Exercise Physiology Flashcards
exam #2
What are the layers of skeletal muscle
skeletal muscle then goes to the–>
Epimysium – The outermost layer of connective tissue that surrounds the entire muscle, protecting it and helping it connect to tendons.
the fascicles then goes to the–>
Perimysium – A layer of connective tissue that surrounds groups of muscle fibers, organizing them into bundles called fascicles.
muscle fibers then go to the–>
Endomysium – The innermost layer that surrounds each individual muscle fiber (muscle cell), providing support and facilitating the exchange of nutrients and waste.
How are the layers of skeletal muscles relative to a cross-sectional area?
Large skeletal muscles are encased by epimysium
Smaller fascicles within are separated by perimysium
Individual muscle fibers within fascicles are each wrapped by endomysium
What do all the connective tissue layer surround?
Epimysium – Surrounds the entire muscle, binding all fascicles together.
Perimysium – Surrounds fascicles, which are bundles of muscle fibers.
Endomysium – Surrounds individual muscle fibers (muscle cells) within each fascicle.
what are the myofibrils in the sarcomere?
Sarcomeres are the basic functional units of muscle contraction, made up of organized myofilaments (actin and myosin).
Thick Filaments (Myosin) – Contain myosin proteins with heads that form cross-bridges for contraction.
Thin Filaments (Actin, Troponin, and Tropomyosin) – Act as binding sites for myosin heads during contraction.
Z-Line (Z-Disc) – Defines the boundary of each sarcomere and anchors actin filaments.
M-Line – Located at the center, anchoring myosin filaments.
A-Band – Contains the entire length of thick filaments (myosin), including the overlapping thin filaments (actin).
I-Band – The light region containing only thin filaments (actin), shrinking during contraction.
H-Zone – The central part of the A-band, containing only thick filaments (myosin) when relaxed.
How is muscle contraction generated
Muscle contraction is generated through the sliding filament theory, which describes how actin (thin) filaments slide past myosin (thick) filaments to shorten the sarcomere. This process is powered by ATP and controlled by calcium ions (Ca²⁺). The steps involved in muscle contraction are:
- Nerve Stimulation (Excitation)
A motor neuron releases acetylcholine (ACh) at the neuromuscular junction.
ACh binds to receptors on the muscle fiber’s sarcolemma, triggering an action potential.
The action potential travels along the T-tubules, reaching the sarcoplasmic reticulum (SR). - Calcium Release
The action potential causes the SR to release Ca²⁺ into the sarcoplasm.
Ca²⁺ binds to troponin, causing a conformational change that moves tropomyosin, exposing myosin-binding sites on actin. - Cross-Bridge Formation (Attachment)
Myosin heads bind to the exposed active sites on actin, forming cross-bridges. - Power Stroke (Pulling)
Myosin heads pivot, pulling actin filaments toward the M-line, shortening the sarcomere.
ADP and Pi are released from the myosin head during this process. - Detachment
A new ATP molecule binds to myosin, causing it to release actin and break the cross-bridge. - Myosin Reset (Reactivation)
ATP is hydrolyzed into ADP and Pi, re-cocking the myosin head into its high-energy state, ready for another cycle. - Muscle Relaxation
When nerve stimulation stops, Ca²⁺ is pumped back into the SR.
Troponin and tropomyosin return to their original positions, covering actin’s binding sites.
Without cross-bridge formation, the muscle relaxes.
Key Points:
ATP is essential for both contraction and relaxation.
Calcium ions regulate contraction by exposing myosin-binding sites on actin.
The cycle continues as long as ATP and Ca²⁺ are available.
what are the different types of muscle contractions
Concentric Contraction (Shortening Muscle)
The muscle shortens while generating force.
Example: Lifting a dumbbell during a bicep curl.
Function: Produces movement and strengthens muscles. h and I band decrease (shorten) and the A band stays the same.
Eccentric Contraction (Lengthening Muscle)
The muscle lengthens while still generating force.
Example: Lowering a dumbbell in a bicep curl.
