The flashcards below were created by user
on FreezingBlue Flashcards.
Initiating, Integrating and Controlling Movements
Cerebrum - responsible for higher mental functions, movement, visceral functions, perception, behavioral reactions, and for the association and integration of these functions.
Motor Cortex - consists of the primary motor cortex and the premotor cortex
Premotor Cortex - causes general patterns of movement involving groups of muscles that perform specific tasks. Involved in the unconscious fine tuning of muscle activity required for highly-skilled movements.
Sensory Cortex - relays information into the motor cortex for control of motor activities
Basal Ganglia - functions in muscle tone, control of movement
Thalamus - acts primarily as a relay station of sensory input as well as interpretation of some sensory input, such as pain, temp, crude pressure and touch
Cerebellum - coordination of movement
Medulla Oblongata - controls heart rate, blood flow, equilibrium, swallowing, salivation and respiration
Pons - controls respiration; also involved in facial/neck sensations and the regulation of facial expressions, eye movement, taste, salivation and equilibrium.
Midbrain - conveys sensation of touch, proprioception and vibrations to the thalamus; also, involved in the regulation of eye movement, pupil size and lens shape.
Pyramidal System - Of the pyramidal motor tracts, 90% cross-over at the decussation of pyramids and 10% are ipsalateral
Extrapyramidal System - general movement patterns (i.e., muscle tone and posture, control of head movement to vision and hearing, and equilibrium), highly-skilled movements which facilitate the execution of whole movement patterns without conscious awareness of the individual parts (i.e., allows for fine tuning)
Sensory receptors that provide feedback to the CNS include:
- Muscle Spindles
- Golgi Tendon Organs
- Bulbs of Krause
- Pacinian Corpuscles
- Ruffini End Organs
Limbic System - provids input to the motor cortex regarding motivation drives and needs
"descend along the same side/do not cross-over)
occurs when only one side of the body is developed through motor training, but due to a cross-transfer effect the other side of the body does receive some neural stimulus and hence, is developed to some extent.
provide sensory information regarding joint angle, acceleration at the joint, and the degree of deformation brought about by pressure.
Greatly contribute to kinesthetic awareness because they prodvide info regarding body awareness
Pacinian corpuscles detect changes in vibrations
Ruffini corpuscles detect changes in temp
in general, sense position, length, tension, pressure and temp in a muscle and hence, regulate rate of change in length as well as facilitating kinesthetic awareness.
Golgi Tendon Organs
proprioceptors located in muscles at their junctions with tendons and in ligaments of joints; if force of contraction and consequently tension is too great, inhibits alpha and gamma motor neuron of contraction muscle thereby reducing excess tension and thus preventing injury (protective mechanism - reflex inhibition).
Also, appear to help equalize the contractile forces of seperate muscle fibers.
Roles of the Muscle Spindle
proprioceptors located in intrafusal muscle fibers which lie parallel to the extrafusal (normal) muscle fibers.
