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Neuromuscular Adaptation
Muscle Physiology 420:289
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Agenda Introduction Morphological Neural Histochemical
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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
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Agenda Introduction Morphological Neural Histochemical
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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
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Hypertrophy and Myofibrillar Proliferation
Two mechanisms in which protein is accumulated muscle growth Increased rate of protein synthesis -Myosin and actin added to periphery of myofibrils Decreased rate of protein degradation -Proteins constantly being degraded -Contractile protein ½ life = 7-15 days -Regular and rapid overturn adaptability
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Hypertrophy and Myofibrillar Proliferation
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
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Figure 8.3 b, Komi, 1996
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Figure 8.3 a, Komi, 1996
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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
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FT ST FOG Figure 8.5, Komi, 1996
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Hypertrophy and Myofibrillar Proliferation
Role of satellite cells History: First identified in 1961 – Thought to be non-functioning Adult myoblasts Believed to be myoblasts that did not fuse into muscle fiber Called satellite cells due to ability to migrate
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Brooks, et al., Fig 17.2, 2000
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Brooks et al., Fig 17.3, 2000
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Hypetrophy and Myofibrillar Proliferation
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
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Figure 5.7, McIntosh et al. 2005
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Hypertrophy and Myofibrillar Proliferation
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
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Hyperplasia 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 . . .
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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)
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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
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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
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Sarcomeres in series displacement and velocity
Sarcomeres in parallel force Figure 17.20, Brooks et al., 2000
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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
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Training?
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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
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Agenda Introduction Morphological Neural Histochemical
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Neural Adaptations Recall:
Motor unit: Neuron and muscle fibers innervated Increasing force via recruitment of additional motor units Number coding
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Figure 9.6, Komi, 1996
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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
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Neural Adaptations Timeline
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Fig 20.8, Brooks et al. 2000
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Neural Adaptations 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
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Neural Adaptations Neural facilitation
Facilitation = opposite of inhibition Enhancement of reflex response to rapid eccentric actions
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Fig 20.10, Brooks et al., 2000
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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
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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
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1. High muscle tension GOLGI TENDON REFLEX 3. GTO activation 4. Inhibition of agonist 2. High tendon tension Figure 4.16, Knutzen & Hamill (2004)
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Neural Adaptations Progressive resistance training may inhibit GTO
Anecdotal evidence: Car accidents Hypnosis
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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
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Agenda Introduction Morphological Neural Histochemical
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Histochemical Adaptations
Histochemistry: Identification of tissues via staining techniques Recall
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Table 12.8, McIntosh et al., 2005
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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
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Histochemical Adaptations
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
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Rapid bursts of stimulation?
Figure 18.2, McIntosh et al., 2005
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