BIO 338 Exam 2

neuroendocrinology

endocrine system releases hormones into circulation (blood stream)

• hormones limited in speed, by cardiac output

• slower

• can give an indication of how nervous system is functioning

nervous system uses neurotransmitters

hormones

several classes

• amino acid derivatives

• peptides

• proteins

• steroids

chemical structure impacts the way they are transported and the way their effects are exerted on a tissue

blood hormone control

effect exerted by a hormone on a tissue is proportional to the concentration of that hormone in the blood and the number of active receptors

concentration of hormone dependent on:

rate of secretion from the gland

rate of metabolism or excretion

quality of transport proteins (steroid in particular)

changes in plasma volume

hormone secretion

rate of secretion dependent on:

• magnitude of input (what is the stimuli?)

• whether the input is stimulatory or inhibitory

input is ALWAYS a chemical, but can be an ion, substance (ex. glucose), neurotransmitter or another hormone

hormone control of processes are redundant with many inhibitors of secretion (one pathway is blocked, the process will continue)

metabolism of hormones

plasma concentration influenced by rate of metabolism

inactivation can take place at or near the receptor or in the liver

kidneys also help in hormone secretion

slow down metabolism; increase concentration of hormone

transport protein

some hormones require transport in blood via binding/transport protein

• steroid hormones require this

hormone must be unbound or active to exert an effect

Amount of free hormone dependent on

quality of transport protein and the capacity and affinity of the proteins to bind the hormone molecules

want a lot of transporters and want them to be able to release their neurotransmitter well

first adaptation to altitude

exercising; more RBC than plasma - increased concentration of hormones in blood; more at higher intensity, higher concentration of O2 (by lessening plasma)

hormone-receptor interactions

carried via the circulation to all tissues, but effect only exerted on those with specific receptors

receptors are not static fixtures

downregulation

decrease in receptor number in response to high concentration of hormone - diminishing response for some hormone concentration (less sensitive)

ex. type II diabetes

upregulation

increase in receptor number in response to low concentration of hormone - enhance sensitivity

saturation

all receptors in or on a cell are bound with a hormone - any additional increase in hormone concentration will have no net effect on the tissue

too much hormone

competition

receptors are specific to chemical shape so two hormones can have a similar chemical shape and thus ‘compete’ for binding (least amount of drug needed to stimulate hormone)

ex. pharmaceuticals

mechanisms of hormone action

several ways by which a hormone can exert a response/effect

mechanism of hormone action 1

altering the activity of DNA in the nucleus to initiate or suppress the synthesis of a specific protein

steroids

mechanism of hormone action 2

activation of special proteins called “second messengers”

lipophobic

mechanism of hormone action 3

alerting membrane transport mechanisms

insulin

altering activity of DNA in the nucleus

lipophilic; steroid, easily diffuses into cell

• steroid hormone binds to a receptor protein in the cytoplasm or nucleus

  • if bound, then complex enters the nucleus

• in nucleus, hormone or hormone receptor complex bind to hormone - responsive elements on DNA

  • directly w/ DNA

• activates or could suppress genes that lead to mRNA synthesis that carry codes from nucleus to cytoplasm where protein in synthesized

cyclic AMP second messenger mechanism

• hormone binds to receptor on cell surface

• activates G protein within cell membrane

  • link between inside of cell and hormone- receptor complex on surface

• G protein activates adenylate cyclase which causes formation of cyclic AMP

• increased cyclic AMP concentration activates protein kinase A

• PKA activates response proteins to alter cellular activity

ion channel second messenger mechanism

• hormone binds to receptor on cell surface

• activates G protein located within cell membrane

  • link between inside of cell and hormone-receptor complex on surface

• G protein activates phospholipase C

• phospholipid on membrane is hydrolyzed into IP3; causing Ca++ release and DAG

• Ca++ binds to an active calmodulin which activates proteins in the cell

  • work in concert with calmodulin effects

membrane transport

• hormone binds to receptor on cell surface, which activates carrier molecules in or near near the membrane to facilitate the movement of substrates/ions into the cells

• relevant for exercise physiology, determines how quickly you can get glucose into a cell

hormones: regulation and action

hormones are secreted from endocrine glands

• hypothalamus and pituitary glands → release hormones to release other hormones; stimulate another endocrine organ to release their hormones

