Transcript Neuromuscular Adaptation

Neuromuscular Adaptation
Muscle Physiology
420:289
Agenda
Introduction
 Morphological
 Neural
 Histochemical

Introduction

The neuromuscular system readily adapts to
various forms of training:
 Resistance
trainin
 Plyometric training
 Endurance training


Adaptations vary depending on type of training
Skeletal muscle adapts in many different ways
 Morphological
 Neural
 Histochemical
Agenda
Introduction
 Morphological
 Neural
 Histochemical

Morphological Adaptations
Morphology: The study of the configuration
of structure of animals and plants
 Most obvious morphological adaptation is
increase in cross-sectional area (CSA)
and/or muscle mass
 Hypertrophy vs. Hyperplasia

Hypertrophy and Myofibrillar
Proliferation

1.
Two mechanisms in which protein is
accumulated  muscle growth
Increased rate of protein synthesis
-Myosin and actin added to periphery of myofibrils
2.
Decreased rate of protein degradation
-Proteins constantly being degraded
-Contractile protein ½ life = 7-15 days
-Regular and rapid overturn  adaptability
Hypertrophy and Myofibrillar
Proliferation

1.
2.
3.
Mechanism of action:
Myofibrils increase in mass and CSA due
to addition of actin/myosin to periphery
Myofibrils reach critical mass where
forceful actions tear Z-lines longitudinally
Myofibril splits
Figure 8.3 b, Komi, 1996
Figure 8.3 a, Komi, 1996
Hypertrophy and Myofibrillar
Proliferation
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Hypertrophy of different fiber types:
Fast twitch:
-Mechanism: Mainly increased rate of synthesis
-Potential for hypertrophy: High
-Stimulation: Forceful/high intensity actions

Slow twitch:
-Mechanism: Mainly decreased rate of degradation
-Potential of hypertrophy: Low
-Stimulation: Low intensity repetitive actions
-FT may atropy as ST hypertrophy
FT ST FOG
Figure 8.5, Komi, 1996
Hypertrophy and Myofibrillar
Proliferation
Role of satellite cells
 History:

identified in 1961 – Thought to be nonfunctioning
 Adult myoblasts
 Believed to be myoblasts that did not fuse into
muscle fiber
 Called satellite cells due to ability to migrate
 First
Brooks, et al., Fig 17.2, 2000
Brooks et al., Fig 17.3, 2000
Hypetrophy and Myofibrillar
Proliferation

1.
2.
3.
4.
Satellite cell activation due to injury:
Dormant satellite cells become activated when
homeostasis disrupted
Satellite cells proliferate via mitotic division
Divided cells align themselves along the
injured/necrotic muscle fiber
Aligned cells fuse into myotube, mature into
new fiber and replace old fiber
Figure 5.7, McIntosh et al. 2005
Hypertrophy and Myofibrillar
Proliferation

1.
2.
Satellite cell activation due to resistance
training:
Resistance training causes satellite cell
activation as well
Interpretation:
-Satellite cells repair injured fibers as a result of
eccentric actions
-Hyperplasia
Hyperplasia

1.
2.
3.
4.
Muscle fiber proliferation during development –
4th week of gestation  several months
postnatal
Millions of mononucleated myoblasts (via
mitotic division) align themselves
Fusion via respective plasmalellae (Ca2+
mediated)
Myotube is formed
Cell consituents are formed  myofilaments,
SR, t-tubules, sarcolemma . . .
Evidence of Hyperplasia
Animal studies:
 Cats: 9% increase in fiber number after
heavy resistance training (Gonyea et al,
1986)
 Quail: 52% in latissimus dorsi fiber number
after 30 days of weight suspended to wing
(Alway et al, 1989)

Evidence of Hyperplasia
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Human study: MacDougall et al. (1986)
Method of estimation:
 Fiber
number Fn of total muscle area (CT scan) and
fiber diameter (biopsy)
 Compared biceps of elite BB, intermediate BB and
untrained controls

Results: Range:
– 419,000 muscle fibers
 Means between groups not significant
 172,000

