Exam 1 Flashcards
(392 cards)
1
Q
Evidence suggests sarcoplasmic hypertrophy coincides with…
A
muscle fiber tissue growth during resistance exercise
2
Q
Other modes of hypertrophy during resistance exercise include
A
A proportional accretion of myofibril protein with fiber or tissue growth
OR
fibril protein accretion preceding fiber or tissue growth
3
Q
Heavy resistance exercise does not change
A
packing density of myofilaments or ratio of actin to myosin
4
Q
Sliding Filament Theory
A
muscle contraction driven by change in structure on myosin and ‘stroke’ to pull actin towards myosin
5
Q
Measuring muscle size
A
DEXA, UWW, BodPod, CT, MRI, Biopsy, Ultrasound, Proteins, Ultra-Microscopic
6
Q
Limitation to measuring techniques
A
Who is doing the measuring, are they an expert, having measurement agreement
7
Q
What forms of muscle size measuring have poor agreement following skeletal muscle hypertrophy
A
macroscopic, microscopic, ultramicroscopic
8
Q
What forms of muscle size measuring have strong correlations in % change increases in thickness but poorly associated with volume
A
ultrasound and MRI
9
Q
What forms of muscle size measuring are highly correlated for muscle area
A
DXA, MRI, CT
10
Q
What forms of muscle size measuring have moderate correlation when assessing changes in muscle mass following resistance training and highest measurement error for determining subtle change in muscle mass over a protocol
A
DXA and CT
11
Q
When measuring muscle thickness
A
multiple sites should be used to capture growth of muscle
12
Q
When does growth occur?
A
4-6 weeks, noticeably, but still grows from the beginning stages of resistance training
13
Q
Muscle growth will
A
plateau
14
Q
After how much time will you have acquired your max hypertrophy
A
1-2 years
15
Q
When pushing the upper limit of hypertrophy
A
the body fights back against growth
16
Q
Training must be __________ to see small changes after max hypertrophy
A
hyperfocused
17
Q
Updated time course operates under same assumption
A
neural adaptation before hypertrophy
18
Q
Muscle quality across time shows
A
by week 3-4. the quality was better (bigger and stronger) which concludes real growth
19
Q
Muscle quality at first has no growth, therefore the strength is explained by
A
neural adaptation
20
Q
Muscle quality then shows growth with a decrease in strength explained by
A
no ‘functional’ hypertrophy a.k.a. swelling
21
Q
Early RT-induced increases in muscle cross-sectional area are concomitant with edema-induced muscle suggests
A
growth cannot be determined as early as 3 weeks due to swelling (seen 10-12 weeks)
22
Q
Early RT-induced increases in muscle cross-sectional area are concomitant with edema-induced muscle shows that
A
muscle damage (swelling) occurs each week, and changes at 3 weeks, which coincides with “growth” from other studies as continued exercise decreases swelling
23
Q
Echo-intensity
A
pixelated images giving each pixel a # based on lightness or darkness of pixel; changes in color determine how much fluid (swelling) there is
24
Q
Differentiating swelling and hypertrophy through indirect assessment of muscle damage in untrained men following repeated bouts of resistance exercise shows a
A
consistent up and down nature, but swelling goes down and does not accumulate when not training (e.g. muscle growth)
25
Can changes in echo-intensity be used to detect the presence of acute muscle swelling?
is able to measure fluid change, but echo-intensity does not change, therefore no consistency (random and meaningless)
26
Role of FFM accumulation and skeletal muscle architecture in powerlifting performance
shows FFM and strength as a correlation, that people with more muscle are stronger (linear relationship)
27
Time course story based on
assumptions of muscle size and strength; change scores instead of baseline, no guarantee that growth means you are the strongest
28
Neuromuscular Adaptations after 2 and 4 weeks of 80% vs. 30% 1 RM RT to failure suggested that
training-induced hypertrophy may cause increases in muscle stiffness which would attenuate the MMG signal
29
Neuromuscular Adaptations after 2 and 4 weeks of 80% vs. 30% 1 RM RT to failure showed a decrease in
MMG AMP at 80% and 90% of MVIC from baseline to week 4 after both 80 and 30% 1 RM training
30
MMG tests for
muscle-tendon stiffness vs. lack of; can infer on muscle activation
31
Neuromuscular Adaptations after 2 and 4 weeks of 80% vs. 30% 1 RM RT to failure show similar
hypertrophy was observed between groups, supporting the hypothesis regarding diminishing need for motor unit recruitment or increased muscle stiffness caused by muscle hypertrophy
32
Muscle fiber hypertrophy in response to 6 weeks of high-volume RT in trained young men is largely attributed to sarcoplasmic hypertrophy study found
no change in muscle size
33
Muscle fiber hypertrophy in response to 6 weeks of high-volume RT in trained young men is largely attributed to sarcoplasmic hypertrophy study limitations
No control group
Random nature of included measures (error or damage from high volume)
Images show great growth which indicates to error (thought to be swelling or damage)
34
Key evidence to conclude that muscle fiber hypertrophy in response to 6 weeks of high-volume RT in trained young men is largely attributed to sarcoplasmic hypertrophy is
a decrease in concentrations of myosin and actin after 6 weeks of training
35
31 subjects from muscle fiber hypertrophy in response to 6 weeks of high-volume RT in trained young men is largely attributed to sarcoplasmic hypertrophy determined
6 weeks did not induce myofiber hypertrophy
36
Evidence level for Longitudinal Growth of Fascicles
High
37
Evidence level of Radial Growth of Fascicles
High
38
Evidence level of Myofiber Splitting
Low
39
Evidence level of Myofiber Hyperplasia
Low & Controversial
40
Evidence level of Longitudinal Growth of Myofibers
Mixed - Model Dependent
41
Evidence level of Radial Growth of Myofibers
Extremely High
42
Evidence level of Sarcoplasmic Hypertrophy
Low and Controversial
43
Evidence level of Myofribril Hypertrophy
Low
44
Evidence level of Myofibril Hyperplasia
Very Low
45
Muscle fiber activation is unaffected by load and repetition duration when resistance exercise is performed to task failure study key points
EMG is not a good tool for activation due to firing inconsistencies in muscle
Performing resistance exercise with heavy loads is proposed to be necessary for the recruitment of larger motor units and activation of T2 muscle fibers leading to T2 fiber hypertrophy
