Anatomy Test 7 - Muscle Energy Source, Fatigue, Neuromuscular Junction

1 ATP Molecule Usage

Everytime myosin and actin filaments engage

What determines the “gentleness” or “strength” of a muscle

how ever many muscle fibers engage

What makes muscles become fatigued

limited amount of oxygen so not enough ATP is produced

How is ATP produced

Proteins, sugars, and fats go through glycolysis (sugar break down) and then if there is enough oxygen, they go through the Krebs cycle (or citric acid cycle), if not Fermentation

Step 1 of Muscle Fatigue

Intense Exercise

Step 2 of Muscle Fatigue

Muscle Fatigue

Step 3 of Muscle Fatigue

Anaerobic Respiration

Step 4 of Muscle Fatigue

Oxygen Debt

1.Intense Exercise

Muscles are worked strenuously and the glucose supply is exhausted

2.Muscle Fatigue

ATP is no longer efficiently being used for cross-bridges

3.Anaerobic Respiration

Muscles begin to burn, causing you to stop exercising before cells are injured

Oxygen Debt

Amount of oxygen available vs. “out of breath”

• Better health = more efficient oxygen transfering

Lactate

molecule produced by muscle cells during anaerobic respiration; important source of fuel for muscles, allowing them to continue working

Lactate Threshold

amount of lactate produced can no longer prevent the muscles from failing

Delayed Onset Muscle Soreness (DOMS)

caused by lactic acid or inflammation at the site of microscopic tears in the muscle fibers

Sarcolemma

Plasma membrane that surrounds each muscle fiber under the endomysium

Neuromuscular Junction

Where the axon terminal (end of motor neuron) meets the sarcolemma

Motor Unit

group of fibers that is collectively controlled by one motor neuron

action potential

the stimulus your brain sends to the motor neuron to initiate muscle contraction.

Synaptic Cleft

The gap between the axon terminal and the muscle fiber

Neurotransmitters

molecule released because action potential can not jump the synaptic cleft

Two types of channel proteins

voltage-gated and chemically-gated

Voltage-Gated Channel Protein

open in response to an action potential

Chemically-Gated Protein Channels

open when a particular molecule attaches to them

Step 1 of Neuromuscular Junction

The action potential arrives at the axon terminal of a motor neuron

Step 2 of Neuromuscular Junction

Calcium channels open, allowing Ca² to enter through the axon terminal

Step 3 of Neuromuscular Junction

Ca²⁺ cause bubble-like vesicles of Acetylcholine (a neurotransmitter) to release their contents into the synaptic cleft

Step 4 of Neuromuscular Junction

Acetylcholine (ACh) binds to ACh receptors on the sarcolemma of the muscle fiber, causing protein channels to open

Step 5 of Neuromuscular Junction

Sodium ions (Na+) enter through the protein channels and Potassium ions (K+) leave through the protein channels, causing the action potential to continue through the muscle fiber

Step 6 of Neuromuscular Junction

As the action potential progresses through the muscle fiber along t-tubules, more Ca² is released causing the actin and myosin fibers to interact, contracting the muscle fiber