• thyroid and parathyroid glands → T3 and T4

• adrenal gland → norepinephrine and epinephrine

• pancreas → insulin, glucagon

• testes and ovaries → sex hormones

hypothalamus and pituitary gland

hypothalamus

• controls secretions from pituitary gland

• located at the base of the brain; attached to the pituitary

anterior pituitary gland

• true endocrine gland

• hormone release controlled via chemicals that originate in neurons in the anterior pituitary

• these chemicals stimulate or inhibit the release of specific hormones from anterior pituitary

posterior pituitary

• also controlled by hypothalamus - hormones move down the axon to blood vessels in pituitary where they discharge into circulation

anterior pituitary gland

adrenocorticotropic hormone (ACTH)

follicle-stimulated hormone (FSH)

luteinizing hormone (LH)

melanocyte-stimulating hormone (MSH)

thyroid-stimulating hormone (TSH)

growth hormone (GH) most relevant for exercise

prolactin

posterior pituitary gland

oxytocin

antidiuretic hormone (ADH)

• reduces water loss (via urine output) to maintain plasma volume

• results in increased water reabsorption from the renal tubules to capillaries

• released stimulated by high plasma osmolarity and low plasma volume

  • due to sweat loss without water replacement

• released during exercise

• osmoreceptors in the hypothalamus sense water concentration in the interstitial fluid

  • osmolality high - release of ADH

  • osmolality normal; plasma volume low - stretch receptors in left atria initiate ADH release

growth hormone

secretion stimulated by exercise (resistant; most potent), sleep, stress, and low plasma glucose

stimulates growth of all tissue through actions of insulin-like growth factors (IGFs)

• stimulates uptake of amino acids. the synthesis of new proteins, and long-bone growth

• spares glucose; goes into circulation

GH release is controlled via negative feedback where GH and IGF concentration inhibit further GH release

role of GH and maintenance of plasma glucose

increases blood glucose

use fatty acids instead of glucose

GH and exercise

very responsive to exercise

increases about by 2000% at max

greater in trained; mobilizing fat

GH and performance

increase protein synthesis and long-bone growth

• used to treat childhood dwarfism, used by elderly, and by most athletes

athletes

• definite history of use

• effects more adverse than beneficial

  • not with micro dosing

• minimal empirical evidence of performance improvement

• can accelerate recovery; won’t directly improve performance but could improve training → negative outcomes

thyroid gland

thyroid stimulated by TSH to synthesize two iodine-containing hormones:

• triiodothytonin (T3)

• thyroxine (T4)

T4 is released from thyroid in greater amounts compared to T3, but most of T4 is converted to T3 which is the more potent of the two

thyroid hormones

central to establishing overall metabolic rate

• related weight control

long latent period between T3 and T4 release and when their effects are observed

• T3 6-12 hours

• T4 2-3 days

controlled via negative feedback

during exercise “free exercise” concentration of hormone increase due to changes in binding characteristics of transport protein, which accelerates uptake by tissues

calcitonin - hormone released from thyroid gland that plays a minor role in Ca ++ regulation

• critical for muscle contraction, bone growth, and bone decay

parathyroid gland/hormone

primary hormone involved in calcium regulation

adrenal gland

relevant for exercise

adrenal medulla

• catecholamine

  • epinephrine and norepinephrine

adrenal cortex

• mineralocorticoids

  • aldosterone - involved in maintenance of plasma Na+ and K+ concentration

• glucocorticoids

  • cortisol - involved in plasma glucose regulation

• sex steroids

  • androgens\ support prepubescent growth; androgens associated with post-pubescent sex drive in women

  • estrogens/

adrenal medulla

part of SNS

• spikes fast; comes down quickly

secretes catecholamines (80% EPI, 20% NE)

• fast-acting hormones

• part of the “fight or flight” response

• have wide acting effects on many different tissues and organs

bind to adrenergic receptors on target tissues

• alpha (a)

• beta (B)

• both can influence blood pressure

effect is dependent upon hormone and receptor type

epinephrine and norepinephrine

fast-acting hormones; appear quickly and disappear quickly

maintain blood glucose during exercise

plasma EPI and NE increase during exercise ( up to 1000 fold increase)

adaptions to training”

• decreased plasma EPI and NE following training

things most important for survival have multiple pathways - REDUNDANT

effect of EPI and NE

different subunits of a and B stimulated by NE and EPI but lead to different effects

aldosterone

similar effects like vasopressin

controls blood volume

• important regulator of Na+ and K+ and thus plays an important part in blood volume and bp regulation

