?
Sarcolemmal enzyme; functional dimer (alpha and beta subunits...both must be present for pump to work)
147
Capacity of Na+-K+-ATPase determined by?
Concentration of pumps (how many pumps there are) and the activity of the pumps (how fast/slow they are working)
148
Alpha subunit of Na+/K+ ATPase has binding sites for?
ATP and Na+/K+
149
Beta subunits in the Na+-K+-ATPase serve what purpose?
Involved in proper insertion of alpha subunit into the plasma membrane and required for proper enzymatic activity
150
Isoforms of alpha subunits in Na+/K+ ATPase?
Alpha 1 and alpha 2
151
Isoforms of Beta subunits in Na+-K+-ATPase?
Beta 1, Beta 2, and Beta 3
152
What happens to the NA+/K+ ATPase during exercise?
E/NE bind to beta2-adrenoreceptors, activate adenylate cyclase and increase cAMP levels. This second messenger activates protein kinase A, which increases Na+-K+-ATPase activity. Alsom alpha-beta subunits are translocated from the SR to the sarcolemma.
153
What is the SR?
Extensive membrane system surrounding each myofibril within muscle cells that plays a critical role in skeletal muscle to regulate intracellular free calcium, and to store Ca2+, release it, and uptake Ca2+ upon relaxation
154
Two parts of the SR?
Terminal Cisternae/Junctional SR and Longitudinal SR
155
Purpose of terminal cisternae/junctional SR?
Forms junction with T-Tubule called triad membrane (10-20 nm gap), contains Ca2+ release channel (Ryanodine Receptor), most Ca2+ is found bound to calsequestrin, and its major function is Ca2+ release
156
Purpose of longitudinal SR?
Contain the Ca2+-ATPase pumps (SERCA), and its major function is Ca2+ UPTAKE
157
Function of calsequestrin?
Found in the SR and has a high capacity Ca2+ binding (storage) in the lumen of SR
158
Phospholamban (PLN)?
Found in SR and regulates SERCA activity; expression is fibre type and species dependent
159
Sarcolipin (SLN)?
PLN homologue that regulates SERCA activity; expression is fibre and species dependent
160
Triadin/Junctin?
2 junctional SR proteins that form complex with CRC and CSQ to regulate CRC function
161
How many Ca2+ can SERCA bring into cell, and for what metabolic cost?
2 Ca2+ per 1 ATP
162
What do PLN and SLN do to the efficiency of SERCA?
Decrease efficiency...but increase BMR
163
Where is the ATP binding site on SERCA?
in the cytosol
164
What is the purpose of the phosphorylation domain in SERCA?
Influences activity and confirmation
165
How transmembrane helices does SERCA have?
10
166
How many binding sites does SERCA have for calcium?
2
167
Elementary steps of Ca2+ translocation?
1. Binding of 2 Ca2+ to the enzyme in a strong binding confirmation towards the cytoplasm (2Ca2+:E1) 2. ATP binds to the enzyme (2CA2+:E1:ATP) 3. ATP is hydrolyzed and a phosphorylated intermediate is formed (2Ca2+:E1~P) 4. Change in the enzyme configuration from the E1 to E2 state with translocation of Ca2+ to the lumen (2Ca2+:E2~P) 5. Release of Ca2+ to the lumen of the SR. Affinity of Ca2+ binding sites reduced by 3-fold (E2~P) 6. Mg2+ dependent hydrolysis of the E2~P intermediate (E2~Pi) 7. Release of inorganic phosphate (E2) 8. Change in enzyme confirmation from E2 to E1 state (E1)
168
RYR1 gene is for expression of ryanodine receptors for what?
Skeletal muscle
169
RYR2 gene is for expression of ryanodine receptors for what?
Cardiac and smooth muscle
170
Malignant hyperthermia?
Defect in ryanodine receptor. Anesthetics or stress lead to prolonged release of Ca2+ and prolonged contraction and damage
171
SR proteins involved in altering efficiency of SERCA?
Phospholamban and sarcolipon
172
Transition of the E1 to the E2 is important in SERCA because?
Decreases affinity for Ca2+ binding to SERCA and the Ca2+ binding site is now facing the lumen
173
Muscle fibers are classified by?
Contractile characteristics, myofibrillar organization, E-C coupling, metabolism, phosphorylation state, membrane transporters, histochemistry, and morphological features
174
2 primary factors that differentiate muscle fibre types?
Rate of speed of contraction (Vmax) and fatigue characteristics
175
Which had faster Vmax type 1 or 2?
Type 2
176
The rate of speed of contraction is directly related to?
Actomyosin ATPase activity, which is determined by the MHC isoform
177
Order fastest to slowest muscle fibre types?
HC2B HC2x(d) HC2a HC1
178
Do humans express HC2b fibers?
No!!! Only rodents
179
At pH 4.6, M-ATPase of type 1 fibers stain?
Dark
180
At pH 4.6, M-ATPase of type 2a fibers stain?
Light
181
At pH 4.6, M-ATPase of type 2b/x fibers stain?
Medium
182
Type 1 fibers are acid what? Alkali what?
Acid stable, alkali labile
183
Type 2 fibers are acid what? Alkali what?
Acid labile, alkali stable
184
Index of fatigue?
Final tension/initial tension x 100
185
Shape of slow, fast resistant, and fast fatigue muscle fatigability graph?
Almost straight line, some what steep, super curved
186
The maximal rate of muscle shortening is influenced by?
Myosin heavy chain expression, which determines which myosin ATPase isoform is present
187
At pH of 7, which fibre type in rats would have the highest ATPase activity?