Roles of the Intrafusal Fibers
involved in gross muscular contraction
Roles of the Gamma Motor Neurons
activate the intrafusal muscle fibers
Roles of the Annulospiral Endings
sensory receptors that detect the length or stretch on the intrafusal muscle fibers
Roles of the Sensory Afferent Neurons
receives and carries information from annulospiral endings via spinal cord
Three Functions of Muscle Spindles
- (1) sense length of fibers
- (2) reflex contraction
- (3) coavtivation
a motorneuron and all the muscle fibers that it innervates
- -each is the same in fiber type composition (either SO, FOG, or FG - no mixtures)
- -each type differs in sensitivity to stimulation (SO is easiest, FG is hardest - size principle)
- -each operates on "all-or-none" principle
- -all fibers in motor unit are equally sensitive to neural stimuli
Force Production Determinants
- -dependent on actin and myosin bonding*
- -# of fibers w/in active motor units (hyperplasia will increase fiber #)
- -# of motor units activated
- -size of fiber wi/in active motor units (hypertrophy)
- -balance between stimulating and inhibiting hormones
- -frequency of impulses
- -speed of movement and fiber type
Roles of Alpha Motor Neurons
innervate the extrafusal muscle fibers
cell body of a neuron
process of a neuron that carries impulses away from the cell body
portion of a neuron that carries impulses toward the cell body
responsible for producing myelin
Node of Ranvier and Saltatory Conduction
portion of a myelinated axon which is not covered by myelin sheath
important for saltatory conduction as impulse "jumps" from one Node of Ranvier to the next allowing for fast nerve impulse conduction
the point of contact where nerve impulses are transmitted from one neuron to another
the membrane proximal to a synapse
the membrane distal to a synapse
gap between pre and post synaptic membrane
vesicles in the axon terminal where neurotransmitters are stored
connective tissue surrounding a muscle; connects into tendon at the origin and insertion of the muscle
connective tissue surrounding a fasciculus or group of muscle fibers
connective tissue surrounding a muscle cell or fiber
muscle cell membrane
cytoplasm of muscle cell; site of anaerobic metabolism
site of cellular oxidation or aerobic metabolism; powerhouse of the cell
threadlike protein strands
functional unit of the muscle cell; runs from Z line to Z line
thin protein myofilaments
thick protein myofilaments
also called S-1 heads; extend from actin and myosin
long, thin molecules that lie on the surface of the actin strand
globular molecules (tropomyosin molecules embedded)
anchored to the sarcolemma
- (1) anchors actin (pulling mechanism)
- (2) keeps actin properly oriented around myosin (surrounding)
- (3) provides pathway for T-tubule system to go deep into muscle tissue
light areas near the Z lines consisting of the thing, actin myofilaments
dark areas consisting of both the thin myofilaments and the thick, myosin myofilaments
slight variation in the shading of the A band due to absence of the actin myofilaments
appear to parallel Z lines (invaginations of the cell membrane)
run parallel to myofibrils
In relationship to the sarcoplasmic reticulum, what is meant by the term "triad?"
collectively, the two cisternae and T tubule are known as the triad
What happens to the H zone and I band during muscle contraction?
the H zone disappears and the I band gets smaller
What is the basic functional unit of a muscle cell?
Events of Muscle Contraction
(1) motor nerve impulse causes depolarization of cell membrane at axon terminal which opens Ca++ gates allowing influx of Ca++ that stimulates reease of acetylcholine (ACH) vesicles via exocytosis.
(2) ACH binds to receptors of sarcolemma opening Na++ channels which depolarizes cell membrane and wave of depolarization spreads inward along T system that invaginates from surface of sarcolemma.
(3) action potential causes release of Ca++ from terminal cisternae of sarcoplasmic reticulum (SR) which travels via the longitudinal tubules into the sarcoplasm around the myofibrils
(4) Ca++ (2 molecules) bind to regulatory sites on troponin (TN-C) changing the troponin-tropomyosin-actin complex which removes the inhibition between actin and myosin (tropomyosin rods are drawn from periphery toward center on groove of actin so that the active sites on actin are exposed.
(5) the S-1 unit head of myosin attaches to the actin filament and changes its orientation to about a 45 degree angle in relation to the actin filament axis. The tilting of the S-1 head is the power stroke of muscle contraction causing the actin filament to be pulled over the myosin filament. The power stroke or forward tilt is driven by previously stored energy that causes the release of ADP and Pi from the S-1 head of myosin resulting in the pulling (sliding) of acting over myosin and hence, muscle contraction.
(6) the S-1 head is then released from the active site on the actin filament by binding with ATP. Myosin ATPase breaks down ATP into ADP and Pi plus energy for it to tilt back to a new angle and react with a new active site on the actin molecule.
(7) The process repeats and the actin filament is pulled over and in on the myosin filament and the sarcomere...fiber....muscle contracts.
