unit 1 Flashcards
study for test
skeletal muscle major functions
force production for locomotion and breathing (movement)
force production for postural support
heat production for maintenance of body temperature (shivering/normal muscle contractions)
anatomy of skeletal muscle
whole muscle, fascicles, muscle fibers/muscle cells, myofibrils, contractile proteins organized into sarcomeres
whole muscle is surrounded by connective tissue called
epimysium
whole muscles are made up of bundles of
Fascicles
fascicles are surrounded by connective tissue called
perimysium
fascices are made up of
muscle fibers/muscle cells
muscle fibers/muscle cells are surrounded by connective tissue called…
endomysium
muscle fiber/ muscle cells are made up of
myofibrils that contain contractile proteins
What do myofibrils contain?
contractile proteins (actin and myosin)
myofibrils have how many nucleus
multi-nucleated
what is the muscle cell membrane?
sarcolemma
What do transverse tubules (T tubules) do?
signal from nervous tissue gets to sarcoplasmic reticulum
continuous with membrane
extends from sarcolemma to sarcoplasmic reticulum
what does the sarcoplasmic reticulum do?
web like structure that is the storage site for calcium
terminal cisternae
what does calcium do in muscle fibers?
signal for muscle to contract
what are the parts that make up myofibril?
sarcomere -> actin/myosin
z line to Z line is
1 sarcomere
Myosin is
thick filament
polymer of 200 myosin molecules; two stands
heads protrude from thick filament axis and interact with actin filaments
has head, body, neck
actin is
think filament
two strands of actin wrap around each other
tropomyosin
protein that covers myosin binding sites
troponin
protein attached to tropomyosin that pulls it away from binding site when bound to calcium
titin
stabilizes myosin along longitudinal axis, largest protein in the body,
involved with increased force during eccentric (stretching or lengthening) contractions
Nebulin
anchoring protein for actin
sliding filament model
muscle shortening due to overlap of myosin and actin
this overlapping creates a cross-bridge and overall creates a power stroke
reduces distance between z lines of sarcomere
Resting position of sliding filament model
tropomyosin is in place blocking myosin binding sites on actin
ATP is bound to myosin, ATPase hydrolyzes ATP into ADP, P, and energy
myosin filament is in high energy state
myosin head is “cocked” - ready to bind/move
calcium signal
calcium ions bind to troponin and move tropomyosin away from binding sites, myosin forms a strong bond (cross-bridge) with actin
P is released and myosin head swivels/pull along actin fiber initiating the power stroke
Power stroke
movement of the myosin head pulls actin filament towards middle of the sarcomere
ADP is also released from myosin
myosin and actin stay bound together - waiting for a new ATP
New ATP
ATP binds to myosin and causes release of cross-bridge
ATPase breaks down ATP to ADP and P returning myosin head to cocked/energized state
relaxation
absence of signal from motor neuron stops the flow of calcium into the cell
active Ca pumps calcium back into sarcoplasmic reticulum, ATP releases myosin from actin binding sites
tropomyosin shifts back to resting position over binding sites
excitation-contraction coupling
excitation: electrical signal from central nervous system is translated into Ca signal that causes mechanical movement (contraction)
signal comes from motor neuron
motor end plates interact w/muscle fibers
excitation
nerve impulse (action potential) originates from the CNS and is transmitted down a motor nerve to the muscle
at the neuromuscular junction, axon terminal releases ACh into synaptic cleft
ACh diffuses across synaptic cleft and binds to receptors on the motor end plate
increased Na+ permeability results in depolarization called the end-plate potential
sarcolemma depolarizes, and action potential conducted along membrane and down the t-tubules
calcium is released from the terminal cisternae
acetylcholine ligand-gated channel
when open, Na rapidly flows into cell causing depolarization of resting membrane potential
calcium release from sarcoplasmic reticulum
involves dihydropyridine receptors in T-tubule and ryanodine receptors in sarcoplasmic reticulum
Role of Ca++ in muscle fiber
calcium stored in the sarcoplasmic reticulum
action potential leads to mass release of Ca2+ into sarcoplasm (100X)
Ca2+ binds to troponin on the thin filament , troponin ca2+ complex moves tropomyosin, myosin binds to actin; contraction can occur
Role of ATP in muscle fiber
ATP triggers myosin-actin dissociation (break up of cross bridges) allowing myosin head to detach from actin
