Test 2

What are the primary differences between the autonomic and somatic divisions?

somatic controls skeletal muscles and is mostly voluntary

autonomic controls smooth and cardiac muscle, many glands, and some adipose tissue and is mainly involuntary

What is antagonistic control?

one autonomic branch is excitatory and another is inhibitory

What are the exceptions to antagonistic control in the autonomic nervous system?

smooth muscle in most blood cells always have some tension and sweat glands always sweat a little

cooperative control

work on different tissues to achieve a common goal

ex. erection (parasympathetic) and ejaculation (sympathetic)

What are the primary differences in the sympathetic and parasympathetic branches?

sympathetic is fight or flight while parasympathetic is rest and digest

sympathetic originates at the thoracic and lumbar regions of the spinal cord while parasympathetic originates in the brain stem and leaves the brain through cranial nerves

What is the central integration location for autonomic control?

hypothalamus, spinal cord, brain stem (pons, medulla)

Where do the primary stimuli come from?

sensory input from somatosensory and visceral receptors

What are the primary responses?

autonomic, endocrine, behavioral responses

What neurotransmitters does the sympathetic branch use?

ACh (acetylcholine) and norepinephrine

What neurotransmitters does the parasympathetic branch use?

ACh (acetylcholine)

What is the difference between muscarinic and nicotinic receptors?

muscarinic are receptive to muscarine and nicotinic and receptive to nicotine

varicosity

swelling at the end of postganglionic neuron; like a net thrown over all receptors, efficient way of getting large area to react at same time

Where do we find varicosities?

found in neuroeffector junction

How do varicosities differ from synaptic clefts?

synaptic cleft is a gap that neurotransmitters diffuse across while varicosities are a net that dumps out neurotransmitters on multiple receptors at the same time

What occurs if we administer alpha beta agonists?

stimulate receptors, increase heart rate and force of contractions, increase blood pressure

What occurs if we administer alpha beta antagonists/blockers?

decrease heart rate and force of contractions; prevent norepinephrine from creating contractions; lower blood pressure

What occurs if we administer muscarinic and nicotinic agonists?

causes bronchoconstriction, increases mucus, increases blood pressure, increases smooth muscle tone

What occurs if we administer muscarinic and nicotinic antagonists?

block synaptic transmission, bronchodilators (used to treat COPD)

What is special about the adrenal medulla (in terms of tissue type)?

neuroendocrine tissue (not true hormonal tissue); innervated by preganglionic fibers; secretes epinephrine into the blood

How is epinephrine released into circulation?

adrenal medulla secretes epinephrine into the blood

spinal cord to preganglionic neuron to adrenal medulla ACh bonds to chromaffin cell (postganglionic) and epinephrine enters blood and blood vessels go to target tissues

How does the efferent pathway of somatic motor neurons differ from autonomic motor neurons?

somatic motor consists of one neuron that is myelinated, long, and excitatory, terminal branches close to target and each terminal innervated and single skeletal muscle fiber

autonomic motor has two efferent neurons and two branches (symp. and parasymp.), it uses a variety of chemical/electrical signals to target smooth and cardiac muscle and glands

Why is acetylcholinesterase so important?

terminates neuronal transmission and signaling to prevent ACh dispersal; inhibits/stops movement; breaks down acetylcholine is synapses

acetylcholine

neurotransmitter used by neurons of CNS and PNS

adrenergic

receptor pertaining to epinephrine or norepinephrine

afferent pathway

pathway that connects receptors to integrating center

efferent pathway

outgoing signal that goes from integrating center to an effector

ganglion

cluster of nerve cell bodies in PNS

motor

control skeletal muscles

motor endplate

on postsynaptic side of neuromuscular junction, muscle cell membrane that lies opposite to axon terminal; series of folds that look like shallow gutters

muscarinic

subtype of cholinergic receptor

nicotinic

nicotine is agonist; cholinergic receptor

neuromuscular junction

synapse of somatic motor neuron and skeletal muscle fiber

postganglionic neuron

autonomic neuron that has its cell body in ganglion and sends axon to target tissue

preganglionic neuron

autonomic neuron that originates in CNS and terminates in an autonomic ganglion

What are the 3 different types of muscles?

skeletal, smooth, cardiac

skeletal muscle

striated, attached to bones, control body movement, voluntary, respond to somatic motor neurons

smooth muscle

internal organs and tubes, involuntary, movement into and out of and within body, respond to autonomic innervation, spontaneous contraction, modulated by endocrine system

cardiac muscle

striated, only in heart, move blood, involuntary, respond to autonomic innervation, spontaneous contraction, modulated by endocrine system

What is muscle antagonism?