2 Roles of Calcium in Muscle Contraction*
- (1) influx of Ca++ into the axon terminal stimulates the release of acetylcholine (contraction - step 1)
- (2) binding of calcium to regulatory sites on troponin remove the inhibition between actin and myosin (contraction - step 4)
3 Roles of ATP in Muscle Contraction*
- (1) the release of previously stored energy drives the power stoke of the myosin S-1 head resulting in the pulling (sliding) of actin over myosin (contraction - step 5)
- (2) new molecule of ATP binds to myosin S-1 head causing the dissociation of actin and myosin; myosin ATPase breaks ATP down into ADP + Pi, heat, and energy which is used to tilt the myosin S-1 head back down and away from actin to the resting, relaxed position (contraction - step 6)
- (3) ATP is used to actively pump Ca++ back into the sarcoplasmic reticulum cisternae when the nerve impulse stops (relaxation - step 1)
How fast can muscle tissue twitch during sustained muscular contraction?
twitches occur at the rate of 100-200 per second during sustained muscular contraction
3 Fundamental Principles of Exercise Physiology
- (1) peak rate of muscle contraction (peak twitch rate) is dependent on myosin ATPase activity and the size (thickness) of the motor axon
- (2) maximal force (tension) that a muscle can generate is dependent on the amount of actin-myosin binding that is taking place
- (3) continuation of muscle contraction is dependent on the ability to recycle ATP
What factors are peak rate of muscle contraction dependent on?
speed of contraction dependent on
- A. size of axon (myelination)
- B. myosin ATPase; FT > ST
FG > FOG > SO
What factors is maximal force (tension) that a muscle can generate dependent on?
maximum tension dependent on action-myosin binding; FT > ST
FG > FOG > SO
What factors are continuation of muscle contraction dependent on?
continuation of muscle contraction is dependent on ability to recycle or regenerate ATP; ST > FT
SO > FOG > FG
How do muscle fiber types relate to the 3 fundamental principles of exercise physiology?
2 Methods to Determine Muscle Fiber Types
myosin ATPase high in FT glycolytic, anaerobic fiber
SDH high in ST fibers
(light circle, dark circle) 50% ST oxidative - aerobic [SO, Type I, Red]
(two dark circles) 30% FT high oxidative glycolytic [FOG, Type IIa, Intermediate]
(dark circle, light circle) 20% FT glycolytic - anaerobic [FG, Type IIb, White]
Rate of Contraction for Muscle Fiber Types
(various physiological mechanism underlying the properties)
Tension of Contraction for Muscle Fiber Types
(various physiological mechanism underlying the properties)
Endurance Properties for Muscle Fiber Types
(various physiological mechanism underlying the properties)
General Neuronal Characteristics of FT and ST Motor Units
- FT motor units
- -neurons have large cell bodies
- -neurons have thicker axons
- -require higher levels or neural stimulation in order to depolarize and propagate neural impulses
- -propagate neural impulses faster than ST motor units
- -therefore, used less frequently, but twitch at faster rates; used during maximal effort (high intensity) slow speeds of movement, high intensity fast speeds of movement, during low intensity, long duration tasks when ST motor units become fatigued, and during the initiation of movement and maintenance of balance.
- ST motor units
- -neurons have smaller cell bodies
- -neurons have thinner axons
- -require lower levels of neural stimulation in order to depolarize and propagate neural impulses
- -propagate neural impulses more slowly than FT motor units
- -therefore, used more frequently, but have slower twitch capabilities; used during high intensity, slow movements and during low intensity, long duration tasks
Recruitment Characteristics of ST and FT Motor Units
motor units whose neurons have a smaller cell body (i.e., ST motor units) are generally recruited first followed by motor units whose neurons have a larger cell body (FT motor units)
motor units whose neurons have a smaller cell body (i.e., ST motor units) are generally recruited first followed by motor units whose neurons have a larger cell body (FT motor units).
Which came first, the motor neuron or the fiber type?
Cross-innervation studies indicate that "neurons dominate the response characteristics of the muscle tissue" due to either (theories) axoplasmic flow of a genetic substance theory or use-disuse theory.
Although traditional thought suggested that ST fibers could not be converted to FT fibers and vice-versa; recent studies indicated that sprint training increase FT fibers and decreased ST fibers
more research is needed to resolve the issue
What do cross-innervation studies indicate?
"neurons dominate the response characteristics of the muscle"
What theories are used to explain the results of cross-innervation studies?
- (1) axoplasmic flow
- (2) use-disuse
Distribution of Fiber Type
Muscle fiber type composition for a muscle shows basically normal distribution in both men and women.
