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
what is the functional organization of the nervous system
CNS (Brain & Spinal Cord):
- Afferent: sensory-> Spinal Cord-> Brain (ascending)
- Efferent: motor= brain-> spinal cord (descending)
PNS (Sensory & Motor Divisions):
-Autonomic Nervous System (ANS): Involuntary, sympathetic: fight or flight, parasympathetic: rest and digest Regulates involuntary body functions (e.g., heart rate, digestion).
-Somatic Nervous System: voluntary
what is the anatomical organization of the nervous system
Central Nervous System (CNS): Includes the brain and spinal cord, responsible for processing information and controlling responses.
Peripheral Nervous System (PNS): Includes all nerves outside the CNS, responsible for connecting the CNS to the rest of the body.
Motor Division: Controls voluntary and involuntary movements (somatic and autonomic).
Sensory Division: Transmits sensory information from receptors to the CNS.
Ganglia: Clusters of neuron cell bodies outside the CNS, acting as relay stations.
Neurons and Glial Cells: Neurons transmit electrical signals, while glial cells provide support and protection.
what are neurotransmitters
Neurotransmitters are chemical messengers that allow communication between neurons and between neurons and target cells (such as muscles and glands). They are essential for a wide range of bodily functions, including mood regulation, movement, cognition, and homeostasis. The balance and proper functioning of neurotransmitters are vital for maintaining health, and disruptions in neurotransmitter systems can lead to various neurological and psychiatric disorders.
how do neurotransmitters affect post-synaptic membranes
A neurotransmitter is released from the presynaptic neuron (or nerve terminal) into the synaptic cleft, it travels across the cleft and binds to receptors on the postsynaptic membrane and causes depolarization.
- Types of Responses in Postsynaptic Cells
Excitatory Postsynaptic Potentials (EPSPs): can promote neural depolarization in 2 ways. Temporal summation- summing serval EPSPs from one presynaptic neuron or Spatial summation- summing EPSPs from several different presynaptic neurons
Inhibitory Postsynaptic Potentials (IPSPs): they prevent synaptic transmission. They cause hyperpolarization (more negative resting membrane potential). Neurons with a more negative membrane potential resist depolarization.
The combined result of all the EPSPs and IPSPs at any given time determines whether the postsynaptic neuron will reach the threshold for firing an action potential (i.e., whether the neuron will send a signal down its axon to communicate with other neurons or muscles).
what are EPSP’s
Excitatory Postsynaptic Potentials (EPSPs): can promote neural depolarization in 2 ways. Temporal summation- summing serval EPSPs from one presynaptic neuron or Spatial summation- summing EPSPs from several different presynaptic neurons more likely to generate an AP
Sodium (Na⁺) enters the neuron, making it less negative (depolarized). Which Increases the chance of firing an action potential. Causing the movement of the membrane potential closer to threshold (-55mV).
Neurotransmitters: Glutamate, Acetylcholine, Dopamine, Norepinephrine.
Result: If the threshold is reached, an action potential occurs.
What are IPSP’s
Inhibitory Postsynaptic Potentials (IPSPs): they prevent synaptic transmission. They cause hyperpolarization (more negative resting membrane potential). Neurons with a more negative membrane potential resist depolarization.
Negative ions (Cl⁻) enter or positive ions (K⁺) leave. Causing the Membrane Potential to becomes more negative (hyperpolarized). Causing a less likely to fire an action potential. Which prevents excessive neural firing or overactivity.
Common Transmitters: GABA, Glycine, Dopamine (in certain regions).
