Lecture Exam #1 Flashcards
6 senses
hearing seeing smell taste touch Kinesthetic awareness
responsibility of kinesthetic awareness
joint receptors
system responsible for motivational drives and needs
Limbic system
functional unit of muscle cell
Sarcomer
two roles of calcium during muscle contraction
Ca+ in axon termianl causes release of acetycholing
Ca+ binds to regulatory site on troponin removes inhibition between actin and myosin
three roles of ATP during muscle contraction
release of energy -> myosin head pulls actin over myosin (powerstroke)
new ATP attaches to myosin head -> seperation of actin and myosin
when nerve impulse stops ATP used to pump Ca+ back to sarcoplasmic reticulum
process that breaks ATP down and moves myosin head
myosin ATPase
muscle fiber types
Fast twitch Glycholiytic (anaerobic)
Fast twitch Oxidative Glycholytic (intermediate - between aerobic and anerobic capilities)
Slow twitch oxidative (aerobic)
size principle
larger cell bodies require greater neural stimulation in order to depolarize (FT muscle fiber)
motor units with smaller cell bodies get recuited first
which muscle fibre type has the largest cell body
Fast twitch Glycholytic
what does the max. tension depent on
actin-myosin binding
muscle fibre type with highest max. tension
fast twitch glycholytic
what does the speed of a contraction depend on
size of axon (myelinated)
myosin ATPase
muscle type with lowest endurance
slow twitch oxidative
what does the length of a msucle contraction depent on
ability to recycle or regnerate ATP (slower endurance)
motor unit
one motor neuron and all by it contolled muscle fibres
rest before muscle contraction
actin and myosin are seperated
tropomyosin blocks actin binding site
Ca+ stored in Sarcoplasmic Reticulum
steps of muscle contraction
release of Ca+ through nerve impulse causes release of acetycholine
ACH attaches to receptors that causes opening of Na+ channels and depolarization
AP causes release of Ca+ from SR
Ca+ binds to troponin receptors and moves tropomyosin away from blocking position
myosin head attaches to actin and pulls it over myosin filament
ATP binds to myosin head and releases it from actin
ATPase causes new attachement and further contraction
power stroke
tilting of myosin head and mpulling of actin filament
what causes power stroke
stored energy
relaxation after muscle contraction
nerve impulse stops
Ca+ released from troponin binding site and transported back to SR
tropomyosin moves into blocking position
myosin head moves back
what system allows Ca+ to travel away and back to the SR
Longitudinal Tubules
why does the right side of the brain controls the majority of our bodie´s left side movement
because 90% of pyramidal motor tracts cross
brain area behind the central sulcus
sensory cortex
brain area prior to central sulcus
primary motor cortex
brain are prior to primary motor cortex
pre motor cortex
responsibility of pre motor cortex
unconcious, fine tuning, highly skilled
responsibility of primary motor cortex
concious, voluntary movement
responsibility of sensory cortex
interprets information
pituitary gland
controlled by hypothalamus
master gland
basal ganglia
grey matter
disease if grey matter is damaged
parkinson - lose muscle control
responsibility of cerebellum
coordination
A band
myosin, overlapping actin
H zone
only myosin area
I Band
lighter area
actin
z lines
attached to sarcolemma
groove for t-tubules to go deep into sarcolemma
where is Acetycholin stored
in synaptic vesicles
where is Ca++ within the muscle fibre stored
sarcoplasmic reticulum
responsibility of the midbrain
visual acuaity
responsibility of the medulla
heart rate
blood flow
respiration rate
responsibility of pons
respiration rate
facial expression
general eye movement
muscle fiber distribution in untrained people (genetic)
almost 50 % FT
50 ST
exceptions exist (some are born with a higher distribtion of one fiber type then others)
difference in gender and fiber type distribution
gender does not affect the fiber type distribution
fiber types in location of body
each individual has different fiber types in different parts of the body
fiber types within a motor unit
only same fiber types within one motor unit
why do motor units operate at “all-or-none” principle
because all are the same muscle fiber types - they need the same stimuli to get depolarized
what determines the force production
Actin and Myosin Binding
# of fibers within a motor unit
# of motor units activated
size of fiber within an active motor unit
balance between stimulating and inhibitory neurotransmitter
stimulating neurotransmitter
Acetycholin (AcH)
inhibitory neurotransmitter
gamma amino butyric acis (GABA)
twitch
a single muscle fiber contraction
summation
new stimuli while muscle fiber is still contracted - next contraction starts at a higher level and is stronger
tetanus
max. contraction
muscle cramp
not desrable
what muscle fiber type has more actin and myosin?
