MUSCULAR SYSTEM (part 2)

Leak

____ ion channels allow for the slow leak of ions down their concentration gradient. Like all membrane transport proteins, these are specific for a particular ion.

Gated

_____ ion channels are most important in stimulated cells. It is their presence that governs the production of action potentials.

The Resting Membrane Potential

In actuality, all cells in the body have this electrical charge difference, but neurons and muscle fibers contain specialized components that allow them to utilize this charge difference. In an unstimulated cell, this charge difference is called the ____________.

The Resting Membrane Potential

__________ is the result of three factors:

• The concentration of K+ inside the cell membrane is higher than that outside the cell membrane

• the concentration of Na+ outside the cell membrane is higher than that inside the cell membrane

• the cell membrane is more permeable to K + than to Na+

Action potential

__________ occurs when the excitable cell is stimulated. This is a reversal of the resting membrane potential such that the inside of the cell membrane becomes positively charged compared with the outside. This charge reversal occurs because ion channels open when a cell is stimulated.

Depolarization

The ___________ phase of the action potential is a brief period during which further depolarization occurs and the inside of the cell becomes even more positively charged. Sodium (Na+) channels open, allowing Na+ ions to enter the cell.

Repolarization

The ___________ phase is the return of the membrane potential to its resting value. It occurs when ligand-gated Na+ channels close and gated K+ channels open. When K+ moves out of the cell, the inside of the cell membrane becomes more negative and the outside becomes more positive.

Slow-Twitch (Type I)

Motor unit characteristics:

• small motor neuron

• High excitability

• Slow Oxidative muscle fiber (SO)

• Low force output

• High fatigue resistance

• Aerobic metabolism

• First recruitment order

• Function: Postural, control, endurance

• Example activities: walking, marathon running

Fast-twitch fatigue resistance (Type IIa)

Motor unit characteristics:

• Medium motor neuron

• Moderate excitability

• Fast Oxidative-Glycolytic muscle fiber (FOG)

• Moderate force output

• Moderate fatigue resistance

• Aerobic and Anaerobic metabolism

• Second recruitment order

• Function: Sustained moderate-intensity activity

• Example activities: cycling, swimming

Fast-twitch fatigable (Type IIb/IIx)

Motor unit characteristics:

• Large motor neuron

• Low excitability

• Fast Glycolytic muscle fiber (FG)

• High force output

• Low fatigue resistance

• Anaerobic metabolism

• Last recruitment order

• Function: Short burst of high-intensity activity

• Example activities: sprinting, weightlifting

Cross-bridge cycling.

The mechanical component of muscle contraction is called __________. This rapid sequence of events will cause the sarcomeres to shorten and the muscle will contract.

ATP

The energy from one ______ molecule is required for each cross-bridge cycle. Before each cycle, the myosin head is in its resting (“high-energy”) position.

Power stroke

Binding of the myosin heads to the attachment sites on the actin forms the cross-bridges and triggers a rapid movement of the myosin heads at their hinged region. The movement of the myosin head is called the _________.

Relaxation

Muscle _________ occurs when acetylcholine is no longer released at the neuromuscular junction.

Muscle fiber

After an action potential has occurred in the __________, the sodium-potassium pump must actively transport Na+ out of the muscle fiber and K+ into the muscle fiber to return to and maintain resting membrane potential.

Myosin heads

ATP is required to detach the _________ from the attachment sites for the recovery stroke.

Sarcoplasmic reticulum

ATP is needed for the active transport of Ca2+ into the ____________ from the sarcoplasm.

Muscle twitch

The response of a muscle fiber to a single action potential along its motor neuron is called a __________.

Phases of twitch

1. lag

2. contraction

3. relaxation.

Lag phase

The __________ or latent phase, is the gap between the time of stimulus application to the motor neuron and the beginning of contraction. This phase is the time during which the action potential is traveling along the axon, the events at the neuromuscular junction occur, and the action potential travels along the sarcolemma and releases Ca 2+ from the sarcoplasmic reticulum.

Contraction phase

The ________ phase commences once the Ca 2+ released from the sarcoplasmic reticulum initiates cross-bridge formation and cross-bridge cycling.

