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three ways ATP can be remade 1. oxidative phosphorylation (electron transport chain)
2. anaerobic glycolysis (no oxygen): pyruvate gets turned to lactic acid
3. stored as phosphocreatine
physiological causes of fatigue -ATP production < ATP demand
-excessive accumulation of lactic acid
-pH levels drop associated with lactic acid
in skeletal muscle, ATP is not generated through
a)Aerobic metabolism
b) Anaerobic metabolism
c) Breakdown of phosphocreatine
d) Lactic acid metabolism d
lactic acid is a by-product of anaerobic metabolism and contributes to muscle fatigue
how could you relieve fatigued muscles rest the muscles to allow blood flow to re-
establish pH and replenish nutrients needed for ATP production
peripheral neuropathy damage to a lower motor neuron or their myelin sheaths. associated
with motor, sensory, and autonomic involvement
Motor diseases progressive loss of lower motor neuron
only *motor* abilities affected
, Bio 253 Lab 1 Test 1 Questions and Answers
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example of autonomic dysfunction: ANS doesn't work sexual dysfunction, abnormal hr,
abnormal blood pressure, decreased ability to sweat, constipation or diarrhea
how does signaling stop (ACH) -neurotransmitter diffuse away
-acetycholinesterase breaks down ACH in synapse
-preventing activation of receptors
-breakdown products taken back into the axon terminal (reuptake)
How is action potential passed from motor neuron to muscle fiber 1. signal from motor
neuron arrives at the nerve terminal
2. calcium moves into the nerve terminal
3. ACh released in the synapse and binds to receptors
4. influx of Na+ initiates an action potential
myasthenia gravis -affects nmj
-antibodies bodies bind to ACh receptors reducing Na influx resulting in lack of AP to muscle
fibers
-fatigue quickly, but improvements after rest
-20% of patients have antibodies
Lambert-Eaton Syndrome results from antibodies that affect voltage sensitive calcium
channels, inhibiting ACh release
-improve with exercise and nerve stimulation
Botulinum toxin Produces muscle paralysis by inhibiting the release of acetylcholine from
muscle endplates.