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Exercise Physiology > Anaerobic glycolytic system > Flashcards

Anaerobic glycolytic system Flashcards

1
Q

where does the energy for phosphorylating ADP during intense and short duration exercise come mainly from?

A

stored muscle glycogen

breakdown via anaerobic/fast glycolysis resulting in lactate formation

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2
Q

power vs capacity and timeline of anaerobic glycolytic

A

moderate to high power, mod to low capacity

peak power - 15-30 seconds
capacity - 45-120 seconds

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3
Q

when does the anaerobic glycolytic system kick in?

A

5 seconds after muscle contraction starts

- overlap between ATPPC capacity and anaerobic glycolytic power

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4
Q

sports using the anaerobic glycolytic system

A 
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
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5
Q

anaerobic glycolytic energy

A

reserve fuel used at the start/end of race

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6
Q

Embden Meyerhof glycolytic pathway

A

Meyerhof - glycogen was precursor of lactate (1920)

Embden - put together a model of all the steps of glycolysis - later adopted and confirmed by meyerhof

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7
Q

glycolysis

requires

A

series of sequential metabolic steps that converts glucose/glycogen into pyruvate to produce ATP

energy to be invested first

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8
Q

net gain of ATP depends in glycolysis depends on

A

if starting substrate is glucose or glycogen

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9
Q

level of ATP phosphorylation

A

substrate level

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10
Q

how much potential ATP is generated?

A

5% of potential 30-33 ATP that is produced through complete aerobic breakdown of glucose

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11
Q

where does glycolysis occur?

A

cytoplasm

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12
Q

Products of glycolysis of glucose vs glycogen

A

2 vs 3 ATP
2 NADHH
2 pyruvate

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13
Q

rate limiting enzyme of glycolysis

A

phophofructokinase

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14
Q

What are cell membranes permeable and not permeable to?

A

glucose and lactate but not phophorylated substances

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15
Q

is glycolysis possible without glucose/glycogen?

A

no

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16
Q

low glycogen induced by

A

fasting, inadequate nutrition, depleted stores from previous exercise

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17
Q

can glycogen move out of muscles?

A

no

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18
Q

muscle glucose transporters

A

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 )

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19
Q

glycogen synthase (5)

A

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
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20
Q

anaerobic glycolysis is regulated by a series of

A 
controls the rate of energy production along the anaerobic metabolic pathway 
glycolytic enzymes 
- hexokinase 
- phophorylase 
- phosphofructokinase (PFK)
- lactate dehydrogenase  (LDH)
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21
Q

hexokinase

A

One ATP required for activation

traps glucose in the cell

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22
Q

Phosphorylase

A

no ATP required for activation
activated by Pi, Ca and cAMP (epinephrine via g-protein receptor- activate energy)
McArdle’s syndrome - dysfunctional phosphorylase

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23
Q

phosphofructokinase

A

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

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24
Q

numbers of ATP produced from heart muscle and skeletal muscle from heart muscle

A

skeletal glucose 30 glycogen 31

Heart glucose 32 glycogen 33

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25
Q

Lactate dehydrogenase and isoforms

A

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

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26
Q

LDH (m)

A

regenerate NAD to faciliate fast glycolysis b/c that doesnt happen without NAD and allows it to continue for minutes instead of seconds

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27
Q

how is lactic acid fromed?

A

when NADHH is oxidized to NAD by transferring H to pyruvic acid (C3H4O3) which turns into lactic acid (C3H6O3)

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28
Q

lactic acid or lactate?

A

99% of lactic acid dissociates into H and lactate immediately

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29
Q

Why is there lactic acid all the time in our blood?

A

RBC, kidneys and certain tissues in the eye will produce lactic acid continuously, always some lactate in circulation

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30
Q

how do lactate levels fluctuate?

A

depends on lactate turnover which is a function of production vs clearnace

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31
Q

5 factors that promote lactate production

A 
muscle contrations 
mass action effect 
muscle fibre type 
increased SNS activation 
insufficient oxygen
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32
Q

muscle contrations and lactate prodution

A

ca activates phosphorylase which leads to glycogenesis

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33
Q

mass action effect and lactate production

A

LDH in glycolysis - any increase in pyruvate and NADHH, regarless of presence of oxygen contributes to lactate production - keep turning pyruvate into lactate

34
Q

muscle fibre type and lactate

A

increased expression of LDHM in fast twitch

35
Q

4 EVENTS THAT clear lactate

A

oxidation
transamination
gluconeogensis/glyconeogenesis
sweat

36
Q

pH regulation in the body

muscle and blood

A 
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
37
Q

2 mechnisms used to regulate pH

A

ventilation - H into H2O and CO 2 through carbonic anhydrase (H+HCO3=H2CO3=H2O and CO2)
Kidneys - secretion of carbonic acid