Function: Controls movement, absorbs impact, and builds strength. H and I band increase (lengthen) and A band stays the same.
- Isometric Contractions (No Change in Muscle Length)
The muscle produces force without changing length (no visible movement).
Example: Holding a plank or pushing against a wall.
Function: Improves stability, endurance, and joint support.
How do the different types of muscle contractions influence muscle tone, length, etc.
- Isotonic Contractions (Changing Muscle Length)
In isotonic contractions, muscle length changes while tension remains constant. These contractions are responsible for movement.
Concentric Contraction (Shortening Muscle)
The muscle shortens as it generates force.
Example: Lifting a dumbbell in a bicep curl.
Influence: Increases muscle mass and strength by promoting hypertrophy.
Eccentric Contraction (Lengthening Muscle)
The muscle lengthens while still producing force.
Example: Lowering a dumbbell during a bicep curl.
Influence: Strengthens muscles more effectively than concentric contractions and plays a major role in muscle damage and repair (leading to soreness and growth).
- Isometric Contraction (Same Muscle Length)
The muscle does not change in length, but it still generates force.
Example: Holding a plank or maintaining posture.
Influence: Improves muscle endurance and stabilizes joints without increasing muscle length.
Impact on Muscle Function & Development
Strength & Growth → Concentric and eccentric contractions build muscle.
Endurance & Stability → Isometric contractions enhance joint stability.
what are the characteristics of muscle fibers
Type I: Slow twitch
- high mitochondria, aerobic, high efficiency, low VO2 max, low ATP-ase activity, low force production, low fatigue (or high fatigue resistance), high sedentary
- endurance based
Type II: Fast Twitch
- low mitochondria, anaerobic, low efficiency, high VO2 max, high ATp-ase activity, high force production, high fatigue (or low fatigue resistance), low sedentary
- sprints
Type IIa: Intermediate Twitch
- 50/50 sedentary, aerobic and anaerobic, Vo2 max is high but not as high as fast twitch
what is the relationship between a motor neuron and a muscle fiber
- Motor Unit: The Functional Connection
A motor neuron and all the muscle fibers it innervates form a motor unit.
Smaller motor units (few fibers per neuron) control precise movements (e.g., fingers, eyes).
Larger motor units (many fibers per neuron) control powerful movements (e.g., legs, back). - Neuromuscular Junction (NMJ): The Communication Site
The axon terminal of a motor neuron releases acetylcholine (ACh) into the synaptic cleft.
ACh binds to receptors on the muscle fiber’s sarcolemma.
This triggers an action potential, leading to muscle contraction. - The All-or-None Principle
When a motor neuron fires, all muscle fibers in its motor unit contract fully.
The strength of contraction depends on the number of motor units activated, not individual fiber contraction. - Motor Unit Recruitment
Smaller motor units are recruited first for light tasks.
Larger motor units are activated for stronger contractions. - Muscle Fiber Type & Motor Neuron Control
Slow-twitch fibers (fatigue-resistant) are controlled by small motor neurons.
Fast-twitch fibers (powerful but fatigue quickly) are controlled by large motor neurons.
what are the different forms of muscle wasting
Sarcopenia:
Age-related muscle wasting
Caused by a decline in muscle mass, strength, and function due to aging.
It often leads to weakness, mobility issues, and frailty in older adults.
-Ages 25-50 (10%), AGES 50-80 YOU lose additional 40%
Cachexia:
A severe form of muscle wasting associated with chronic diseases like cancer, chronic kidney disease, heart failure, and AIDS.
Characterized by involuntary weight loss (muscle and fat), fatigue, and weakness.
Involves both muscle protein breakdown and fat loss, driven by inflammatory responses.
how is muscle force generated
Muscle force is generated through the interaction of actin (thin) and myosin (thick) filaments within the sarcomere, the basic functional unit of muscle contraction. This process, known as the sliding filament theory, involves several key steps:
- Motor Neuron Activation
A motor neuron sends an electrical signal (action potential) to a muscle fiber.