MHCIIb
188
At a pH of 7 what fibre type in humans would have the highest ATPase activity?
MHCIIx
189
What does SAG refer to?
The time it takes to observe a reduction in force output
190
How is SAG determined?
Using a protocol of continuous tetanic stimulations (muscle contraction) for a period of time (until force begins to drop)
191
Based on metabolic characteristics, fibres are classified as?
Fast-Glycolytic, Fast-Oxidative-Glycolytic, or Slow-Oxidative
192
For an an oxidative test, SO fibres will stain?
Dark
193
For an oxidative test, FOG (IIa) fibres will stain?
Medium
194
For an oxidative test, FG (IIx/d) will stain?
Medium-light
195
For a glycolytic test a SO (I) fibre will stain>
Light
196
For a glycolytic test a FOG (IIa) fibre will stain?
Med/Med-light
197
For a glycolytic test FG (IIx/d) will stain?
Medium
198
Histochemical stains for metabolic characteristics are only what type of measures?
QUALITATIVE measures of aerobic/anaerobic potential
199
Can metabolic properties be used to determine a fibre type?
NO!! Due to the diversity found within individual fibre types (as determined by myosin ATPase activity)
200
Oxidative potential from least oxidative to most oxidative?
Type IIb (IIdx), Type IIa, Type I
201
Glycolytic potential from least to most glycolytic?
Type I, Type IIa, Type IIb (IIdx)
202
Phosphorylation Potential for ATP from least to most?
Type I = Type IIa = Type IIx (IIdx)
203
Phosphorylation potential for PCr form least to most?
Type I, Type II
204
Fibre type classification schemes?
Type I = Slow-Oxidative = Slow Fatigue
Type IIa = Fast-Oxidative-Glycolytic = Fatigue Resistant
Type IIb = Fast-Glycolytic = Fast Fatigue
205
Morphological characteristics of muscle fibre types?
Muscle fibre diameter (size), capillary density (muscle blood flow), and myoglobin content (cellular O2 transport)
206
Size of human muscle fibres from smallest to biggest?
Type I, Type IIa, Type IIx
207
Size in rat muscle size from smallest to biggest?
Type IIa, Type I, Type IIb
208
Least oxidative to most oxidative fibres in rats?
Type IIb, Type I, Type IIa
209
Capillaries/area from least to most?
Type IIx, Type IIa, Type IIax, Type I
210
SDH concentration from least to most?
Type IIx, Type IIax, Type IIa, Type I
211
What is the purpose of hybrid fibres (Type IIax)?
Contains MHC a and MHC x, allows the muscle to be "in the middle," allows for diversity and a continuum of properties
212
The maximal rate of muscle shortening is influenced by?
Myosin heavy chain expression, which determines which myosin ATPase isoform is present
213
At pH of 7, which fibre type in rats would have the highest ATPase activity?
MHCIIb
214
At a pH of 7 what fibre type in humans would have the highest ATPase activity?
MHCIIx
215
What does SAG refer to?
The time it takes to observe a reduction in force output
216
How is SAG determined?
Using a protocol of continuous tetanic stimulations (muscle contraction) for a period of time (until force begins to drop)
217
Based on metabolic characteristics, fibres are classified as?
Fast-Glycolytic, Fast-Oxidative-Glycolytic, or Slow-Oxidative
218
For an an oxidative test, SO fibres will stain?
Dark
219
For an oxidative test, FOG (IIa) fibres will stain?
Medium
220
For an oxidative test, FG (IIx/d) will stain?
Medium-light
221
For a glycolytic test a SO (I) fibre will stain>
Light
222
For a glycolytic test a FOG (IIa) fibre will stain?
Med/Med-light
223
For a glycolytic test FG (IIx/d) will stain?
Medium
224
Histochemical stains for metabolic characteristics are only what type of measures?
QUALITATIVE measures of aerobic/anaerobic potential
225
Can metabolic properties be used to determine a fibre type?
NO!! Due to the diversity found within individual fibre types (as determined by myosin ATPase activity)
226
Oxidative potential from least oxidative to most oxidative?
Type IIb (IIdx), Type IIa, Type I
227
Glycolytic potential from least to most glycolytic?
Type I, Type IIa, Type IIb (IIdx)
228
Phosphorylation Potential for ATP from least to most?
Type I = Type IIa = Type IIx (IIdx)
229
Phosphorylation potential for PCr form least to most?
Type I, Type II
230
Fibre type classification schemes?
Type I = Slow-Oxidative = Slow Fatigue
Type IIa = Fast-Oxidative-Glycolytic = Fatigue Resistant
Type IIb = Fast-Glycolytic = Fast Fatigue
231
Morphological characteristics of muscle fibre types?
Muscle fibre diameter (size), capillary density (muscle blood flow), and myoglobin content (cellular O2 transport)
232
Size of human muscle fibres from smallest to biggest?
Type I, Type IIa, Type IIx
233
Size in rat muscle size from smallest to biggest?
Type IIa, Type I, Type IIb
234
Least oxidative to most oxidative fibres in rats?
Type IIb, Type I, Type IIa
235
Capillaries/area from least to most?
Type IIx, Type IIa, Type IIax, Type I
236
SDH concentration from least to most?
Type IIx, Type IIax, Type IIa, Type I
237
What is the purpose of hybrid fibres (Type IIax)?
Contains MHC a and MHC x, allows the muscle to be "in the middle," allows for diversity and a continuum of properties
238
Name 2 factors that can influence SDH levels
Fibre type (higher in Type I than Type II) and training status (endurance training increased SDH by increasing mitochondria levels)
239
What are the definitive ways to determine a fibre type?