38
Q

acid

A

compound that donates a H in solution

39
Q

base

A

roems a hydroxyl when dissolved in water

40
Q

pH calculation

A

-log[H+]

41
Q

why dont you wanna drink before you compete in your short distance event

A

NAD is required for alcohol breakdwon which will take away from glycolysis

42
Q

concern with acid

A

metabolic acidosis if H+ exceeds buffering capacity which is linked to fatigue

43
Q

buffering capacity

A

ability to neutralize a decrease in pH experienced during anaerobic glycolytic exercise

44
Q

8 metabolic effects of reduced pH/increased H+

A

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

45
Q

4 metabolic effects of increased lactate

A

increased oxidation of lactate in muscles
efflux into blood
efflux to other muslce cells where it can be oxidized
may interfere with crossbridge cycling

46
Q

oxidation of lactate

A

done by LDH h to regenerate pyruvate

47
Q

lactate efflux into blood -5

A

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

48
Q

lactate and crossbridge cycling

A

binding to thick and thin filaments - fatigue

49
Q

does lactate induce fatigue?

A

no - but its highly associated with fatigue related factors i.e. hydrogen

50
Q

evaluating anerobic glycolytic power and capacity -3

A

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

51
Q

fatigue index =

A

% of peak power drop off during high intensity, short duration work

52
Q

lactate testing for anaerobic glycolytic power

A

8mmol/L - someone who’s working maximally
can go up to 32,
resting level 1-2

53
Q

limitation of lactate testing

A

lactate can move easily between muslce and bloodstream but takes time to equilibrate (5-10min)

54
Q

range of lactic anaerobic exercise response

A

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

55
Q

high intensity, short duration and supramaximal activity results in what VO2 max?

A

105-110

56
Q

stress hormones activate

A

glycolysis - lactate goes up

57
Q

diff goals =

A

diff training and diff results

58
Q

What kind of athletes would have higher buffering capacity?

A

athletes that rely on anaerobic glycolytic power

- so they can neutralize the acid and increase the workload

59
Q

Buffering capacity and training

A

specific training and enhance it but theres a limit to adpatton

60
Q

Function of buffering agents

A

artificially increase ability of body to buffer metabolic acidosis in an effort to delay fatigue and increase performance

61
Q

2 commonly used buffering agents

A

sodium bicarbonate/citrate

beta alanine

62
Q

purported mechanism of sodium bicarbonate -2

A

increased extracellular HCO3 to increase arterial blood pH

gradient to draw out H

63
Q

Ergogenic dose of sodium bicarbonate and sodium citrate

A

sodium bicarbonate - .2-.4g/kg
sodium citrate 0.6-0.6 g/kg
60-90 min before exercise

64
Q

research of ergogenic benefits of sodium buffering agents

why ?

A

mixed results - some say bicarbonate enhances performance in short term intense tests while others have no benefits
hydrogens are in the cell

65
Q

3 ergogenic benefits of sodium agents

A

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

66
Q

side effect of sodium agents

A

GI upset - 10% are intoleratn
leads to vomiting and diarrhea
more pronounced with bicarbonate
so dont try it before a competition

67
Q

beta alanine proported mechanism 2

A

increased intracelluar buffering capacity

delayed fatigue during intense aerobic exercise

68
Q

dose of beta alanine

A

65mg/kg/day once a day for 4-10 weeks

69
Q

ergogenic benefits of beta alanine

A

mixed results - may improve performance with repeated bouts of high intensity exercise
often consumed with creatine so heard to distinguish

70
Q

side effect of beta alanine

A

paresthesia - pins and needles feeling on the face and skin

71
Q

beta alanine and carnosine

A

combines with histidine to get carnosine - so you can stockpile as it is the limiting substrate for the carnasine molecule

72
Q

buffering agents legal?

A

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

73
Q

how to train the anaerobic glycolytic system

A

work duration between 30s-2min

repeat intervals - lactate stacking which gives you a higher blood lactate than just one all-out

74
Q

5 metabolic adaptations of anaerobic glycolytic system training

A

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

75
Q

peak power in females -

A

65 of peak in males
83 relative to total weight
94 relative to lean mass

76
Q

mean power in females

A

68 of peak
87 relative to total weight
98 relative to lean mass

77
Q

what accounts for the different power value in sex

A

different hormonal profiles
more adipose tissue in females
utilize different fules

78
Q

what stimulates PFK?

A

high ADP because ATP needs to be made

79
Q

low pH and PFK

A

low levels means PFK has been working hard so lots of ATP

80
Q

citrate vs PFK

A

citrate is the downstream product of PFK

Exercise Physiology (17 decks)

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