Neuromuscular Adaptation Muscle Physiology 420:289.

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Neuromuscular Adaptation Muscle Physiology 420:289

Transcript of Neuromuscular Adaptation Muscle Physiology 420:289.

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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

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

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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

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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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Figure 8.5, Komi, 1996FT ST FOG

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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

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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: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

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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:1. Resistance training causes satellite cell

activation as well2. 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

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 . . .

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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-bridgesMore sarcomeres in parallel

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Figure 17.20, Brooks et al., 2000

Sarcomeres in series displacement and velocity

Sarcomeres in parallel force

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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 unitsMaximal 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:

1. Increase ability to recruit highest threshold motor units

2. Increase rate coding of all motor units

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Neural Adaptations

Neural facilitationFacilitation = opposite of inhibitionEnhancement 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 antagonistsEnhancement of agonist/antagonist control

during rapid movementsJoint protectionEvidence: Sprinters greater hamstring EMG

during knee extension compared to distance runners

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http://www.brianmac.demon.co.uk/sprints/sprintseq.htm

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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

2. High tendon tension

3. GTO activation

4. Inhibition of agonist

GOLGI TENDON REFLEX

Figure 4.16, Knutzen & Hamill (2004)

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Neural Adaptations

Progressive resistance training may inhibit GTO

Anecdotal evidence:Car accidentsHypnosis

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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

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

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Figure 18.2, McIntosh et al., 2005

Rapid bursts of stimulation?