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Part 4 3/27/2016

Kathleen Cercone PT, PhD

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Glycolysis

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The production of lactate during peak activity, its conversion to glucose in the liver, and the rebuilding ofglycogen reserves in the muscles during recovery

Lactate

Pyruvate Glucose

Glucose

Pyruvate

Lactate

Glucose

70–80%

20–30% LIVER

MUSCLE

Glycogen reserves in muscle

Peak Activity RecoveryMuch of the large amounts of lactateproduced during peak exertion diffusesout of the muscle fibers and into thebloodstream. The liver absorbs this lactateand begins converting it into pyruvate.

This process continues after exertion has ended, because lactatelevels within muscle fibers remain relatively high, and lactatecontinues to diffuse into the bloodstream. After the absorbedlactate is converted to pyruvate in the liver, roughly 30 percent ofthe new pyruvate molecules are broken down in themitochondria, providing the ATP needed to convert the remaining 70 percent of pyruvate molecules into glucose. The glucose molecules are then released into the circulation, where they are absorbed by skeletal muscle fibers and used to rebuild their glycogen reserves.

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Slow (R)—more mitochondria (M) and capillaries (cap) than fast (W)

Table 10-2

Intermediate

Intermediate

Intermediate

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Figure 10-22

• individual cells (NOT fused into fibers)

• connected by intercalated discs• striated, with single central nucleus• short, broad T tubules encircle Z

lines• no terminal cisternae in SR• rich in mitochondria and myoglobin• totally dependent on aerobic

metabolism-functional syncitium

19

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Factors and clinical conditions affecting muscles

• Hypertrophy– Increase in muscle size due to:

• Increase in myofilaments• Increase in myofibril size• Increase in mitochondria• More glycogen and glycolytic enzymes

– As a result of repeated exhaustive stimulation• Can be promoted by administration of steroid hormones

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Factors and clinical conditions affecting muscles

• Atrophy– Decrease in muscle size, tone, and power– As a result of decreased stimulation such as during:

• Paralysis by spinal injury• Damage to nervous system• Having body part in cast after bone fracture

– Initially reversible, but after prolonged disuse, muscle fibers can die and not be replaced

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Factors and clinical conditions affecting muscles

• Clinical conditions– Polio

• Virus attacks motor neurons of brain and spinal cord causing paralysis (lost of voluntary movement)

– Tetanus• Toxin from bacteria (Clostridium tetani) that suppresses the

mechanism inhibiting motor neuron activity• Thrives in low-oxygen areas like deep punctured tissues• Results in sustained, powerful contractions of affected muscles• Severe tetanus can have 40%–60% mortality

– Deaths rare due to immunization in U.S.

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Factors and clinical conditions affecting muscles

• Clinical conditions • Botulism

• Toxin from bacteria (Clostridium botulinum) that blocks ACh release at neuromuscular junctions

• Acquired through bacteria-contaminated food– Myasthenia gravis

• Loss of ACh receptors at neuromuscular junctions• Results in progressive weakness

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Factors and clinical conditions affecting muscles

• Clinical conditions Rigor mortis• Generalized muscle contraction shortly after death

(2–7 hours)• Begins with small muscles of face, neck, and arms• Due to depletion of ATP, leaving myosin cross-bridges

attached to actin• Ends 1–6 days later as muscular tissue decomposes

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Four clinical conditions thataffect skeletal muscles

Polio: a virus affects motor neurons in thespinal cord and brain, causing muscleatrophy and paralysis

Tetanus: the bacterium Clostridium tetani releases apowerful toxin that suppresses the mechanism thatinhibits motor neuron activity, causing sustained, powerful contraction of skeletal muscles throughoutthe body

Botulism: ingestion of a toxin produced by the bacteriumClostridium botulinum paralyzes skeletal muscles by preventingACh release at neuromuscular junctions

Myasthenia gravis: loss of ACh receptors at the neuromuscularjunctions results in progressive muscular weakness