Anaerobic glycolytic system Flashcards
where does the energy for phosphorylating ADP during intense and short duration exercise come mainly from?
stored muscle glycogen
breakdown via anaerobic/fast glycolysis resulting in lactate formation
power vs capacity and timeline of anaerobic glycolytic
moderate to high power, mod to low capacity
peak power - 15-30 seconds
capacity - 45-120 seconds
when does the anaerobic glycolytic system kick in?
5 seconds after muscle contraction starts
- overlap between ATPPC capacity and anaerobic glycolytic power
sports using the anaerobic glycolytic system
15-120 seconds 1500m speedskating 200m track - 800m capacity 100m swimming slalom and downhill skiing gymnastic - floor routine or parallel barrs round of boxing period of wrestling track cycling - kilo race
anaerobic glycolytic energy
reserve fuel used at the start/end of race
Embden Meyerhof glycolytic pathway
Meyerhof - glycogen was precursor of lactate (1920)
Embden - put together a model of all the steps of glycolysis - later adopted and confirmed by meyerhof
glycolysis
requires
series of sequential metabolic steps that converts glucose/glycogen into pyruvate to produce ATP
energy to be invested first
net gain of ATP depends in glycolysis depends on
if starting substrate is glucose or glycogen
level of ATP phosphorylation
substrate level
how much potential ATP is generated?
5% of potential 30-33 ATP that is produced through complete aerobic breakdown of glucose
where does glycolysis occur?
cytoplasm
Products of glycolysis of glucose vs glycogen
2 vs 3 ATP
2 NADHH
2 pyruvate
rate limiting enzyme of glycolysis
phophofructokinase
What are cell membranes permeable and not permeable to?
glucose and lactate but not phophorylated substances
is glycolysis possible without glucose/glycogen?
no
low glycogen induced by
fasting, inadequate nutrition, depleted stores from previous exercise
can glycogen move out of muscles?
no
muscle glucose transporters
Glut 1 (glucose transporter type 1)
- steady flow
- non insulin regulated
moves glucose into muscles during rest
GLUT 4
- stored in intracellular vesicles
- moves glucose into cells after a meal and during exercise
- insulin regulated - postprandially (after a meal)
- activated by muscle contractions - (increased intracellular calcium )
glycogen synthase (5)
used in glycogenesis
- enzymes that convert glucose into glycogen (long chains)
- active in postprandial period
- glycogen close to active site of muscles
- too much glucose gets turned into fat
anaerobic glycolysis is regulated by a series of
controls the rate of energy production along the anaerobic metabolic pathway glycolytic enzymes - hexokinase - phophorylase - phosphofructokinase (PFK) - lactate dehydrogenase (LDH)
hexokinase
One ATP required for activation
traps glucose in the cell
Phosphorylase
no ATP required for activation
activated by Pi, Ca and cAMP (epinephrine via g-protein receptor- activate energy)
McArdle’s syndrome - dysfunctional phosphorylase
phosphofructokinase
one ATP for activation
rate limiting for glycolysis
allosteric regulation - enzyme bind and changes active site
-inhibited by ATP, citrate, free FA and decreased pH
-activated by ADP, Pi, AMP and increased pH
numbers of ATP produced from heart muscle and skeletal muscle from heart muscle
skeletal glucose 30 glycogen 31
Heart glucose 32 glycogen 33
Lactate dehydrogenase and isoforms
LDH 4&5 predominate in fast twitch to convert pyruvate to lactate “m” for muscle form
LDH 1&2 predominate in cardiac - slow twich to convert lactate to pyruvate “h” for heart form
LDH (m)
regenerate NAD to faciliate fast glycolysis b/c that doesnt happen without NAD and allows it to continue for minutes instead of seconds
how is lactic acid fromed?
when NADHH is oxidized to NAD by transferring H to pyruvic acid (C3H4O3) which turns into lactic acid (C3H6O3)
lactic acid or lactate?
99% of lactic acid dissociates into H and lactate immediately
Why is there lactic acid all the time in our blood?
RBC, kidneys and certain tissues in the eye will produce lactic acid continuously, always some lactate in circulation
how do lactate levels fluctuate?