Hydrolysis of STP provides energy required to cock the myosin head into the “high energy” position
ATP necessary for active transport of Ca2+ back into sarcoplasmic reticulum where it is stored/concentrated
Resting membrane potential
Difference in electrical charge between the inside and outside of a cell (due to different qualities of ions (sodium and potassium)
Depolarization
reversal of the membrane potential. Rapid influx of Na+ changes makes inside cell more positive
Action potential
electrical signal transmitted by a wave of depolarization along the membrane
repolarization
restoring of the membrane potential. Outflow of K, then active pump to restore resting concentration of both Na+ and K+
Myosin ATPase function
breakdown of ATP provides energy to “cock” myosin head
Calcium ATPase function
Breakdown of ATP provides energy to re-sequester calcium in sarcoplasmic reticulum
oxidative capacity depends on
mitochondria, capillaries, myoglobin, myosin isoforms, sarcoplasmic reticulum and contractile proteins
Force
specific force (aka specific tension): How much force is generated relative to muscle cross sectional area (how big muscle is)
Speed of contraction
shortening velocity (aka Vmax): how quickly a muscle can contract/shorten
muscle power
force x shortening velocity
efficiency
force relative to amount of ATP used
fatigue resistance
how well can contraction be sustained over time
oxidative capacity contributes to
greater fatigue resistance and fiber efficiency
more developed sarcoplasmic reticulum contributes to
faster calcium release, faster shortening velocity, greater power
greater ATPase activity contributes to
faster shortening velocity (and therefore greater power)
More contractile proteins (actin and myosin) contribute to
greater specific force, greater power
Type 1 fibers
“slow twitch” fibers
large amount of oxidative enzymes
greater capillary density and contraction of myoglobin
ATP produced by aerobic processes - oxygen is required
Type 2 fibers
“fast twitch” fibers
large amount of glycolytic enzymes
more developed sarcoplasmic reticulum
ATP is produced through anaerobic pathways- oxygen is not required
Type IIx = fast
type IIa = intermediate
Muscle fiber types info
properties of different fiber types exist on a continuum
each person has unique ratio
no sex differences
different muscles will have different ratio
individual muscle fibers can exhibit blended qualities and fiber types/characteristics can change
fiber type and athletic performance
VO2max is strongly correlated with proportion of slow fibers
but there is a large amount of variety between similarly successful athletes. Fiber type is not the best predictor of performance
Static: force production with no movement or change in length
isometric
dynamic: force production with change in muscle length
isotonic (eccentric and concentric)
isotonic
eccentric and concentric
isometric contraction
static contraction
cross-bridge formation and force production without change in muscle length
force is equal to or insufficient to overcome resistance
concentric contraction
dynamic muscle contraction
cross-bridge formation with overall muscle shortening
sarcomeres shorten and actin filaments slide toward center
eccentric contraction
dynamic muscle contraction
cross bridge formation with overall sarcomere and muscle lengthening
greater force production, but potential for high stress or injury
speed of muscle action
muscle twitch: isolated, rapid muscle contraction and relaxation from a single action potential in 1 motor unit
speed of contraction is variable and depends on different muscle fiber properties: fiber type, speed of ca release, ATPase activity
muscle twitch steps graph
stimulus received from motor neuron action potential
brief latent period (time for action potential to spread through sarcolemma, ca be released and tropomyosin to be uncovered)
contraction: 40 milliseconds
relaxation: 50 milliseconds
forced regulation in whole muscle depends on
motor unit recruitment: how many, what type
neural stimulation
initial muscle length
prior contractile activity of the muscle
motor units
one alpha motor neuron and all muscle fibers it innervates
- the muscle fibers within a single motor unit will have similar biochemical and contractile properties
smallest motor unit size
Type S: show twitch
includes type 1 muscle fibers
intermediate motor unit size
type FR: fast, fatigue resistant
includes type IIa muscle fibers
Largest motor unit size
type FF: Fast fatigable
includes: Type IIx muscle fibers
key principle of motor unity recruitment
recruit smallest first and goes up from there
Neural stimulation (another way to generate force)
1 action potential from alpha motor neuron produces a simple muscle twitch
additionally, stimuli produce subsequent muscle twitches