Function: Promotes relaxation, reduces muscle contraction, limits brain overactivity.
what is muscle fiber recruitment
Muscle fiber recruitment, also known as motor unit recruitment, is the process by which the nervous system activates motor units to generate force in a muscle. A motor unit consists of a motor neuron and all the muscle fibers it controls, and when the motor neuron fires, all its muscle fibers contract simultaneously. According to the size principle, recruitment occurs in a specific order based on force demand: small motor units (Type I, slow-twitch fibers) are recruited first for low-force, endurance activities, followed by medium motor units (Type IIa, fast-twitch oxidative fibers) for moderate force, and finally large motor units (Type IIx, fast-twitch glycolytic fibers) for maximum force output during heavy lifting, sprinting, or explosive movements. If more force is needed, the brain recruits more motor units to increase contraction strength. Muscle recruitment also adapts with training, allowing athletes to recruit more muscle fibers during high-intensity tasks, enhancing strength, power, and performance. Additionally, during prolonged exercise, fatigue in slow-twitch fibers can trigger the recruitment of fast-twitch fibers to sustain muscle output. This sequential recruitment system is designed to conserve energy, prevent fatigue, and maximize force production when necessary.
Match the following exercise durations with their primary source of ATP production and the main factor limiting performance.
Ultra-short duration exercise (<10 seconds)
Short duration exercise (10-180 seconds)
Moderate duration exercise (2-10 minutes)
Ultra-short (<10 sec) A. Phosphagen system i. Phosphocreatine depletion
Short (10-180 sec) B. Anaerobic glycolysis ii. Lactic acid accumulation
Moderate (2-10 min) C. Aerobic metabolism iii. Cardiovascular system limitations
Define membrane potential and describe the changes in resting membrane potential that result in
an action potential
Membrane potential refers to the electrical charge difference across a cell membrane, resulting from the uneven distribution of ions (Na⁺, K⁺, Cl⁻) inside and outside the cell. In a resting neuron, the resting membrane potential is typically around -70mV, meaning the inside of the cell is more negative relative to the outside. This resting potential is maintained by the sodium-potassium pump (Na⁺/K⁺ pump), which actively moves 3 Na⁺ out and 2 K⁺ in, and the membrane’s permeability to K⁺ leakage, allowing potassium to slowly diffuse out of the cell. When a stimulus reaches the neuron, voltage-gated sodium channels open, allowing Na⁺ to rush into the cell, causing depolarization — the membrane potential becomes more positive (around +30mV). If the depolarization reaches the threshold (-55mV), an action potential is triggered, resulting in a rapid electrical impulse along the neuron. Following this, repolarization occurs as K⁺ channels open, allowing potassium to flow out of the cell, restoring the negative charge. Finally, a brief hyperpolarization may occur, where the membrane becomes slightly more negative than the resting potential before returning to its resting state. This rapid change in membrane potential, known as an action potential, is essential for transmitting electrical signals in neurons.
Describe the motor unit, and how a lifetime of exercise or sedentary behavior can impact motor
unit aging.
A motor unit consists of a motor neuron and all the muscle fibers it innervates, and it is responsible for generating muscle contractions. When the motor neuron sends an electrical signal (action potential), all the muscle fibers within that motor unit contract simultaneously. Motor units vary in size, with small motor units controlling slow-twitch (Type I) muscle fibers for endurance activities, and large motor units controlling fast-twitch (Type II) muscle fibers for power and strength movements. Over a lifetime, sedentary behavior can lead to motor unit loss (motor neuron death), particularly affecting fast-twitch fibers, resulting in muscle atrophy, decreased strength, and slower reaction times. Additionally, surviving motor neurons may attempt to reinnervate abandoned muscle fibers, converting them into slow-twitch fibers, causing a decline in power output. In contrast, a lifetime of exercise, especially strength and high-intensity training, can help preserve motor unit function, maintain muscle mass, and slow down motor unit loss, promoting better mobility, strength, and balance as a person ages. Exercise also helps enhance motor unit recruitment, allowing for more efficient muscle contractions, reducing the effects of sarcopenia (age-related muscle loss), and promoting overall neuromuscular health.
Describe the principal functions of skeletal muscles.