Relaxation phase

The __________ phase is much longer than the contraction phase, because the concentration of Ca 2+ in the sarcoplasm decreases slowly due to active transport into the sarcoplasmic reticulum.

Rigor Mortis

Stiffening of muscle, 12-24 hours post-mortem

• Loss of ATP production → Failure of Cross Bridge Detachment & Calcium Ion Accumulation → PERSISTENT MUSCLE CONTRACTION

Isometric

In ____________ contractions, the muscle does not shorten. This type of contraction increases the tension in the muscle, but the length of the muscle stays the same.

Isotonic

In ___________ contractions, the muscle shortens. This type of contraction increases the tension in the muscle and decreases the length of the muscle. Isotonic contractions happen any time you move your limbs in order to lift an object and move it.

Muscle contraction

The change in __________ strength depends on two factors:

• summation

• recruitment.

Summation

factor that change muscle contraction strength: the amount of force in an individual muscle fiber called _________

Recruitment

factor that change muscle contraction strength: the amount of force in a whole muscle _________

Motor unit

consists of a single motor neuron and all the muscle fibers it innervates.

Muscle tone

There are variations in motor unit recruitment when muscles stay contracted for long periods of time. This constant tension is called __________ and is responsible for keeping the back and lower limbs straight, the head upright, and the abdomen flat.

Concentric

__________ contractions are isotonic contractions in which tension in the muscle is great enough to overcome the opposing resistance, and the muscle shortens. This contraction result in an increasing tension as the muscle shortens.

Eccentric

_____________ contractions are isotonic contractions in which tension is maintained in a muscle but the opposing resistance is great enough to cause the muscle to increase in length.

ATP-dependent proteins

Skeletal muscle fibers have three major ________________:

• the myosin head

• the Na + /K + pump, which maintains the resting membrane potential

• the Ca 2+ pump in the sarcoplasmic reticulum

First step

skeletal muscle contraction: Acetylcholine (ACh) is released from the motor neuron at the neuromuscular junction.

Second step

skeletal muscle contraction: Calcium (Caz*) binds to troponin, exposing myosin-binding sites on actin.

Third step

skeletal muscle contraction: The myosin head forms a cross-bridge with actin.

Fourth step

skeletal muscle contraction: ATP is hydrolyzed, energizing the myosin head.

ATP hydrolysis

It directly supplies the energy needed for the power stroke of the myosin head during muscle contraction

Atrophy

Muscle shrinkage due to loss of protein and fiber size

• cause: Disuse, aging, malnutrition, denervation, disease

• mechanism: Decreased protein synthesis, increased degradation

• functional impact: Decreased strength, endurance, and metabolic rate

Hypertrophy

Increase in muscle fiber size

• cause: Resistance training, mechanical overload, hormones

• mechanism: Increased protein synthesis via mTOR, IGF-1, and satellite cell activation

• functional impact: Increased muscle mass, strength, and metabolism

Hyperplasia

Increase in the number of muscle fibers

• cause: Controversial in humans; possible extreme training response

• mechanism: Possible fiber splitting or new fiber formation from satellite cells

• functional impact: Possible contribution to long-term muscle mass increase

Strain

an injury to a muscle or tendon.

• caused by sudden forceful movements or repetitive stress.

• Symptoms include localized pain, swelling, inflammation, muscle weakness or spasms, limited range of motion (ROM), and bruising (in severe cases).

• Management typically involves rest, ice, compression, elevation (RICE), physical therapy (PT), and in some cases, surgery.

Sprain

an injury to a ligament.

• caused by sudden twisting or impact, joint overextension, or direct trauma.

• Symptoms include localized pain, swelling, bruising, joint instability or weakness, and difficulty bearing weight or moving the affected joint.

• Management involves the RICE method (rest, ice, compression, elevation), physical therapy (PT), medication ("meds"), and potentially surgery.

Fatigue

a decline in a muscle's ability to generate force over time.

• Causes include energy depletion, lactic acid accumulation, electrolyte imbalance, dehydration, and neuromuscular dysfunction.