• chronically tend to increase over time; less negative consequences from higher blood pressure (temporary) than lower blood pressure

renin-angiotensin-aldosterone system

ACE inhibitors bring blood volume down

B blockers - reason why some need to try many medications

cortisol

mineralocorticoid

controls blood glucose during long-term fasting and exercise

promotes breakdown of tissue protein to form amino acids

• more in circulation; keep it from entering cells

increases lipolysis

simulates liver enzymes involved in metabolic pathways leading to glucose synthesis

pancreas

blood glucose control

protects brain

• insulin - secreted from B (beta) cells of the pancreas

  • facilitates movement of glucose from circulation to inside of cells

  • stimulated by plasma amino acid concentration, plasma glucose concentration, parasympathetic tone

  • inhibited by sympathetic outflow, EPI low plasma glucose

• glucagon - secreted from a (alpha) cells of pancreas

  • opposite effect of insulin

  • stimulated by low plasma glucose, EPI

hormonal control of substrates during exercise

type of substrate and rate of utilization is the dependent upon the intensity and duration of exercise

intense = more carbohydrates

prolonged = more fats

control of muscle glycogen utilization

exercise intensity is inversely related to duration

higher intensity = shorter duration; quicker depletion

plasma EPI is powerful stimulator of glycogen breakdown

blood glucose homeostasis during exercise

all pathways in place to keep blood glucose in range

exercise provides a significant challenge to blood glucose control

plasma glucose maintained through 4 processes:

• mobilize glucose from hepatic glycogen stores

• mobilize FFA from adipose tissue and spare plasma glucose

• synthesize new glucose via hepatic gluconeogenesis from amino acids, lactate, and glycerol

• block glucose entry into cells to force the use of FFA as fuel

obviously goal is to maintain plasma glucose AND sustain work

permissive/slow acting hormones

thyroxine

thyroid hormones

• T3 and T4 responsible for establishing basal metabolic rate and allow other hormones to have their full effect (permissive)

• impacting number of receptors at the cell surface or altering the affinity of the receptor for a hormone

  • EPI has a minimal effect on FFA mobilization from adipose tissue in the absence of T3

cortisol

• stimulates FFA mobilization from adipose tissue

• slows uptake of glucose

GH

• decreases glucose uptake by tissues

• increases FFA mobilization

• enhances hepatic gluconeogenesis

• increases substantially during exercise and to a greater extent in trained vs. untrained

• direct slow effect on blood glucose during exercise

fast acting

EPI and NE

• mobilization of glucose from liver

• mobilization of FFA from adipose tissue

• interference with the uptake of glucose by tissues

• NE taken to reflect SNS activity

• EPI viewed as primary catecholamine in the mobilization of glucose

• responsive to endurance training

• plasma glucose still maintained; less needed at given workload

• at maximal exercise is greater following training

insulin and glucagon

• same sensed variable but opposite effect

• insulin - increases glucose storage; lowers blood glucose concentration

  • involved in glucose uptake in ALL tissue

  • concentration decreases during graded exercise

• glucagon - increases glycogen breakdown; increases blood glucose concentration

  • increases during exercise and favors FFA mobilization and hepatic glycogen breakdown

  • type 2 diabetes improves with exercise

SNS modifies the secretion of insulin and glucagon

skeletal muscle

human body contains over 600 skeletal muscles

• 40-50% body mass (change w/ phenotype)

functions

• force production for locomotion and breathing

• force production for postural support

• heat production during cold stress

  • support of blood and lymphatic system

connective tissue covering skeletal muscle

epimysium - outer layer

perimysium - connective tissue that surrounds bundles of muscle fibers (fascicles)

endomysium - connective tissue that surrounds each muscle fiber within the fascicles

basement membrane - protective tissue around every fiber under the endomysium

sarcolemma - cell membrane of muscle cells

satellite cells

*precursor cells

• undifferentiated cells, flexible fate contribute nuclei to muscle fibers

located above the sarcolemma but below the basement membrane

play a key role in muscle growth and repair

addition of nuclei increases capacity for protein synthesis

important adaption to strength training

myonuclear domain - volume of cytoplasm to nucleus; more nuclei, more capacity for growth

