• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/40

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

40 Cards in this Set

  • Front
  • Back
Slow Twitch Fibers (Type 1)
*High Oxidative Capacity
* High mitochondrial density because slow twitch fibers use alot of energy constantly.
*Have high capillary density b/c they have a high amount of blood flow
*High myoglobin levels: high oxygen storage and transfer.
Slow twitch fibers have low glycolytic capacity
They also have a relatively slow contractile speed because:
1. myosin ATPase activity is low
2. Little SR (slow Calcium release and uptake)
*Also les than 300 fibers per motor neuron
Fast twitch (type 2a)
*They have a high oxidative capacity and are fatigue resistant.
*High glycolytic capacity
*Theres high glycolytic enzymes, thus high lactic acid production
*Fast contractice speed of type 2a fibers
This is due to high myosin ATPase activity. and high density of SR.
*relatively large motor units
Fast twitch (type 2x)
*Low oxidative capacity & low fatigue
*High glycolytic capacity & high lactate production when active
*fast contractile speed
*relatively large motor units, greater than 300 muscle fibers per motor neuron
*very hard to activate
Theres a higher isometric force in type 2 then type 1 due to more muscle fibers per motor neuron and larger size of the fibers.
Cross-innervation of slow and fast muscles shows us that the alpha motoneuron
Genes determine which motor neurons innervate individual muscle fibers and generally MU's are made up of homogenous fiber composition. They also determine how fast the ATPase is.
Fibers in a motor unit are recruited when an alpha motorneuron carries an action potential from the CNS.
Principle of orderly recruitment states that motor units are activated in a fixed order
The size principle states that the order of recruitment is directly related to the motor neuron size
Cerebrum:
Site of intellect; primary motor and sensory area
Diencephalon:
Location of the hypothalamus, which is essential to homeostasis.
Cerebellum:
Important for coordinating movement.
Brain Stem:
Connects the brain to spinal cord; coordinates skeletal muscle Fx and maintains muscle tone.

It also contains regulators for respiratory and cardiovascular systems.
Nervous System is divided into two distinct subsystems: The Central Nervous System and the Peripheral.
The peripheral is further divided into the Sensory and Motor Divisions. Motor division is efferent, takes info from PNS to the tissues. Sensory division is afferent, takes info from body and relays to PNS.
Motor Division is further divided into Autonomic and Somatic: Somatic controls skeletal muscles and the Autonomic is fuether divided into ParaSympa and Sympa
There are 12 pairs of cranial nerves and 31 pairs of spinal nerves.

The autonomic system controls involuntary internal functions.
Sympathetic:
*fight or flight; norepinephrine is neurotransmitter; also stimulates release of catecholamines (norep and Epi) from adrenal medulla.
Sympathetic NS reacts to the motor response by increasing HR, BP, strength of heart contraction, blood supply to heart and active muscles, rate of gas exchange, mental alertness
Parasympathetic NS reacts to the motor response by:
*slowing down HR, constricts coronary vessels, constricts tissues in lungs.
Parasympathetic is known as the Internal "Housekeeping".
*controls digestion, urination, gland secretion and energy conservation. It uses ACh mostly
Types of Sensory Receptors:
Mechano: pressure, touch, stretch, vibration...
Thermo: Temperature changes
Nocio: Painful stimuli
Photo: respond to light to allow vision
Chemo: chemical stimuli from foods, odors, blood concentrations
Proprio: body mvmt and positio
Muscle Spindles sense muscle length and how much it changes during contraction.