Immunofluroescence and pre-incubation to determine the MHC isoform/myosin ATPase
240
What is the purpose of myoglobin?
Intracellular oxygen buffer and facilitates oxygen delivery to mitochondria
241
What type of fibres have the most myoglobin?
Type I
242
What type of fibres have the highest Na+/K+ ATPase activity?
Type I because they are used more throughout the day, so there MP is disturbed more, making the Na+/K+ ATPase work more
243
Subunits of Na+/K+ ATPase found in Type I fibres?
Alpha 1 and Beta 1
244
Na+/K+ ATPase isoform found in Type II fibres?
Alpha 2 and Beta 2
245
SERCA isoform in Type I fibres?
SERCA2
246
SERCA isoform in Type II fibres?
SERCA1
247
RYR Isoform in Type I fibres?
RYR1-Slow
248
RYR Isoform in Type II fibres?
RYR1-Fast
249
What fibres have the highest Ca2+-ATPase activity?
Type II
250
Fibre type that has the fastest Ca2+ uptake?
Type II
251
Which fibre has the fastest Ca2+ release and most number of RYR channels?
Type II
252
Isoforms of tropomyosin?
alpha, beta, and gamma
253
Predominant isoform in Type II fibres?
Alpha subunit
254
Predominant isoform in Type I fibres?
Beta subunit
255
What does the beta subunit do to cross-bridge development?
Slows the rate of cross-bridge development, causes a slower rate of force development, and decreases steady-state level of force
256
How do different troponin isoforms influence contraction?
The different isoforms respond different to Ca2+ and how it acts with tropomyosin
257
Z-disk width in fibres from least to greatest?
FG, FOG, and SO
258
Lipid droplets in fibres from least to most?
FG, FOG, and SO
259
Glycogen granules in fibre types from least to greatest?
SO, FOG, and FG
260
What is a motor unit?
A set of muscle fibres innervated by a single motor neuron that have: 1. a certain capacity for producing tension 2. A particular contraction speed 3. A characteristic range of firing rate 4. A specific susceptibility to neuromuscular and contractile fatigue 5. A distinctive hitsochemical profile 6. Well-defind morphological properties
261
The characteristics of moto units are matched to the activity of the?
Motoneurons. EXAMPLE, a motor unit that is constantly stimulated will be different than one that isn't stimulated as much, even if they are the same fibre type makes up the motor unit
262
Are all muscle fibres in a motor unit the same fibre type?
YES! And, they share other properties, like oxidative capacity, etc.
263
Smallest amount of muscle that can be activated voluntarily?
The motor unit
264
How do you increase force in muscle?
Recruit more motor units and increase the frequency of stimulation
265
Once a motor unit is recruited, how many fibres within the unit will contract?
ALL OF THEM!!
266
Graduation od force in skeletal muscle is coordinated largely by?
The nervous system
267
What motor units are recruited first?
Slow-oxidative followed by FOG, and finally SO
268
Which of the following would influence absolutre force generation and/or contraction in a fibre?
Myosin isoform, tropomyosin isoform, troponin isoform
269
What motor units have the most fibres per unit? The least?
Fast fatiguable have the most fibres per motor unit, and slow have the least amount of fibres
270
What kind of muscles have the fewest numbers and sizes of motor units?
Muscles that require strict control over the amount of force produced, such as the eye muscles.
271
Motor neuron for Type I fibres?
Alpha 2
272
Motor neuron for FOG fibres?
Alpha 1
273
Motor neuron for FG fibres?
Alpha 2
274
Neuron size of Type 1 fibres?
Small
275
Neuron size of fast fibres?
Large
276
Conduction velocity of slow fibres?
Slow
277
Conduction velocity of fast fibres?
Fast
278
Recruitment threshold of slow fibres?
Low
279
Recruitment threshold of fast fibres?
High
280
Can MHC isoform change in response to the activity of the motorneuron?
YES!!! MN signal dictates property of fibres
281
Power athletes have majority of what type of fibres?
Fast fibres
282
Endurance athletes have majority of what type of fibres?
Slow fibres
283
Non-athletes and weightlifters have majority of what type of fibre?
Have about 50% slow and 50% fast
284
Is fibre type the most important thing in determining what makes an elite athlete?
NO! Abilitiy to recruit, metabolic properties, biomechanics, etc. are more important
285
Most malleable tissue in body?
Skeletal muscle
286
At 25% of pool recruited how many slow fibres are activated?
ALL OF THEM
287
At 50% of pool recruitment, how many type IIa fibres are activated?
ALL OF THEM
288
Name 2 experimental models that show it's possible to change a Type II into a Type I fibre
Chronic low frequency stimulation and surgically switching the MN
289
What light chain isoform increases Vmax?
LC 3 (alkali light chain)
290
All fibres must have what light chain?
LC2 (regulatory/phosphorylatable)
291
What do the varying isoforms of the light chain do?
They can change the Vmax independent of the heavy chain
292
Reasons to assess muscle/group of muscles ability to generate force?
1. To evaluate effects of any acute perturbation on muscle function (exercise, hypoxia, etc) 2. To evaluate muscle adaptations to exercise training or chronic exposure to different environments 3. To determine the effects of different chemical stimuli (drugs) on muscle function 4. To determine role of different genes in muscle function **Use a Pre-Test vs. Post-Test
293
Isotonic contraction?
Contraction at near constant tension
294
Primary function of muscle?
To generate force
295
Isokinetic?
Contraction near a constant velocity
296
Power = ?
Force x Velocity
297
At maximal velocity of contraction what is the theoretical force produced?