Subjects perform resistance exercises to failure with heavy and light loads with both normal and longer repetition duration (time under tension)
T1 & 2 muscle fiber glycogen depletion was determined by neither load nor repetition duration
Surface EMG amplitude is not related to muscle fiber glycogen depletion or anabolic signaling
Performing resistance exercises to failure, regardless of load or repetition duration, necessitates activation of T2 fibers
46
How we adapt to exercise
exercise generates signals that are sensed by sensor proteins, conveyed and computer by signal transduction proteins
47
Why do we adapt
based on overload, linking loading of bones (and other organs) to their adaptation
48
Supercompensation
describes a decline in an undefined y-axis variable during exercise and recovery after exercise
Recovery does not reach baseline, but overshoots initial value
49
Exercise Adaptation has 4 fundamental flaws
1. happens for muscle glycogen after endurance exercise and feeding
2. is a time-course but not a mechanism
3. implies recovery periods are essential for adaptation
4. little evidence that supercompensation time course is essential for adaptation
50
General Adaptation Syndrome
Alarm Phase: initial phase of training when stimulus is first recognized and performance generally decreases in response to fatigue
Resistance Phase: 2nd phase, adaptation occurs, system is returned to baseline or elevated
Supercompensation Phase: new level of performance capacity, occurs in response to adaptive response
Overtraining Phase: stressors are too high, performance can be suppressed
51
General Adaptation Syndrome is
NOT a great model for adaptation
52
Limitations in delayed myonuclear addition, myofiber hypertrophy, and increases in strength with high-frequency low-load blood flow restricted training to volitional failure study
should be individualized to THEIR cut-off points for BFR and NOT standardized cutoff points
small sample size
if 3 weeks is "too soon" for growth, two-a-day training may not show more adaptation
several muscle biopsies
53
In delayed myonuclear addition, myofiber hypertrophy, and increases in strength with high-frequency low-load blood flow restricted training to volitional failure study, supercompensation
doesn't change until 10 days post, no growth during protocol
54
Why does supercompensation not change in delayed myonuclear addition, myofiber hypertrophy, and increases in strength with high-frequency low-load blood flow restricted training to volitional failure study
most likely due to muscles still recovering and building proteins; T2 fibers overworked and they take longer to recover
55
Change in strength in delayed myonuclear addition, myofiber hypertrophy, and increases in strength with high-frequency low-load blood flow restricted training to volitional failure study occured
20 days post
56
Which muscle fibers increased over 10 days post in delayed myonuclear addition, myofiber hypertrophy, and increases in strength with high-frequency low-load blood flow restricted training to volitional failure study
T1 fibers
57
Signal Transduction Hypothesis
specific sensor proteins detect exercise-related signals, which are computed by transduction pathways or networks; early signals downstream events including gene transcription, translation, or protein synthesis and breakdown
58
Mechanical load leads to ______ which leads to _____ or ______ which creates ________
signaling; transcription & post-transcriptional modifications; translation & posttranslational modifications; proteins
59
Results of RT variable manipulations are less relevant than intrinsic biology in affecting muscle fiber hypertrophy study
groups similar across time, no significant difference in proteins; frequent manipulation of RT variables does not enhance hypertrophy response at fiber level when RT is performed, or near to, concentric failure
60
Gene
stretch of DNA that encode mostly proteins
major building blocks of cells
61
For genes to be expressed as a protein
DNA needs to be transcribed into RNA
62
RNA polymerase scans along chosen gene to
read DNA and synthesize an RNA copy of the DNA
63
Newly synthesized RNA is spliced by
splicesomes
64
Splicesomes are
enzymes complexes that cut and join RNA
65
During splicing...
RNA is turned to mRNA
66
The concentration of each mRNA depends on
rates of transcription, splicing, and degradation
67
Ribsomes are ________ that bind to _______, read the _______ and add, for each three-base combo, one ________ to the __________
organelles; mRNA; mRNA; amino acid; nascent protein
68
Amino acids are bound to
tRNAs
69
Amino acids bound to tRNA works because
tRNA is paired with the triplet in mRNA and ribosome then attaches amino acid on tRNA to the nascent
70
After ribosomes bind to mRNA they
move along it until release factor enters A-site of ribosome and translation is terminated
71
DNA to Protein Steps
1. Newly synthesized RNA spliced by spliceosomes to make mRNA
2. During translation, mRNA translated to a protein
3. Ribosomes bind to mRNA
4. Release factor enters A-site and translation terminates
72
mRNA translation is
primary process necessary for the development of compensatory hypertrophy
73
Protein degradation primarily responsible for
removal of proteins that are no longer functioning
74
In what scenario does protein degradation not change meaningfully to predict growth overtime
anabolic
75
Mechanisms of protein synthesis include
translation of mRNA combined with posttranslational processing and transport of polypeptide process
76
Short-term, translation increases in protein synthesis can be accomplished via
an increase in translational efficiency
77
Complex networks regulate which steps in the translation process
preferential recognition of specific message, preparation of mRNA, and assembly of the translation machinery
78
Translation increases in protein synthesis regulated via
changes in signaling activity focused on existing components of translational machinery
79
Long term, increases in translational capacity may be required to
support a sustained increase in protein synthesis
80
Increasing translational capacity requires
synthesis of additional copies of translational components such as ribosomal subunits, ribosomal proteins, initiation, and elongation factors
81
More ribosomes =
more proteins
82
The benefits of higher resistance-training volume are related to ribosome biogenesis study results showed