Conclusion:
 Large
variation between individuals
 Variation due to genetics
Other Morphological Adaptations
Angle of pennation
 In general  as degree of pennation
increases, so does force production
 Why?
 More muscle fibers/unit of muscle volume

 More
cross-bridges
 More sarcomeres in parallel
Sarcomeres in series  displacement and velocity
Sarcomeres in parallel  force
Figure 17.20, Brooks et al., 2000
Figure 17.22, Brooks et al., 2000
Muscle length (ML) to
fiber length (FL) ratio
also an indicator of
force and velocity
properties of muscle
Training?
Other Morphological Adaptations

Capillary density:
 High
intensity resistance training: Decrease in
capillary density
 Endurance training: Increase in capillary density
(body building)

Mitochondrial density:
 High
intensity resistance training: Decrease in
mitochondrial density
 Endurance training: Increase in mitochondrial density
Agenda
Introduction
 Morphological
 Neural
 Histochemical

Neural Adaptations
Recall:
 Motor unit: Neuron and muscle fibers
innervated
 Increasing force via recruitment of
additional motor units  Number coding

Figure 9.6, Komi, 1996
Neural Adaptations
Recall:
 Increasing force via greater neural
discharge frequency  Rate coding
 Maximum force of any agonist muscle
requires:

 Activation
of all motor units
 Maximal rate coding
Neural Adaptations

Timeline
Fig 20.8, Brooks et al. 2000
Neural Adaptations
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
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1.
2.
Increased activation of agonist motor units:
Untrained subjects are not able to activate all
potential motor units
Resistance training may:
Increase ability to recruit highest threshold
motor units
Increase rate coding of all motor units
Neural Adaptations

Neural facilitation
 Facilitation
= opposite of inhibition
 Enhancement of reflex response to rapid
eccentric actions
Fig 20.10, Brooks et al., 2000
Neural Adaptations

Co-contraction of antagonists
 Enhancement
of agonist/antagonist control
during rapid movements
 Joint protection
 Evidence: Sprinters greater hamstring EMG
during knee extension compared to distance
runners
http://www.brianmac.demon.co.uk/sprints/sprintseq.htm
Neural Adaptations

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Neural disinhibition:
Golti tendon organs (GTO):
 Location:
Tendons
 Role: Inhibition of agonist during forceful movements
 Examples:
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
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Muscle weakness during rehabilitation
Arm wrestling
1RM
1. High muscle tension
GOLGI TENDON REFLEX
3. GTO
activation
4. Inhibition of agonist
2. High tendon tension
Figure 4.16, Knutzen & Hamill (2004)
Neural Adaptations
Progressive resistance training may inhibit
GTO
 Anecdotal evidence:

 Car
accidents
 Hypnosis
Neural Adaptations

Resistance training vs. plyometric training
 Load:
RT: Heavy
 PT: Light

 Velocity
of movement:
RT: Low
 PT: High

 Stretch
shortening cycle (SSC):
RT: Minimal
 PT: Yes

Agenda
Introduction
 Morphological
 Neural
 Histochemical

Histochemical Adaptations
Histochemistry: Identification of tissues via
staining techniques
 Recall

Table 12.8, McIntosh et al., 2005
Histochemical Adaptations
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Muscle fiber distribution shifts
Generally believed that ST do not change to FT
and vice-versa
Several studies have observed IIB  IIA in
humans
Fiber shifts from ST to FT and vice-versa have
been observed in animals under extreme
conditions
Histochemical Adaptations

1.
2.
3.
4.
Chronic long term low frequency (10 Hz)
stimulation of rabbit tibialis anterior
3 hours: Swelling of SR
4 days: Increased size/# of mitochondria,
increased oxidative [enzyme], increased
capillarization
14 days: Increased width of Z-line, decreased
SERCA activity
28 days: ST isoforms of myosin and troponin,
decreased muscle mass and CSA
Rapid bursts of stimulation?
Figure 18.2, McIntosh et al., 2005