as the frequency of stimulation increases, muscle does not have time to relax in-between
summation: repeated stimulation that results in force accumulation
Tetanus
individual contractions are blended into a single sustained contraction
continues until muscle fatigues or stimuli are stopped
Length tension relationship
each muscle has an optimal resting length that allows for the greatest force generation (80-120%) due to optimal overlap between actin and myosin filaments so most cross bridges
prior contractile active of muscle
exercise that causes fatigue: decrease force production
low level exercise increases force production due to post-activation potentiation (increase muscle sensitivity)
Force velocity relationship (concentric muscle actions)
maximal velocity occurs at lowest force
maximal force occurs at slowest velocity
each muscle group has an optimal speed of movement that gives optimal power output
for any given force, speed of movement will be faster in muscles with more fast-twitch fibers, and slower in muscles with more slow-twitch fibers
Bioenergetics
the process of converting foodstuffs into usable energy for cell work
substrates
fuel sources from which we make energy ex. Carbohydrates, fat, protein
energy
the ability to perform work
for body movement to take place…
chemical energy must be transformed into physical energy
metabolism
sum of all chemical reactions that occur in the body; two general categories - anabolic and catabolic
anabolic reactions
synthesis of molecules
catabolic reactions
breakdown molecules
exergonic
chemical reactions that release energy
endergonic
energy-requiring reactions
oxidation
removing an electron
reduction
addition of an electron
- oxidation and reduction are coupled reactions
Nicotinamide adenine dinucleotide
oxidized form: NAD+
reduced form: NADH
Flavin adenine dinucleotide
Oxidized form: FAD
reduced form: FADH2
- NAD+ and FAD play a critical role in the transfer of electrons during bioenergetic reactions
enzymes function
-do not cause chemical reactions
- do facilitate breakdown of substrates
- lower the activation energy for a chemical reaction
enzymes
regulate the rate at which a chemical reaction occurs; speed up the reaction without being used up themselves
Regulation of enzyme activity
enzyme concentration, allosteric regulation, covalent modification
enzyme concentration
amount of enzyme available changes by altering transcription rates of genes that encode for specific enzymes
allosteric regulation
non-covalent interaction where a compound binds to a site distinct from active site and changes activity; may inhibit or activate
covalent modification
reversible addition of a chemical group to an enzyme that changes its activity
Allosteric effects in energy metabolism
-end products of an individual reaction or pathway (inhibition and negative feedback)
- substrate of a reaction pathway (stimulation)
-common indicators of cellular energy status: ATP,ADP, and AMP NADH or NAD
Rate- limiting enzymes
found early in a metabolic pathway
activity is regulated by modulators
transferases
catalyze transfer of atoms from one molecule to another
dehydrogenase
remove hydrogen atoms
oxidases
catalyze oxidation-reduction reactions
isomerase
rearrange the structure of molecules
influences on enzyme activity
temperature (increase generally), PH (increase when optimal)
carbohydrates
converted into glucose
extra glucose stored as glycogen
fat
efficient substrate, efficient storage
high ATP yield, but slow to produce
protein
minor energy source
converted into glucose or FFA
using food to make energy
Chemical (bond) energy of ATP is transformed into kinetic energy as well as allowing cell processes to occur
amount of ATP stored in muscles
limited amount
how much ATP is used in turnover?
10g/sec
Breakdown of ATP to release energy equation
ATP + water +ATPase -> ADP + Pi + energy
Synthesis of ATP from by-products
ADP + Pi + energy -> ATP (via phosphorylation)
- can occur in either absence or presence of O2
What are the three ATP synthesis pathways?
ATP-Phosphocreatine (PC) - anaerobic metabolism
Glycolytic system - anaerobic metabolism
oxidative system - aerobic metabolism
ATP-pc system
main energy source for maximal effort lasting approx. 5-15 sec
anaerobic, substrate-level phosphorylation
most rapid source of ATP, but low yield
stored, pre-existing ATP (depleted in 1-2 sec)
rapid synthesis from phosphocreatine and ADP
Rapid synthesis from 2 ADP
occurs at the beginning of any exercise
phosphocreatine equation
PC + ADP -> ATP + C
Creatine kinase
PC breakdown catalyzed by Creatine Kinase
creatine kinase controls the rate of ATP production
- neg feedback system
when ATP dec. ADP incr. CK activity incr.