• need nuclei for growth (hypertrophy)

microstructure of skeletal muscle

multi-nucleated

thick filament - myosin

thin filament- actin

striated appearance

sarcomere - functional component, separated by z line

sarcoplasmic reticulum and transverse tubules

SR is membrane channel surrounding myosin fibril

• storage of Ca++

• transverse tubules pass through fiber -sandwiched between terminal cisternae of SR

neuromuscular junction

junction between motor neuron and muscle fiber (where motor neuron meets muscle cell)

motor neuron - where nerve meets contractile component

• motor unit = motor neuron and all fibers it innervates

motor end plate = pocket formed around motor neuron by sarcolemma

neuromuscular cleft = short gap between neuron and muscle fiber

acetylcholine is released from the motor neuron

• causes end-plate potential (EPP)

• results in depolarizing of muscle fiber

muscular contraction

end result is actin ‘sliding’ over myosin which causes the muscle to shorten (contract) and develop tension

crossing of thick and thin filaments

process of muscular contraction is explained by sliding filament theory

sliding filament theory

muscle fibers contract by a shortening of their myofibrils due to actin sliding over the myosin

results in a reduction in the distance between Z lines

formation of cross-bridges between actin and myosin

rigor mortis - no ATP (dead), muscles stay contracted

energy for contraction

energy required at several steps

breakdown of ATP is done via ATPase (present at myosin head)

this release of energy serves to energize the myosin cross-bridge which results in the pulling of actin towards the center, shortening the fiber

power stroke -single contraction, of all the cross bridges in a muscle would only shorten the muscle ~1% and some can shorten up to 60%, must be done many times

excitation

process begins when a nerve impulse arrives the the neuromuscular junction

depolarization is conducted down the transverse tubules deep into the muscle fiber

end result - release of Ca++ from SR

contraction

released Ca++ diffuses into the muscle and binds to troponin

troponin is directly on tropomyosin which lies in the grooves of the double strand of actin

• in relaxed muscle there is no cross-bridge formation because tropomyosin is in the way of the binding sites

attachment of a fresh ATP breaks the actin-myosin cross-bridge

ATPase again hydrolyzes ATP and provides energy for a new ’cocking’ of the myosin head and reattachment of the cross-bridge to a new site and generation of another power stroke

lack of Ca++ or accumulation of H+ and Pi, impair cross bridge movement and ability to generate force

relaxation

signal to stop contraction is the absence of impulse

• triggers an energy-requiring Ca++ pump within the SR to requestor Ca++ back to the SR

this will remove Ca++ from troponin causing tropomyosin to roll back and cover binding sites on actin

important to get into relaxed state

steps of skeletal muscle contraction

excitation

1. nerve impulses reaches the neuromuscular junction

2. depolarization sweeps through the transverse (T) tubules

3. Ca++ is released from SR

contraction

4. Ca++ binds to troponin

5. tropomyosin rolls and reveals site of cross-bridge formation

6. ATP binds to myosin, energy is released, and myosin is cocked and energized

7. without tropomyosin in the way, myosin binds to actin

8. Pi is released, myosin rotates toward midline and shortening occurs

9. ADP is released and myosin remains bound to actin until another ATP binds to myosin - once new ATP binds to myosin the bridge is broken

10. ATP is broken down my myosin ATPase and myosin is re-cocked and shortening occurs

Relaxation

11. nerve impulse is gone triggering the re-sequestration of Ca++ into the SR

12. once Ca++ is pulled back into the SR the contraction is over and myosin can’t bind anymore because tropomyosin is in the way

muscle function

motor unit - one motor nerve and all the muscle cells it innervates

ratios from 1:1 to 1:2,000 or more

muscle fatigue

decline in muscle power output; inability to maintain a specified power output

• or perception of increased effort when maintaining power output (can be central fatigue)

• decrease in force generation

• decrease in shortening velocity

high intensity exercise ~60 sec

prolonged submaximal exercise ~2-4 hrs

CNS factors for fatigue

central fatigue

brain or spinal chord sends less signal to the muscle (less force generated)

more peripheral feedback, less central drive—very difficult to dissociate

fatigue neuromuscular junction

rapid, repeated contractions causes depletion of acetylcholine a neuromuscular junction

• leads to less stimulus going to the muscle and thus a reduction in force generation

fatigue contractile apparatus

don’t want high acidity in muscle

something at the level of muscle inhibits contraction or development of energy

lactic acid accumulation; buildup of H+

• inhibits Ca++ release from SR

• negatively affects ca++ binding to troponin

• H+ ions inhibit PFK

• fatigue tries to prevent too high [H+]

