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Ex Phys > Bioenergetics > Flashcards

Bioenergetics Flashcards

1
Q

metabolism defn

A

sum of all chemical reactions that occur within the body

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2
Q

anabolic reaction

A

synthesis of molecules, requires energy

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3
Q

catabolic reaction

A

breakdown of molecules, releases energy

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4
Q

bioenergetics defn

A

converting food fuels (CHO, lipids, proteins) into energy

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5
Q

energy to perform work - ATP

A

energy is stored in chemical bonds within molecules, the energy is released when the bonds are broken.
ATP (adenosine triphosphate) is the energy currency of the cell, due to its energy rich phosphate bond

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6
Q

enzymes defn

A

complex protein structures, biological catalysts that regulate the rate of a reaction by lowering the activation energy (Ea)

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7
Q

enzyme action - induced fit model

A

enzyme binding to substrate causes active site to be altered, allowing binding of substrate and active site. enhances catalysis, as the enzyme converts the substrate to product

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8
Q

kinases function

A

add phosphate group to the substrates, eg creatine kinase

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9
Q

dehydrogenase function

A

removes hydrogen from the substrate eg lactate dehydrogenase

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10
Q

factors that alter enzyme activity

A

temperature: small rise in body temp inc enzyme activity, eg temp inc d/t exercise. large rise in body temp results in decreased enzyme activity (denatures protein)
pH: Change in pH reduces enzyme activity (denatures protein) eg acid produced during exercise

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11
Q

control of bioenergetics - rate limiting enzymes

A

enzyme that regulates the rate of a metabolic pathway. increase opportunity for the reaction to progress. increases the number of enzymes.

modulator: switch enzymes off when required. modulators of RLE include levels of ATP and ADP + Pi. high ATP inhibits ATP production. low ATP and high ADP + Pi stimulate ATP production

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12
Q

energy systems (fn and list)

A

all ES function to restore ATP, to be used as energy for muscular contraction

ATP, CP, glycolysis, oxidative phosphorylation & ETC, B-oxidation & ETC

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13
Q

order of dominant energy systems

A

ATP –> ATP-CP –> ATP-CP & GLYC –> OXID PHOS –> AEROBIC/FFA

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14
Q

ATP hydrolysis

A

ATP –> ADP + Pi + free energy
enzyme ATPase breaks down the chemical bond of ATP

repletion occurs rapidly via ATP-CP, lactic acid system and aerobic system

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15
Q

Phosphocreatine system (PC/CP)

A

energy rich phosphate bond, most readily available fuel source for muscle contraction. stored within muscle fibre, ~5-10sec worth.

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16
Q

ATP-PC system

A

immediate source of ATP
PC + ADP –> ATP + C, facilitated by creatine kinase enzyme
creatine kinase activated by inc ADP and inhibited by ATP (ADP inc triggers breakdown of CP to replenish ATP)

rapid as it is a short, uncomplicated reaction that doesn’t require O2 and is easily accessible.

sport eg: throws, jumps sprints, power lifts (less than 10s events)

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17
Q

glucose and glycogen

A

glucose general formula = C6H12O6

glycogen is a more compact storage form of glucose

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18
Q

glycogenesis

A

formation of glycogen from glucose (gluc –> glyc)

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19
Q

glyconeogenesis

A

formation of glycogen from substrates other than glucose

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20
Q

gluconeogenesis

A

formation of glucose from glycogen breakdown (glyc –> gluc)

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21
Q

glycolysis

A

breakdown of glucose or glycogen to form pyruvate. occurs within the sarcoplasm (outside the mitochondria)

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22
Q

glycolysis - energy investment phase

A
  1. glucose phosphorylation by ATP: glucose –> glucose-6-phosphate
  2. rearrangement and 2nd phosphorylation by ATP: glucose-6-phosphate –> fructose-6-phosphate
  3. 6C mol split into 2x 3C mol: fructose-6-phosphate –> fructose-1,6-biphosphate
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23
Q

glycolysis - energy generation phase

A

not added yet

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24
Q

H+ and e- carrier molecules (NAD and FAD)