when ATP levels incr. CK activity decr.
creatine supplementation
limit performance for short-term, high intensity exercise (reduced rate of ATP production) but leads to increased stores of muscle PC and is effective in improving strength, fat free mass, and performance in very high-intensity exercise)
Adenylate Kinase equation
ADP + ADP - (adenylate kinase) -> AMP + ATP
Glycolysis
main energy source for max effort lasting 1-2 min
uses glucose or glycogen as its substrate
- must covert to glucose-6-phosphate
occurs in sarcoplasm; anaerobic pathways
has energy investment and generation phase
two phases of glycolysis
result of glycolysis is a net positive in ATP
must be “primed” by using ATP in energy investment phase
investment doffers with glucose vs. glycogen
breakdown of glycogen is referred to as…
glycogenolysis
glycolysis inputs
glucose and glycogen
glycolysis outputs
2 pyruvate
2 NADH
2 or 3 ATP (if glycogen is used it’s 3)
glycolysis regulatory enzymes: Hexokinase
(-) glucose 6-phasphate
glycolysis regulatory enzymes: glycogen phosphorylase
(+) ADP, AMP, Pi, Ca, Epi
(-) ATP, citrate
glycolysis regulatory enzymes: phosphofructokinase
(+) ADP, AMP, pi
(-) ATP, Citrate
glycolysis regulatory enzymes: pyruvate kinase
(-) ATP
glycolytic system - key takeaways
Rate-limiting enzyme: phosphofructokinase (PFK)
- decreased ATp = increased ADP means increased PFK activity
- increased ATP means decreased pfk activity
permits, shorter-term, higher-intensity exercise without utilization of oxygen-requiring systems
relatively low ATP yield, inefficient use of substrate
What is the ATP yield of glycolysis?
32 ATP
electron carrier molecules
Transport hydrogens and associated electrons
NAD+
for glycolysis to proceed NAD+ must accept 2 hydrogens
this is necessary to keep glycolysis ongoing
What does lactate dehydrogenase do?
turns NADH into NAD+ to make lactate in an anaerobic pathway
Formation of lactate
if O2 is not available to accept hydrogens in the mitochondra, pyruvate will form lactate
recall that oxidation is loss of electrons and NAD+ is reformed and is now available
recall that reduction is gain of electrons and pyruvate reduced to become lactate
THIS IS ALL SO THAT GLYCOLYSIS CAN CONTINUE
Lactate
mostly seen as bad but important for cell fueling and microbiome ect.
lactate utilization
lactate is an important fuel during exercise and is handled in three ways: intracellular lactate shuttle, intercellular shuttle and cori cycle
intracellular lactate shuttle
lactate produced in the cytoplasm enters mitochondria in the same muscle fiber, converted back into pyruvate and then oxidation
intercellular lactate shuttle
lactate is transported, but to an adjacent muscle fiber (ex. produced in type 2 and transported into type 1 fiber)
cori cycle
lactate is exported, circulates in blood from muscle to the liver where it undergoes gluconeogenesis
aerobic metabolism
main energy source for maximal efforts lasting more then 2 minutes
two cooperating systems:
- citric acid cycle (Krebs cycle)
- electron transport chain - oxidative phosphorylation
occurs in mitochondria
ATP yield depended on substrate/fuel utilized, more efficient compared to glycolysis
aerobic metabolism process
pyruvate from glycolysis is transported into mitochondrial matrix where it is converted into acetyl-coA
- catalyzed by pyruvate dehydrogenase
- generates NADH
citric acid (Krebs) cycle produces
1 ATP (GTP)
3 NADH
1 FADH2
2 CO2
* X2 for 2 pyruvates
citric acid cycle rate limiting enzyme
isocitrate dehydrogenase
(+) ADP, Ca, NAD+
(-) ATP, NADH
electron transport chain
uses potential energy available in reduced carrier molecules (electron chemical gradient)
electrons revomed from NADH and FADH2 are passed along a series of electron carriers known as cytochromes
- recall 2 NADH rormed in glycolysis (cytosol): must be “shuttled” across mitocondrial membrane