move in opposite directions

structure of skeletal muscle

muscle cells are muscle fibers (long and cylindrical, fused cells with many nuclei), fibers bundled together into fascicles surrounded by CT sheath, CT surrounds entire muscle (fascia; continuous with CT sheath, holds muscle to bone with tendon)

organization of sarcomere

sliding filament theory

overlapping actin and myosin myofibrils slide past each other in energy dependent process

describes mechanism that allows muscles to contract

myosin binds to actin, myosin alters its configuration resulting in a stroke that pulls on actin and causes it to slide across myosin filament

How does muscle cross bridging work?

as active muscle lengthens/shortens and filaments slide, cross bridges detach and reattach to new positions

powerstroke repeated multiple times

move actin filaments

powerstroke

myosin cross-bridge swivels and pulls actin toward M-line (sarcomere shortens)

movement of mysoin head that is basis for muscle contraction

end of powerstroke

myosin releases actin and resets and binds to another actin (heads are not released in unison)

Explain excitation contraction coupling

somatic motor neuron releases ACh at neuromuscular junction; net entry of Na+ through ACh receptor channel initiates a muscle action potential; action potential in T-tubule alters conformation of DHP receptor; DHP receptor opens RyR Ca2+ release channels in sarcoplasmic reticulum and Ca2+ enters cytoplasm; Ca2+ binds to troponin allowing myosin-actin binding; myosin heads execute powerstroke; actin filaments slide toward center of sarcomere

explain contraction-relaxation cycle

muscle twitch is a single cycle; can be summed

sarcoplasmic reticulum Ca2+ -ATPase pumps Ca2+ back into SR; decrease in free cytosolic (Ca2+) causes Ca2+ to unbind from troponin; tropomyosin recovers binding site; when myosin heads release elastic elements pull filaments back to relaxed position

contraction: muscle generating tension

relaxation: muscle returning to normal length

What actions required for skeletal muscle contraction require ATP?

1. ATP hydrolysis provides energy for myosin head to rotate and reattach to actin
2. ATP powers pump that transports Ca2+ from cytosol back into SR


1. ATP binding to myosin causes detachment from actin after powerstroke

What path does a signal take (how does a signal for muscle contraction go from CNS to sarcomere)?

CNS to action potential along motor neuron to neuromuscular junction to excitation-contraction coupling to muscle twitch

How is calcium removed from the cytosol?

sarcoplasmic Ca2+ -ATPase pumps Ca2+ back into SR

What are the 3 energy systems for muscle contraction?

phosphocreatine, anaerobic glycolysis, aerobic respiration

phosphocreatine

produces short burst of energy by breaking down, muscle molecule that stores energy in high-energy phosphate bonds

anaerobic glycolysis

produces lactate and acid, quick, no oxygen required, small amount of energy released

aerobic respiration

citric acid cycle and electron transport chain, slow, oxygen required, large amount of energy released

How does phosphocreatine renew ATP?

breakdown of phosphocreatine produces a short energy burst

What is the difference between central and peripheral fatigue and what are causes for both?

central fatigue is due to CNS, giving up; chemoreceptors release when something is working to hard

peripheral fatigue is due to neuron or muscle; extended submaximal exercise leads to depletion of glycogen stores; short-duration maximal exertion leads to increased levels of phosphate buildup; maximal exercise leads to ion imbalances

What are the different types of muscle fibers?

type 1 (slow-twitch), type 2 (fast-twitch) (fast-twitch oxidative-glycolytic fiber and fast-twitch glycolytic fibers)

type 1 (slow-twitch) fibers

rely primarily on oxidative phosphorylation (lots of capillaries, mitochondria, oxygen, myoglobin), have low ATPase activity, high oxidative and low glycolytic capacity, relatively fatigue resistant, small diameter, longest contraction duration, oxidative/aerobic, high capillary density, numerous mitochondria, dark red in color; develop tension slowest

use: posture

type 2 (fast-twitch) fibers

develop tension faster (split ATP more rapidly), pumps Ca 2+ into SR more rapidly

fast-twitch oxidative-glycolytic fiber

fast-twitch glycolytic fiber

muscle fibers that develop tension rapidly

fast-twitch oxidative-glycolytic fiber

use oxidative and glycolytic metabolism, red muscle, moderate mitochondria, medium capillary density, glycolytic metabolism but becomes more oxidative with endurance training, fatigue resistant, short contraction duration, medium diameter

use: standing and walking

fast-twitch glycolytic fibers

rely primarily on anaerobic glycolysis; fastest, large diameter, short contraction duration, easily fatigued, glycolytic metabolism, low capillary density, few mitochondria, pale color

use: least used; jumping; quick, fine movements

How does muscle fiber length affect muscle tension?

sarcomeres contract with optimum force if at optimum length (not too short or too long) before contraction begins

tension generated directly proportional to number of cross bridges

What is summation?