out of 34 participants, 13 displayed clear benefit of MOD on muscle hypertrophy, and 16 clear benefits of MOD on muscle strength gains
83
The benefits of higher resistance-training volume are related to ribosome biogenesis study results coincided with
greater total RNA accumulation in early phase of training period, suggesting ribosomal biogenesis regulates the dose-response relationship between training volume and hypertrophy
84
On the individual level in the benefits of higher resistance-training volume are related to ribosome biogenesis study, higher training volume was associated with
increased ribosomal biogensis
85
The ability to induce superior increases in ribosomal content in response to higher mechanical and metabolic stress of accompanying higher training volume is necessary to induce
subsequent superiority in growth and strength increases
86
Two general mechanisms of translational initiation
cap dependent & internal ribosome entry site (IRES)
87
Both mechanisms of translational initiation rely on
host of mRNA binding proteins that coordinate recruitment of mRNA to 40s ribosomal unit
88
Binding of mRNA to 40s is typically considered
rate-limiting step in initiation
89
Under pro growth conditions, which mechanism of translational initiation predominates
cap dependent
90
During cell stress, which mechanism of translational initiation is suppressed and which is enhanced
cap dependent suppressed; translation of IRES mRNA enhanced
91
Cap-dependent mechanism is estimates to account for
over 90% of translation
92
Initiation is regulated by what two parallel processes
joining of Met-tRNA and the "activated" mRNA with the 40s subunit of the ribosome
93
Parallel processes are mediated by
two highly regulated eukaryotic initiation factor complex (eIF2 and eIF4F)
94
Function of eIF4F
involves recognition of binding sites on 5' cap structure of mRNA and formation of initiation complex that properly locates mRNA in 40s ribosomal subunit
95
5' cap is where
ribosome attaches on mRNA
96
eIF4F includes
eIF4-A (helicase = unwinds)
eIF4-G (scaffolding)
eIF4-E (cap binding)
97
A critical regulatory step in the formation of eIF4F is the
removal of inhibitor of eIF4e binding protein 4E-BP
98
In an unstimulated state, 4E-BP is
hypo-phosphorylated and binds to eIF4E
99
Binding of 4E-BP to eIF4E prevents
formation of initiation complex by blocking access to eIF4G to eIF4E
100
Dissociation of 4E-BP fromeIF4E is accomplished via
multiple phosphorylationa
101
Multiple phosphorylations allow eIF4G to
bind with eIF4E and assemble the initiation complex to proceed to small subunit of the ribosome
102
In the GTP-dependent process, eIF2 binds to
the initiator tRNA (Met-tRNAi)
103
Binding of eIF2 GTP (Met-tRNAi) forms the
ternary complex
104
The ternary complex binds to _____ and leads to
40s; 43s preinitiation complex
105
As eIF4F-bound mRNA is delivered to 43s
the ternary complex scans the mRNA for its initiator codon and binds to it
106
Once bound, GTP is
hydrolyzed to GDP by eIF2, leading to release of eIF2 GDP and other components, and binding of 60s
107
Alt to mTOR leads to _____ which _______
S6K1; initiates translation
108
mTORC1 is
key mediator of hypertrophy following RT
109
An increase in mTOR phosphorylation in response to
muscle loading
110
Primary action of mTOR
regulate and promote hypertrophy via S6K through regulation of cap-dependent translation and increased expression of components of translational machinery
111
S6K phosphorylation is a marker of
mTOR kinase activity
112
mTOR kinase activity is both necessary and sufficient to
induce hypertrophy which is independent of Akt
113
Propose role of S6K1
phosphorylation of ribosomal S6 protein
114
RPS6 phosphorylation levels are essentially _____ in S6k-deficient mice
normal
115
Under unstimulated conditions, S6k is bound to
eIF3, which is not present in ribosomal pool
116
eIF3 is released following phosphorylation which leads to
further sequential phosphorylations required for full activation
117
Activity of S6K is regulated via
phosphorylation/dephosphorylation
118
Fully activated S6K
phosphorylates a number of initiation factors promoting preparation of transcript and formation of initiation complex
119
S6K participates in
regulation of translation initiation for mRNAs that have 5' cap structures and potentiating elongation process
120
Translation of specific mRNA
can increase in absence of changes in amount of that specific mRNA
121
Following a bout of mRNA in rats, it was found that
rate of muscle protein synthesis per unit RNA was increased
122
Primary mechanism of increased translation efficiency is thought to involve
initiation
123
One level of regulation of initiation efficiency for majority of eukaryotic mRNA is imposed by
size of 5' UTR and level of structural complexity present
124
Code for components of translational machinery
ribosomal proteins, poly (A)-binding proteins, elongation factors
125
An increase in efficiency of translation of 5' TOP mRNAs would contribute to enhancement of
translational capacity
126
Primary limitations that might be imposed by the bulk amount of DNA present in a given myofiber is
the ability to sustain large increases in translation
127
of copies of rRNA and tRNA genes can only be increased via
acquisition of additional copies of template DNA
128
Evidence suggests general increase in translational efficiency occurs at
onset of hypertrophy
129
Early adaptations in protein production may include an
increase in translational efficiency and an acceleration of synthesis of new ribosomes
130
Six weeks of low-load blood flow restricted and high-load resistance exercise training produce similar increases in cumulative myofibrillar protein synthesis and ribosomal biogenesis in healthy males study findings support
notion that BFFRE provides a low-load approach to stimulate long-term protein turnover
131
In rats subjected to synergistic ablation (cut) to produce muscle hypertrophy, there was an approximately ______ increase in the RNA: DNA ratio after ______ of overloading
30%; 15 days
132
After 90 days of overload, in rates, the RNA content of the muscles was increased by approximately ________, however, the RNA:DNA ratio was __________ relative to control values due to the acquisition of new nuclei
1.8-fold; no longer elevated
133
Why can’t a given myofiber just turn up the production of the translational apparatus until sufficient amounts of protein have been produced?