The principal functions of skeletal muscles are to facilitate movement, maintain posture, stabilize joints, and generate heat. Skeletal muscles attach to bones via tendons and produce movement by contracting and pulling on bones, allowing for activities such as walking, running, and lifting objects. They also play a critical role in maintaining posture by continuously contracting to keep the body upright and balanced, especially during sitting or standing. Additionally, skeletal muscles stabilize joints by supporting and reinforcing the bones, preventing dislocation or abnormal movement during physical activity. Another essential function is heat production, as muscle contractions generate body heat (thermogenesis), which helps maintain normal body temperature, especially during cold environments. Skeletal muscles also assist in protecting internal organs by providing a cushioning effect and supporting bodily structures. Beyond physical movement, skeletal muscles contribute to venous return, assisting blood flow back to the heart through rhythmic contractions during movement. Collectively, these functions are vital for mobility, stability, and overall body function.
Outline the contractile process. Use a step-by-step format illustrating the entire process,
- Nerve Impulse Reaches the Neuromuscular Junction
A nerve impulse (action potential) travels down the motor neuron to the neuromuscular junction (where the neuron meets the muscle fiber).
This triggers the release of the neurotransmitter acetylcholine (ACh) from the axon terminal (end of the neuron) into the synaptic cleft (gap between neuron and muscle fiber). - Acetylcholine Binds to Receptors on the Sarcolemma
Acetylcholine (ACh) diffuses across the synaptic cleft and binds to acetylcholine receptors on the sarcolemma (muscle cell membrane).
This opens sodium (Na⁺) channels, allowing Na⁺ ions to rush into the muscle fiber, causing depolarization (a shift in electrical charge inside the muscle fiber). - Action Potential Travels Along Sarcolemma and T-Tubules
The depolarization generates a muscle action potential (electrical impulse) that travels along the sarcolemma.
The impulse travels deep into the muscle fiber through T-tubules (transverse tubules), ensuring the signal reaches the entire muscle fiber. - Sarcoplasmic Reticulum Releases Calcium Ions
When the action potential reaches the sarcoplasmic reticulum (SR), it triggers the release of calcium ions (Ca²⁺) into the sarcoplasm (muscle cell cytoplasm).
The influx of calcium ions is critical for initiating muscle contraction. - Calcium Binds to Troponin (Exposure of Binding Sites)
Calcium (Ca²⁺) binds to a protein called troponin, which is attached to tropomyosin on the actin (thin) filament.
This changes the shape of troponin, causing tropomyosin to shift and expose the myosin-binding sites on actin. - Cross-Bridge Formation (Myosin Attaches to Actin)
The myosin head (from the thick filament) binds to the exposed binding site on actin, forming a cross-bridge.
The myosin head is already “cocked” with energy from the breakdown of ATP (adenosine triphosphate).
Define muscle fatigue. Discuss those factors that contribute to skeletal muscle fatigue during
exercise lasting: (1) 1–10 minutes and (2) >60 minutes.
fatigue is defined as a decline in muscle power. A decline in muscle power output occurs due to: decrease in muscle force production at the cross bridge level. A decrease in muscle shortening velocity. The cause of muscle fatigue is dependent on the exercise that produces the fatigue
Very heavy exercise (1-10 mins): causes of fatigue are multifactorial-range from decreased Ca2+ release from SR to accumulation of metabolites that inhibit myofilament sensitivity to Ca2+. Key metabolites that contribute to fatigue include increases in Pi, H+ and free radicals, H= ions bind to Ca2+ binding sites on troponin-preventing Ca2+ binding and contracting, both Pi and free radicals modify cross-bridge head and reduces number of cross-bridges bound to actin.
moderate intensity exercise (>60 min): causes of fatigue during prolonged endurance exercise include increase radical production and glycogen depletion. Accumulation of Pi and H+ in muscle do not contribute fatigue during moderate intensity exercise. Radical accumulation in muscle fibers modifies cross-bridge head and reduces number of cross-bridges bound to actin 9force production reduces). Depletion of muscle glycogen reduces TCA cycles intermediates and decreases ATP production via oxidative phosphorylation.