0
298
At the maximal isometric force what is the velocity?
0
299
The force-velocity curve is defined by what equation?
Hill Equation Velocity = (max isometric force - Force/load on muscle) / Force on muscle V = (Po-P)/P
300
In a concetric contraction, as velocity increases, what happens to force?
Decreases
301
What fibre type can produce more power?
Type II x
302
What fibre type can produce more force at a particular speed?
Type II x
303
Max power in most muscles occurs at a velocity between?
200-300 degrees per second
304
What is maximal isometric strength defined as?
The maximal force that can be generated with a maximal voluntary contraction in a given muscle or muscle group under a given set of conditions (i.e. fixed length or joint angle)
305
Force is greatest during what type of contraction?
Eccentric
306
Considering only myosin heavy chain and light chain, what fibre type would have the highest Vmax?
(HCIIb)(HCIIb) and (LC3F)2(LC2F)2
Humans: (HCIIx)(HCIIx) and (LC3F)2(LC2F)2
307
2 ways mechanical properties of specific muscles or muscle groups can be measured voluntarily?
Performance based on tasks involving maximal efforts: isometric (maximal voluntary contraction) and dynamic (maximal POWER output at constant velocity (isokinetic) or constant force (isotonic))
308
Mechanical output in muscles depends on?
Both the neural commands to the muscle (activation) and the muscle itself (response) to neural command
309
Fatigue?
A decrement in force or power output
310
Central fatigue?
A failure to maximally activate the muscle
311
Peripheral fatigue>
Failure at the level of the muscle itself (muscle not able to appropriately respond to the neural stimulus)
312
Central fatigue happens above where?
Above the sarcolemma
313
Latent period?
Time it takes for stimulus (electrical) to travel to and cause changes in the muscle
314
Contraction time?
Time it takes to generate Pt starting from the point in time when force first begins to increase
315
+dF/dt ?
Maximal RATE of force development...slope of twitch curve
316
-dF/dt?
Maximal rate of force decline...RELAXATION from max force to 0 force
317
1/2 RT?
Time it takes for force to decline to 50% of Pt during relaxation
318
Twitch response is determined by?
Both the contractile and series elastic elements
319
Parallel Elastic Elements?
Elastic elements in parallel with contractile elements. Epimysium, perimysium, endomysium, sarcolemma, SR, capillaries, and titin. Responsible for the passive tension in muscle. Run ALONG myofibrils.
320
Series Elastic Elements?
Elastic elements in series with contractile elements. Z-line and tendon. Helps smooth out the rapid changes in tension for gradual transition in force
321
Force development with shortening contraction only occurs after slack in what is taken up?
SEE
322
How does increasing frequency of stimulation increase force output?
Summation. Stimuli that are closer together do not allow muscle to fully relax.
323
What does repetitive stimulation do to force production?
Causes saturating levels of cytoplasmic Ca2+, leading to tetanus.
324
Force is greatest during what type of contraction?
Eccentric
325
Considering only myosin heavy chain and light chain, what fibre type would have the highest Vmax?
(HCIIb)(HCIIb) and (LC3F)2(LC2F)2
Humans: (HCIIx)(HCIIx) and (LC3F)2(LC2F)2
326
2 ways mechanical properties of specific muscles or muscle groups can be measured voluntarily?
Performance based on tasks involving maximal efforts: isometric (maximal voluntary contraction) and dynamic (maximal POWER output at constant velocity (isokinetic) or constant force (isotonic))
327
Mechanical output in muscles depends on?
Both the neural commands to the muscle (activation) and the muscle itself (response) to neural command
328
Fatigue?
A decrement in force or power output
329
Central fatigue?
A failure to maximally activate the muscle
330
Peripheral fatigue>
Failure at the level of the muscle itself (muscle not able to appropriately respond to the neural stimulus)
331
Central fatigue happens above where?
Above the sarcolemma
332
Latent period?
Time it takes for stimulus (electrical) to travel to and cause changes in the muscle
333
Contraction time?
Time it takes to generate Pt starting from the point in time when force first begins to increase
334
+dF/dt ?
Maximal RATE of force development...slope of twitch curve
335
-dF/dt?
Maximal rate of force decline...RELAXATION from max force to 0 force
336
1/2 RT?
Time it takes for force to decline to 50% of Pt during relaxation
337
Twitch response is determined by?
Both the contractile and series elastic elements
338
Parallel Elastic Elements?
Elastic elements in parallel with contractile elements. Epimysium, perimysium, endomysium, sarcolemma, SR, capillaries, and titin. Responsible for the passive tension in muscle. Run ALONG myofibrils.
339
Series Elastic Elements?
Elastic elements in series with contractile elements. Z-line and tendon. Helps smooth out the rapid changes in tension for gradual transition in force
340
Force development with shortening contraction only occurs after slack in what is taken up?
SEE
341
How does increasing frequency of stimulation increase force output?
Summation. Stimuli that are closer together do not allow muscle to fully relax.
342
What does repetitive stimulation do to force production?
Causes saturating levels of cytoplasmic Ca2+, leading to tetanus.
343
Force is greatest during what type of contraction?
Eccentric
344
Considering only myosin heavy chain and light chain, what fibre type would have the highest Vmax?
(HCIIb)(HCIIb) and (LC3F)2(LC2F)2
Humans: (HCIIx)(HCIIx) and (LC3F)2(LC2F)2
345
2 ways mechanical properties of specific muscles or muscle groups can be measured voluntarily?