Could be a form of functional compartmentation resulting from limitations in movement of gene products
134
Types of muscle
skeletal, cardiac, smooth
135
Characteristics of skeletal muscle
multinucleate, mitochondria, t-tubules, myofibrils, and sarcomeres, specific terms for intracellular structures
136
Specific terms for intracellular structures
sarcolemma = plasma membrane
sarcoplasm = cytoplasm
sarcoplasmic reticulum = smooth ER
137
Connective tissue coverings
epimysium (large), perimysium (fascicles), endomysium (end)
138
Satellite cells (location & role)
located in the sarcolemma, regenerative cell growth, role in hypertrophy
139
Myofibrils
give striated appearance, arrangements of actin and myosin filaments
140
Myofibrils are made of
myosin & actin
141
Myosin is
thick
142
Actin is
thin
143
Tropomyosin
covers myosin binding sites on actin
144
Troponin
binds to tropomyosin and holds it over the myosin binding site
145
Skeletal muscle structure
muscle on bone, muscle, fascicle, myofibril, sarcomere, proteins
146
Study: Human Striated Muscle Ultrastructural changes accompanying increases in strength without hypertrophy --> Limitation
Only study like this
147
Study: Human Striated Muscle Ultrastructural changes accompanying increases in strength without hypertrophy --> methods
2 biopsies prior to training, 1 after
Leg circumference, subcutaneous fat, leg ext strength
Five days/week for 10 weeks
Five reps 2/3 max leg ext & 5 max isometric contractions at 125º
20 round trips on stairs covering 3 floors
Remeasured for strength for new max loads
148
Study: Human Striated Muscle Ultrastructural changes accompanying increases in strength without hypertrophy --> results
No sig change in diameter of cells
Three sig measures: myosin filament concentration, distance between myosin filaments, # of actin around myosin
Change in ratio if unexplainable
149
Muscle Chemical Composition
75% water, 20% protein, 5% other
150
Neurotransmitter Release and Action (6 steps)
1. AP reaches terminal
2. Voltage-gated Ca channels open (Ca enters synaptic terminal and increases cytosolic Ca concentration)
3. Ca enters terminal
4. Release of ACh and diffuses into the cleft
5. ACh binds to postsynaptic receptors
6. ACh removed from synaptic cleft
151
Synaptic Transmission at NMJ (3 steps)
1. Postsynaptic receptor (NAChR) allows diffusion of Na into the cell and K out
2. Inactivation - ACh Esterase (AChE) is localized in folds of endplate and hydrolyses the ACh to choline and acetate
3. Choline is taken back into the nerve terminal and is used to synthesize new ACh
152
Generation of action potentials
Current produced by EPP spreads to the surrounding muscle membrane
Local current depolarizes surrounding muscle membrane to a threshold and activates voltage-gated Na channels to produce action potentials
153
Voltage-dependent Ca channels located in
t-tubules
154
Activation of Ca release channels allows Ca to flow out of
cytosolic Ca into SR
155
Ca-ATPase in the SR membrane pumps out
cytosolic Ca into SR
156
Events of excitation-contraction coupling (6 steps)
1. Action potential travels down into t-tubules
2. Ca released from lateral sac
3. Ca binds to troponin removing tropomyosin
4. Cross-bridge binds and generates force
5. Ca taken up
6. Ca removal from troponin which restores tropomyosin
157
Sliding Filament Theory
Force generation produces shortening of skeletal muscle fiber, the overlapping of the thick and thin filament in each sarcomere propelled by movements of the cross-bridge
Ability of muscle fiber to generate force and movement depends on contractual proteins actin and myosin
158
A-band
thick
159
I-band
thin without thick
160
H Zone
thick without thin
161
Steps of Cross-Bridge Cycle (4)
1. Cross bridge binds to actin
2. Power stroke pulls actin toward the center of the sarcomere
3. ATP binds to the myosin head and causes cross bridge to detach
4. Hydrolysis of ATP energizes cross-bridge
162
Role of ATP in Cross Bridge Cycle
Hydrolysis of ATP energizes the cycle
Binding of ATP breaks the linkage
No ATP means cross-bridge remains attached to actin producing rigor mortis
163
Rigor Mortis
peaks 12 hours after death and disappears 48-60 hours after death due to breakdown of muscle
164
Troponin's three subunits
Inhibitory
Calcium-binding
Tropomyosin-binding
165
Calcium binding sites are on
troponin
166
Binding of calcium to the C subunit of troponin causes
conformational change of troponin which causes tropomyosin to move and expose myosin binding sites on actin
167
As long as binding sites on actin remain exposed
cross-bridges will repeat and result in large displacements of the filaments
168
SR
endoplasmic reticulum - like organelles that store calcium in skeletal muscle (and cardiac) muscle fibers
Surrounds myofibrils
169
Lateral Sacs
enlargements at the end of ST and associated with t-tubules
170
T-tubules
invaginations of muscle plasma membrane (sarcolemma)
171
Sequence of Events in Activating Skeletal Muscle (13 steps)
1. Activation of motor neuron cell body leads to action potential
2. Action potential at the nerve terminal of a motor neuron causes the release of ACh at the neuromuscular junction
3. ACh activated nicotine receptors in the endplate producing end-plate potential
4. The end-plate potential depolarizes surrounding muscle membrane and produces an action potential
5. Action potential propagates to the end of muscle fiber
6. Action potential enters t-tubules and activates voltage-gated calcium channels
7. Calcium is released from SR via calcium release channels
8. Ca binds to troponin
9. Tropomyosin moves to uncover myosin binding sites on actin
10. Cross bridge cycling begins
11. Calcium ATPase pumps calcium back into SR
12. Calcium dissociates from troponin
13. Tropomyosin covers myosin binding sites and cross-bridge cycling ends
172
The plateau and descending limb of isometric/concentric force-length relationships are explained by
the amount of overlap between actin and myosin filaments
173
When a muscle is stretched while activated and held at a final length long enough for force transients to cease, the steady force achieved is
always higher than steady force developed when the muscle is activated when held isometrically at the same final length
174
When lengthened into a position you produce ______ force; after relaxing there is
greater; more tension in the muscle that was lengthened to get into position
175
Force enhancement after active muscle stretching was maintained when muscles were
deactivated
176
Passive force after deactivation of myofibrils was increased after
active stretching
177
Passive force enhancement in muscle and fiber preparations occurs in
single myofibrils
178
What is the main source of passive force in myofibrils it may be responsible for passive force enhancement in myofibrils
Titin
179
Titin extends from ____________ & is fixed to the thick filament in the _______
sarcomere Z-disc to M band; A-band
180
Titin runs freely in the
I-band region
181
Skeletal muscles are activated by the release of
Ca from the SR
182
Titin’s stiffness might be changed by
bringing calcium to specific attachment sites
183
Stretching myofibrils results in
higher passive forces
184
Passive structures of muscles are ____________ when passively stretched and become _____________ during active stretching
soft and compliant; hard and stiff
185
Titin forces increase when _________ decreases
actin-myosin force
186
Titin provides stability for sarcomeres on
descending limb of force-length relationship
187
When titan is eliminated, all passive and active force transmission across sarcomeres is
lost
188
Titin could increase its inherent stiffness upon activation and stretch by
binding calcium upon activation
189
Titin could shorten its active spring length, becoming stiff, by
binding proximally to actin
190
Training eccentrically is a longer energy demand for a
greater force output
191
Genetics
Science focused on the transmission of traits of phenotypes across generations
192
Quantitative traits such as _____________________ exhibit large inter-individual differences
total adiposity, heart size, or VO2max
193
Evidence suggests there is a significant genetic component to human variation in
skeletal muscle strength and endurance
194
Acute intervention data implies genes regulating translation initiation signaling influence progressive skeletal muscle hypertrophy in response to
RT
195
Myostatin gene is expressed almost exclusively in cells of ___________ throughout embryonic development
skeletal-muscle lineage
196
Systemic over-expression of the myostatin gene leads to a ________ characterized by extensive muscle loss
wasting syndrome
197
A basic argument against generalized reliance on transgenic and/or knockout animals is that
rarely does a single gene control complex physiological systems
198
What type of contractions tend to produce the greatest amount of muscle damage
lengthening
199
What contractions produce minimal muscle damage
maximal isometric contractions at 90 degrees elbow flexion
200
What contractions produce muscle damage
maximal isometric contraction at 20 degrees elbow flexion
201
Direct marker of muscle damage
muscle biopsy
202
Factors that contribute to EIMD
number of contractions
203
As number of lengthening contractions increases
greater amount of EIMD is found
204
High forces do not necessarily dictate the amount of muscle damage produced, but
muscle fiber strain produced during the lengthening contractions
205
What speed of lengthening velocities produce more muscle damage
faster
206
DOMS is due to
inflammation of the connective tissue in or around the muscle
207
Inflammation from DOMS appears to ______, probably situated in _________ which respond
sensitize mechanoreceptors; connective tissue sheaths; excessively when the muscle is stressed and massaged
208
What is more related to induction of DOMS and accounts for the poor relationships observed between soreness, plasma CK activity, and decrement of muscle function?