fast twitch
when is max. tension of a muscle gnerated
when length reaches peak tension range
120% of resting muscle
how can max tension of a muscle be increased
prestretch before movement
what kind of training can improve prestretch
biometric training
what 3 factors additionally affect force production
initial length of muscle fiber
angle of pull
architecture of tendon and muscle fiber
angle of pull
different angles determine different force production
muscle types
Fusiform
Penniform
Fusiform muscles
parallel fibers running length of muscle
fibers insert into tendon
greater range of motion
less strangth and resistance to pull - greater risk to insure
Penniform muscles
fibers arranged diagonal to the direction of pull
fibers attached to tendon in small spaces
short range of movement
great strength and great resistance to injury
subdivisions of fusiform muscle
fusiform
bicipital
triangular
subdivisions of penniform
unipennate
bipennate
multipennate
metabolic by-products of muscle fatigue
lactic acid
ketone bodies
what causes muscle fatigue
metabolic by-products -> decrease of pH -> interference of Ca+ release Actin-Myosin binding & ATP breakdown
depletion (Abbau) of Neurotransmitter (neural fatigue)
depletion of phosphagen (PC & ATP)
what leads to an increase in force
hypertrophy (increase in muscle size) hyperplasia (increase in muscle fiber #) increase in motor unit recruitment prestretch change of fibertype
agonist
contracting muscle
antagonist
relaxing muscle
high intensity speed training forms what kind of muscle fiber
fast twitch, decreases % slow twitch muscle fibers
low intensity endurance training forms what kind of muscle fiber
slow twitch, decreases % fast twitch muscle fiber
what is the most documented muscle fiber conversion due to training
SO to FOG
what does a reduced neural inhibition lead to
increase in motor unit recruitment
addition of strength training within endurance training
increase time to exhaustion while performing submax workload
addition of endurance training to strength program
may reduce strength gains from strength training
ATP use per day
at rest 40 kg
heavy exercise 720 kg
phosphagen metabolism
highest power
lowest capacity
breakdown of ATP into ADP + Pi + E
extremely low ATP earned
enzyme within phosphagen metabolism
Myosin ATPase to breakdown ATP
CPK and AK
formation of ATP
CP + ADP -> ATP + C (use of CPK Enzyme)
ADP +ADP -> ATP +AMP (use of AK Enzyme)
when is phosphagen metabolism used
0-30 sec
high intensity
location of phosphagen metabolism
sarcoplasm
energy pathway of phosphagen metabolism
phosphogen breakdown
starting product of phosphagen metabolism
ATP and CP
location of anaerobic glycolysis
sarcoplasm
energy pathway of anaerobic glycolysis
glycolytic (breakdown of glucose or glycogen)
starting product of anaerobic glycolysis
carbohydrate (CHO)
enzymes of anaerobic glycolysis
H-LDH (phosphorylase) M-LDH (Hexokinase HK) PFK (phosphofructokinase) PK (pyruvate kinase) A.T. (alanine transaminase)
by-product of anaerobic glycolysis
pyruvate broken down into lactic acid and alanine to live
relationship between lactic acid and pH
increase in lactic acid -> decrease in pH
earned ATP from anaerobic glycolysis
first 2 ATP invested, later 4 earned
Net +2 ATP
when is the anaerobic glycolysis used
30sec. - 3-4 min
high intensity
starting product of aerobic glycolysis/oxydative metabolism
pyruvic acid transformed into acetyl CoA
location of aerobic glycolysis
starts in sarcoplasm, end in mitochondra
eneryg pathway of aerobic glycolysis/oxidative metabolism
Glycolytic (breakdown of glycogen and glucose) in sarcoplasm
Krebs cycle and Electron Transport System in Mitochondria
enzymes of aerobic glycolysis/oxidative metabolism
CS (Citrate synthase)
SDH (succinate dehydrogenase)
IDH (isocitrate dehydrogenase)
earned ATP with the aerobic glycolysis/oxydative metab.