depends on lactate turnover which is a function of production vs clearnace
5 factors that promote lactate production
muscle contrations mass action effect muscle fibre type increased SNS activation insufficient oxygen
muscle contrations and lactate prodution
ca activates phosphorylase which leads to glycogenesis
mass action effect and lactate production
LDH in glycolysis - any increase in pyruvate and NADHH, regarless of presence of oxygen contributes to lactate production - keep turning pyruvate into lactate
muscle fibre type and lactate
increased expression of LDHM in fast twitch
4 EVENTS THAT clear lactate
oxidation
transamination
gluconeogensis/glyconeogenesis
sweat
pH regulation in the body
muscle and blood
homeostatic mechanisms resting muslce - 6.9-7 extreme exercise 6.4 resting blood - 7.4-7.45 exercise rarely below 7 extreme exercise 6.74
2 mechnisms used to regulate pH
ventilation - H into H2O and CO 2 through carbonic anhydrase (H+HCO3=H2CO3=H2O and CO2)
Kidneys - secretion of carbonic acid
acid
compound that donates a H in solution
base
roems a hydroxyl when dissolved in water
pH calculation
-log[H+]
why dont you wanna drink before you compete in your short distance event
NAD is required for alcohol breakdwon which will take away from glycolysis
concern with acid
metabolic acidosis if H+ exceeds buffering capacity which is linked to fatigue
buffering capacity
ability to neutralize a decrease in pH experienced during anaerobic glycolytic exercise
8 metabolic effects of reduced pH/increased H+
decreased PFK
decreased phosphorylate
acclerated break down of PC
decreased activity of ATPase on mysoin head
-decrease in myosinATPase, Na/k ATPase, SR ATPase
altered membrane transport
central fatigue - pain receptors triggered by H
Decreased Ca binding to troponin
decreased O2 binding to hemoglobin - dump more oxygen
4 metabolic effects of increased lactate
increased oxidation of lactate in muscles
efflux into blood
efflux to other muslce cells where it can be oxidized
may interfere with crossbridge cycling
oxidation of lactate
done by LDH h to regenerate pyruvate
lactate efflux into blood -5
moves out of cell, circulates and gets picked up by others
increased oxidation in other tissues
heart likes lactate during exercise - usually FA but can take lactate
loss to sweat and urne
liver picks it up - gluconeogensis - cori cycle to make glucose
lactate and crossbridge cycling
binding to thick and thin filaments - fatigue
does lactate induce fatigue?
no - but its highly associated with fatigue related factors i.e. hydrogen
evaluating anerobic glycolytic power and capacity -3
Wingate - 30 seconds for anaerobic glycolytic power
- first five is alactic power, then fast glycolysis
modified 90s- anaerobic glycolytic capacity
cunningham faulkner treadmill test - lactic anaerobic capacity
fatigue index =
% of peak power drop off during high intensity, short duration work
lactate testing for anaerobic glycolytic power
8mmol/L - someone who’s working maximally
can go up to 32,
resting level 1-2
limitation of lactate testing
lactate can move easily between muslce and bloodstream but takes time to equilibrate (5-10min)
range of lactic anaerobic exercise response
short term light to moderate submax aerobic
short term mod to heavy submax aerobic
incremental exercise - exponential curve
dynamic resistance training
short term high intensity anaerobic
longterm mod to heavy submax aerobic depends
high intensity, short duration and supramaximal activity results in what VO2 max?
105-110
stress hormones activate
glycolysis - lactate goes up
diff goals =
diff training and diff results
What kind of athletes would have higher buffering capacity?
athletes that rely on anaerobic glycolytic power
- so they can neutralize the acid and increase the workload
Buffering capacity and training
specific training and enhance it but theres a limit to adpatton
Function of buffering agents
artificially increase ability of body to buffer metabolic acidosis in an effort to delay fatigue and increase performance
2 commonly used buffering agents
sodium bicarbonate/citrate
beta alanine
purported mechanism of sodium bicarbonate -2
increased extracellular HCO3 to increase arterial blood pH
gradient to draw out H
Ergogenic dose of sodium bicarbonate and sodium citrate
sodium bicarbonate - .2-.4g/kg
sodium citrate 0.6-0.6 g/kg
60-90 min before exercise
research of ergogenic benefits of sodium buffering agents
why ?
mixed results - some say bicarbonate enhances performance in short term intense tests while others have no benefits
hydrogens are in the cell
3 ergogenic benefits of sodium agents
results in increased blood HCO3 and reduced blood H but skeletal muscle H is not altered
increased power output with repeated sprints
both sodium agents are effective
side effect of sodium agents
GI upset - 10% are intoleratn
leads to vomiting and diarrhea
more pronounced with bicarbonate
so dont try it before a competition
beta alanine proported mechanism 2
increased intracelluar buffering capacity
delayed fatigue during intense aerobic exercise
dose of beta alanine
65mg/kg/day once a day for 4-10 weeks
ergogenic benefits of beta alanine
mixed results - may improve performance with repeated bouts of high intensity exercise
often consumed with creatine so heard to distinguish
side effect of beta alanine
paresthesia - pins and needles feeling on the face and skin
beta alanine and carnosine
combines with histidine to get carnosine - so you can stockpile as it is the limiting substrate for the carnasine molecule
buffering agents legal?
not banned but may be considered a violation of doping rule because you arent allowed to use any physiological substance to enhance performance - human thresholds are hold to test but they are illegal in horse racing
how to train the anaerobic glycolytic system
work duration between 30s-2min
repeat intervals - lactate stacking which gives you a higher blood lactate than just one all-out
5 metabolic adaptations of anaerobic glycolytic system training
increased buffering capacity
increased enzyme activity - PFK, Hexokinase, Phosphorylase, LDH5m
increased glycogen storage
decreased lactate accumulation at same absolute workload
no change at same relative intensity for resistance exercise
peak power in females -
65 of peak in males
83 relative to total weight
94 relative to lean mass
mean power in females
68 of peak
87 relative to total weight
98 relative to lean mass
what accounts for the different power value in sex
different hormonal profiles
more adipose tissue in females
utilize different fules
what stimulates PFK?
high ADP because ATP needs to be made
low pH and PFK
low levels means PFK has been working hard so lots of ATP
citrate vs PFK
citrate is the downstream product of PFK