This action potential travels along the sarcolemma and through the T-tubules to reach the sarcoplasmic reticulum (SR), stimulating the release of calcium ions (Ca²⁺). - Calcium Release and Binding to Troponin
The release of Ca²⁺ from the SR binds to the troponin complex on the actin filament.
This causes a conformational change in troponin, which moves tropomyosin away from the myosin-binding sites on actin, exposing the sites for myosin attachment. - Cross-Bridge Formation
The myosin heads bind to the exposed actin binding sites, forming cross-bridges between myosin and actin. - Power Stroke (Force Generation)
The myosin head pivots, pulling the actin filament toward the center of the sarcomere (M-line).
This movement is powered by the hydrolysis of ATP (adenosine triphosphate), which is broken down into ADP (adenosine diphosphate) and inorganic phosphate (Pi). - Detachment and Resetting
After the power stroke, a new ATP molecule binds to the myosin head, causing it to detach from actin.
The ATP is hydrolyzed, which re-energizes the myosin head, positioning it for another cycle of attachment and movement along the actin filament. - Muscle Shortening (Contraction)
The continuous cycling of cross-bridge formation and power strokes shortens the sarcomere, resulting in muscle contraction and force generation.
The more cross-bridges formed, the greater the force generated. - Recruitment of Motor Units
The force generated by a muscle depends not only on the number of cross-bridges but also on how many motor units are activated.
Small motor units (with fewer muscle fibers) are activated for fine movements.
Larger motor units (with more muscle fibers) are recruited for stronger, more powerful movements. - Rate of Stimulation (Twitch Summation)
If a motor unit is stimulated repetitively, the individual contractions can summate (add together), increasing the overall force.
Tetanus occurs when the muscle is stimulated at a high frequency, resulting in a smooth, sustained contraction.
Summary of Key Points:
Force is generated through the interaction of actin and myosin, powered by ATP.
The more motor units recruited and the faster the stimulation, the greater the force generated.
Muscle length and tension also influence the amount of force produced (optimal length-tension relationship).
what are the characteristics of muscle fiber types
- Type I Fibers (Slow-Twitch)
Contraction Speed: Slow
Force Production: Low
Fatigue Resistance: High
Mitochondria Density: High (lots of mitochondria for aerobic metabolism)
Primary Energy Source: Primarily aerobic metabolism
Function: Endurance and sustained activities (e.g., long-distance running, swimming, maintaining posture) - Type II Fibers (Fast-Twitch)
Type II fibers are divided into two subtypes based on their specific characteristics: Type IIa (fast oxidative) and Type IIb (fast glycolytic).
Type IIa Fibers (Fast Oxidative)
Contraction Speed: Fast
Force Production: Moderate to high
Fatigue Resistance: Moderate (more resistant to fatigue than Type IIb, but less than Type I)
Primary Energy Source: Combination of aerobic and anaerobic metabolism (oxidative and glycolytic pathways)
Function: Activities requiring both endurance and power (e.g., middle-distance running, cycling, weightlifting)
Key Feature: Flexible and adaptable; can function in both aerobic and anaerobic conditions.
what are the mechanisms of muscle fatigue
Muscle fatigue occurs when a muscle loses its ability to generate force, reducing its capacity for prolonged activity. This phenomenon can result from various mechanisms that affect the muscle’s energy production, nerve signaling, and contractile function. Below are the primary mechanisms of muscle fatigue:
Long Term:
-free radicals develop over along term
-glycogen depletion
Short term:
- decrease Ca2+ in SR
- hydrogen ions accumulation
- inorganic phosphate formed as result of breakdown of ATP; ATP can’t bind as easily
how does muscle repair occur?
satellite cells proliferate into myoblasts and myotubes to help form muscle fibers or repair the growth of a muscle fiber
what evidence supports muscle cramps
Electrolyte Imbalances: Disruptions in sodium, potassium, calcium, and magnesium levels can trigger cramps.
Dehydration: Fluid loss during exercise or heat stress increases cramp occurrence.
Neurological Factors: Nerve hyperexcitability or irritation can lead to involuntary muscle contractions.
