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Signal Transmission overview (contraction)
nerve impulse (AP) travels from motor neuron to NMJ
At the NMH: ach is released into synaptic cleft
Ach binds to receptors on the sarcolemma
Na+ channels generate new AP in the muscle fiber
AP runs along sarcolemma and into T tubules
T-tubules (muscle contraction)
The electrical signal in the t-tubules triggers the SR to release calcium into the sarcoplasm
Contraction (CA is released into sarcoplasm)
Ca binds to troponin
tropnin pulls tropomyosin away from myosin-binding sites
Myosin attaches and cross-bridges are formed
ATP is hydrolysed into ADP and Pi
the myosin head pivots, and actin is pulled inwards
Shortening=contraction
Detachement and reactivation
After first CB cycle, atp binds to new head
if ca is present cycle will continue
If CA is not available
nerve signal ends
Ach is broken down
Co2+ is pumped back into SR
muscle relaxes
Glycogen (net atp)
3 atp
Glucose net atp
2 net
PFK inhibited
atp levels are increased
glycolysis is inhibit
PFK is activated
decreased levels of atp in body
allows glycolysis
fate of pyruvate
becomes lactate or can entre the TCA
what keeps the tca going
oxaloacetate
lactate produced by glycolysis
trained people are good at clearing lactate
can go to the cori cycle in the liver
anaplerosis
a metabolic process involving chemical reactions that synthesize intermediates for the Citric Acid Cycle (TCA cycle). (protein support)
Chemical energy is stored
in the bonds of nutrients (CHO, protein, fats)
chemical energy is released
released through
metabolic pathways
manageable energy bursts
extracted energy becomes
ATP
immediate enrgy
Atp and creatine phosphate
creatine is 4-6x greater than atp
lasts only for a few seconds
increased energy means increased use of
intramuscular components
increased carbohydrate use
intramuscular energy
muscular glycogen
intramuscular triglycerides
muscle glycogen
stored CHO
rapid ATP source
used locally in muscle
important for high intensity, prolonged workout
intramuscular triglycerides
stored fat in muscle fibers
used for oxidative, anaerobic processes
How is glucose stored and why
glucose is stored as part of a glycogen ball, so we can store more and decrease osmolarity issues.
glucose is a highly soluble molecule and increases osmotic pressure, meaning storing glucose chains would be inefficient
what triggers glycogenphosphorylase
glucagon
epinephrine
glucagon
activates liver glycogenolysis
triggered by low blood glucose
epi and glycogenolysis
activates glycogen phosphorylase in the in muscle and some liver
cleaving glycogenolysis (stored glycogen balls)
glycogen phosphorylase removes glucose from glycogen branches at the end
glycogen phos removes glucose and hexokinase turns in immeditaley into G-6-p
muscle and g6p
g6p enters glycolysis to make ATP
it cannot leave as glucose
will be g6p forever
liver and G6P
NADH (aerobic vs anaerobic conditions)
can help with continuing glycolysis (anaerobic)
can also (under aerobic conditions) can be transformed into ATP through the ETC
the ETC
NADH/FADH (from gly/tca) passes through complexes
energy is released, pumping H+ from mitochondrial matrix into the intermembrane space
H+ accumulates in intermembrane space (creating conc/electrical gradient)
H+ needs to flow back into matrix through ATP synthase which means ATP is created
fuel from lipids is plentiful
estimated 90 000-110 000 kcal
compared to glucose at 2000 kcal (not enough for long period/high intensity)
Adreanline and fat
stimulated during exercise
triggers the mobilization of energy stores
lipolysis
lipolysos
releases free fatty acids and glycerol into the blood stream
lipid usage
adrenaline activates hormone-sensitive lipase
fatty acids are taken up by the muscle cell (mediated by lipoprotein lipase)
fatty acids are transported into the mitochondria (limiting step, transport)
Hormone sensitive lipase
breaks fown stored triglycerides into glycerol and 3 FFA
sources of lipids
intramuscular TG
TG in lipoprotein complexes
FFA from adipose tissue
Beta oxidation creates
creates acetyl coa
each cycle = 1 NADH and FADH (5 ATP)
Acetyl CoA goes to crebs and produces more NADH/FADH
Acetyl coa is formed by
cleaving of 2 C from FA
oxaloacetate must be available for
acetyl coa to enter the krebs cycle (limiting step)
Lipid - glucose shift
reduced blood flow to adipose tissue (reducsed ffa to muscle)
reductions in lipid transport
reduction in intramuscular tg hydrolysis due to decrease in hormone sensitive lipase (due to energy shift)
Protein usage in energy
Protein contributes very little to energy
can play a role in breakdown and TCA
Transamination
anapleurosis
glucose-alanine cycle
transamintaion
changing available amino acids into keto acids to make the AA we need
some AA we can’t make
free AA pool
small and comes from liver and non-contractile muscles
training effects on metab — endurance
reduction in rer
reduction in glucogenolysis
inc lactate clearance
inc fat oxidation
reductions in rer
downward shift at the same absolute workload
RER shifts towards 0.7 (fat usage)
Rer is the ratio of vco2 and co2
why see reductions in glycogenolysis with metabolism training
increase in # of oxidative fibers
reductions in adrenaline spike
decrease glycogenphosphorylase activity
increase fat burn
inc lactate clearance
lactate can be filtered to supply muscles by making glu/gly
inc training inc lactate clearance
athlete paradox
athletes often have increased levels of intramuscular fat because their body stores and uses it so efficiently
