ENS 304 Exam 1

central nervous system

brain and spinal cord

peripheral nervous system

afferent nerves (periphery to central); efferent nerves (central to periphery)

afferent nerves (periphery to central)

sensory nerves (senses and proprioception)

efferent nerves (central to periphery)

autonomic (sympathetic and parasympathetic); somatic (motor; voluntary and involuntary)

parts of a neuron

dendrites; soma (cell body); axon; collateral axon; myelin sheath; node of Ranvier

nerve signals

electrical and chemical

membrane depolarization can lead to:

the formation of an action potential

action potential steps 1-4

resting membrane potential → stimulus initiates depolarization causing Na⁺ channels to open → membrane potential reaches threshold causing voltage-gated Na⁺ channels to open allowing influx of Na⁺. K⁺ channels open slowly → rapid Na⁺ entry into cell

action potential steps 5-9

Na⁺ channels close and slower K⁺ channels open → rapid K⁺ exit from cell → some K⁺ channels remain open and additional K⁺ leaves cell hyperpolarizing it → some K⁺ channels have still not closed → all Na⁺ and K⁺ channels closed, cell returns to resting ion permeability and resting membrane potential

clinical application of propagation of an action potential

multiple sclerosis; amyotrophic lateral sclerosis (ALS)

multiple sclerosis

destroys myelin on neurons; ataxia (loss of coordination); paresis (muscle weakness or partial paralysis)

amyotrophic lateral sclerosis (ALS)

degeneration of motor neurons responsible for controlling voluntary muscle movement; loss of strength and ability to speak, eat, move, breathe; worsens with time; most die of respiratory failure within 3-5 years of first symptoms

2 major neurotransmitters involved in regulating multiple physiological responses to exercise

acetylcholine and norepinephrine

neuron communication is facilitated by:

neurotransmitters, which are released from synaptic vesicles into the synaptic cleft

these neurotransmitters then bind to postsynaptic receptors, influencing:

the behavior of the other cell

if the postsynaptic cell is excitable (another neuron, muscle fiber, etc.) and the depolarization exceeds the threshold, then:

an action potential occurs

certain drugs that interact with acetylcholine receptors (curare and tubocurarine):

block muscle fiber stimulation at the neuromuscular junction (NMJ)

neuromuscular transmission failure

during high-intensity exercise, with a high rate of contractions, failure in NMJ activation contributes to muscle fatigue; most prevalent in fast-twitch muscle fibers

neuromuscular transmission failure involves

a decrement in motoneuron discharge rate (leading to a decrease in acetylcholine release); a reduced sensitivity of acetylcholine receptors to acetylcholine

motor units can innervate:

different number of muscle fibers

large motor units innervate a great number of muscle fibers

associated with gross movements (higher force and velocity)

small motor units innervate a low number of muscle fibers

associated with fine movements (greater coordination)

motor units within one muscle

many motor units of different fiber types

connective tissue layers

epimysium, perimysium, endomysium

epimysium

surrounds the entire muscle and defines its volume

perimysium

sheath of connective tissue that groups muscle fibers into bundles or fascicles

endomysium

surrounds individual muscle fibers and contains the vessels (arterioles, capillaries, and venules), muscle satellite cells and nerves that supply the muscle fibers

muscles are mostly composed of:

muscle fibers, adipocytes, connective cells (ex. fibroblasts), myogenic cells (ex. satellite cells)

muscle fibers are the functional cells of the muscles and are composed of:

sarcolemma, myofibrils, sarcoplasmic reticulum, hundreds or thousands of nuclei, cell components and compartments that are also present in other cells (ex. mitochondria)

sarcoplasmic reticulum

storage depot for intracellular Ca²⁺

ryanodine receptor (RYR)

Ca²⁺ channels release Ca²⁺ into sarcoplasm

SERCA (Ca²⁺ -ATPase)

pumps return Ca²⁺ to sarcoplasmic reticulum (SR)

T tubules

responsible for transmitting the action potential to inner parts of the muscle fibers

voltage gated dihydropyridine (DHP)

Ca²⁺ receptors (channels) line t-tubules

ryanodine (RYR)

Ca²⁺ receptors (channels) are on SR across from DHP channels

SERCA

are present in the membrane of the SR and uses ATP to pump Ca²⁺ back into SR

contractile proteins

responsible for muscle force production; thick filament, thin filament, z-lines

thick filament

composed mostly of myosin; myosin heads attach to “active” sites on actin (thin) filament; myosin heads contain myosin ATPase to hydrolyze (break down) ATP to ADP + Pi

thin filament

actin, tropomyosin, troponin

actin

two protein strands twisted around each other, contain binding sites to myosin

tropomyosin

thin strand that lays in groove of actin strands and covers binding sites

troponin

attached to actin and tropomyosin strands; has strong affinity for Ca²⁺

Ca²⁺ couples:

excitation, contraction, and relaxation

if the action potentials continues:

Ca²⁺ is released into the sarcoplasm, activating muscle contraction

when action potentials cease:

SERCA pumps return Ca²⁺ to SR, ceasing contractions and promoting relaxation

necessary for myosin head to release from actin

ATP

excitation-contraction coupling steps 1-3

action potential at axon terminal causes ACh release that causes new action potential generation at neuromuscular junction → action potential travels along plasma membrane and down t-tubules → action potentials stimulate voltage-gated dihydropyridine (DHP) Ca²⁺ channels to open that stimulate ryanodine (RYN) channels to open

excitation-contraction coupling steps 4-7

Ca²⁺ diffuses from the sarcoplasmic reticulum to cytosol → Ca²⁺ binds to troponin, moves tropomyosin to uncover actin binding sites → myosin heads hydrolyze ATP and bind to actin → power stroke of myosin heads on actin causes sarcomeres to shorten

if isometric force is measured:

force will be dependent on the length of the muscle (due to the length of the sarcomeres)

there is an optimal sarcomere length (and muscle length)

for force production

skeletal muscle fiber types

isoform of myosin heavy chain differences help explain performance characteristics

identifying muscle fiber types

determined by the expression of specific isoforms of myosin heavy chain (MHC)

type 1 muscle fiber type

expressing MHC type 1

type 2a muscle fiber type

expressing MHC type 2A

type 2x muscle fiber type

expressing MHC type 2X (= 2B in rodents)

type 2c muscle fiber type

expressing MHC type 2c (very rare)

fiber type identification of skeletal muscle based on:

myosin ATPase activity at different pre-incubation acidity

hybrid muscle fibers

express 2 or more isoforms of MHC; considered “less specialized” muscle fibers; more present in untrained (or sedentary) individuals, or during the aging process (in aging, there is a fiber-type shift (II to I) of some fibers); exercise training reduces the proportions of hybrid fibers

association of skeletal muscle fiber types with:

performance for specific tasks

having a higher proportion of certain fiber-type in muscles is:

not a guarantee of success in sports activities (other physiological factors, skills, etc.)

researchers found that there is a chance that exercise training:

had changed the individual’s proportion of fiber-types, but it is not known how long it takes (if it does) for training to modify this proportion

power =

work / time

work =

force x distance

velocity =

distance / time

power =

force x velocity

power generated by fast twitch muscle fibers

significantly higher than slow twitch fibers, due to the lower force type I and IIa fibers produce vs type IIx

since power depends on force and velocity (power = force x velocity), and force produced decays at higher velocities of contraction:

power is maximal at submaximal force and velocity of contraction

recruitment of motor units during exercise follows the principle of orderly recruitment based on:

size of the motor neuron, force produced needed, fatigue of muscle fibers

size of the motor neuron (muscle recruitment by fiber type)

number of muscle fibers innervated (low to high)

force produced needed (muscle recruitment by fiber type)

that will require more type I or type IIa or type IIx

fatigue of muscle fibers (muscle recruitment by fiber type)

if type I fibers become fatigued, then type II are recruited

when fast-twitch muscle fibers are recruited during exercise

only at higher intensities of exercise

strength gains can be achieved without structural changes in muscle:

but not without neural adaptations

synchronization of motor units

allows greater number of motor units recruited with lower muscle fatigue; also increases movement economy and better skills

neural drive

more motor units are recruited to a given task which increases total force

neural gain strength most proven so far by:

synchronization of motor unit recruitment and increased neural drive

muscle hypertrophy

increase in myofiber cross-sectional area (CSA) and total muscle CSA

transient hypertrophy

edema within and between myofibers; reversed just a few minutes or hours later

chronic hypertrophy (or simply hypertrophy)

increase in myofiber CSA (volume) by increasing protein synthesis and metabolic substrates; greater number of myofibrils; greater amounts of creatine kinase and glycolytic enzymes; increase in muscle phosphocreatine and glycogen concentration

resistance training and protein metabolism

increased myofibrillar proteins → increased cross-sectional area of muscle fibers (hypertrophy) → increased cross-sectional area of muscle

endurance training and protein metabolism

increased muscle mitochondrial proteins → increased muscle mitochondrial content → increased aerobic ATP resynthesis

muscle hypertrophy mostly occurs by:

hypertrophy of fast-twitch muscle fibers

muscle fiber-type hypertrophy/atrophy

resistance exercise leads to greater changes in muscle fiber CSA in “fast-twitch” muscle fibers than in slow-twitch fibers; also applies to muscle atrophy (loss of muscle fiber CSA)

key to understanding hypertrophy

muscle fibers do not suffer mitosis (are not able to produce a new muscle fiber); muscle fibers contain a large number of nuclei

muscle fibers synthesizing proteins in response to exercise training

nuclei are responsible

proteins are synthesized on ribosomes, which translate:

the mRNA produced by gene transcription

ribosomes will connect amino acids to:

form the primary structure of a protein

mechanical loading does not need to be excessive to stimulate muscle hypertrophy

some studies show loads as low as 30% 1RM can trigger a hypertrophy response

maximizing hypertrophy

achieved through higher loads, such as 60-90% 1RM

anabolic hormones

testosterone, growth hormone (GH), insulin growth factor-1 (IGF-1) are important for muscle growth and hypertrophy (ex. puberty and men x women)

resistance exercise acutely increases anabolic hormone production:

but the increase in anabolic hormone after exercise is not the ultimate predictor of hypertrophy

the use of massive doses of anabolic steroids coupled with resistance exercise leads to:

muscle hypertrophy (and increase in several side effects)

loss in anabolic hormone production during aging:

contributes to the muscle atrophy

muscle satellite cell incorporation hypothesis

muscle fiber protein synthesis depends on gaining new nuclei from muscle satellite cells around muscle fibers

effect of acquiring new nuclei due to training

real, but it is not clear whether this affects muscle hypertrophy

stimuli and sensors that initiate skeletal muscle hypertrophy following resistance exercise

hypertrophy stimulus → hypertrophy signal transduction → hypertrophy

hypertrophy stimulus

mechanical load; anabolic hormones

hypertrophy signal transduction

mechanosensors; recruitment of additional muscle fibers; hormone signaling

mTOR (mechanistic target of rapamycin)

an enzyme that is an important regulator of muscle protein synthesis

activation of mTOR in muscle is dependent on the combination of multiple events

repeated muscle stress; low-level sustained events of anabolic hormone production; amino acid availability; insulin signaling in muscle