Does the distribution of muscle fiber types vary between as well as within individuals? EXPLAIN
average person has 40-60% of FT, ST (even distribution)
gender doesnt affect fiber type distribution
Determinants of Force Production
1-5, 1-5A, 1-5B
- A. Number of fibers within an active motor unit
- B. Number of motor units activated within a muscle
- C. Size of fibers within an active motor unit
- D. Balance between stimulating (acetylcholine) and inhibition (GABA) neurotransmitters
- E. Frequency of neural impulses
- F. Synchronous, coordinated firing of motor units
- G. Motor unit recruitment patterns
- H. Speed of movement and fiber type
- I. Initial length of the muscle fibers
- J. Angle of pull
- K. Architecture (configuration) of tendon and muscle fibers
Various Effects of Fatigue on Force Production
(1) Metabolic by-products, such as lactic acid accumulation from anaerobic glycolysis or the accumulation of ketone bodies from the breakdown of fatty acids in the absence of the needed carbohydrates to prime the pump for fat utilization, will decrease the pH of muscle tissue; a decrease in pH will interfere with Ca++ release from the sarcoplasmic reticulum, actin-myosin binding, and ATP breakdown for energy
(2) Deletion of the neurotransmitter acetylcholine in the motor neuron axon terminal
(3) Depletion of the intramuscular phosphagen stores
(4) A greater relative distribution of FT muscle fibers in the working muscles will result in an earlier onset of fatigue; FT muscle fibers (particularly FG) have much lower oxidative capabilities and consequently endurance capabilities than the ST oxidative muscle fibers and to a certain extent, the FOG muscle fibers
Factors Influencing Speed of Movement
(1) FT muscle fibers have faster speeds of movement capabilities than ST muscle fibers; consequently, an individual with a relatively high distribution of FT muscle fibers can potentially move at faster speeds of movement than an individual with a relatively high distribution of ST muscle fibers. About 25% of the difference in speed of movement capabilities can be attributed to amount of FT muscle fiber types
(2) The greater the force production capabilities relative to resistance, the greater the potential speed of movement; similarly, the greater the force production capabilities relative to body weight, the greater the potential acceleration of the body and consequently, the greater the potential speed of movement. Hence, an increase in force production capabilities or a decrease in excess fat weight will increase the potential speed of movement.
(3) The greater the coordination via synchronous recruitment of agonist and antagonist muscle groups, the greater the potential speed of movement.
How does training affect contractile-related factors?
high intensity speed training has been reported to increase the % of FT fibers and decrease the % of ST fibers; conversely, low intensity endurance has been reported to increase the % of ST fibers and decrease the % of FT fibers
How does training affect muscle fiber type composition?
It appears that some transformation in muscle fiber type with chronic activity is in fact possible.
Does strength training compliment endurance training and does endurance training compliment strength training?
The addition of strength training to an endurance training program will increase time to exhaustion while performing a submaximal workload.
The addition of endurance training to a strength program may reduce or compromise the potential strength gains from strength training.
How does fatigue affect force production?