Net in skeletal muscle 36 ATP
Net in cardiac muscle 38 ATP
when is oxydative metabilism used
3-4 min. - 2-3 h.
moderate intensity
by products of oxydative metabolism
CO2 and H2O
what is beta fat oxidation based on
triglycerides = glycerol + 3 fatty acids
location of beta (fat) oxidation
TG starts in Sarcoplasm
Beta oxidation in mitochondria
pathway of beta (fat) oxidation
beta oxidation, kreb´s cycle, Electron transport system all in mitochondria
starting product of beta (fat) oxidation
Acyl CoA
Carnitine - transporter
enzymes within the beta (fat) oxidation
lipase (HSL) thiokinase thiolase carnitine fatty acid transferase
by-product of beta (fat) oxidation
ketone bodies (decrease in pH)
ATP earned by beta (fat) oxidation
1 Fatty acid = 100-150 ATP
when is the beta (fat) oxidation used
during continous low activity
factors that determine lactate production
oxidative metabolism´s ability to accept pyruvate into krebs cycle
ability of the ETS to accepts NADH+H+ and FADH+H+
ability to form alanine from the breakdown of carbohydrates
ratio of M-LDH (forms lactate) to H-LDH (clears lactate)
factors of phosphagen metabilism to increase capacity
increase in training
increase in muscle mass
increase in creatine ingestion
factors of anaerobic glycolysis to increase capacity
increase in muscle mass
increase in alanine transaminase
increase ratio of H-LDH and M-LDH
factors of aerobic glycolysis/oxidative metabolism to increase capacity
capacity is based on muscle and liver glycogen stores
increase in training
increase in CHO loading
increase in fluid ingestion
factors of beta (fat) metabolism to increase capacity
increase CHO
power
speed ATP can be produced and released at
what is power of phosphagen metabolism based on
enzyme activities
what is power of anaerobic glycolysis based on
enzyme activities
what is power of aerobic glycolysis(oxidative metabolism based on
O2 delivery rate
enzyme activity
what is power of beta (fat) metabolism based on
fat mobilization
enzyme activity
O2 delivery rate
H+ and e- carrier within the ETS
cytochromes
when do NAD carrier take action
glycolysis of cardiac muscle, in krebs cylce, beta (fat) oxidation, and conversion of pyruvate to acetyl CoA
how many ATP can be earned when NAD dropps of H+
3 ATP
when do FAD carrier take action
in glycolysis of skeletal muscle, krebs cycle, and beta (fat) oxidation
molecule for carbohydrates and fat to enter krebs cycle
Acetyl CoA
how many ATP are in aerobic glycolysis already formed before entering the mitochondria
cardiac muscle 2 invested, 10 formed
Net of 8 ATP
skeletal muscle 2 invested, 8 formed
Net of 6 ATP
where do NAD and FAD carry H+ and e- to to form ATP
Electron Transport System (ETS)
Mitchell´s Chemiosmotic Hypothesis
electron transfer leads to pumping of protons out of matrix generating proton gradient which leads to phosphorylation of ATP
how many ATP are formed in pyruvate oxidation in the Krebs cycle and ETS
15 ATP x 2 rounds = 30 ATP
Fat metabolism energy yield
Fat 9 Kcal/gm
Carbohydrates 4 Kcal/gm
protein 4 Kcal/gm
alcohol 7 Kcal/gm
how many carbons are in each fatty acid
12-18
what does free fatty acid needs to get formed to, to enter the mitochondria in beta oxidation
acyl CoA
carrier of Acyl CoA into mitochondria
carnitine
why do energ systems respond in a certain order
by- or end-products of energy systems stimulat enzymes of other nergy systems
quick energy systems are often less complex
slower energy systems depend often on intramuscular metabolic factors and other systems likecardiorespiratory and circulatory systems
HSL stimulating hormones and fat mobilization
thyroxine cortisol glucagon epinephrine norepinephrine
hormones that inhibit HSL and fat mobilization
Insulin
what increases stimulating hormone release
exercise