stronger contraction when muscle doesn’t relax completely between action potentials

What is tetanus?

maximal contraction; sustained muscle contraction

What is a motor unit?

one motor neuron and its muscle fiber

How do we get our skeletal muscles to generate a greater force?

recruitment of additional motor units increase contraction force

What is asynchronous recruitment?

recruiting different motor neurons at different times; motor neurons “take turns” to give time to rest to help avoid fatigue

What is nerve-to-muscle ratio for generating force?

larger number, up to 150

What is nerve-to-muscle ratio for fine motor control?

smaller number, as low as 3

What are the elastic elements of skeletal muscle contraction?

tendons, aponeuroses, connective tissue

How are we able to generate force if our limbs aren’t moving (isometric contraction)?

series elastic elements; sarcomeres shorten while elastic elements stretch resulting in little change to overall length, force created cannot move load, movement at microscopic level

Know how to calculate force generation to move a weight at a joint

F1 x D1 = F2 x D2

What is the load velocity relationship of skeletal muscle?

as load increases, velocity is slower

How does smooth muscle differ from skeletal muscle?

smooth is involuntary and not striated; smooth responds to autonomic innervation and is modulated by endocrine system; smooth controls materials into and out of and within body; smooth is in internal organs and tubes; more variable, must operator of a range of lengths within organ layers and must run several directions; contract and relax more slowly, use less energy, maintain given amount of force, small spindle-shaped cells with single nuclei connected by gap junctions; initiated by chemical/electrical signals; ANS control, lacks specialized receptor regions; Ca2+ from SR and extracellular fluid; Ca2+ signal initiates cascade that ends with phosphorylation of myosin light chain and activation of myosin ATPase

What are the two ways phasic smooth muscle can act?

usually relaxed (esophagus) or cycles between contraction and relaxation (intestine)

What are the two ways tonic smooth muscles can act?

usually contracted (sphincters that relax to allow material to pass i.e. esophageal and urinary sphincter) and contraction is varied as needed (vascular smooth muscle)

Why do smooth muscles have gap junctions?

single-unit smooth muscle cells use gap junctions to connect to each other to contract as a single unit

allow rapid spread of depolarization; permit flow between neighboring cells

How does the contraction unit of smooth muscle differ from skeletal muscle sarcomeres?

uses contraction of myosin and actin

actin is more plentiful and associated with tropomyosin (smooth doesn’t have troponin)

myosin filaments are longer and entire surface is covered in myosin heads

no t-tubules; amount of SR varies and is less organized

extensive cytoskeleton (intermediate filaments and dense bodies)

smooth muscles lack sarcomeres

How does the calcium source of smooth muscle differ from skeletal muscles?

Ca2+ in smooth muscle comes from extracellular fluid and sarcoplasmic reticulum while in skeletal in comes only from SR

How does the contraction cycle of smooth muscle differ from skeletal muscle?

electrical signaling causes electromechanical coupling; chemical signaling causes pharmacomechanical coupling; skeletal is excitation-contraction coupling

What are the different smooth muscle channels?

voltage-gated, ligand-gated, stretch activated

voltage-gated Ca2+ channels

triggered by self or gap junctions

ligand-gated Ca2+ channels

receptor operated calcium channels (ROCC)

stretch-activated Ca2+ channels

open when pressure or other force distorts cell membrane (muscle fights strong force to prevent it from breaking); myogenic contraction (tissue protects itself after being stretched further than it should have)

Why do some smooth muscle cells have varying resting potentials?

due to ion channels spontaneously opening and closing (create slow wave and pacemaker potentials)

some smooth muscles have unstable membrane potentials

pacemaker potentials

always depolarize to threshold

A-band

band of striated muscle sarcomere whose length equals that of the thick filament

actin

a globular protein that polymerizes to form thin filaments

calmodulin

intracellular second messenger that binds Ca2+

central fatigue

subjective feeling of fatigue during exercise

concentric action/contraction

muscle tension rises to meet resistance then remains stable as muscle shortens

contraction

creation of tension in muscle

contraction-relaxation cycle

can be explained by sliding filament theory at molecular level and at muscular level is a muscle twitch

cytoskeleton

internal scaffolding of cell, composed of microfilaments, intermediate filaments, and microtubules

dihydropyridine (DHP)

calcium channel blocker

eccentric action-contraction

muscle lengthens as resistance becomes greater than force the muscle is producing

excitation-contraction coupling

sequence of action potentials and Ca2+ release that initiated contraction

extensor

a muscle that move bones away from each other when muscle contracts

flexor

muscle that brings connected bones closer together when it contracts

glycogen granule

independent metabolic unit composed of a highly branched polysaccharide and various proteins involved in its metabolism