ATP-PC depletion (ATP not depleted, but PC is)

glycogen depletion (longer duration exercise)

Pi causes fatigue

muscle cramps

spasmodic involuntary muscle contractions (don’t know exact reason why)

electrolyte depletion and dehydration theory

• water and sodium loss via sweating causes spontaneous muscle contractions

• Na+ accumulates in interstitial space resulting in excess Ach release into synapse

altered neuromuscular control theory

• muscle fatigue causes abnormal activity in muscle spindle and golgi tendon organ

• leads to increased firing of motor neurons

• hypocapnia - (possible cause) low CO2 in body

  • clear effect of CO2 on cramps

stretching of a muscle activates

golgi tendon organ which inhibits motor neurons, allows muscle to relax and stops cramps temporarily

characteristics of muscle fiber types

biochemical properties

• oxidative capacity

  • number of capillaries, mitochondria, and amount of myoglobin

• type of myosin ATPase

  • speed of ATP degradation

contractile properties

• maximal force production

• speed of contraction (Vmax - velocity)

  • myosin ATPase activity

• muscle fiber efficiency

characteristics of individual fiber types

type I fibers (endurance athletes)

• slow-twitch fibers

• slow oxidative fibers

type IIa fibers (anaerobic and aerobic glycolysis)

• intermediate fibers

• fast-oxidative glycolytic fibers

type IIx fibers (fatigue a lot faster)

• intermediate fibers

• fast-glycolytic fibers

fiber types and performance

no sex difference in fiber type distribution

• mostly genetic; some plasticity w/training

sedentary individuals posses approximately 50% slow twitch fibers

power athletes have a high percentage of type II fibers

endurance athletes have high percentage of type I fibers

muscle twitch

if muscle given a single stimulus; responds with a simple twitch

• twitch characteristics dependent of proportion of fiber types

latent period - immediately after stimulus; lasts a few milliseconds

contraction phase - muscle shortening; lasts ~40 milliseconds

relaxation phase - return to original length; lasts ~50 milliseconds

force regulation in muscle

w/in single fiber, force related to actin-myosin contact

number and type of motor units required

initial muscle length overlap of actin and myosin)

• ideal length for force generation

nature of neutral stimulation of motor units

• frequency of stimulation

  • simple twitch

  • summation

  • tetanus

prior contractile activity

• can help or hinder; ex. post-activation potential

relationship between stimulus strength and force of contraction

length-tension relationship on skeletal-muscle

optimal length

simple twitch, summation, and tetanus

prior contractile activity

if a muscle performs a fatiguing exercise, subsequent force production is decreased

short period of non-fatiguing exercise can enhance force production ex. warm-up

• post-activation potential (PAP)

• phosphorylation of myosin light chains increases sensitivity of Ca++ release

force-velocity relationship

ideal speed of contraction for force generation

at any absolute force, the speed of movement is greater in muscle with the higher percent of fast-twitch fibers

the maximum velocity of shortening is at the lowest force

• true for both slow and fast-twitch fibers

force-power relationship

at any given velocity of movement, the power generated is greater in a muscle with a higher percent of fast-twitch fibers

peak power increases with velocity up tp movement speed of 200-300 degrees/sec

• power decreases beyond this velocity because force decreases with increasing movement speed

general nervous system functions

control of the internal environment w/ the endocrine system

voluntary control of movement

programming spinal cord reflexes

assimilation of experiences necessary for memory and learning

organization of the nervous system

central nervous system

• brain and spinal cord

peripheral nervous

• neurons outside of the CNS

• sensory division

  • afferent fibers transmit impulses from receptors to CNS

    • afferent - arrives to brain and spinal chord

• motor division

  • efferent fibers transmit impulses from CNS to effector organs

    • efferent - exits from brain and spinal chord

somatic - skeletal muscles, external

autonomic - smooth muscle, cardiac, glands, often not voluntary

structure of the neuron

cell body - center of operation and contains nucleus

dendrites - narrow cytoplasmic connections; serve as receptive area that can conduct electrical impulses towards the cell body; receives information

axon - carries electrical message away from cell body towards another neuron or effector organ; axon transmitting action potential

synaptic connections lost as you age

schwann cells

insulating layer of cells covering axons (white matter of brain)

contain large amount of myelin (lipid protein structure)