Performance based on tasks involving maximal efforts: isometric (maximal voluntary contraction) and dynamic (maximal POWER output at constant velocity (isokinetic) or constant force (isotonic))
346
Mechanical output in muscles depends on?
Both the neural commands to the muscle (activation) and the muscle itself (response) to neural command
347
Fatigue?
A decrement in force or power output
348
Central fatigue?
A failure to maximally activate the muscle
349
Peripheral fatigue>
Failure at the level of the muscle itself (muscle not able to appropriately respond to the neural stimulus)
350
Central fatigue happens above where?
Above the sarcolemma
351
Latent period?
Time it takes for stimulus (electrical) to travel to and cause changes in the muscle
352
Contraction time?
Time it takes to generate Pt starting from the point in time when force first begins to increase
353
+dF/dt ?
Maximal RATE of force development...slope of twitch curve
354
-dF/dt?
Maximal rate of force decline...RELAXATION from max force to 0 force
355
1/2 RT?
Time it takes for force to decline to 50% of Pt during relaxation
356
Twitch response is determined by?
Both the contractile and series elastic elements
357
Parallel Elastic Elements?
Elastic elements in parallel with contractile elements. Epimysium, perimysium, endomysium, sarcolemma, SR, capillaries, and titin. Responsible for the passive tension in muscle. Run ALONG myofibrils.
358
Series Elastic Elements?
Elastic elements in series with contractile elements. Z-line and tendon. Helps smooth out the rapid changes in tension for gradual transition in force
359
Force development with shortening contraction only occurs after slack in what is taken up?
SEE
360
How does increasing frequency of stimulation increase force output?
Summation. Stimuli that are closer together do not allow muscle to fully relax.
361
What does repetitive stimulation do to force production?
Causes saturating levels of cytoplasmic Ca2+, leading to tetanus.
362
Force is greatest during what type of contraction?
Eccentric
363
Considering only myosin heavy chain and light chain, what fibre type would have the highest Vmax?
(HCIIb)(HCIIb) and (LC3F)2(LC2F)2
Humans: (HCIIx)(HCIIx) and (LC3F)2(LC2F)2
364
2 ways mechanical properties of specific muscles or muscle groups can be measured voluntarily?
Performance based on tasks involving maximal efforts: isometric (maximal voluntary contraction) and dynamic (maximal POWER output at constant velocity (isokinetic) or constant force (isotonic))
365
Mechanical output in muscles depends on?
Both the neural commands to the muscle (activation) and the muscle itself (response) to neural command
366
Fatigue?
A decrement in force or power output
367
Central fatigue?
A failure to maximally activate the muscle
368
Peripheral fatigue>
Failure at the level of the muscle itself (muscle not able to appropriately respond to the neural stimulus)
369
Central fatigue happens above where?
Above the sarcolemma
370
Latent period?
Time it takes for stimulus (electrical) to travel to and cause changes in the muscle
371
Contraction time?
Time it takes to generate Pt starting from the point in time when force first begins to increase
372
+dF/dt ?
Maximal RATE of force development...slope of twitch curve
373
-dF/dt?
Maximal rate of force decline...RELAXATION from max force to 0 force
374
1/2 RT?
Time it takes for force to decline to 50% of Pt during relaxation
375
Twitch response is determined by?
Both the contractile and series elastic elements
376
Parallel Elastic Elements?
Elastic elements in parallel with contractile elements. Epimysium, perimysium, endomysium, sarcolemma, SR, capillaries, and titin. Responsible for the passive tension in muscle. Run ALONG myofibrils.
377
Series Elastic Elements?
Elastic elements in series with contractile elements. Z-line and tendon. Helps smooth out the rapid changes in tension for gradual transition in force
378
Force development with shortening contraction only occurs after slack in what is taken up?
SEE
379
How does increasing frequency of stimulation increase force output?
Summation. Stimuli that are closer together do not allow muscle to fully relax.
380
What does repetitive stimulation do to force production?
Causes saturating levels of cytoplasmic Ca2+, leading to tetanus.
381
List and explain 3 factors that would influence force and/or power in muscle in which all fibres are fully activated and not fatigued.
1. Velocity of movement...Power is a function of FxV, and therefore, is usually maximal around 200-300 degrees per second 2. Muscle length...optimal length will produce the most force 3. Fibre type composition...For a given velocity, both force and power are higher in Type II compared to Type I 3.Fibre size...bigger = more force
382
In mammailian muscle, the twitch force is what percent of the tetanic force?
10-20% Important because it allows for gradual, controlled increases in force.
383
Why do slow twitch fibres generate more force at lower frequency stimulation than fast twitch fibres?
They exhibit slower relaxation rates, so fused tetanus occurs at lower frequency of stimulation.
384
Why do Type II fibres need higher frequency of stimulation to reach tetanus than a Type I fibre?
SERCA 1, found in Type II fibres, can uptake Ca2+ faster, meaning it can relax faster than Type I. So, a high frequency is needed to reach saturating sarcoplasmic levels
385
What is weakness?
Persistent loss of force (extended time)
386
What fibre type shows greater decreased in velocity and power when fatigued?
Type II
387
Why do Type II fibres fatigue faster?
Inherent biochemical properties
388
The duty cycle?
Tc/(Tc+Tr) The higher the duty cycle the faster you fatigue or shorter you can produce desired force
389
Tension Time Index (TTI)?
(F/MVC) x Tc/(Tc+Tr) ...determines fatigue. If TTI > 0.15 or 15%, fatigue will occur
390
Sites of fatigue for central fatigue in a voluntary activity?