resistance exercise- metabolic change
inc glycogen stores
anaerobic increases
increase in storage and maximized glycogen levels
inc in muscle protein synthesis after exercise (depending on vol and freq)
Muscle protein synthesis
dependent on vol/freq
too little = no inc
too much = reductions in MPS
MPS peak
trained
2-3 peak, quick revert to baseline
untrained
peaks at 16 hours, and reverts back to baseline slowly
two most important factors of optimizing nutrition for performance
fluid and fuel
fluid factors
#1 thermoregulation
cognitive fx can decrease with 1% dehydration
water is the medium where everything takes place
sweat rate
cools us down
highly individual
decrease water, blood vol, blood to skin and cooling
loosing high amounts of water and salt decreases
perfusion
how much we need to drink is determined by
sweat rate
determining sweat rate
determined by change in body weight before and after an activity
ideally, no weight loss (ideally no more than 1.5-2% BW) loss
need to be as close to nude weight as possible
arrive to activity
hydrated
before exercise adults drink
500-700ml (3 cups)
60-90 min before
before exercise athletes drink
5-7 ml/kg 4 hr before
if urine is dark/MIA need another drink of 3-5ml/kg 2 hr before
(won’t calcualte for the average adult or rec athlete)
children drink before exercise
400 ml of fluid the night before
Drink regardless of thirst
urine gets lighter with hydration
thirst mechanism 2/3 of the way and then turns off
After exercise Hydration
intake to replenish BW
1-1.2kg/bw loss
hydration should be as early as tolerated
should account for epoc
accounting for epoc in hydration
increased sweat rate after exercise
add 30-50% to calculated intake
methods for rehyrdation
bolus
metered
Bolus
replenish all at once
drink it all in an hour
most won’t tolerate
metered
drink over 4-5 hours
more effective than bolus
more tolerated
Dehyrdation and env
heat is bad
cold env equipment can trap sweat and decrease cooling
hydration during activity
drink enough to prevent body weight loss (150-350 ml/fluid every 15-20 min)
consider tolerance, temp and workload
training the gut
gut will adapt
gastric empting
receptors in the gut can change
during exercise BF is diverted, and stuff is not absorbed and digested as well but this can be trained.
heat stroke
body temp = 40c or higher
heat stroke signs and symptoms
altered mental state (confusion/agitation/seizures/irritable
Alteration in sweating (hot weather, skin is hot and dry) (strenuous, skin is hot and moist)
Nausea and vomiting
flushing
rapid and shallow breathing
inc hr
headache
if heatstroke what to do
call 911, cold compress, layers, shade
rhabdomyolysis
Condition where muscle breakdown leads to accumulation of CK and Heme in the muscle
caused by overexertion and dehydration
typically in inactive person
symptoms
soreness, swelling, weakness
dark urine
Kidney failure
why kidney failure and rhabdomyolysis
dehyrdation means we are no longer producing urine, or producing a shit ton less
bad shit then accumulates in the liver.
electrolytes
maintainable in a diet, but we can consider supplementing in ultra athltetes
sweat rate and salt intake makes this highly variable
electrolytes depending on
length of exercise
temperature
Hypotranemia
increased sweating but only replacing the sweat with water
too much water and too much sweat
Hypotranemia symptoms
cramps, dizzy, weak, vomiting, fatigue, decreased appetite
fuel with serious athletes
heavy carb reliance (85%+)
Athletes need 5-7g/kg of carbs per day
1.2-2g protein
Muscle glycogen
liver gets first dibs on gly/glu coming into the body, and then filters the rest out to muscles
unless there is an emergency and very low levels in the muscle
fueling for exercise carbs and fluid
consumed until exercise
carbs should get more simple as game gets closer
dec volume and how complex they are
protein and fuel for exercise
until 30 min- 1hr before
fats fuel for exercise
1-2 hours before
gold standard fluid status
isotope/total body water
plasma osmolarity (blood test) (euhy level = 285 Mosm/kg)
Simple measurements for fluid status
urine (lags response to hypovolumia/euhydration)
BW
plasma conc of sodium
BIA
Saliva
Symptoms
field test and fluid status
-whole body sweat test (loss of bw, account fluid in and out)
local sweat Na2 conc
Gatorade/sport beverages
not designed for electrolytes
meant to drive thirst and CHO intake
thirst mech and fatorate
sometimes water only will turn off mechanism early, and when we start balancing water and salt after sweat.
Adding salt to our fluid will extend thirst mechanism
CES studies and intake
Studies support that ces drives people to drink more/hydrate
better net fluid balance
rehydration agents
better in hydration terms
1g salt lost/L sweat, CES = 400mg/L
can use medical rehydrants
Blood glucose supplied by
liver glucose
external sources
gluconeogenesis
liver glycogen
Liver glycogen gets way low overnight
so need to replenish in the morning so the liver gets first dibs
how to slow/stop Gluconeogenesis
need to supply enough CHO so protein isn’t broken down
muscle glycogen can take up to
18 hours to replenish
fueling during 45-60 min
not required unless high intensity (75% vo2)
wouldn’t be necessary for completion, just would increase performance
Activities 30-75 min (fuel during)
could do a salivary rinse
activates salivary amylase
Activities 1-2 hours, fuel during activity
not required but will enhance performance
30g of carb
activies 2-3 hours plus
should fuel prob
60g