Chapter 8 Flashcards
human body contains over how many skeletal muscles and what do they weigh
over 600 skeletal muscles that way 40-50% body weight
how are skeletal muscles attached to bones
through connective tissue called tendons
origin
the end of the muscle that is attached to bone and DOES NOT move
insertion
the opposite end to the origin that is moved during a muscular contraction
structure of skeletal muscle- superficial to deep
muscle
muscle bundle
fascicle
muscle fiber
myofibril
sarcomere with thick and thin filaments
major organelles within a muscle cell
have many nuclei along the entire length of the muscle fiber
lots of mitochondria
2 subpopulations of mitochondria in skeletal muscle
subsarcolemmal (SS) mitochondria
intermyofibrillar (IMF) mitochondria
subsarcolemmal (SS) mitochondria
located directly beneath cell membrane (sarcolemma)
produce cellular energy needed to maintain active transport of ions across the sarcolemma
*needs to establish a [ ] gradient with action potentials to be able to propagate along the surface
intermyofibrillar (IMF) mitchondria
next to contractile proteins (myofibrillar proteins)
provide energy needed to sustain muscle contraction
*supply ATP so we can get myosin head to release from actin
satellite cells
play a role in muscle growth and repair - during muscle growth, satellite cells increase the # of nuclei which helps with hypertrophy (increasing the size of the muscle fiber)
more nuclei allow for greater protein synthesis which is important for muscle growth in response to strength training
3 functions of skeletal muscle
1) force production for locomotion and breathing
2) force production for postural support
3) heat production during cold stress (shivering thermogenesis)
what is produced in skeletal muscle as a result of contractions
myokines and cytokines
role of myokines in skeletal muscle contraction
stimulate glucose uptake and fatty acid oxidation
promote blood vessel growth in muscle
promote liver glucose production and triglyceride breakdown
role of cytokines during skeletal muscle contraction
might have a pro-inflammatory response
as you increase the duration of an exercise, what happens to myokine production during skeletal muscle contraction
increase duration
increase myokines
increase glucose uptake and fat oxidation
*crossover effect (switch from CHO to FATs as duration increases)
what is the main cytokine produced during a skeletal muscle contraction
IL6
both pro-inflammatory and anti-inflammatory
*IL6 produced during exercise promotes anti-inflammatory effect
regular exercise promotes a anti-inflammatory environment by
reducing chronic inflammation and reduced risk of heart disease, type 2 diabetes, and certain cancers
flexors
decrease joint angle
extensors
increase joint angle
static
not changing the angle of a joint
muscle exerts force without changing length
pulling against immovable object
postural muscles
ex) pressing on a well
types of dynamic muscle contractions
concentric and eccentric
concentric contraction
muscle shortens during force production
eccentric contraction
muscle produces force but length increases
associated with muscle fiber injury and soreness (growth and repair)
PNS controls
everything other than brain and spinal cord
CNS controls
brain and spinal cord
somatic motor neurons of PNS
responsible for carrying neural messages from spinal cord to skeletal muscles
motor unit
motor neuron and all the muscle fibers it innervates
neuromuscular junction
junction between motor neuron and muscle fiber
motor end plate
pocket formed around motor neuron by sarcolemma
where NT release occurs
myofibrils can be further subdivided into
individual sarcomeres
sarcomeres
contain specialized arrangement of thin and thick filaments
includes: Z line, M line, I band (light zone), A band (dark zone), H zone (middle of A band)
thin filament consists of
actin, tropomyosin, troponin
thick filament consists of
myosin
the sliding filament model
muscle shortening occurs due to the movement of the thin (actin) filament over the thick (myosin) filament
formation of cross bridges between thick and thin filaments (myosin head has to hold onto actin to pull it together towards the M line) - * in order to move actin over, cross bridge must be formed
sarcomere shortening during muscle contraction involves
reduction in the distance between Z lines of the sarcomere
what happens to the width of the A band with a concentric contraction
does not change
what happens to the width of the H-zone with a concentric contraction
decreases
what happens to the width of the I band with a concentric contraction
decreases
what happens to the width of the sarcomere with a concentric contraction
decreases
what happens to the width of the thin and thick filaments with a concentric contraction
does not change
what is required for muscle contraction
ATP
how do we acquire ATP for a muscle contraction
Myosin ATPase breaks down ATP as fiber contracts
(ATP breakdown -> power stroke -> ADP + Pi)
breakdown of ATP equation
ATP+water –> (via ATPase)—> ADP +Pi + energy
sources of ATP for muscle contraction
ATP-Pc system
Glycolysis
Oxidative Phosphorylation
7 stages of cross bridge cycling
1)Action potential stimulates ACh release from alpha motor neuron at neuromuscular junction
2) ACh induces an action potential in the muscle fiber. Action potential spreads down sarcolemma and T tubules. Myosin binding sites on the actin molecule are covered in resting fibers (tropomyosin intertwined with actin)
3) the action potential releases Ca2+ from sarcoplasmic reticulum
4) calcium binds troponin on tropomyosin. Tropomyosin moves, revealing myosin binding sites.