connective tissue damage
209
Possible that what contributes to the sensation of DOMS
afferents from muscle spindles
210
The study of the development of skeletal muscle hypertrophy through RT: the role of muscle damage and muscle protein synthesis states
damage is not necessary for growth
211
Exercise-Induced Muscle Damage and Hypertrophy: A Close Look Reveals the Jury is Still Out discusses
what leads to maximum muscle hypertrophy (metabolic stress, mechanical tension, muscle damage)
212
Does blood flow restriction result in skeletal muscle damage
available evidence does not support that BFR in combination with low-intensity exercise increases the incidence of muscle damage
available literature suggests that minimal to no muscle damage is occurring with this type of exercise
213
Which contractions produce greater levels of force while recruiting fewer motor units
lengthening
214
High levels of tension in stretched sarcomeres can cause
overlap between myofilaments to become disrupted
215
Z-disk streaming
the cytoskeletal protein matrix of the muscle fiber will bear added tension from disruption in overlap between actin and myosin
216
Muscle injuries that result from eccentric contractions involve extensive disruptions to
the intermediate filament system
217
The intermediate filament system contributes to
passive stiffness of muscle and maintaining the architecture of myofibrils
218
Desmin
most prevalent intermediate filament protein in skeletal muscle
219
Desmin links
Z-disks to one another and to cell membrane at costameres at myotendinous junction
220
Eccentric contractions can cause a selective and rapid damage to
the desmin intermediate filament lattice
221
Desmin filaments are degraded selectively by
proteases
222
Mechanical stress to the muscle fiber can damage the
excitation-contraction coupling complex resulting in a loss of force
223
Excitation-contraction coupling complex is disrupted specifically in
the connection between the t-tubules and ryanodine receptors of sarcoplasmic reticulum membrane
224
Junctophilin allows
direct connection between t-tubule and ryodine receptor
225
Junctophilin levers are significantly reduced following
50 lengthening contractions
226
Junctophilin damage was significantly associated with
decline in force
227
Junctophilin keeps what on path to ryanodine receptor
Ca
228
Cell membrane of muscle cells also experiences extensive damage during
acute muscle injuries
229
Membrane lesions are large enough to
allow the unregulated influx of extracellular marker dyes bound to albumin and unregulated efflux of muscle cytosolic proteins (i.e., creatine kinase)
230
Increased accumulation of __________ into injured muscle fibers and the increased ________________in the extracellular space is progressive for days following increased muscle loading or after eccentric contractions
extracellular marker dyes; concentration of cytosolic proteins from muscle
231
Delay in the days following increased muscle loading or after eccentric contractions indicate
much of the damage to the cell membrane
232
Unregulated influx of Ca leads to
immense disruptions or normal homeostasis
233
Activation of calcium-dependent proteases (calpains) within the muscle cytosol is an
important pathogenic consequence of membrane damage during muscle injury
234
Calpain activation in injured muscle can
promote muscle damage
235
Elevations in cytosolic calcium concentration would be a key event in
the rapid activation of calpain proteolytic activity
236
Eccentric contractions produce rapid elevations in
cytosolic calcium
237
In the presence of elevated cytosolic calcium, calpain activity can be regulated by
calpastatin
238
Both desmin and α-actinin (the major structural protein in Z-disks) can be injured with
eccentric exercise
239
Exercise-induced muscle injury: A calpain hypothesis study states
Ca is agent for destruction in the muscle cell in days following exercise
240
Unregulated calcium influx into injured muscle fibers can promote
muscle damage through mechanisms that are independent of calpain-mediated proteolysis
241
Activation of _______________ may be especially important for increasing membrane damage in muscle following eccentric contractions or other injuries
phospholipase A2 (PLA2) by calcium
242
PLA2 is expressed constitutively in
muscle and other cells of vertebrates
243
PLA2 hydrolyzes
glycerol at the cell membrane to generate arachidonic acid
244
Arachidonic acid can function as
a second messenger or be metabolized
245
Arachidonic acid promotes
inflammation
246
Increases in PLA2 activation can cause damage to
the structure of myofibrils; resembles defects caused by damaging eccentric contractions
247
Production of free radicals in skeletal muscle is modulated by
the contractile state of muscle
248
Production of free radicals provides a mechanism through which
signaling pathways can be regulated as a function of muscle activity
249
Production of _______ and ___________ is low in resting muscle but increases rapidly to levels 10-fold greater soon after the onset of contraction
superoxide; nitric oxide
250
The delay in the appearance of cytosolic proteins from muscle in the serum of animals following increased muscle use or muscle injury indicates that
much of the membrane damage is not a direct consequence of mechanical stresses, but instead, membrane damage is largely attributable to some other injury mechanism
251
The first morphologically discernible signs of muscle damage postexercise coincided with
the invasion of neutrophils into the muscle
252
Biggest culprit to muscle membrane damage
neutrophils
253
Exercise-induced muscle damage
Delayed onset muscle soreness
Decreased force production
Decreased range of motion
Swelling of exercised limb
Increased muscle proteins in blood
254
The most reliable marker of indicating muscle damage is
sustained decreases in force production
255
Decrement in muscle force production is highly correlated with
myofibrillar damage
256
Nosaka et al. examined the association between indirect markers of muscle damage and soreness levels and determined
no difference found between soreness
soreness did not correlate well with other indirect markers of muscle damage
257
Using DOMS alone to assess magnitude of muscle damage would
not be correct given DOMS does not correlate well with other indirect markers of muscle damage
258
Repeated bout effect
refers to protection of attenuation in muscle damage markers observed following a second bout of exercise
259
A damaging bout of exercise through eccentric actions will result in
protective effect in subsequent repeated bouts
260
Protective effect of repeated bouts also occurs from