A

transport hydrogens and associated e- to:

  1. mitochondria for ATP generation (aerobic)
  2. convert pyretic acid to lactic acid (anaerobic)

NAD: nicotinamide adenine dinucleotide
NAD+ + H –> NADH

FAD: flavin adenine dinucleotide
FAD + 2H –> FADH2

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25
Q

conversion of pyruvic acid to lactic acid - NADH and mitochondria

A

NADH produced by glycolysis must be converted back to NAD+. achieved by converting pyruvic acid to lactic acid, via shuttling of H+ back into the mitochondria. a specific transport system shuttles H+ across the mitochondrial membrane.
NADH + H+ NAD
pyretic acid —————————-> lactic acid

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26
Q

Lactic acid and reaction

A

lactic acid is not actually formed within the cell, rather the salt lactate is. Lactate is produced in quantities equivalent to the amount of H+ so it remains a good indirect marker. lactate is a valuable fuel source.

Pyruvate lactic acid reaction: consumes 2xH+ so actually increases pH (decreases acidity). converts NADH to NAD+ allowing glycolysis and ATP generation to continue.

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27
Q

glycolysis regulatory factors

A 
[glycogen phosphorylase]
[hexokinase] (HK)
[phosphofructokinase] (PFK)
[pyruvate kinase]
O2 levels
fructose 1,6 diphosphate levels
28
Q

glycogen phosphorylase

A

converts glycogen –> glucose

activation: inc ADP, Ca2+, adrenaline
inhibition: inc ATP, inc FA

29
Q

hexokinase (HK)

A

converts glucose –> glucose-6-phosphate
has a high affinity for glucose
inhibition: inc FA and its product (-ve feedback) - important because ATP used in this step, prefer to use glycogen to produce product so HK is inhibited to spare blood glucose and ATP

30
Q

phosphofructokinase (PFK)

A

converts fructose-6-phosphate –> fructose1,6biphosphate
key rate limiting step
activation: inc fructoste-6-phospahte, inc ADP, dec CP
inhibition: inc H+, inc citrate, inc ATP, inc FA

31
Q

pyruvate kinase

A

converts phosphoenolpyruvate into pyruvate
final glycolytic step
activation: inc fructose-6-phosphate
inhibition: inc ATP, alanine

32
Q

lactate system and performance

A

the lactate system supplements for ATP-PC system when O2 supply rate is inadequate for the energy demand. primarily recruited for max efforts lasting 20-50s.

dec pH inhibits PFK. extended reliance on glycolysis for energy production results in fatigue. aerobic enzyme concentrations increase with anaerobic training.

33
Q

removal of lactate and H+ following exercise

A

following severe exercise: lactate lost in sweat, urine. glyconeogensis in liver removes 20% lactate. majority (70%) is re-oxidised to pyruvate then enters the Krebs cycle - often occurs in non working muscles and the heart.

recovery exercise: light to moderate exercise (30-50% VO2 max) improves recovery by maintaining high blood flow and oxidative functioning of working muscles. 
intense exercise (70% VO2 max) may result in further lactate production - counter productive
34
Q

aerobic energy system

A

oxidative energy system, occurs only in the mitochondria. interaction of 2 separate pathways:

  1. krebs cycle
  2. ETC

utilised for longer energy production (60+ sec), requires O2

35
Q

krebs cycle

A

citric acid cycle/tricarboxylic acid cycle (TCA)

function: complete oxidation of CHO, fats (sometimes protein). Uses NAD+ and FAD+ as H+ carriers.