• Symptoms are a gradual loss of muscle strength, muscle weakness and sluggishness, increased exertion, and difficulty sustaining activity.

• Management and prevention involve adequate hydration and electrolyte balance, proper nutrient intake, sufficient rest and sleep, gradual training progression, and cooling down and stretching after exercise.

Cramps

sudden, involuntary, and painful muscle contractions.

• Causes include dehydration and electrolyte depletion, muscle overuse or prolonged static contractions, neuromuscular excitability, and underlying medical conditions.

• Symptoms involve sudden, sharp muscle pain, visible or palpable muscle hardening or twitching, and temporary muscle stiffness after the cramp subsides.

• Management and prevention strategies include hydration and electrolyte replenishment, stretching and massaging the affected muscle, applying heat or cold therapy, adjusting posture and sleeping position, and magnesium supplementation.

Fibrillation

a spontaneous, involuntary contraction of a single muscle fiber.

• caused by denervation of muscle fibers, spinal cord injuries, poliomyelitis, muscle diseases (myopathy), and electrolyte disturbances.

• Symptoms are not visible on the skin and can only be detected through electromyography (EMG); there is no visible muscle movement.

• clinical significance of fibrillation is that it indicates severe nerve damage, chronic denervation, or motor neuron diseases; it's not observed in healthy individuals.

Fasciculation

a spontaneous, involuntary contraction of a group of muscle fibers.

• causes are categorized as benign and pathological.

• Symptoms include visible muscle twitching without loss of muscle strength; fasciculations may persist in neurodegenerative disorders.

• Clinically, fasciculations can be benign (harmless) or, if persistent with muscle weakness, may indicate ALS or other serious neuromuscular disorders.

Denervation

a loss of nerve supply to a muscle. It can be partial or complete. Causes include neurological, traumatic, systemic, and other factors.

Disuse

a lack of physical activity or reduced muscle engagement.

• Causes include immobilization and physical inactivity, neurological and systemic conditions, microgravity and spaceflight, and aging.

• Effects involve structural and functional changes in muscles, metabolic consequences, and changes in bone and connective tissue.

Toxins

originating from bacteria, plants, animals, or chemicals, can cause muscle paralysis, spasms, weakness, or necrosis. Three types of toxins are listed: neurotoxins, myotoxins, and metabolic toxins.

Neurotoxins

block or enhance the action of acetylcholine (ACh) at the neuromuscular junction (NMJ), causing flaccid or spastic paralysis.

• Botulinum toxin: flaccid paralysis.

• Tetanus toxin: spastic paralysis.

• α-latrotoxin (Black Widow spider venom): full muscle spasm.

• Curare (plant-derived toxin): flaccid paralysis and respiratory failure.

• Snake venom neurotoxins: paralysis.

Myotoxins

damage muscle membranes, leading to muscle necrosis and rhabdomyolysis.

• Snake venom myotoxins (viper & rattlesnake) and Bee and wasp venom: These toxins degrade muscle cell membranes.

Metabolic toxins

inhibit ATP production, resulting in muscle fatigue and weakness.

• Cyanide: Blocks ATP production, leading to muscle weakness.

• Carbon monoxide: Binds to hemoglobin, reducing oxygen delivery to muscles.

• Statins: Can cause myalgia (muscle pain) due to mitochondrial dysfunction.

Bacterial Infection

Direct muscle invasion by bacteria.

• Symptoms: Fever, swelling, abscess formation.

• Treatment: Intravenous (IV) antibiotics and drainage of abscesses.

Viral Infection

Inflammatory myopathy (muscle inflammation) and neuronal damage.

• Symptoms: Myalgia (muscle pain), weakness, and potentially paralysis.

• Treatment: Antiviral medications and supportive care.

Parasitic infection

Parasites encyst (form cysts) within muscle tissue.

• Symptoms: Muscle pain and the formation of nodules (small lumps).

• Treatment: Antiparasitic medications (such as albendazole).

Fungal Infection

Opportunistic fungal infection of muscle tissue.

• Symptoms: Muscle abscesses and pain.

• Treatment: Intravenous (IV) antifungal medications.