Overuse/Fatigue: Muscle fatigue and overexertion contribute to cramping.
Muscle Length Changes: Excessive muscle lengthening or shortening during exercise or stretching can trigger cramps.
Underlying Health Conditions: Diabetes, neurological, and circulatory disorders increase the risk of cramps.
Medications: Diuretics and statins can cause cramps as side effects.
Hormonal Factors: Pregnancy, menstruation, and hormone-related changes can contribute to cramping.
what evidence does not support muscle cramps
Dehydration Alone: Dehydration contributes but is not the sole cause of cramps.
Low Sodium Alone: Low sodium is not consistently linked to muscle cramps.
Lack of Stretching: Stretching may relieve cramps but doesn’t directly cause them.
Low Magnesium Alone: Magnesium deficiency is not always the cause of cramps.
Poor Circulation: Muscle cramps are generally not caused by circulatory problems.
Overuse Alone: Muscle cramps can occur with or without overuse.
Lack of Oxygen: Oxygen deprivation is not typically responsible for muscle cramps.
Psychological Stress Alone: Psychological stress may contribute but is not the direct cause of muscle cramps.
what happens with skeletal muscle as we age?
Muscle Atrophy: A decline in muscle mass and size.
Weakness: Reduced muscle strength, making physical tasks more difficult.
Decreased Power: Reduced ability to generate rapid or forceful muscle contractions.
Slower Recovery: Prolonged recovery times after exercise and muscle injury.
Decreased Functionality: Reduced muscle endurance, strength, and coordination, leading to a higher risk of falls, injuries, and disability.
How to Mitigate Muscle Decline with Age
While aging leads to natural muscle changes, there are several ways to counteract or slow down muscle loss:
Regular Exercise:
Strength training (resistance exercises) is particularly effective in maintaining and even increasing muscle mass and strength in older adults.
Aerobic exercise can help improve cardiovascular health, which supports muscle function.
Stretching exercises improve flexibility and joint mobility.
Adequate Protein Intake: Consuming more protein-rich foods helps stimulate muscle protein synthesis and prevent muscle loss.
Hormonal Therapy: In some cases, hormone replacement therapy (HRT), like testosterone replacement, may be considered to support muscle health, although this is typically a decision made on an individual basis with a healthcare provider.
Adequate Sleep: Rest is critical for muscle recovery and repair.
Nutrition and Supplements:
Creatine supplementation may help improve muscle strength and endurance.
Vitamin D and calcium are important for bone and muscle health.
Omega-3 fatty acids may help reduce inflammation and support muscle function.
what are nerve fibers
Nerve fibers are extensions of neurons responsible for transmitting electrical impulses.
They are primarily axons and can be myelinated or unmyelinated.
Nerve fibers are classified by their size, myelination, and speed of impulse transmission: Type A (fastest, large), Type B (medium, slower), and Type C (small, slowest).
Nerve fibers play key roles in sensation and motor control throughout the body.
how do nerve fibers send signals
Resting Potential: The neuron has a negative charge inside and a positive charge outside, maintained by ion pumps.
Stimulation: A stimulus causes depolarization, where the inside of the neuron becomes more positive.
Action Potential: An electrical impulse travels down the axon as sodium ions rush in and potassium ions rush out.
Propagation: The action potential travels down the axon by triggering adjacent segments to depolarize.
Saltatory Conduction: In myelinated fibers, the signal jumps between nodes, speeding up transmission.
Synapse: The action potential triggers neurotransmitter release, passing the signal to another neuron or muscle.
Muscle Contraction: In motor neurons, acetylcholine stimulates muscle fibers to contract.
what are the charges of neurons
- Resting Potential (At Rest)
Resting Membrane Potential: A neuron, when not transmitting a signal, has a resting membrane potential of about -70 millivolts (mV). This means the inside of the neuron is more negative relative to the outside.
Ions Involved:
Inside the neuron: There is a high concentration of potassium ions (K⁺), which are positively charged, and negatively charged proteins.
Outside the neuron: There is a high concentration of sodium ions (Na⁺), which are also positively charged, and chloride ions (Cl⁻), which are negatively charged.
