First Exam Flashcards
anabolic reations
synthesis of molecules
catabolic reactions
breakdown of molecules
metabolism
sum of all chemical reactions that occur in the body (anabolic and catabolic reactions)
bioenergetics
process of converting foodstuffs into usable energy for cell work
endergonic reaction
require energy to be added to the reactants, endothermic
exergonic reaction
release energy, exothermic
coupled reactions
liberation of energy in an exergonic reaction drives an endergonic reaction
Oxidation
removing electron (hydrogen atom)
Reduction
adding electron
Nicotinamide adenine dinucleotide (NAD)
carrier molecule
– Oxidized form: NAD+
– Reduced form: NADH
Flavin adenine dinucleotide (FAD)
carrier molecule
– Oxidized form: FAD
– Reduced form: FADH2
enzymes
facilitate faster reactions by locking with specific substrates
enzyme activity in blood
damaged cells release enzymes into the blood, so the level of enzymes in blood can serve as biomarkers of disease or damage
kinases
add phosphate group
dehydrogenase
remove hydrogen atoms
oxidases
catalyze oxidation-reduction reactions involving oxygen
isomerases
rearrangement of structure of molecules
effect of temp on enzymes
-small rise in temp increases enzyme activity (warmup)
-large increase in body temp decreases activity
effect of pH on enzymes
production of lactic acid and CO2 during exercise lowers pH and decreases enzyme acivity
protein as fuel for exercise
-some amino acids can be converted to glucose in the liver (gluconeogenesis)
-others can be converted to metabolic intermediates, contribute as fuel
anaerobic cycles occur in…
…cytoplasm
aerobic cycles occur in…
…mitochondria
energy system for short, explosive exercise
ATP-PC system
energy system for moderate exercise
Glycolysis
energy system for prolonged exercise
oxidative phosphorylation
ATP-PC system
use ATP stored in skeletal muscle and phosphocreatine to create ATP
creatine supplemenation
increases performance in short-term, high-intensity exercise
glycolysis
-glucose -> 2 pyruvate or 2 lactate
-two phases, energy investment (2 ATP used) and energy generation (4 ATP produced and 2 NADH produced)
blood glucose vs glycogen
1 ATP is used to come from glucose vs no energy needed to come from glycogen because free phosphates are used
reason to produce lactic acid
to convert NADH to NAD so the energy generation phase in glycolysis can take place and produce ATP
Hydrogens and electrons shuttled to mitochondria
for ATP generation, aerobic, slower process
Hydrogens and electrons shuttled to convert…
…convert pyruvate to lactate, anaerobic, faster process
two steps of aerobic ATP production
citric acid cycle and electron transport chain
steps leading to oxidative phosphorylation
glycolysis occurs in cytoplasm breaking glucose into pyruvate and ATP, pyruvate goes through membrane of mitochondria and produces CO2 and becomes 2 acetyl CoA, goes through citric acid cycle, then electron transport chain which produces ATP
primary molecule for energy production
acetyl-CoA
beta oxidation
process of converting fatty acids to acetyl-CoA
- activated fatty acid (fatty acetyl-CoA) enters mitochondrion where it is broken down into 2 carbon fragments forming acetyl-CoA which is then used as fuel for the citric acid cycle
Electron transport chain
electrons are removed from NADH and FADH and are passed along a series of carriers (cytochromes) to produce ATP
How much ATP does NADH and FADH produce
NADH: 2.5 ATP
FADH: 1.5 ATP
(called chemiosmotic hypothesis)
Functions of the three pumps in oxidative phosphorylation
1.First pump moves H+ into the intermembrane space using NADH (which is converted to NAD)
2. Second pump moves H+ into intermembrane space (FADH is converted to FAD)
3. Third pump moves H+ into intermembrane space (O2 produces H2O with H+)
4. As H+ crosses into the mitochondria through channels, ATP synthase is activated, converting ADP + Pi to create ATP
Free radicals
- molecules with unpaired electron in outer orbital which can be produced by the leakage of e- along electron chain
- react with and damage other molecules in the cell
- aerobic exercise promotes the production of free radicals
number of ATP produced by 1 glucose
32 ATP
High energy products made by glycolysis
2 ATP, 2 NADH
(2 ATP if anaerobic, 7 if aerobic)
high energy products made by converting pyruvate to acetyl-CoA
2 NADH
high energy products made by the citric acid cycle
2 GTP, 6 NADH, 2 FADH
efficiency of oxidative phosphorylation
34% efficiency
66% energy expended as heat
Rate limiting enzyme regulates the rate of metabolic pathways, with what levels of ATP/ADP Pi?
