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?