Failure within nervous system, reduced central drive (motor unit recruitment, firing frequency), and feedback from muscle to inhibit activation (i.e. the muscle spindle)
391
Sites of fatigue in voluntary or involuntary activity for peripheral fatigue?
Excitation: sarcolemms, t-tubule, SR, or something with increasing Ca2+ levels
Contraction: regulatory proteins (TN-C) or hte cross-bridge cycle (actin and myosin)
392
Perihperal sites of fatigue divided into what 2 kinds?
Excitation and Contraction
393
What is an interpolated twitch?
A single supramaximal stimulus is superimposed on a MVC
394
If an interpolated twitch it applied during an MVC and there is no measurable increase in force, what does this mean?
Maximal activation is believed to occur (no central fatigue)
395
MVC depends on what in the individual?
MOTIVATION to recruit all motor units...last 5% of motor units are very difficult to recruit
396
What are 2 properties of the isometric twitch that can be measured to assess muscle relaxation?
1/2 RT and -dF/dt
397
4 things that affect central fatigue?
1. Motivation...TMS increases force generation in participants experiencing fatigue, and serious athletes show less fatigue 2. Perceived Pain...distraction helps maintain force 3. Brain activity...decreased neural activity in the brain motor cortex during and following exhaustive exercise 3. Neurotransmitters....Decreased ACh release following repeated stimulation and HIGH serotonin levels are associated with fatigue and lethargic behaviour
398
2 components of metabolic peripheral fatigue?
1. Reduced energy supply (ATP, PCr) 2. Build-up of metabolic by-products (ADP, Pi, H+)
399
Non-metabolic peripheral fatigue?
Due to structural alterations to proteins and/or membranes involved in excitation and contraction processes (i.e. damage due to mechanical disruption) from eccentric exercise, free radicals, or proteolytic enzymes that increase activity during exercise
400
What is low-frequency fatigue?
Failure to generate the same force at low frequencies of stimulation (10, 20 Hz)
401
What causes low frequency fatigue?
Failure to activate the muscle despite adequate excitation...Ca2+ sensitivity or Ca2+ release
402
Is low frequency fatigue long or short lasting?
Long lasting...may take several hours to days to regain original force
403
What helps overcome low frequency fatigue?
Caffeine...open RyR channels and keep them open
404
High frequency fatigue?
Failure to generate the same force at high frequencies of stimulation (50, 100 Hz)
405
What causes high-frequency fatigue?
Likely due to failure of the APs along the sarcolemma or T-tubular system, which could be due to the accumulation of K+ in the T-tubules (T-tubular block)
406
Is high frequency fatigue short or long lived?
Short lived because gradients are restored very rapidly following exercise
407
How is calcium related to peripheral fatigue?
It may also be due to reduced Ca2+ sensitivity or responsiveness of regulatory proteins (TN-C)
408
Force-pCa relationship?
At low frequency, a decline in pCa will cause a big decrease in force, since the TN-C is not saturated with Ca2+. At high frequency, though, a decline in Ca2+ there is no decline in force output when pCa2+ declines because TN-C is already saturated.
409
List and explain 3 factors that would influence force and/or power in muscle in which all fibres are fully activated and not fatigued.
1. Velocity of movement...Power is a function of FxV, and therefore, is usually maximal around 200-300 degrees per second 2. Muscle length...optimal length will produce the most force 3. Fibre type composition...For a given velocity, both force and power are higher in Type II compared to Type I 3.Fibre size...bigger = more force
410
In mammailian muscle, the twitch force is what percent of the tetanic force?
10-20% Important because it allows for gradual, controlled increases in force.
411
Why do slow twitch fibres generate more force at lower frequency stimulation than fast twitch fibres?
They exhibit slower relaxation rates, so fused tetanus occurs at lower frequency of stimulation.
412
Why do Type II fibres need higher frequency of stimulation to reach tetanus than a Type I fibre?
SERCA 1, found in Type II fibres, can uptake Ca2+ faster, meaning it can relax faster than Type I. So, a high frequency is needed to reach saturating sarcoplasmic levels
413
What is weakness?
Persistent loss of force (extended time)
414
What fibre type shows greater decreased in velocity and power when fatigued?
Type II
415
Why do Type II fibres fatigue faster?
Inherent biochemical properties
416
The duty cycle?
Tc/(Tc+Tr) The higher the duty cycle the faster you fatigue or shorter you can produce desired force
417
Tension Time Index (TTI)?
(F/MVC) x Tc/(Tc+Tr) ...determines fatigue. If TTI > 0.15 or 15%, fatigue will occur
418
Sites of fatigue for central fatigue in a voluntary activity?
Failure within nervous system, reduced central drive (motor unit recruitment, firing frequency), and feedback from muscle to inhibit activation (i.e. the muscle spindle)
419
Sites of fatigue in voluntary or involuntary activity for peripheral fatigue?
Excitation: sarcolemms, t-tubule, SR, or something with increasing Ca2+ levels
Contraction: regulatory proteins (TN-C) or hte cross-bridge cycle (actin and myosin)
420
Perihperal sites of fatigue divided into what 2 kinds?
Excitation and Contraction
421
What is an interpolated twitch?
A single supramaximal stimulus is superimposed on a MVC
422
If an interpolated twitch it applied during an MVC and there is no measurable increase in force, what does this mean?
Maximal activation is believed to occur (no central fatigue)
423
MVC depends on what in the individual?
MOTIVATION to recruit all motor units...last 5% of motor units are very difficult to recruit
424
What are 2 properties of the isometric twitch that can be measured to assess muscle relaxation?
1/2 RT and -dF/dt
425
4 things that affect central fatigue?
