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where does our energy come from
carbs, lipids and protein converted to ATP for energy
ATP can be generated by
ADP + PC > C +ATP, anaerobic respiration/glycolysis, or aerobic respiration (maintaining blood glucose is critical)
carbohydrates
preferred fuel source of body for max activity, less O2 required compared to fat, only substrate that can be used in anaerobic metabolism
glucose
simple CHO (what we break down from carb sources of food)
1g glucose =
4kcal of energy
normal fasting blood glucose
80-100
normal blood glucose after eating
170-200
normal blood glucose 2-3 hours after eating
120-140
plasma glucose
only substrate that can be used by the brain or RBCs for energy
glucose in excess is
cytotoxic - dont want too much of a good thing
hemorrhagic stroke
blood interaction in brain allows glucose to kill brain cells, downstream is not perfused so no glucose
ischemic stroke
not perfused, getting no glucose or O2 and no aTP production is possible
CHO that is not used or circulating is
stored as glycogen in the muscle or liver (more in muscle - about 400g muscle 100g liver)
with a 24 hour fast
it would be expected to dip into glycogen stores
glycogenesis
formation of glycogen from glucose via glycogen synthase stimulated by eating
is CHO is not circulated or stored, it is
converted to adipose tissue
glycogenolysis
breakdown of glycogen to glucose via glycogen phosphorylase, stimulated by EPI, glucagon, and cA2+ released with muscle contraction
gluconeogenesis
creation of glucose from non-CHO sources, stimulated by depletion of glycogen stores or protein breakdown (why fasting decreases muscle mass), can use backbone of triglyceride, pyruvate or lactate
role of CHO in the body
energy source, protein sparer, primer for fat catabolism
lipids
long hydrocarbon chains, insoluble in water
lipids are found where in the body
intramuscular, circulating in blood as FFA, stored as adipose tissue, or as circulating triglycerides/lipoproteins (10%)
triglyceride
simple lipid, glycerol backbone with 3 fatty acid chains - major storage compound for lipids, # of carbons they have determine how much energy they will produce
enzymes that catalyze breakdown of triglycerides
adipose triacylglycerol (ATGL) and hormone sensitive lipase (HSL)
glycerol
soluble in blood, can enter glycolysis in cytoplasm, not typically in skeletal muscle, can be converted to glucose in liver
free fatty acids
must be bound to albumin to be transported in blood, receptors in muscle cell membrane bring FFA into cytoplasma then they're translocated or transported into mitochondria
beta oxidation
cyclic series of steps that breaks off successive pairs of carbon atoms from FFA which are used to form acetyl CO A
role of lipids in the body
energy source and reserve (primary source at rest or with lower intensity exercise - 90% of total energy), protects vital organs, thermal insulation, vitamin carrier
1g fat
9kcal energy
fat is stored
dry
when CHO availability is inadequate
oxaloacetate is converted to glucose, Acetyl CoA cant enter krebs without oxalocetate, so liver converts Acetyl CoA into ketones
ketones can be used as
fuel by muscles, nerves and brain - but accumulation increases acidity and puts body into ketosis which can disrupt physiological function (decrease enzyme function, etc)
proteins
chains of amino acids - 20AAs that we need that can form >80000 proteins
complete proteins
have all 20AA's, 8AA's can be produced by the body, 12AA's have to be gotten through dietary intake (essential)
AAs are never
stored - body is always using them for something
role of protein in the body
structural components, cellular transporters, enzymes, blood clotting, form contractile appratus of muscle, energy (if using for energy, stealing it from another function)
1g protein
4kcal energy
ATP is a universal
energy donor - in energy requiring and energy yielding reactions
coupled reactions
energy required and energy releasing
ADP to ATP takes
7kcals of energy
ATP gets broken down via
ATPase
ATP supply
enough for a 6 sec sprint, not a lot stored, must be constantly producing for demand (depletes but never drops because of constant reproduction)
ATP production in the mitochondria
citric acid cycle/electron transport chain uses fatty acids, pyruvate from glucose, deaminated AA's
ATP production in the cytosol
glycolysis/anaerobic, phosphocreatine, glucose/glycogen, glycerol, deaminated AA's
daily ATP production is a combination of
high production at a slow rate, low production fast rate
high production at slow rate is
aerobic metabolism
low production at fast rate is
anaerobic metabolism
three energy systems
phosphagen system, anaerobic glycolysis, aerobic
phosphagen system
ADP and PCr converting to ATP and creatine via creatine kinase
ATP-PC provdes
immediate energy supply for the first 10-15sec
glycolysis becomes the primary energy supply
about 10 sec in
aerobic is dominant energy supply
at 90 seconds onwards
time-energy system continuum
50/50 aerobic and anaerobic contribution of energy at 75 sec
alactic anaerobic metabolism
body can store 90-160mmol/kg in muscle of creatine in dry muscle (reversible), creatine broken down to creatinine (irreversible)
95% of creatine stroage is in
muscle
glycolysis is stimulated via
insulin, EPI, presence of AMP and ADP
glycolysis is inhibited by the
presence of ATP, low pH and citrate
anaerobic glycolysis converts six carbon molecule
2 three carbon molecules
oxidation-reduction reactions
oxidation of glucose, takes an H off and allows NAD+ to form with the e- and make NADH via reduction