- bulk of NADH and FADH formed via citric acid cycle
- series of oxidation-reduction reactions
utilizes chemiosmotic hypothesis to generate ATP
electron transport chain continued
electron pairs from NADH and FADH2 used to pump H+ out of matrix
creates electriochemical gradient
o2 serves as final electron accepter forms h2o
gradient energy used to synthesize ATP from ADP + Pi
electron transport chain ATP production
1 NADH = 2.5 ATP
- passes through all 3 pumps
1 FADH2 = 1.5 ATP
- bypasses first proton pump
electron transport chain rate limiting enzyme
cytochrome C Oxidase
(+) ADP, pi
(-) ATP
aerobic ATP tally
32/33( if start from glycogen)
Notice: results from 1 glucose (6c) -> 2 pyruvate (3C)
subcutaneous and visceral (adipose) lipid sources
very large fuel reserve (73,320 kcal)
requires mobilization to blood then uptake by muscle
some can be stored in muscle
intramuscular lipid source
smaller lipid reservoir (1,513 Kcal)
less mass vs. muscle glycogen, but nearly as much energy due to higher energy content in lipid
Adipose tissue steps
Mobilization: lipolysis of triglyceride & transport of FFA into blood
circulation: transport of FFA from adipose to muscle
uptake: transport of FFA into muscle
activation: raises energy level of FFA in preparation from catabolism
translocation: transport form cytosol into mitochondrial matrix
oxidative phosphorylation: ATP synthesis
beta-oxidation -> Krebs cycle -> electron transport chain
Beta oxidation steps
starts with activated fatty acid (uses ATP like glycolysis)
fatty acid is “chopped” into two-carbon fragments
- number of steps/”turns” varies based on number of carbons
each “turn” forms 1 NADH & 1 FADH2
final product is an acetyl-coA for each pair of carbons
acetyl-COA progresses through citric acid cycle
ATP total from atty acid activation, beta-oxidation and Kreb cycle
106
direct calorimetry
measurement of heat production as an indication of metabolic rate
- precise, but expensive; measurement during exercise imperfect
indirect calorimetry
measurement of oxygen consumption as an estimate of metabolic rate
- rate of oxygen consumption proportional to energy expenditure
therefore, VO2 is an “indirect” measure of EE
roughly 5 kcal/L O2 consumed (substrate dependent)
steady state must be achieved
not as accurate
steady state
constant level of some physiological variable
- not the same as homeostatis
stead state work rate is required for and precedes attainment of steady state physiology
energy requirements at rest
almost 100% of ATP produced by aerobic metabolism
- aerobic metabolism uses oxygen and produces carbon dioxide
resting )2 consumption (VO2) for a 70 kg adult:
- .25 L/min - absolute
- 3.5 ml/kg/min - relative - 1 Met (metabolic equivalent)
how to measure oxygen consumption?
(how much air did the subject inspire (breathe in) x What fraction of that air was made up of oxygen?) - (How much air did the subject expire (breathe out) x What fraction of that air was made up of oxygen (21%))
Exercise Intensity
Amount of oxygen consumption
- relative to resting value (METs)
- relative to subject’s maximal capacity (%VO2 max)
Transition from rest to exercise for speed and ATP
Running speed increases immediately
ATP requirement increases immediately
rest to exercise: aerobic pathways
oxygen consumption (VO2) increases rapidly
- reaches steady state within 1 to 4
- after SS is reached, ATP requirement is met through aerobic ATP production
- Trained individuals reach SS sooner
Aerobic pathway canno meet the immediate demand for ATP
Rest to exercise: ATP-PC system
rapid availability of ATP
Production is highest at onset of exercise, then drops as levels of PC in muscle decline
Rest to exercise: Glycolysis
second bioorganic pathway
ATP production increases at onset of exercise and peaks around 2 min
VO2 during moderate exercise
at onset of exercise, oxygen demand is greater than oxygen consumption