exercise that does not produce severe muscle damage
261
Initial exercise stimulus may induce
cellular or neural adaptations that produce a protective effect
262
Potential candidates for the protective effect
Heat Shock Proteins
Increased cytoskeletal proteins
Strengthening of extracellular matrix
263
Heat Shock Proteins may protect muscle from future damage by aiding in
refolding of damaged proteins and folding of newly synthesized proteins after exercise
264
What levels significantly increase after 2 bouts of exercise, particularly at z-disks and sites of myofibrillar disruption and suggested they play a role in protecting the muscle from future damage
HSP27 & HSP70
265
Using proteomic technique, a damaging bout of downhill running significantly increased
desmin and actin protein expression
266
increases in desmin, dystrophin, and titin mRNA levels have been shown to increase following
downhill running
267
Downhill running findings suggest that
cytoskeletal proteins may play a role in future protection of the muscle
268
Mackey et al. used intermittent electrical stimulation of the gastrocnemius to produce muscle damage and found
a significant decrease in heat shock proteins and tenascin C after the 2nd bout of exercise when compared to the 1st bout of exercise 30 days earlier
20 days after 1st bout, stellite cells were significantly elevated, and also extracellular matrix lamin-B1 and collagen types 1 and 2 were elevated 6-9 fold
269
For a given force production, less motor unit activation is required for what type of contractions?
eccentric
270
Pierrynowski et al. suggested that
increased synchrony of motor unit firing may reduce myofibrillar stresses during a repeated bout
271
Bigland and Lippold suggested that
less motor unit activation associated with eccentric contractions may provide the opportunity to learn more efficient recruitment for a repeated bout
272
Hortobágyi et al. demonstrated similar neural adaptations in women, with only 6 weeks of eccentric & concentric training
eccentric: strength increased by 42% while iEMG increased by 89%
concentric: strength increased by 36% and iEMG increased by 39%
273
Nosaka and Clarkson have suggested
neural adaptation would better distribute the workload among fibers
274
Komi and Buskirk noted
a large increase in iEMG at 3 weeks into training, suggesting that increases in strength were not due to hypertrophy
275
Muscle damage has been referred to as _________________ consistent with materials fatigue typical of ductile material subjected to cyclic tensile loading
mechanical failure of individual myofibrils
276
Materials fatigue refers to structural failure caused by ___________________ and is distinct from failure caused by the application of a single stress that exceeds the materials ultimate tensile strength
cumulative tensile stress
277
Lieber and Fridén demonstrated
damage to rabbit tibialis anterior muscles was a function of the length to which the muscle was elongated during stimulation rather than the magnitude of the contractile stimulus
278
Traditional Sarcopenia Model of Skeletal Muscle loss shows
a linear decline
279
Catabolic Sarcopenis Model of Skeletal Muscle loss shows
a decline in function with various incidents/accidents; retrain to get stronger, but never recover back to baseline; leads to less confidence, less training, and more muscle loss
280
For both men and women, the decrease in lean body mass is greater in the
lower limbs than in the upper limbs
281
Studies showed that motor unit number remained fairly constant up to the __________ but from _________ it declined by _________
sixth decade of age; 60-80 years of age; 50%
282
Lexell found using whole muscle cross-sectional slices rather than bioptic samples that there was a similar decline in the number of ________________
type 1 and type 2 fibers
283
Greater loss of ___________ may occur up to the late ________________, also ____________ are lost and a new “balance” between the two types is reached as suggested by the similar Type ½ fiber ratio in individuals aged ________
Type II fibers ; 70’s, past 80 years; type 1 fibers; 85-97 years
284
Original studies reported that postabsorptive MPS was reduced with aging which may be related to
Health status
Physical activity levels
Sensitivity of tests
285
When showing the muscle protein synthesis (%/hr) over 3, 6, and 24 hours post,
the older population had a harder time showing the same response; to facilitate MPS there needs to be more protein intake
286
Aging is associated with an
impaired skeletal MPS response to resistance exercise only, this impairment is overcome with postexercise nutrient ingesting
287
Increased hepatic first-pass uptake of amino acids may limit the stimulus required to
trigger MPS in the elderly
288
Elderly requires relatively larger quantities of protein after exercise to robustly stimulate ________ relative to their younger counterparts
MPS rates
289
Young people who consumed _______ of protein were observed to be sufficient to induce __________
20g; maximal stimulation of MPS
290
Whey protein >< soy protein for inducing increases in muscle protein synthesis
whey > soy
291
Why is whey protein better for inducing increases in muscle protein synthesis
likely due to leucine
292
Leucine is the
key amino acid that triggers the stimulation of key regulatory proteins and the initiation of MPS from a state of net negative protein balance
293
Potency of leucine was shown when subjects consumed a ___________ of protein (6g) with _________ and elicited the ___________ as an optimal dose
lower dose; added leucine; same MPS response
294
No benefit has been observed in terms of leucine promoting lean mass or strength gains due to
elderly consuming adequate protein
supplementation of leucine resulted in reducing systemic valine and isoleucine concentrations
295
Long-term leucine supplementation (7.5 g/d) does or does not augment skeletal muscle mass or strength and does or does not improve glycemic control or the blood lipid profile in healthy elderly men
does not; does not
296
Aging is associated with impairment in the _____________________ and _____________ to both resistance and endurance type exercise
muscle protein anabolic response to feeding; the muscle protein synthetic response
297
Kumar reported
a blunting of MPS and mTORC1 signaling in the elderly compared to the young
298
A doubling of resistance exercise volume (from 3 to 6 working sets) substantially
increased MPS rates in the elderly, but not in the young
299
Abrupt muscle disuse is known to reduce
postabsorptive and postprandial rates of MPS in both young and old
300
14 days of reduced ambulatory activity via forced step reduction reduced/introduced/increased...