Golgi Tendon Organs: detect the tension of a muscle on its tendon, thus provides info on strength of muscle contraction.
Muscle Spindles: A group of4-20 small muscle fibers called INTRAFUSAL fibers with Sens/Mtr nerve endings, connected in parallel with regular muscle fibers, aka EXTRAFUSAL.
The middle of the muscle spindle stretches but doesn't contract because it contains little to no actin/myosin.
When extrafusal muscle fibers attached to the spindle are stretched, sensory neurons on the spindle transmit information to the CNS about the muscles length
Gamma motorneurons activate intrafusal fibers, making the spindle sensitive to small degrees of stretch.
GTO's are encapsulated sensory organs that muscle tendon fibers pass thru.
They sense small changes in muscle tension and can inhibit contracting (agonist) muscles and excite the antagonist muscles to prevent injury
Different Integration Centers are utilized by the nervous system for different neural inputs.
*Spinal Cord - Simple motor reflexes such as pulling your hand away after touching a stovetop
*Lower Brain stem - more complex subconscious mtr reactions such as posture control
*Cerebellum - subcon control of movement such as what would be needed to coordinate multiple movements at once.
*Thalamus - Conscious distinction among sensations, such as feeling hot or cold.
* Cerebral cortex - cons. awareness of a senstation and the location within body where it originates.
The closer to the brain, or the higher in the brain that the sensory impulse stops, the more complex the motor reaction is.
*a mtr reflex is preprogrammed and happens without cons thought
Neurons originating in the primary motor cortex control voluntary muscle movement. Also called cerebro-spinal motorneurons, pyramidal, or upper motorneurons.
Clusters of nerve cells in the basal ganglia initiate sustained and repetitive movements such as runnig, walking, maintaining posture, and muscle tone
The cerebellum compares the actual movement with the intended movement. It is nicknamed the "Comparator."
Engrams are 'learned motor patterns' that are stored in the cortex
Resistance training can lead to:
*alterations of neural control of the trained muscle.
*and increased muscle size
Muscular Endurance can be increased by(2):
*through gains in muscular strength.
*through changes in local muscular metabolic and circulatory capacity
Neural Adaptations that take effect with gains in muscle strength:
*There will be synchronization & recruitment of additional mtr units
*decreased neural inhibition(ex: decreased GTO effects)
*a decrease in co-activation of antagonist muscles during stress
*increased rate coding
*fiber hypertrophy yes, hyperplasia? probably not.
for muscle size increases while training: more than 3 sets of 6RM to 12RM loads with short rests
for muscular endurance (20RM used)
Muscle Hypertrophy can either be transient(short term) or chronic(long term)
transient is the pumping up of muscle due to squeezing of fluid from the blood plasma into interstitial spaces of muscle due to high muscle pressures.
Chronic muscle hypertrophy happens due to changes in muscle fiber number(fiber hyperplasia) or muscle fiber size(fiber hypertrophy)
With muscle fiber hypertrophy the # of myofibrils and actin/myosin filaments increase so theres more cross-bridges which allows for a greater amt of strength to be utilized.
Muscle fibers MAY experience Hyperplasia(split in two) during intense weight training. Each half would ten increase in size. Hasn't been demonstrated clearly in humans.
For double muscled animals: within the embryo, the myotome(composed of myoblasts) which the myoblasts form myotubes, which go on to form myofibers.
myostatin either signals for cells to stop dividing or signals for satellite cells to remain quiescent. In dbl muscled animals, myostatin isnt activated so you get constant reproduction of muscle cells, so u get dbl muscled animals.
intersting..
Ways to study muscular inactivity:
In Humans: Casting/bed rest
In Animals: hindlimb suspension, casting, denervation
Acute Muscle Soreness - usually goes away right after exercise due to diffusion of waste from muscle
due to accumulation of EDEMA(water) or waste products in muscles such as lactic acid, pyruvate, CO2.
DOMS - primarily from eccentric contractions.
*assoc with dmg or injury to muscle fibers.
Can be due to edema, inflammation..felt 12 to 48 hours.
Satellite Cells - Adult stem cells available to maintain a relatively constant nucleus to muscle mass ratio
If muscle injury is bad enough, S cell fuses in with myofiber and you see the nucleus of S cell being added to myofiber nuclei.
S cells get to site thanks to chemotaxia.
This could be a different type of hyperplasia too, this theory says that the satellite cells once done proliferating turn into new fibers. Just a theory. But more accepted.
Sequence of events leading to DOMS
* Structural damage to muscle fibers
*impaired calcium homeostsis resulting in necrosis(cell death)
*inflammation occurs as macrophages invade the damaged tissue
*accumulation of irritants stimulate nociceptors(dull aching pain) within muscle
Muscle injury causes a reduction in force-generating capacity of muscles due to:
1. physical disruption of the muscle.
2. failure in the excit/contrac coupling process.
3. loss of contractile protein
*muscle glycogen synthesis is impaired
Muscle glycoggen synthesis is impaired because it costs the cell energy to build glycogen, which your body has to focus first on repairing muscle tissue.
To Reduce DOMS affect:
1. reduce eccentric workouts during early training
2. gradual increase in training
3. begin with high intensity eccentric workout so you can just get it over with and then hit it hard they recover.
Exercise induced muscle cramps
May be due to fluid/electrolyte imbalances and/or sustained alpha motor neuron activity from increased muscle spindle activity and/or GTO activity
electrolyte imbalance that increases muscle contraction: Calcium excess in cell would cause contraction, thus a cramp.
decrease in sSTR after injury mostly due to E-C Coupling failure.