Neuromuscular Adaptation Muscle Physiology 420:289.
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Transcript of Neuromuscular Adaptation Muscle Physiology 420:289.
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 Two mechanisms in which protein is
accumulated muscle growth
1. 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 Mechanism of action:
1. Myofibrils increase in mass and CSA due to addition of actin/myosin to periphery
2. Myofibrils reach critical mass where forceful actions tear Z-lines longitudinally
3. Myofibril splits
Figure 8.3 b, Komi, 1996
Figure 8.3 a, Komi, 1996
Hypertrophy and Myofibrillar Proliferation 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
Figure 8.5, Komi, 1996FT ST FOG
Hypertrophy and Myofibrillar Proliferation Role of satellite cells History:
First identified in 1961 – Thought to be non-functioning
Adult myoblastsBelieved to be myoblasts that did not fuse into
muscle fiberCalled satellite cells due to ability to migrate
Brooks, et al., Fig 17.2, 2000
Brooks et al., Fig 17.3, 2000
Hypetrophy and Myofibrillar Proliferation Satellite cell activation due to injury:1. Dormant satellite cells become activated when
homeostasis disrupted 2. Satellite cells proliferate via mitotic division3. Divided cells align themselves along the
injured/necrotic muscle fiber4. Aligned cells fuse into myotube, mature into
new fiber and replace old fiber
Figure 5.7, McIntosh et al. 2005
Hypertrophy and Myofibrillar Proliferation Satellite cell activation due to resistance
training:1. Resistance training causes satellite cell
activation as well2. Interpretation:
-Satellite cells repair injured fibers as a result of eccentric actions
-Hyperplasia
Hyperplasia
Muscle fiber proliferation during development – 4th week of gestation several months postnatal
1. Millions of mononucleated myoblasts (via mitotic division) align themselves
2. Fusion via respective plasmalellae (Ca2+ mediated)
3. Myotube is formed4. 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 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:
172,000 – 419,000 muscle fibers Means between groups not significant
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-bridgesMore sarcomeres in parallel
Figure 17.20, Brooks et al., 2000
Sarcomeres in series displacement and velocity
Sarcomeres in parallel force
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 unitsMaximal rate coding
Neural Adaptations
Timeline
Fig 20.8, Brooks et al. 2000
Neural Adaptations
Increased activation of agonist motor units: Untrained subjects are not able to activate all
potential motor units Resistance training may:
1. Increase ability to recruit highest threshold motor units
2. Increase rate coding of all motor units
Neural Adaptations
Neural facilitationFacilitation = opposite of inhibitionEnhancement of reflex response to rapid
eccentric actions
Fig 20.10, Brooks et al., 2000
Neural Adaptations
Co-contraction of antagonistsEnhancement of agonist/antagonist control
during rapid movementsJoint protectionEvidence: Sprinters greater hamstring EMG
during knee extension compared to distance runners
http://www.brianmac.demon.co.uk/sprints/sprintseq.htm
Neural Adaptations
Neural disinhibition: Golti tendon organs (GTO):
Location: Tendons Role: Inhibition of agonist during forceful movements Examples:
Muscle weakness during rehabilitation Arm wrestling 1RM
1. High muscle tension
2. High tendon tension
3. GTO activation
4. Inhibition of agonist
GOLGI TENDON REFLEX
Figure 4.16, Knutzen & Hamill (2004)
Neural Adaptations
Progressive resistance training may inhibit GTO
Anecdotal evidence:Car accidentsHypnosis
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
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
Chronic long term low frequency (10 Hz) stimulation of rabbit tibialis anterior
1. 3 hours: Swelling of SR2. 4 days: Increased size/# of mitochondria,
increased oxidative [enzyme], increased capillarization
3. 14 days: Increased width of Z-line, decreased SERCA activity
4. 28 days: ST isoforms of myosin and troponin, decreased muscle mass and CSA
Figure 18.2, McIntosh et al., 2005
Rapid bursts of stimulation?