- high levels of ATP inhibit ATP production
- High levels of ADP+Pi stimulate ATP production
- calcium stimulates aerobic ATP production (a lot of calcium indicates rapid muscle contraction)
structural organization of skeletal muscle (superficial to deep)
tendon connects muscle to bone
- fascia
- epimysium
- perimysium
- endomysium
- sarcolema
–muscle fibers
myosin
thick filaments
actin
thin filaments
satellite cells (muscle growth)
- can increases the number of nuclei in muscle fibers
- more nuclei allows for greater protein synthesis and more myonuclear domain (the volume of cytoplasm around each nucleus)
satellite cells (muscle repair)
- injury to muscle
- fusion to injured myofiber
- produce new myofibers
- regenerated
Neuromuscular junction
site where motor neuron and muscle cell meet
neuromuscular junction (functions)
action potential travels to t-tubule which activates calcium storage site in the sarcoplasmic reticulum
(muscle will not do anything until action potential comes down the motor neuron axon)
sliding filament (swinging lever-arm) model of muscle contraction
reduction in the distance btweem z lines of the sarcomere
muscle shortening occurs due to
the movement of actin filament over myosin filament
power stroke
formation of cross-bridges between actin and myosin filaments
excitation-contraction coupling
depolarization of motor end plate (excitation) is coupled to muscle contraction
- CA++ binds to troponin causing change in tropomyosin, exposing myosin binding sites on actin
tropomyosin
blocks actin so myosin cannot connect
troponin
when calcium binds to troponin, tropomyosin unblocks actin
cross bridge cycling steps (6)
- Resting fiber, myosin is not attached to actin (ADP + Pi on myosin head
- Myosin head binds to actin and forms cross bridge to actin
- Pi is released from myosin head causing conformational change in myosin
- Power stroke causes filaments to slide, ADP is released
- A new ATP binds to myosin head allowing it to release from actin
- ATP is hydrolyzed and Pi binds to myosin causing it to return to its original state
muscular fatigue
decline in power output due to decrease in force generation and decrease in shortening velocity
muscular fatigue in high-intensity exercise
due to accumulation of waste products which diminishes cross bridges bound to actin
(lactate & H+, ADP & Pi, free radicals)
muscular fatigue in long duration exercise
- accumulation of free radicals which attack muscles
- electrolyte imbalance (nerve conduction needs sodium + potassium)
- glycogen depletion
exercise-associated muscle cramps
likely due to excessive firing of motor neurons in the spinal cord
- muscle spindle (excitatory) and golgi tendon organ (inhibitory) functions get messed up
- possible relief research with spices,, sending strong inhibitory stimulus to the spinal cord to prevent motor neurons from firing
steady state
balance between demands on body and response, physiological variable is unchanging but not “normal”
biological control system parts
- sensor or receptor, detects change in variable
- control center, assesses input and initiates response
- effector, changes internal environment to normal
(work through negative feedback)
positive feedback
response increases the original stimulus
ex) childbirth
“gain” of a control system
- degree to which a control system maintains homeostasis
- system with large gain is more capable of maintaining homeostasis than one with a low gain (pulmonary and cardiovascular systems have large gains)
- gain= correction/error
hormesis
process where a low to moderate dose of stress (exercise) results in beneficial adaptive response on cell or organ system
stress proteins
cells synthesize stress proteins when homeostasis is disrupted
ex) heat shock proteins repair damaged proteins in cells
increase tension in skeletal muscle by
- increase frequency of stimulation
- increase strength of stimuli
- change length of muscle
low frequency of neural stimulation of motor unit
causes simple twitch
three stimuli of motor unit
summation
continual stimulation motor unit
tetanus
types of muscle action
isometric, isotonic (dynamic), isokinetic
isometric muscle action
muscle exerts force without changing length
isotonic (dynamic) muscle action
concentric (muscle shortening)
eccentric (muscle lengthening)
isokinetic muscle action
movement of labor is constant no matter how much force is exerted
how muscle fiber types are observed
- muscle biopsy
- staining for myosin ATPas isoform
–immunohisotchemical staiing
–gel electrophoresis
type i fibers
slow-twitch fibers
slow-oxidative fibers
type iia fibers
intermediate fibers
fast-oxidative glycolytic fibers
type iix fibers
fast-twitch fibers
fast-glycotic fibers
oxidative capacity of muscle fiber
the number of capillaries, mitochondria and amount of myoglobin (oxygen storage molecule)
(high in slow twitch)
type of myosin ATPase isoform of muscle fiber
speed of ATP degradation
how fast you contract muscles
abundance of contractile protein in muscle fiber