Reduced leg lean mass
Reduced postabsorptive/postprandial insulin sensitivity
Introduced Anabolic resistance to amino acids
Increased circulating markers of inflammation
301
Elderly muscle is less sensitive to the
antiproteolytic effects of insulin
302
Wilkes compared groups of young and elderly participants during a euglycemic, hyperaminoacidemic clamp and reported that insulin concentrations at ~15 uIU/mL (similar to a low glycemic meal) were
less effective in elderly compared to young in reducing net negative protein balance
303
At moderate availability, the effect of insulin on LPB is ________________, and this effect may be mediated through blunted Akt-PKB activation
diminished in older humans
304
The normal insulin-mediated increase in endothelial-dependent vasodilation has been reported to be
impaired in aging
305
Impaired insulin-mediated endothelial-dependent vasodilation may be expected to result in
reduced capillary recruitment and skeletal muscle microvascular perfusion and subsequently reduced amino acid availability
306
Growing evidence suggests a possible link between
endothelial dysfunction and anabolic resistance of skeletal muscle
307
A prior bout of aerobic exercise increases the anabolic effect of nutrient intake in
older adults
308
The increases in the anabolic effect of nutrient intake prior to aerobic exercise appear to be mediated by
exercise-induced improvement in nutrient-stimulated vasodilation and nutrient delivery to muscle rather than to improved insulin signaling
309
Mixed nutrient ingestion and the resulting hyperinsulinemia can promote increases in the
microvascular perfusion in the young
310
When blood flow and microvascular perfusion are maximally stimulated pharmacologically, MPS is stimulated to
an equivalent extent in young and old via insulin
311
Insulin may promote skeletal MPS, but the ability to do so may be contingent upon its ability to stimulate
endothelial-dependent nitric oxide generation and an increase in muscle microvascular perfusion and amino acid delivery
312
Pharmacological enhancement of muscle perfusion and amino acid availability during hyperinsulinemia improves the
muscle protein anabolic effect of insulin in older adults
313
Blood flow, muscle perfusion, phenylalanine increased significantly in
insulin plus sodium nitroprusside (SNP)
314
The effects of consuming a high protein diet (4.4 g/kg/d) on body comp in resistance-trained individuals study found
no significant changes in the control group for any variable
significant increase in total energy and protein intake in the high protein group
315
The effects of consuming a high protein diet (4.4 g/kg/d) on body comp in resistance-trained individuals study key finding
consuming a hypercaloric high protein diet has no effect on body comp in resistance-trained individuals
316
Myofibrillar muscle protein synthesis rates subsequent to a meal in response to increasing doses of whey protein at rest and after resistance exercise study found
20 g and 40 g had greater response of myofibrillar than low 10 g
MPS reached upper limit with 20 g
40 g failed to further augment postabsorptive rates and elicited marked increase in rate of indicators of whole-body amino acid catabolism
increase in amino acid oxidation greater with ingestion of 40 g whey
Ureagenesis was greater with ingestion of 20-60 g whey
317
A Moderate Serving of High-Quality Protein Maximally Stimulates Skeletal Muscle Protein Synthesis in Young and Elderly Subjects study found
A large (340 g) serving of lean beef increase mixed muscle protein synthesis by approx. 50% in young and elderly
A moderate portion (113 g) represents an equally effective and more energetically efficient means of stimulating MPS than three-fold larger serving
Multiple moderate-sized servings of high-quality protein-rich foods over the course of the day may represent an effective means of optimizing potential for muscle growth while permitting greater control over total energy and nutrient intake
318
Nutritional interventions to augment resistance training-induced skeletal muscle hypertrophy
Pre-exercise: high effort. time under tension, volume, frequency of bouts, training 'age' = negative net protein balance
Post-exercise: 0.4 g/kg/meal (young), leucine (3g / meal), 4 meals/day, pre-sleep (0.5-0.6 g/kg) = positive net protein balance
319
Negative net protein balance
breakdown and removal of damaged and/or dysfunctional proteins
320
Positive net protein balance
synthesis of new proteins for repair and growth
321
Muscle full effect after oral protein: time-dependent concordance and discordance between human muscle protein synthesis and mTORC1 signaling study found at 45-90 minutes after oral protein bolus,
Mean concentrations remained elevated
322
Muscle full effect after oral protein: time-dependent concordance and discordance between human muscle protein synthesis and mTORC1 signaling study found increases in
phosphorylation of ribosomal protein kinase S6 and 4E-binding protein 1 was superimposable with MPS responses until 90 min
322
Muscle full effect after oral protein: time-dependent concordance and discordance between human muscle protein synthesis and mTORC1 signaling study found MPS decline in face of
continued availability of activating stimulus, it is likely that muscle possesses a mechanism to gauge its capacity to synthesize new proteins
323
Muscle full effect after oral protein: time-dependent concordance and discordance between human muscle protein synthesis and mTORC1 signaling study found activity of
protein kinase B (PKB) and phosphorylation of eukaryotic initiation factor 4G preceded rise of MPS
324
The corticospinal tract controls
voluntary movement; particularly fine, isolated movements of fingers and hands
325
The corticospinal tract cell body is located
in the cerebral cortex in an area called "primary motor cortex"
326
The corticospinal tract axons descends to
lower medulla and spinal cord
327
The corticospinal tract axons synapse on
skeletal motor neurons (alpha)
328
Axons of alpha motor neurons innervate
skeletal muscle
329
Any interruption in the corticospinal tract will produce
weakness (partial damage) or paralysis (total damage)
330
Axons from neurons in the brainstem form pathways that descend into the spinal cord to influence ___; pathways are referred to as _______
motor neurons; extrapyramidal system
331
Most axons of the brainstem remain
uncrossed; affect muscles on same side of the body
332
What large muscle groups do brainstem pathways coordinate for?