oxygen deficit
anaerobic pathways make up the difference in ATP production: EPOC
oxygen deficit
the difference between the amount of oxygen required and the actual amount of oxygen consumed
Post-exercise: O2 uptake > O2 demand
O2 needs to drop rapidly because ATP hydrolysis and production drop rapidly when muscle contraction stops
VO2 decreases slowly
originally referred to as oxygen debt
excess post- exercise oxygen consumption (EPOC)
Terminology reflects that only approximately 20% elevated O2 consumption used to “repay” O2 deficit
Rapid portion of EPOC
Elevated O2 consumption used for:
- resynthesis of stored PC in muscle
- replenish muscle (myoglobin) and blood (hemoglobin) O2 stores
slow portion of EPOC
increased O2 needed for elevated heart rate and breathing
increased body temperature = increased metabolic rate
increased blood levels of E and NE = increased metabolic rate
conversation of lactic acid to glucose (gluconeogenesis)
VO2 during max exercise
VO2 way higher
greater EPOC components as body takes longer to go to resting levels
EPOC key takeaways
Metabolic rate (oxygen consumption remains elevated for a period of time after stopping exercise
EPOC is greater and takes longer after high intensity exercise
Overall, EPOC represents a small portion of the total exercise oxygen consumption
Metabolic responses to exercise
influenced by intensity, duration, and environment
short, intense exercise: anaerobic systems dominate
prolonged exercise: ATP needs are met by aerobic pathways and VO2 remains at SS
- hot, humid environment causes upward “drift” in VO2
- increasing exercise intensity causes similar rise in VO2
incremental exercise
methodically increasing exercise intensity over stages
Graded exercise test
subject completes series of 1-3 minute exercise states
work rate increases until subject cannot maintain intensity
oxygen consumption (VO2) increases in direct proportion to exercise intensity
Maximal oxygen uptake (VO2 max)
point at which an increase in power output does not lead to increase in oxygen consumption: VO2 max
“physiological ceiling” for oxygen delivery to muscle: maximal aerobic capacity
influenced by genetics and training
higher type 1 muscle fibers have higher VO2 max
Factors that influence VO2 max: oxygen transport/delivery
body’s ability to bring oxygen in (pulmonary system) and circulate (cardiovascular system) to working muscle and other tissues
factors that influence VO2 max: oxygen utilization
body’s ability to extract oxygen and use it to create ATP through aerobic metabolism
Verification of VO2 max
Gold standard for verification of VO2 max is a plateau in O2 consumption will increase in work rate
most subjects do not achieve a plateau in O2 consumption during an incremental exercise test
secondary criteria for verification of VO2 max
reaching age-predicted max heart rate (+/- 10 b/m)
achieving blood lactate concentration of 8 mM or higher
attaining a respiratory exchange ratio of 1.15 or higher
blood lactate during incremental exercise
as exercise intensity increases, blood lactate begins to rise exponentially
sharp inflection point is called the lactate threshold (LT)
LT is usually expressed as a percentage of VO2 max
lactate threshold + related concepts: sharp inflection
sharp inflection point that indicates rapid increase in blood lactate levels
- untrained subjects: LT at 50-60% VO2 max
- trained subjects: LT at 65% - 80% VO2 max
lactate threshold + related concepts: “anaerobic threshold”
original name for lactate threshold
assumed that LT represented switch from aerobic to anaerobic metabolism because of insufficient oxygen in muscle
lactate threshold + related concepts: Onset of Blood lactate accumulation (OBLA)
lactate exceeds a pre-determined concentration (usually 4.0mM/l
What contributes to rise in lactate during exercise?