The resting potential is maintained by the sodium-potassium pump, which actively moves 3 sodium ions out of the neuron and 2 potassium ions in. This creates an imbalance, with more positive charges outside the neuron than inside.
- Depolarization (During Action Potential)
Action Potential: When a neuron receives a strong enough stimulus, it undergoes a rapid change in membrane potential, known as depolarization.
Sodium channels open: Sodium ions (Na⁺) rush into the neuron due to the electrical and concentration gradient. This causes the inside of the neuron to become more positive (or depolarized).
The voltage inside the neuron quickly rises from about -70 mV to as high as +30 mV. - Repolarization (Return to Resting State)
Potassium Channels Open: After the peak of the action potential, potassium ions (K⁺) move out of the neuron, driven by both the concentration gradient and the electrical gradient, which helps restore the negative charge inside the neuron.
This causes the neuron to become more negative again, returning the voltage toward -70 mV (this is known as repolarization). - Hyperpolarization (After Action Potential)
After repolarization, the neuron may temporarily become more negative than the resting potential (around -80 mV to -90 mV). This is called hyperpolarization and ensures that the neuron cannot immediately fire another action potential.
Potassium channels slowly close, and the sodium-potassium pump helps to restore the resting membrane potential.
Ions in relations to resting and stimulated neuron
Resting Neuron:
Sodium (Na⁺): High concentration outside; low concentration inside.
Potassium (K⁺): High concentration inside; low concentration outside.
Depolarization: Sodium ions (Na⁺) rush into the neuron, making the inside more positive.
Repolarization: Potassium ions (K⁺) move out of the neuron, making the inside negative again.
Hyperpolarization: Potassium continues to exit the neuron, making the inside more negative than the resting potential.
Restoration: The sodium-potassium pump works to restore the original ion concentrations, returning the neuron to its resting state.
Sodium Potassium ATP-ase pump: 3 sodium out of the cell and 2 potassium into the cell
what are the types of joint receptors
- Golgi Type Receptors (GTO)
They provide information about joint compression and the force applied to the joint (rate of force development). They are inhibitory muscle contractions so we don’t create to much force and cause damage to the muscle. They stimulate results in reflex relaxation of muscle: inhibitory neurons send IPSPs to muscle alpha motor neurons - Muscle Spindle: provides information about muscle shortening rate. they stimulate contractions hyperactive muscles (cramps), proprioception- detects muscle length. Intrafusal fibers- run parallel to normal muscle fibers (extrafusal fibers). Gamma motor neurons- stimulate intrafusal fibers to contract in concert with extrafusal fibers. They are responsible for stretch reflex: stretch on muscles stimulates muscle spindles and promotes a reflex contraction (knee-jerk reflex)
what are joint receptors
Joint receptors are specialized sensory receptors found in the joints (articulations) of the body. They play a crucial role in proprioception, which is the sense of the position and movement of our body parts in space. Joint receptors help the brain understand the state of the joints and contribute to coordinating movements and maintaining balance.
what is equilibrium and balance
- Equilibrium
Equilibrium refers to the state of balance in the body, where all forces acting on the body are balanced so that the body remains stable.
There are two main types of equilibrium:
a. Static Equilibrium
Static equilibrium is the state of balance when the body is stationary, such as when standing still or sitting.
In static equilibrium, the center of mass of the body is aligned over the base of support (e.g., feet on the ground), and the body’s internal forces and gravity are in balance.
b. Dynamic Equilibrium
Dynamic equilibrium refers to the balance the body maintains during movement. This is important for activities like walking, running, or making quick directional changes.
The body continuously adjusts to changes in position and movement to prevent falling and to keep the body stable while in motion.
Key Components of Balance:
Sensory Input: Balance relies on the brain receiving information from several sensory systems:
Visual system: Eyes provide visual cues about the environment and the body’s position in space.
Vestibular system: The inner ear’s semicircular canals and otolith organs detect changes in head position and motion. This system is key to maintaining balance, particularly when the body is moving or in motion.
Proprioception