Upright posture, locomotion, balance
333
Motor Neuron
neurons that innervate skeletal muscle fibers
334
Motor neurons have a
large diameter, are myelinated, and have fast conduction
335
Cell bodies of motor neurons are located in
brainstem and spinal cord
336
Motor unit
innervated by motor neuron and muscle fiber
337
Motor neurons can innervate
small numbers of muscle fibers (fine control) or large numbers of muscle fibers (gross control)
338
Major sites of fatigue (4)
excitatory input to higher motor centers, excitatory drive to lower motor neurons, motor neuron excitability, neuromuscular transmission
339
Identification of specific sites involved in central fatigue is problematic as
it's difficult to separate factors mediated by changes in afferent inputs from suprasegmental alterations
340
Proponents of a significatn role for central fatigue suggests
the decline in alpha motor neuron firing rate is excessive and results in reduced force caused by too low a firing rate and/or a reduction in number of active motor neurons
341
Net decline in alpha motor neuron facilitation ue to
combined effects of reduced 1a (muscle spindle) afferent input and increased activation of group III and IV muscle afferents activating inhibitory interneurons
342
Firing rate of alpha motor neurons decreases due to
altered ionic currents (increases potassium and decreased sodium) that are intrinsic properties of the motor neuron
343
Changes in alpha motor neuron facilitation reduces likelihood of
an MVC producing optimal activation of alpha motor neuron pool
344
Group 3 muscle afferents are
mechanical
345
Group 4 muscle afferents are
metabolic
346
Central fatigue can be estimated by
twitch interpolation
347
Twitch interpolation delivers
maximal electrical stimulus to motor nerve or contracting muscle
348
During twitch interpolation, look for
superimposed twitch during an MVC
349
If twitch is observed during twitch interpolation
not all motor neurons have been recruited & some motor neurons are not firing at optimal frequency
350
Prolonged endurance exercise (2 hours) can
decrease brain stores of glycogen
351
Brain stores of glycogen are important because if depleted it manifests in
decrease ability for recall on memory tests
352
Across 120 minutes of exercise, glycogen content in areas of brain
increased
353
Decrease in brain glycogen is a possible factor for
exercise-induced central fatigue
354
Exercise-induced fatigue defintion
acute impairment of exercise performance that includes both an increase in perceived effort and eventual inability to produce force/power output
355
What central catecholamines are though to play main roles in central fatigue
dopamine and noradrenaline
356
Administration of noradrenaline (reboxetine) decreased
time trial performance
357
Inhibition of dopamine reuptake did not
delay onset of fatigue
358
Piacentini administration of serotonin/noradrenaline reuptake inhibitor shows
no difference in performance
359
Piacentini acute administration of reboxetine showed
a decrease in performance
360
Roelands administration of reboxetine found a
10% slower time trial performance
361
Neurobiological mechanisms of central fatigue
argues that willingness/motivation to maintain central motor drive is most likely explanation
362
Bigland-Ritchie proposal
inhibition of motor neuron firing rates may results from a reflex involving feedback from mechanoreceptors or group II or IV free nerve endings
363
Nociceptors alert us to
potentially damaging stimuli at skin by detecting extremes in temp and pressure and injury-related chemicals
364
Greater EMG activity of which individuals during maximal voluntary isometric contractions
long term resistance trained
365
M-wave represents properties of the
peripheral
366
M-wave properties no indicative of
increase in motor units (central)
367
Knowing response of muscle might tell if EMG amplitude driven by
peripheral or central systems
368
Detection of surface EMG signals during electrical stimulation of muscle allows for assessment of
peripheral properties without direct involvement of central nervous system
369
Properties of M-wave depends on (7)
number of active motor units, dispersion of innervation zones, distribution of motor unit conduction velocity, location of motor units in muscle, thickness of subcutaneous layers, orientation of detection system, and intracellular action potential shape
370
Less amplitude if signal has to travel through more
subcutaneous fat
371
When correcting for M-wave, no difference for
taking out peripheral, therefore difference are peripheral not central
372
Neural can be linked to
morphological due to adaptations in size
373
EMG commonly used as
surrogate
374
Voluntary EMG normalized to Mmax appears to provide
best index of central neural activation
375
Training at 80% 1 RM induces
greater strength gains and greater neural adaptations
376
lower PTT:MVIC ratio means
greater influence of the central nervous system on activating muscle fibers/units (greater CNS adaptations)
377
MVIC (central) increases disproportionately to
PTT (peripheral)
378
Myofibrillar hypertrophy has a causal impact on
gains in muscular strength (contributory causal)
379
Upon neural recruitment, calcium release, and actin exposure
a specific amount of force is produced by myosin-actin interaction
380
An increase in myosin and actin filaments in parallel can
increase capacity of a myofibril to produce force
381
More sarcomeres in a myofibril through training-induced hypertrophy increases
force production of myofibril
382
Direct trasnfer of force production is
best transfer
383
Myofibers are
multinucleated cells encased by a layer of connective tissue (endomysium), surrounded by interstitial cells such as fibroblasts, immune cells, pericytes and fibro-adipogenic progenitors
384
Satellite cells reside between
endomysium and plasma membrane of myofibers
385
Endomysium is physically coupled to
sarcolemma and everything residing underneath the sarcolemma (sarcoplasm)
386
Myofibers are composed of and surround by
long in-series array of force generating elements called sarcomeres; mitochondrial reticulum and membranous structure called sarcoplasmic reticulum
387
Sarcomeres within myofibrils enact their function through and have regions called
active sliding of thick and thin myofilaments; z-disc, I-band (actin), A-band (myosin)
388
Growth resulting in length is referred to as
longitudinal growth
389
Mechanical load-induced growth can be mediated by
increase in length and/or increase in cross-sectional area
390
Two predominant ways in which mechanical load-induced increases in whole muscle CSA
longitudinal growth of fascicles or radial growth of fascicles
391
Hierarchy of contractile machinery
myofilaments --> myofibrils --> myofibers --> fascicles --> whole muscle