5) cross bridge forms when myosin head (with ADP + Pi bound) binds actin
6) myosin head pivots (with ADP + Pi bound) (power stroke), moving actin. ADP and Pi dissociate from myosin head
7) myosin head releases actin when a fresh ATP binds to the myosin head allowing myosin head to release from actin
8) myosin head binds next actin. The ATP on myosin head is cleaved to ADP + Pi and cycle repeats
muscle cramps
aka spasmodic, involuntary muscle contractions
often associated with prolonged, high intensity exercise (but not always)
electrolyte depletion and dehydration theory - muscle cramps
water and sodium loss via sweating causes spontaneous muscle contractions
more likely in a hot environment
what are some limitations of the electrolyte depletion and dehydration theory to explain muscle cramps?
1) altered neuromuscular control theory
2)increased muscle spindle activity
3) decreased golgi tendon organ activity
altered neuromuscular control theory
abnormal spinal reflex due to fatigue
results in increased excitatory activity of muscle spindles and reduced inhibitory effect of Golgi tendon organ
increased muscle spindle activity
1) muscle spindles detect stretch of the muscle
2) sensory neurons conduct action potentials to the spinal cord in order to get muscle to contract
3) sensory neurons synapse with alpha motor neurons
4) stimulation of the alpha motor neurons causes the muscle to contract and resist being stretched
decreased golgi tendon organ activity
*make it easier to hold contraction and causes cramps
Muscle contraction increases tension applied to tendons:
1) golgi tendon organ detects tension applied to a tendon
2) sensory neurons conduct action potentials to the spinal cord
3) sensory neurons synapse with inhibitory interneurons that synapse with alpha motor neurons
4) inhibition of alpha motor neurons causes muscle relaxation, relieving the tension applied to the tendon
what helps muscle cramps
passive stretching
activates golgi tendon organ inhibits motor neurons in spinal cord, resulting in muscle relaxation
type I fiber primary pathway for ATP synthesis
aerobic
type IIa fiber primary pathway for ATP synthesis
combination of aerobic and anaerobic
type IIx fiber primary pathway for ATP synthesis
anaerobic
Type I myoglobin content/# of mitochondria
high
Type IIa myoglobin content/# of mitochondria
intermediate
Type IIx myoglobin content/# of mitochondria
low
Type I speed of contraction
slow
Type IIa speed of contraction
fast
Type IIx speed of contraction
fastest
Type I maximal force production and power output
moderate
Type IIa maximal force production and power output
high
Type IIx maximal force production and power output
highest
Type I rate of fatigue
slow
Type IIa rate of fatigue
intermediate
Type IIx rate of fatigue
fast
Type I type of motor unit innervating muscle
type S
Type IIa type of motor unit innervating muscle
type FR
Type IIx type of motor unit innervating muscle
type FF
recruitment order of muscle fibers
1st- Type I
2nd- Type IIa
3rd- Type IIx
activities best suited for Type I muscle fibers
endurance type fibers (slow fatigue rate)
activities best suited for Type IIa and IIx muscle fibers
power type activities
how are skeletal muscle fibers typed
via muscle biopsy
(small piece of muscle removed - may not be representative of entire body)
characteristics of type I fibers
slow twitch fibers
slow-oxidative fibers
characteristics of type IIa fibers
intermediate fibers
fast-oxidative glycolytic fibers
characteristics of type IIx fibers
fast twitch fibers
fast-glycolytic fibers
speed of shortening is greater in
fast fibers
SR releases Ca2+ at a faster rate
higher ATPase activity
force production: larger vs smaller fibers
larger muscle fibers produce more force than smaller fibers because they have more actin and myosin than small fibers
men have significantly greater___
total, upper body, and lower body skeletal muscle mass
who generates more absolute force production (men or women)
men generate more absolute force production
power output between fiber type equation
power= force x shortening velocity
sprinters have more
fast fibers
power athletes
distance runners have more
slow fibers
endurance athletes
force regulation in muscle
1) types and number of motor units recruited
2) initial muscle length
3) nature of neural stimulation of motor units
more motor units =
greater force
fast motor units =
greater force
recruitment pattern of motor units during graded exercise
Type S then Type FR then type FF (generate the most force)
progressive recruitment of motor units begins with
smallest motor units and progressing to larger and larger motor neurons
increasing stimulus strength recruits more
motor units and produces more force
normal body movements involve sustained contractions that are
NOT simple twitches
muscle twitch
contraction as the result of a single stimulus
increasing the frequency of the stimulus results in
summation of the twitches and tetanus
DOMS
delayed onset muscle soreness
appears 24-48 hours after strenuous exercise
due to microscopic tears in muscle fibers or connective tissue
what causes more damage: concentric or eccentric exercises
eccentric exercise causes more damage than concentric exercise
exercise induced muscle injury
sarcomere damage (Hrs to Days)
immune cell infiltration (Days)
satellite cell activation (Days to Weeks)
how do muscle fibers repair themselves
using resident satellite populations
procedures leading to DOMS
strenuous exercise
structural damage to muscle fibers
membrane damage
CA2+ leaks out of SR
protease activation resulting in breakdown of cellular proteins
inflammatory response
edema and pain
a bout of unfamiliar exercise results in
DOMS
following recovery of DOMS
another bout of same exercise results in minimal injury