Describe the mechanical and biochemical properties of human skeletal muscle fiber types.
Discuss those factors thought to be responsible for regulating force during muscular contractions.
Human skeletal muscle fibers are classified into three main types based on their mechanical and biochemical properties: Type I (slow-twitch), Type IIa (fast-twitch oxidative), and Type IIx (fast-twitch glycolytic) fibers. Type I fibers are highly efficient at using oxygen to generate ATP through aerobic metabolism, making them suited for endurance activities. They have slow contraction speeds, but high endurance and are fatigue-resistant. Type IIa fibers have a moderate contraction speed and are capable of generating both aerobic and anaerobic energy, making them ideal for activities requiring both strength and endurance. Type IIx fibers generate rapid, forceful contractions but rely on anaerobic metabolism (mainly glycolysis), leading to rapid fatigue. These fibers are suited for short bursts of high-intensity efforts like sprinting or weightlifting.
The regulation of force during muscular contractions is influenced by several key factors. The number of motor units recruited (motor unit recruitment) is a primary factor, with more motor units being activated for greater force. The frequency of action potentials (rate coding) also plays a role, where a higher frequency of neural firing leads to greater force production. Fiber type composition and the cross-sectional area of muscle fibers determine the maximum force a muscle can generate, with larger fibers producing more force. The length-tension relationship also affects force generation, as muscles generate the most force when they are at an optimal length for overlap between actin and myosin filaments. Additionally, muscle temperature, electrolyte balance, and neural drive can modify the force produced during contractions. Together, these factors work in coordination to regulate muscle force efficiently and adapt to varying demands.
Describe the pattern of recruitment of motor unit recruitment during aerobic activities of
progressively greater intensity. Based on muscle fiber type, what is the progression of motor unit
recruitment?
During aerobic activities of progressively greater intensity, the recruitment of motor units follows a specific pattern based on the muscle fiber types involved. Initially, during low-intensity exercise, the body primarily recruits Type I (slow-twitch) fibers. These fibers are efficient at using oxygen and are highly resistant to fatigue, making them ideal for endurance activities such as walking or light jogging. As the intensity of the activity increases, the body progressively recruits Type IIa (fast-twitch oxidative) fibers. These fibers are capable of both aerobic and anaerobic metabolism, allowing them to sustain moderate-intensity efforts while also contributing to strength and power. At higher intensities, Type IIx (fast-twitch glycolytic) fibers are recruited to meet the demand for rapid, forceful contractions. These fibers rely on anaerobic energy systems, providing quick bursts of power but fatiguing rapidly. The progression of motor unit recruitment follows a size principle, where smaller, slower motor units (innervating Type I fibers) are recruited first, and larger, faster motor units (innervating Type IIa and IIx fibers) are recruited as the intensity of the activity increases. This systematic recruitment ensures efficient energy use and optimal performance across various intensity levels.
Factors that influence VO2max in untrained and trained individuals in endurance training
program
VO2max is the maximum rate at which an individual can utilize oxygen during intense exercise, and it is a key indicator of cardiorespiratory fitness. Several factors influence VO2max in both untrained and trained individuals undergoing an endurance training program. In untrained individuals, VO2max is typically lower due to less efficient cardiovascular and muscular systems. Factors such as heart rate, stroke volume (amount of blood the heart pumps per beat), and oxygen delivery to tissues are not optimized, leading to a lower VO2max. However, with endurance training, adaptations occur that improve cardiac output, mitochondrial density in muscle fibers, and aerobic enzyme activity, all contributing to an increase in VO2max. Trained individuals generally exhibit a higher VO2max due to increased stroke volume, greater capillary density in muscles, and more efficient oxygen utilization by muscle fibers. The degree of adaptation is influenced by factors such as genetics, age, sex, and training intensity. The duration and frequency of training also play a significant role; consistent and progressive endurance training increases VO2max over time. Moreover, muscle fiber type and dietary factors (e.g., iron levels) can further impact an individual’s ability to improve VO2max. Overall, while both untrained and trained individuals benefit from endurance training, the extent of improvement in VO2max is generally more pronounced in those who are initially untrained.