role of caffein
stimulates HSL and fat mobilization
stimulates phosphoralyse in glycolysing and glycogen mobilization
what does an increase in carbohydrate loading lead to
increases aerobic glycolysis and beta (fat) oxidation capacity due to an increase in muscle glycogen
best way for a carbohydrate loading program before a competition
1-2 days long hard exercise - exhaustion
2-3 days low carbohydrate diet
2-3 days high carbohydrate diet
competition
what can carbohydrate loading be used for
to improve endurance performance in events longer than 60-80 min at 65-85% of VO2max or 75-85% of max HR
what is understood as a low CHO diet
50 % of calories from CHO
4g of CHO per kg of BW
high CHO diet
70% of calories from CHO
10G of CHO per kg of body weight
CHO and fluid during exercise
event < 90 minutes -> 4-8 ounces of cold water every 10-15 minutes
event > 90 minutes -> 4-8 ounces of cold water containing 5-10% glucose solution every 10-16 minutes
what does the ingestion of caffeine prior to exercise lead to
5g/kg of BW 40 min prior to event
improves fat mobilization -> power of fat ocidation
enhance mobilization of muscle glycogen
critical aspect of caffeine ingestion prior to event
neg. diuretic effect -> dehydration
critical to maintain fluid during exercise
how does creatine monohydrate ingestion help prior to an event
maintain higher muscle creatine levels
increase phosphocreatine resynthesis -> allows high intensity for longer time
allows to shorten resting time between high intensity exercise
increase phosphagen and anaerobic glycogen capacity
how does CHO loading benefits high intensity, short duration athletes
increasing work time to exhaustion
what needs to be considered as important with CHO loading for sprinters
important to not gain BW
poitive effects of sodium bicarbonate ingestion
buffering of H+ released from lactic acid
increase lactic acid tolerance and capacity of anaerobic glycolysis
changes in phosphagen metabolism due to endurance training
increase in [ATP], CP, CPK, AK
increase in reaction time -> increase in power
changes in oxydative metabolism due to endurance training
increase [myoglobin], O2 delivery increase in krebs cycle enzyme, ETS cytochrome and beta oxidation enzyme activity increase in Lipase (HSL) activity mucle [glycogen] Triglyceride in muscle
oxidative changes in fiber type specificity
greater in SO and FOG than in FG
glycolytic changes in fiber type specificity
greater in FT than in ST
phosphagen changes due to endurance training in children
increase in [ATP] and [CP], increase in capacity
glycolysis changes due to endurance training in children
increase in power
changes in phosphagen metabolism following strenth training
increase ATP and CP level
increased myosin ATPase CPK and AK levels
increased capacity
changes in anaerobic glycolysis due to strength training
increased enzyme levels
increased power
changes in oxidative metabolism due to strength training
increase muscle glycogen decreased [mitochondria/fiber volume ratio
increased FT fiber area/ST fiber ratio
muscle hypertrophy
when does strength training in children show an effect
after puberty
peripheral sensory receptors
muscle spindles
golgi tendon organs
joint receptors - proprioreceptors
muscle spindles
operate functional spinal cord level
sense length of muscle fibres
reflex contraction
co-activation of extra- and intrafusal fibers
golgi tendon organs
reflex inhibition (inhibits muscle to overcome to high force
input into motor coretx
sensory cortex
limbic system
proprioreceptors
feedback to sensory cortex = kinesthetic awareness
gamma efferent
nerves from from spinal cord coming
afferent from muscle spindle
nerves to spinal cord going
top one primary annulospinal ending
bottom secondary flower spray endind