glucose oxidation byproduct is
pyruvate
oxidation
loss of hydrogen/electrons in several intermediary steps in cellular respiration
electron donors
organic fuels
nicotinamide adenine dinucleotide (NAD) and flavin adenine dinucleotide (FAD)
2 most important hydrogen carriers in cellular respiration, can accept 2 electrons and 2 protons from 2 H atoms
FAD binds with
both H atoms to form FADH2
NAD+ is the
more important H carrier in human metabolism
pyruvate turns into
acetyl CoA when exposed to oxygen, and lactate without oxygen
lactate dehydrogenase
responsible for lactate production from pyruvate with no O2 present, and when NADH is present to donate the E to make lactate
at rest, lactate and pyruvate levels in the body are
at equal amounts
lactic acid at physiological pH
is broken down almost immediately into H and La - constant production of lactic acid in the body is always occuring and increases during anaerobic metabolism to fuel exercise performance
before lactate begins to accumulate, it either
is converted back to pyruvate with sufficient O2 and NADH present, or it diffuses out of the muscle to be buffered in the blood or interstitial fluid
lactate clearance is via
transamination, sweat, stays circulating as resting lactate level, oxidation (primary)
transamination
forms keto acids and amino acids
intracellular lactate shuttle
MCT1 moves lactate between cytoplasm and mitochondria, lactate oxidized in mitochondria to pyruvate for aerobic metabolism
extracellular lactate shuttle
MCT1/4 moves lactate in and out of tissues - either out of FOG/FG and into SO or into cardiac muscle or liver via bloodstream
lactate can also be involved in the liver via
cori cycle doing gluconeogenesis to create glucose as a nonCHO
intense exercise leads to lactate accumulation becauce
anaerobic is working quickly
lactic acid production is via
muscle contraction, enzyme activity and based on muscle fiber type
muscle contraction causes
Ca2+ release from SR activating glycogen phosphate which facilitates glycogenolysis and produces lactate
lactic dehydrogenase
(converts pyruvate to lactate) highest rate of function of all glycolytic enzymes, increased pyruvate and NADH means greater LDH activity, maintaining the redox potential to keep cell glycolysis going (making H available, etc)
pyruvate dehydrogenase
converts pyruvate to acetyl coa
fast glycolytic muscle fibers rely on
glycolysis (because non oxidative) - resulting in lactic acid production, LDH enzymes are predominant in FG fibers too (facilitating conversion of pyruvate to lactate)
sympathetic neurohormonal activation for lactic acid production
increased EPI and glucagon causes decreased insulin and increased glycogen breakdown which increases G6P which increases rate of glycolysis leading to increased pyruvic acid production and eventually lactic acid production
insufficient oxygen levels
O2 not available in mitochondria as final e acceptor in ETS so cell must rely on anaerobic glycolysis leading to lactic acid production
lactate accumulation is caused by
decreased redox potential, increased activcation of fast twitch muscle fibers and rate of lactae production exceeding removal
lactate threshold
exponential increase in lactate threshold where production exceeds clearance, usually at about 50% Vo2max (higher in atrained athlete)
good aspect of lactic acid
used for energy n slow twitch fibers, for gluconeogenesis, cardiac cycle, takes H- with it when it leaves the cell eventually allowing pH to drop which shifts the O2 curve and permits more O2 into cell to allow aerobic metabolism
lactic acid does not cause
DOMS
lactic acidosis
decreased pH will decrease enzyme function, and pulmonary patients will struggle because lungs are a buffer for lactate
lactic acidosis can be a predictor of
mortality (increased blood lactate = increased risk of death)
normal blood lactate
hyperlactemia
2-4mmol/m
severe lactic acidosis
>4mmol/m (increases mortality)
lab procedures to measure anaerobic metabolism
ATP-PC and lactate blood tests, wingate anaerobic test (gold standard), stair climb, vertical jump, etc.
variance in females vs males for anaerobic characteristics
males have more stored PCr due to more muscle mass, and accumulate more lactate in adulthood due to testosterone (no difference when you normalize to muscle mass)
when you normalize to lean body mass, mechanical power and capacity
is basically equal between males and females
anaerobic characteristics of children
slightly lower availability and utilization of PCr, less lactate accumulation than adults but rate of clearance is similar, lactate threshold occurs at a higher % of VO2max because lower anaerobic capacity and more reliance on aerobic metabolism, lower mechanical power and capacity
muscle enzyme theory for children
producing less but oxidative enzymes are more robust
muscle characteristics theory for children
more FOG (type 2A) which means less lactate production (FG produces the most)
sexual maturation theory for children
teststerone influences muscle mass - increases with puberty
neurohormal regulation theory for children
decreased NS and endocrine activation with exercise (liver is better at gluconeogenesis because more bloodflow)
anaerobic characteristics of older adults
less ATP-PC stores but increased ADP/creatine in muscles, lower lactate accumulation at relative workloads (higher at absolute workloads because working harder), lower max lactate levels, lactate threshold at higher %vo2max, less mechanical power and capacity