Increased lactate production
- low muscle oxygen
- hormones: epinephrine stimulates more rapid rate of glycolysis
- recruitment of fast- twitch muscle fibers
decreased or insufficient lactate removal
accelerated glycolysis = more lactate
increase in epinephrine around 50-65% VO2 max causes faster rate of glycolysis
rapid glycolysis exceeds they hydrogen shuttle capacity and results in extra lactate production
Muscle fiber type matters
different fiber types have different isozymes of lactate dehydrogenase
Reaction that converts pyruvate to lactate is reversible
- LDH in fast fibers promotes lactate formation
- LDH in slow fibers promotes pyruvate formation
Lactate removal after exercise
After 70% of lactate produced during exercise is oxidized
- converted to pyruvate to be used as a substrate
about 20% is converted to glucose in the liver
remaining 10% is converted to amino acids
blood lactate typically returns to resting levels within about 60min
these processes contribute to EPOC
Enhancing lactate Removal: cool down
continuous light exercise facilitates more rapid removal of lactate when compared to stopping exercise entirely
- should be slightly below LT
around 40-50% VO2 max
Returning to lactate threshold
VO2 max sets the physiologic ceiling for aerobic ATP production
lactate threshold sets the ceiling for sustainable exercise
- higher LT = greater endurance performance
- LT is a marker of training intensity
- select training HR based on LT
- training just below LT is effective in shifting threshold to right
Estimating fuel utilization
ratio between CO2 production and O2 consumption
more carbon atoms in each molecule = more oxygen needed
carbon to oxygen relationship
the more carbon, the more oxygen needed
carbon vs. Fat utilization
100% fat: R= 0.70
500% fat, 50% carbs: R = 0.85
100% carbs: R = 1.00
Respiratory Exchange ratio key points
Exercise has to be steady state and below lactate threshold to determine utilization
assume protein isn’t a fuel source
R may be greater than 1
- intense incremental exercise
- VCO2 measures amount of CO2 exhaled - not an exact measure of CO2 produced
- “nonmetabolic CO2” causes increased CO2 exhalation but from sources other than macronutrient oxidation
Factors involved in fuel selection
intensity and duration of exercise
availability of fuels
diet
endurance training status
low intensity exercise (< 30% VO2 max)
fats are primary fuel
especially true during prolonged duration, low intensity
high intensity exercise (>70% VO2 max)
carbohydrates are primary fuel
crossover concept
there is a progressive shift from fat to carbohydrates as exercise intensity increases
exercise intensity and lipid oxidation
delivery of free fatty acids from adipose tissue has an upper limit
process depends upon mobilization and blood flow
as exercise intensity increases:
- mobilization of FFA increases (mostly due to epinephrine)
- blood flow to adipose tissue decreases (blood is diverted to working skeletal muscle)
at high intensity: reduced blood flow limits use of fat as a substrate, despite continued increase in mobilization
low intensity exercise
fat is the preferred substrate
greater proportion of fuel comes from fat
high intensity exercise
carbohydrate is the preferred substrate
greater proportion of fuel comes from carbohydrates
at 20% VO2 max
R = .80
2/3 fat, 1/3 carbs
2 kcals fat and 1 kcal carb
at 60% VO2 max
R = .9
1/3 fat, 2/3 carb
3kcal fat, 6 kcal carb
Relative vs. Absolute fat oxidation
lower intensity exercise: greater relative fat oxidation
higher intensity: greater absolute fat oxidation
peak fat oxidation occurs around 60% VO2 max (at a similar point to lactate threshold!)
exercise duration and fuel selection
prolonged, low to moderate-intensity exercise: substrate shift
- decrease in carbohydrate metabolism
- increase in fat metabolism
due to increased rate of lipolysis
- breakdown of triglycerides to glycerol and free fatty acids
- catalyzed by enzymes called lipases
- stimulated by rising levels of various hormones
- lipolysis is a slow process - begins 10-20 min after onset of exercise
factors that influence lipolysis
stimulated by:
epinephrine
glucagon
inhibited by:
blood glucose
insulin
inadequate levels of Kreb cycle intermediates
carbohydrate fuel for exercise comes from muscle glycogen and blood glucose
muscle glycogen is immediately available
liver glycogen must undergo glycogenolysis and circulate to active muscles in blood
how does the body use carbs
Low- intensity exercise- carb uses: primary carbohydrates fuel source is blood glucose
high intensity exercise: primary carbohydrates fuel source is muslce glycogen
prolonged submaximal exercise: muscle glycogen is used in first hour; shift to BG as these stores are depleted
carbohydrate supplementation
ingestion of carbs can improve endurance performance
- during submaximal, long-duration exercise (especially beyond 90 min
- 30-60 g of carb per hour
lipid fuel for exercise comes from adipocytes, muscle triglycerides
triglycerides are more rapidly available
fat stored in adipocytes must be broken down (lipolysis) and circulated as free fatty acids in blood plasma
How does the body use fats?
low- intensity exercise: primary fat fuel source is plasma FFA
high- intensity exercise: primary fat fuel source is muscle triglycerides
prolonged submaximal exercise: plasma FFA are predominant fuel source
How does the body use protein
protein is broken down into amino acids
- alanine can be converted to glucose in the liver
- other amino acids can be converted to various intermediates in metabolic pathways
for exercise less than 1 hour: protein contributes <2% of overall fuel
for exercise of 3-5 hours or longer: protein may provide up to 5-10% of overall fuel