(1) local muscle fatigue - low pH interferes with Ca++ release, action-myosin binding, ATP breakdown and lower myosin ATPase activity
(2) neural fatigue - depletion of neurotransmitters
(3) local muscle fatigue - depletion of phosphagens (ATP-CP)
Is the rate of fatigue related to muscle fiber type? EXPLAIN
increase in speed of movement = increase in FT
- increase in force and actin/myosin binding:
- -muscle unit recruitment
- -pre stretch muscle
- -distribution of muscle fiber types
more FT % and less ST %
Primary Factors Influencing Speed of Movement
- (1) myosin ATPase
- (2) thickness of axon (myelination)
Anaerobic Metabolic Pathways
- Phosphagen or ATP-PC System
- -energy pathway = phosphogen breakdown
- -starting product = ATP + CP
- -by products = ADP, AMP, Pi
- -ATP yield = limited
- -capacity total Kcal increased by = training status, muscle mass, creatine ingestion (#4)
- Anaerobic Glycolytic or Lactic Acid
- -energy pathway = glycolytic in sarcoplasm
- -starting product = glucose or glycogen
- -by products = lactic acid (low pH), alanine to liver
- -ATP yield = net 2 ATP
- -capacity total Kcal increased by = muscle to L.A. ratio, alanine transaminase, increased H-LDH, decreased M-LDH
- -when used = 30 seconds to 3-4 minutes, high intensity
Aerobic Metabolic Pathways
- Aerobic Glycolytic System
- -energy pathway = glycolytic in sarcoplasm, Kreb's Cycle & ETS in mitochondria
- -starting product = pyruvic acid into acetyl CoA or oxaloacetic acid
- -by products = CO2 & H2O
- -ATP yield = net 36 ATP in skeletal muscle, net 38 ATP in cardiac muscle
- -capacity total Kcal increased by = training, CHO loading, CHO ingestion (#2)
- -when used = 3-4 minutes to 2-3 hours, moderate intensity
- Beta or Fat Oxidative System
- -energy pathway = beta oxidation, kreb's cycle, ETS in mitochondria
- -starting product = acetyl CoA, carnitine (transporter), glycerol in liver
- -by products = ketone bodies (low pH)
- -ATP yield = 1 fatty acid yields about 100-150 ATP
- -capacity total Kcal increased by = unlimited, need CHO (#1)
- -when used = continuous low intensity
- Electron Transport System
- -starting product = needs O2
- -by products = H2O
- -ATP yield = NADH+H (3 ATP), FADH+H (2 ATP)
Key Substrates and Enzymes in Each Energy System or Cycle
- Phosphagen ATP-CP or Alactate
- -substrates = ATP-PC or CP
- -enzymes = myosin ATPase, CPK (creatine phosphokinase), AK (adenylate kinase)
- Anaerobic Glycolysis or Lactic Acid
- -subtrates = CHO, glucose or glycogen
- -enzymes = phosphorylase, HK (hexokinase), PFK (phosphofructokinase), PK (pyruvate kinase), alanine transaminase, M-LDH, H-LDH
- Aerobic Glycolysis or CHO Oxidation
- -substrates = CHO, glucose or glycogen
- -enzymes = CS (citrate synthase), SDH (succinic dehydrogenase), IDH (isocitrate dehydrogenase)
- Beta (fat) Oxidation
- -substrates = triglycerides (glycerol + 3 FA's)
- -enzymes = lipase, thiokinase, thiolase, fatt acetyl CoA, carnitine fatty acid transferase
- Electron Transport System
- -substrates = NADH+H (3 ATP) FADH+H (2 ATP)
- -enzymes = cytochromes carry electrons
*Which of the metabolic pathways are located in the sarcoplasm and mitochondria?
- -phosphagen ATP-CP or alactate
- -anaerobic glycolysis or lactic acid
- -aerobic glycolysis or CHO oxidation STARTS in sarcoplasm
- -beta (fat) oxidation TG's start in sarcoplasm
- -aerobic glycolysis or CHO oxidation ENDS in mitochondria
- -beta (fat) oxidation
- -Kreb's cycle in matrix
- -ETS inside inner membrane of mitochondria
citrate from inhibits PFK to slow down glycolysis to spare CHO to prime the pump for fat usage
Priming the Pump for Fat Usage
pyruvate converted to oxaloacetate to combine with acetyl CoA from fat to form citrate
How many net ATP can be synthesized from anaerobic glycolysis (lactic acid system) in skeletal and cardiac muscle?
cardiac muscle = 38 ATP
skeletal muscle = 36 ATP
How many net ATP can be synthesized from aerobic glycolysis (CHO oxidation) in skeletal and cardiac muscle?
For every molecule of acetyl CoA that enters the Krebs Cycle, how many ATP can be synthesized?
How many acetyl CoA molecules can be formed from a triglyceride molecule (assume all the fatty acids are either 12, 14, 16, or 18 carbons in length)?
formula for this is:
# of acetyl CoA = # of carbon/2
Triglyceride = glycerol + 3 fatty acids (12-18C)
(1) investment = -2 ATP
(2) # of acetyl CoA? #C/2 = 12C/2 = 6 x 12 ATP = +72 ATP
(3) # of trips? (#C/2)-1 = 12/2-1 = 5 trips x 5 ATP = +25 ATP
So, (-2) + (+72) + (+25) = 95 ATP x 3 = 285 ATP from one tryglyceride
Other than the acetyl CoA fatty acids, what are two other sources of fuel substrate and/or ATP from fat metabolism?