Factors that influence strength in untrained and trained individuals in a strength training program Training principles
Strength development in both untrained and trained individuals is influenced by several key factors during a strength training program. For untrained individuals, the initial gains in strength are largely due to neurological adaptations such as improved motor unit recruitment, coordination, and neuromuscular efficiency. These neural adaptations enable better activation of muscle fibers and more effective force production. Additionally, muscle hypertrophy (increase in muscle size) starts to occur with continued training, further contributing to strength gains. For trained individuals, improvements in strength are more gradual and are driven primarily by muscle hypertrophy, which occurs due to the overload principle—progressively increasing the weight or intensity of the exercises. Trained individuals also experience muscle fiber adaptation, with Type II fibers (which generate more force) becoming more active in response to heavy lifting.
Several training principles guide strength development, including the specificity principle, where the type of exercise should align with the goals (e.g., powerlifting or bodybuilding); the overload principle, which ensures the muscles are stressed beyond their usual capacity to promote growth and strength; and the progressive overload principle, which involves gradually increasing the intensity, volume, or load over time. The reversibility principle highlights that gains in strength will decrease if training stops, while the individualization principle acknowledges that training programs should be tailored to each individual’s needs, taking into account factors like age, sex, and fitness level. Proper recovery, periodization (cycling through various intensities), and nutrition (adequate protein intake) are also crucial in maximizing strength gains in both untrained and trained individuals.
Cross education
Cross education refers to the phenomenon where training one limb or side of the body leads to strength and performance improvements in the untrained opposite limb. This occurs due to the neural adaptations that take place in the central nervous system. When one limb is trained, the motor cortex in the brain becomes more efficient at recruiting motor units, and this improved neural pattern can transfer to the opposite, untrained limb, even without direct training. This effect is particularly noticeable when strength training is focused on one arm or leg, resulting in some increase in strength or performance on the contralateral side. Cross education is thought to be beneficial in rehabilitation, as it can help maintain strength in an injured or immobilized limb by training the opposite limb. Factors influencing cross education include the type of training, the intensity, and the duration of the exercise. The effect is generally stronger for strength gains and less pronounced for endurance or skill-related tasks. This neural adaptation can help preserve functional capacity during recovery periods and may be used to speed up rehabilitation.
FITT principle and US guidelines for physical activity
The FITT principle is a framework used to design effective exercise programs by adjusting Frequency, Intensity, Time, and Type of physical activity to meet individual goals. Frequency refers to how often an individual engages in physical activity (e.g., number of sessions per week), intensity is the level of effort required (e.g., low, moderate, or vigorous), time refers to the duration of each exercise session, and type refers to the kind of activity performed (e.g., aerobic, strength training, flexibility exercises). This principle helps tailor exercise programs to enhance fitness, improve health, and prevent injury.
The U.S. guidelines for physical activity recommend that adults engage in at least 150 minutes of moderate-intensity aerobic activity or 75 minutes of vigorous-intensity aerobic activity per week, combined with muscle-strengthening activities on two or more days per week. For additional health benefits, the guidelines suggest increasing aerobic activity to 300 minutes of moderate-intensity or 150 minutes of vigorous-intensity weekly. These guidelines emphasize the importance of regular physical activity for maintaining overall health, reducing the risk of chronic diseases (e.g., heart disease, diabetes), improving mental health, and enhancing quality of life. Following the FITT principle in combination with these guidelines ensures a balanced and sustainable approach to fitness.