actin and myosin
fast twitch fibers contract faster because they have more actin and myosin to exert greater force
force-velocity relationship
the greatest force production has the lowest velocity and the greatest velocity of shortening is at the lowest force
*slow twitch fibers can exert greater velocity or greater force at the same speed
*the speed of movement is greater in muscles with higher % of fast twitch fibers
force-power relationship
there is an optimal velocity for the greatest power output
when velocity is low, power is low, and when velocity is too high power goes down
sarcopenia
age related loss of muscle mass
delay age related muscle loss
resistance training
diabetes and muscle loss
muscles become insulin resistant so insulin cannot stimulate muscle to bring glucose or amino acids into cell
aerobic and resistance training are protective
muscular distrophy
hereditary defects in muscle protein resulting in loss of muscle fibers and weakness
cancer and muscle loss
cachexia is rapid loss of muscle mass that 50% of cancer patients suffer from
regular exercise and nutrition can counteract
energy at rest comes from
oxidative phosphorylation, anaerobic, blood lactate levels are low
resting oxygen consumption
3.5 ml/kg/min (I MET)
oxygen required to burn fat
23 O2
oxygen required to burn carbohydrates
6 O2
Respiratory exchange ration (RER or R)
R=VCO2/VO2
determines how many calories you burn either using fat or carbs
time it takes to reach steady state
1-4mins
oxygen deficit
lag in oxygen uptake at the beginning of exercise
initial ATP comes from anaerobic pathways
primary source of fat in low intensity exercise
plasma FFA
primary source of fat during higher intensity exercise
intramuscular triglycerides
primary source of carbohydrates during high-intensity exercise
muscle glycogen
primary source of carbohydrates during long duration exercise
blood glucose
cardiovascular and muscular adaptations for better aerobic bioenergetic capacity in trained subjects
- higher enzyme activity to raise metabolic functions
- more capillaries and more mitochondria to transport more oxygen and nutrients to cells
(results in less production of lactate and H+ and PC)
oxygen debt
repayment for oxygen deficit at onset of exercise
also called excess post-exercise oxygen consumption (EPOC)
- 20% elevated O2 uptake during recovery to make up for O2 deficit
Rapid portion of O2 debt
- first portion
- resynthesis of PC
- replenishing muscle and blood O2 stores (myoglobin + hemoglobin)
slow portion of O2 debt
- second portion
- elevated heart rate and breathing = greater energy need
- elevated body temp = greater enzyme activity = higher metabolic rate
- elevated epinephrine and norepinephrine = higher metabolic rate
- conversion of lactic acid to glucose (gluconeogenesis)
conversion of lactic acid to glucose
gluconeogenesis
why is oxygen consumption (EPOC, excess post-exercise oxygen consumption) greater following high intensity exercise?
- higher body temp
- greater depletion of PC, additional O2 required for resynthesis
- greater blood concentrations of lactic acid, additional O2 required for greater level of gluconeogenesis
- higher levels of blood epinephrine and norepinephrine
removal of lactic acid following exercise (percentages)
- 70% of lactic acid is oxidized by cells used as a substrate by heart and skeletal muscle
- 20% is converted to glucose
- 10% converted to amino acids
lactic acid and cooldown
light exercise (30-40% VO2 max) during recovery removes lactic acid more rapidly from the blood
short term, high intensity exercise first 1-5 seconds metabolic response
ATP produced from ATP-PC system
short term, high intensity exercise over 5 seconds metabolic response
shift ATP production to anaerobic glycolysis
short term, high intensity exercise over 45 seconds metabolic response
60 seconds, 70% anaerobic/30% aerobic
2 mins, 50% anaerobic/50% aerobic
prolonged exercise (over 10mins) metabolic response
- ATP production from aerobic metabolism
- steady state oxygen uptake can generally be maintained during submaximal exercise (below lactate threshold)
cardiovascular drift
- upward drift in oxygen uptake due to increases in body temp and epinephrine and norepinephrine (from prolonged exercise in hot/humid environments or high intensity exercise >75% of VO2 max)
metabolic response to incremental exercise
oxygen uptake increases linearly until maximal oxygen uptake (VO2 max) is reached, even if work increases there is no further increases in VO2
VO2 max
- “physiological ceiling” for delivery of O2 to muscle, affected by genetics and training
- tight association between VO2 max and endurance performance
physiological factors influencing VO2 max
- max ability of cardiorespiratory system to deliver O2 to the muscle
- ability of muscles to use oxygen and produce ATP aerobically
lactate threshold
the point at which blood lactic acid rises systematically during incremental/graded exercise
sports drinks —
maintain blood glucose levels (above 1.5 hour exercise)