For each gram of fat and CHO, approximately how many kcal can be yielded?
Fat = 9 Kcal/gram
CHO = 4 Kcal/gram
4 Fates of Pyruvate
(1) Lactate (anaerobic); decreases the pH of the muscle tissue thereby interfering with muscle contraction. Lactate is converted back into pyruvate for entrance into the Kreb's cycle in the heart, liver, kidneys, and high oxidative ST skeletal muscle
(2) alanine (anaerobic); acts as a temporary reservoir for the excessive breakdown of CHO under anaerobic conditions, thereby minimizing the formation of lactate; alanine is converted back into glucose in the liver.
(3) acetyl CoA (aerobic); acetyl CoA is the common entry molecule for both fats and CHO's into the Kreb's cycle.
(4) oxaloacetate (aerobic); the conversion of pyruvate to oxaloacetate in order to cmobine with acetyl CoA from fat breakdown is known as priming the pump for fat usage.
Factors That Affect the Power (kcal/min) and Capacity (kcal) of the Various Energy Systems
- Phosphagen ATP-CP (#1)
- -myosin ATPase
- -CPK (creatine phosphokinase)
- -AK (adenylate kinase)
- Anaerobic Glycolysis (#2)
- -HK (hexokinase)
- -PFK (phosphofructokinase)
- -PK (pyruvate kinase)
- Aerobic Glycolysis (#3)
- -CS (citrate synthase)
- -SDH (succinate dehydrogenase)
- -ETS cytochromes
- -kreb's cycle enzymes
- Beta Oxidation (#4)
- -ETS cytochromes
- -kreb's cycle enzymes
General Metabolic Responses of the Energy Systems to Exercise
At the onset of exercise, the energy system respond in the following order in reach steady state exercise:
- (1) phosphagen metabolism
- (2) anaerobic glycolysis
- (3) oxidation metabolism
- (3a) anaerobic glycolysis - CHO oxidation (moderate intensity)
- (3b) beta oxidation (low intensity)
During what time frame is the phosphagen (ATP-PC) system the primary source of energy production during sustained maximal effort activities?
During what time frame is the glycolytic system the primary source of energy production during sustained maximal effort activities?
During what time frame is the oxidative energy system the primary source of energy production during sustained maximal effort activities?
greater than 4 minutes
Hormones that Influence the Mobilization of Fat From Adipose Tissue
- Insulin - inhibits HSL (hormone sensistive lipase) & decreases fat mobilization
- Caffeine - stimulates HSL (also stimulates phosphorylase in glycolysis)
Exercise decreases insulin release from pancreas
Basic Principles of CHO Loading
CHO Loading Prior to Exercise
approximately 1-week prior to a major endurance event, perform a long workout to deplete the muscle glycogen stores. Then for the next 3 days eat a low CHO diet. Then, switch to a high CHO diet for the 3 days prior to the major endurance competition.
CHO Fluid Ingestion During Exercise
During exercise, drink 4-8 ounces of cold water every 10-15 minutes containing a 5-10% glucose concentration.
Both CHO loading prior to exercise and the ingestion of CHO fluids during exercise will significantly increase muscle glycogen levels thereby enhancing performance during moderate intensity, long duration exercise. The capacity of aerobic glycolysis will be increased as well as the capacity of fat oxidation due to an increase in muscle glycogen which is also needed to prime the pump for fat utilization.
Does CHO loading enhance sprint and endurance performance? Why?
Recent research indicates that CHO loading prior to high intensity, short duration exercise enhances performance by increasing work time to exhaustion before fatigue occurs.
Recent research also indicates that CHO fluid ingestion will enhance intermittent high intensity exercise performance by increasing work time to exhaustion before fatigue occurs.
This type of intermittent high intensity exercise is similar to what is experienced by athletes in sports such as basketball, soccer and hockey. During high intensity, short duration exercise, CHO loading prior to exercise and CHO fluid ingestion during exercise appears to enhance CHO availability and hence anaerobic work capabilities.