1. Motivation...TMS increases force generation in participants experiencing fatigue, and serious athletes show less fatigue 2. Perceived Pain...distraction helps maintain force 3. Brain activity...decreased neural activity in the brain motor cortex during and following exhaustive exercise 3. Neurotransmitters....Decreased ACh release following repeated stimulation and HIGH serotonin levels are associated with fatigue and lethargic behaviour
426
2 components of metabolic peripheral fatigue?
1. Reduced energy supply (ATP, PCr) 2. Build-up of metabolic by-products (ADP, Pi, H+)
427
Non-metabolic peripheral fatigue?
Due to structural alterations to proteins and/or membranes involved in excitation and contraction processes (i.e. damage due to mechanical disruption) from eccentric exercise, free radicals, or proteolytic enzymes that increase activity during exercise
428
What is low-frequency fatigue?
Failure to generate the same force at low frequencies of stimulation (10, 20 Hz)
429
What causes low frequency fatigue?
Failure to activate the muscle despite adequate excitation...Ca2+ sensitivity or Ca2+ release
430
Is low frequency fatigue long or short lasting?
Long lasting...may take several hours to days to regain original force
431
What helps overcome low frequency fatigue?
Caffeine...open RyR channels and keep them open
432
High frequency fatigue?
Failure to generate the same force at high frequencies of stimulation (50, 100 Hz)
433
What causes high-frequency fatigue?
Likely due to failure of the APs along the sarcolemma or T-tubular system, which could be due to the accumulation of K+ in the T-tubules (T-tubular block)
434
Is high frequency fatigue short or long lived?
Short lived because gradients are restored very rapidly following exercise
435
How is calcium related to peripheral fatigue?
It may also be due to reduced Ca2+ sensitivity or responsiveness of regulatory proteins (TN-C)
436
Force-pCa relationship?
At low frequency, a decline in pCa will cause a big decrease in force, since the TN-C is not saturated with Ca2+. At high frequency, though, a decline in Ca2+ there is no decline in force output when pCa2+ declines because TN-C is already saturated.
437
List and explain 3 factors that would influence force and/or power in muscle in which all fibres are fully activated and not fatigued.
1. Velocity of movement...Power is a function of FxV, and therefore, is usually maximal around 200-300 degrees per second 2. Muscle length...optimal length will produce the most force 3. Fibre type composition...For a given velocity, both force and power are higher in Type II compared to Type I 3.Fibre size...bigger = more force
438
In mammailian muscle, the twitch force is what percent of the tetanic force?
10-20% Important because it allows for gradual, controlled increases in force.
439
Why do slow twitch fibres generate more force at lower frequency stimulation than fast twitch fibres?
They exhibit slower relaxation rates, so fused tetanus occurs at lower frequency of stimulation.
440
Why do Type II fibres need higher frequency of stimulation to reach tetanus than a Type I fibre?
SERCA 1, found in Type II fibres, can uptake Ca2+ faster, meaning it can relax faster than Type I. So, a high frequency is needed to reach saturating sarcoplasmic levels
441
What is weakness?
Persistent loss of force (extended time)
442
What fibre type shows greater decreased in velocity and power when fatigued?
Type II
443
Why do Type II fibres fatigue faster?
Inherent biochemical properties
444
The duty cycle?
Tc/(Tc+Tr) The higher the duty cycle the faster you fatigue or shorter you can produce desired force
445
Tension Time Index (TTI)?
(F/MVC) x Tc/(Tc+Tr) ...determines fatigue. If TTI > 0.15 or 15%, fatigue will occur
446
Sites of fatigue for central fatigue in a voluntary activity?
Failure within nervous system, reduced central drive (motor unit recruitment, firing frequency), and feedback from muscle to inhibit activation (i.e. the muscle spindle)
447
Sites of fatigue in voluntary or involuntary activity for peripheral fatigue?
Excitation: sarcolemms, t-tubule, SR, or something with increasing Ca2+ levels
Contraction: regulatory proteins (TN-C) or hte cross-bridge cycle (actin and myosin)
448
Perihperal sites of fatigue divided into what 2 kinds?
Excitation and Contraction
449
What is an interpolated twitch?
A single supramaximal stimulus is superimposed on a MVC
450
If an interpolated twitch it applied during an MVC and there is no measurable increase in force, what does this mean?
Maximal activation is believed to occur (no central fatigue)
451
MVC depends on what in the individual?
MOTIVATION to recruit all motor units...last 5% of motor units are very difficult to recruit
452
What are 2 properties of the isometric twitch that can be measured to assess muscle relaxation?
1/2 RT and -dF/dt
453
4 things that affect central fatigue?
1. Motivation...TMS increases force generation in participants experiencing fatigue, and serious athletes show less fatigue 2. Perceived Pain...distraction helps maintain force 3. Brain activity...decreased neural activity in the brain motor cortex during and following exhaustive exercise 3. Neurotransmitters....Decreased ACh release following repeated stimulation and HIGH serotonin levels are associated with fatigue and lethargic behaviour
454
2 components of metabolic peripheral fatigue?
1. Reduced energy supply (ATP, PCr) 2. Build-up of metabolic by-products (ADP, Pi, H+)
455
Non-metabolic peripheral fatigue?
Due to structural alterations to proteins and/or membranes involved in excitation and contraction processes (i.e. damage due to mechanical disruption) from eccentric exercise, free radicals, or proteolytic enzymes that increase activity during exercise
456
What is low-frequency fatigue?
Failure to generate the same force at low frequencies of stimulation (10, 20 Hz)
457
What causes low frequency fatigue?