nodes of ranvier

gaps between myelin segments

play an important role in neural transmission

larger the nerve fiber, the faster the transmission

saltatory transduction

impulse ‘jumps’, fast from node to node

electrical activity in neurons

neurons are an excitable tissue

irritability

• ability to respond to a stimulus and convert it to a neural impulse

conductivity

• transmission of the impulse along the axon

resting membrane potential

cells negatively charged

polarized

attracts positively charged cations on outside of neurons

-5 to -100 mv determined by

• permeability of the cell membrane to different ions

• differences in ion concentrations between the intracellular and extracellular fluids

many ions present, but Na+, K+, and Cl- exist in the highest concentrations and play the most important role

more negative - hyperpolarization

more positive - depolarization

concentrations of ions across a cell membrane

resting membrane potential specifics

permeability of a neuron membrane to K+, Na+, and other ions regulated via ion channels

• can be opened or closed by gates within the channel

• when open, ions move from high to low concentration (increase permeability)

at rest, almost all Na+ channels are closed (some K+ open)

negative resting membrane potential in neurons is maintained by:

• higher permeability of the membrane for K+ compared to Na+

• concentration gradient for K+ promotes movement of K+ out of the cell

• Na+ wants in; K+ wants out

cell membrane has a Na/K pump that uses ATP to maintain the intracellular/extracellular ion concentrations by pumping Na out and K in

• energy consuming; against concentration gradient

• 3 Na+ for every 2K+

Na/K pump

action potential

stimulus of sufficient strength depolarizes the cell; all or nothing

• opens Na+ channels (reaches threshold) and Na+ moves in to the cell —> depolarization

• when critical threshold is reached, more Na+ gates open; action potential occurs

• ionic exchanges along axion occur to propagate the nerve impulse sequentially along nodes of ranvier

repolarization

• return to resting membrane potential- occurs immediately after depolarization

  • K+ leaves cell rapidly (increased permeability)

  • Na+ channels close, few positive ions enter the cell

all or none law

if threshold is not reached; nothing happens

if impulse occurs; it will travel entire length of axon without a decrease in voltage; does not lose strength

depolarization/repolarization of a nerve fiber

neurotransmitters and synaptic transmission

neurons communicate using synaptic transmission

• requires sufficient amount of neurotransmitter from synaptic vesicles into synapse

synapse - small gap between presynaptic neuron and postsynaptic neuron

neurotransmitter

• acetylcholine (most common in muscle)

• chemical messenger released from presynaptic membrane

• binds to receptor on postsynaptic membrane

• causes depolarization of postsynaptic membrane (excitatory neurotransmitters)

excitatory postsynaptic potentials (EPSP)

causes depolarization of entire cell body/neuron

can bring postsynaptic neuron to threshold by:

• temporal summation - rapid, repetitive excitation from a single excitatory presynaptic neuron

• spatial summation - sum EPSPs from several different presynaptic inputs/axons

inhibitory postsynaptic potential (IPSP)

cause hyperpolarization (more negative) making it more difficult for threshold to be reached

proprioceptors

receptors that provide CNS with information about body position

located in joints and muscles

kinesthesia

conscious recognition of the position of body parts

• reason the brain has such a high metabolic rate

limb movement rates

joint proprioceptors

free nerve endings

• most abundant

• sensitive to touch and pressure

• strongly stimulated at movement initiation, then adapt

golgi-type receptors

• found in ligaments around joints (stress on ligaments)

• similar to free nerve endings; not as abundant

pacinian corpuscles

• in tissues around joints

• detect rate of joint rotation

muscle proprioceptors

provide sensory feedback to nervous system; required for properly controlled movements

mechanoreceptors

• tension development by muscle

• account of muscle length

muscle spindle (stretch)

golgi tendon organ (tension)

muscle spindle

respond to changes in muscle length

primary endings (respond to dynamic changes)

secondary endings (provide information about static muscle length)

intrafusal fibers - run parallel to normal muscles (extrafusal fibers)

gamma motor neurons - stimulate intrafusal fibers to contract with extrafusal fibers by alpha motor neurons to tighten the spindle

stretch reflex - stretch on muscle causes reflex contraction

• knee-jerk reflex

golgi tendon organ

monitors tension developed in muscle

• prevents muscle damage during excessive force generation

stimulation results in reflex relaxation of muscle

• inhibitory neurons send IPSPs to muscle fibers

ability to voluntarily oppose GTP inhibition may be related to gains in strength (muscle hypertrophy)