Failure to activate the muscle despite adequate excitation...Ca2+ sensitivity or Ca2+ release
458
Is low frequency fatigue long or short lasting?
Long lasting...may take several hours to days to regain original force
459
What helps overcome low frequency fatigue?
Caffeine...open RyR channels and keep them open
460
High frequency fatigue?
Failure to generate the same force at high frequencies of stimulation (50, 100 Hz)
461
What causes high-frequency fatigue?
Likely due to failure of the APs along the sarcolemma or T-tubular system, which could be due to the accumulation of K+ in the T-tubules (T-tubular block)
462
Is high frequency fatigue short or long lived?
Short lived because gradients are restored very rapidly following exercise
463
How is calcium related to peripheral fatigue?
It may also be due to reduced Ca2+ sensitivity or responsiveness of regulatory proteins (TN-C)
464
Force-pCa relationship?
At low frequency, a decline in pCa will cause a big decrease in force, since the TN-C is not saturated with Ca2+. At high frequency, though, a decline in Ca2+ there is no decline in force output when pCa2+ declines because TN-C is already saturated.
465
What happens to force production when there is a rundown of Na+ and K+ gradients due to repetitive muscle activation?
Action potential propagation in sarcolemma and in t-tubules impaired or abolished. Reduced Ca2+ release from SR. Reduced tension development.
466
Role of the SR in fatigue is due to?
Activation failure (reduced Ca2+ release) and Impaired relaxation (reduced Ca2+ uptake)
467
Metabolic fatigue in the SR is due to?
Decreasd ATP can reduce SERCA activity, AMP/IMP/Mg2+ directly inactivate Ca2+ release channel, and Pi can enter SR, interact with Ca2+ and cause Ca2+ precipitation (Ca2+ cannot be released so less force production)
468
Is the metabolic contribution to reduced Ca2+ from SR fatigue recovered quickly or slowly?
Quickly upon the cessation of exercise. Although, Ca2+ free concentration and force (low-frequency) can be depressed for greater than 24 hours (long lasting fatigue), which must involve non-metabolic mechanisms
469
Non-metabolic fatigue in the SR is due to?
O2 free radicals and proteolytic enzymes can cause damage to SERCA and RyR. NOTE: These same non-metabolic mechanism may also effect fatigue independent of the SR, since they can also damage other pumps and contractile proteins
470
Changes in muscle twitch due to fatigue?
Decreased peak tension, decreased +dF/dr and -dF/dt, and increaed CT and 1/2 RT
471
Where does post-tetanic potentiation occur?
In FAST TWTICH fibres only at LOW frequencies of stimulation
472
What does post-tetanic potentiation do to the muscle twitch?
Increased Pt and Increased rate of contration
473
What causes post-tetanic potentiation?
Increased Ca2+ in sarcoplasm bind to calmoudlin, which activated MLCK. MLCK phosphorylates LC2. Myosin filament is pushed away from backbone because the negative charge on phosphate repels it. The myosin head is now closer to actin, meaning the probability of crossbridge formation increases and hte rate of force development is increased because myosin is now closer to actin.
474
Why doesn't post-tetanic potentiation happen in slow twitch fibres?
Myosin Light Chain Phosphatase works to fast, so Ca2+ is removed before repulsion has a chance to occur
475
Metabolic fatigue can be due to?
Decreased ATP availability and the buildup of ATP breakdown products
476
What happens to force production when there is a rundown of Na+ and K+ gradients due to repetitive muscle activation?
Action potential propagation in sarcolemma and in t-tubules impaired or abolished. Reduced Ca2+ release from SR. Reduced tension development.
477
Role of the SR in fatigue is due to?
Activation failure (reduced Ca2+ release) and Impaired relaxation (reduced Ca2+ uptake)
478
Metabolic fatigue in the SR is due to?
Decreasd ATP can reduce SERCA activity, AMP/IMP/Mg2+ directly inactivate Ca2+ release channel, and Pi can enter SR, interact with Ca2+ and cause Ca2+ precipitation (Ca2+ cannot be released so less force production)
479
Is the metabolic contribution to reduced Ca2+ from SR fatigue recovered quickly or slowly?
Quickly upon the cessation of exercise. Although, Ca2+ free concentration and force (low-frequency) can be depressed for greater than 24 hours (long lasting fatigue), which must involve non-metabolic mechanisms
480
Non-metabolic fatigue in the SR is due to?
O2 free radicals and proteolytic enzymes can cause damage to SERCA and RyR. NOTE: These same non-metabolic mechanism may also effect fatigue independent of the SR, since they can also damage other pumps and contractile proteins
481
Changes in muscle twitch due to fatigue?
Decreased peak tension, decreased +dF/dr and -dF/dt, and increaed CT and 1/2 RT
482
Where does post-tetanic potentiation occur?
In FAST TWTICH fibres only at LOW frequencies of stimulation
483
What does post-tetanic potentiation do to the muscle twitch?
Increased Pt and Increased rate of contration
484
What causes post-tetanic potentiation?
Increased Ca2+ in sarcoplasm bind to calmoudlin, which activated MLCK. MLCK phosphorylates LC2. Myosin filament is pushed away from backbone because the negative charge on phosphate repels it. The myosin head is now closer to actin, meaning the probability of crossbridge formation increases and hte rate of force development is increased because myosin is now closer to actin.
485
Why doesn't post-tetanic potentiation happen in slow twitch fibres?
Myosin Light Chain Phosphatase works to fast, so Ca2+ is removed before repulsion has a chance to occur
486
Metabolic fatigue can be due to?
Decreased ATP availability and the buildup of ATP breakdown products