36
Q

oxidation

A

the removal of H+ from a compound, or addition of O to it. (loss of e-)

37
Q

reduction

A

addition of H+ or removal of O from a compound. (gain of e-)

38
Q

reduction/oxidation NAD, FADH and fuel

A

NAD+ and FAD+ are reduced to NADH and FADH2, fuel is oxidised. as the H+ are high energy molecules, H+ carried by NADH and FADH2 to the ETC

39
Q

krebs cycle products per glucose molecule

A

acetyl CoA function: acetyl (2C) + oxaloacetate (4C) –> citrate (6C)

9 steps and 2 ‘laps’ per glucose molecule
- 4 to oxidise the fuel: 2 CO2 given off, left with 4C compound and produces 2x NADH
- 5 to regenerate the oxaloacetic acid, rearranges the compound to give 1x FADH2 and 1x NADH
(Repeat for other pyruvate)

each pyruvate produces:
1x FADH2
3x NADH
1x ATP

40
Q

ETC - e- function

A

oxidative phosphorylation occurs in the mitochondria. NADH and FADH release H+ and e- to ETC. e- are passed along a series of carriers (cytochromes)

41
Q

chemiosmotic hypothesis of ATP formation

A

e- transport causes cytochromes to pump H+ across inner mitochondrial membrane, results in H+ gradient across membrane. As H+ transported back across membrane energy released to form ATP (chemiosmotic hypothesis)
H+ and e- are accepted by O2 to form water

42
Q

factors that stimulate & inhibit glycolysis, Krebs cycle and ETC

A

inc ADP + Pi: enhances rate of glycolysis
inc NADH + H+: inhibition of Krebs cycle and inhibition of ETC
dec O2: inhibition of ETC

43
Q

ATP yield per 1 glucose

A 
glycolysis: 2x ATP, 2x NADH
pyruvate conversion to acetyl CoA: 2x (1x NADH) = 2x NADH
Krebs cycle: 
2x (3x NADH) = 6x NADH
2x (1x FADH) = 2x FADH
2x (1x ATP) = 2x ATP

total
10x NADH
2x FADH
4x ATP

total ATP = 10 x 2.5 x 2 x 1.5 + 4 = 32 ATP

44
Q

fat metabolism

A

triglyceride: glycerol + fatty acid
many different FA: differ in bonding and lengths

ATP variation varies with length of FA chain

less efficient than glucose, 15% more O2 required for FA oxidation (compared to glycolysis)

45
Q

beta (B) oxidation

- where from, activation and inhibition

A

FA broken down to acetyl CoA 2C at a time
1x ATP used
1x FADH2 and 1x NADH generated
then enters the Krebs cycle

FA utilised for energy by muscle come from

  1. triglyceride (TG) from muscle
  2. TF stored in body fat
  3. TG or FA circulating in the blood stream

lipases split FA from glycerol portion of TG

activation: inc adrenaline, inc noradrenaline, inc cortisol, inc glucagon and dec insulin
- inc SNS activity and inc release of FA and TG stores

46
Q

aerobic and anaerobic metabolism interaction (rest vs exercise)

A

at rest: most energy from aerobic metabolism: 2/3 from fats, 1/3 from CHO. VO2 = 0.3L/min, blood lactate: 1mmol/L

exercise: relative contributions dependent on mostly intensity of exercise performed, but also training state and diet of athlete

47
Q

intensity continuum

A

0-7secs: ATP-PC system. fatigue: depletion of ATP and PC
90s-6min: anaerobic glycolysis. fatigue: H+ accumulation
20min-2hr: aerobic oxidation. fatigue: dehydration, hyperthermia, depleted substrate, enzyme activity

48
Q

determining exercise intensity with tests

A 
peak power (6s sprint)
anaerobic capacity (30s Wingate)
%VO2 max
blood lactate concentration
% critical power
49
Q

VO2 max values

A

F vs M

sedentary: 2.2L/min vs 3.2L/min
trained: 3.0L/min vs 5.0L/min
endurance: 4.0L/min vs 6.0L/min

relative values important for weight bearing activities

50
Q

steady state

A

characterised by a stable VO2. HR and Ve may drift but appear stable over consecutive minutes. takes 2-3mins for O2 consumption to stabilise to new, higher level exercise demands

51
Q

limitations during aerobic exercise

A

performance limited by oxygen delivery and utilisation
VO2 = SV x a-vO2

limitations during endurance exercise (lead to exhaustion): depleted muscle and liver glycogen stores, muscle fatigue to to trauma, dehydration and electrolyte loss, inc body temperature

52
Q

blood lactate

A

marker of glycolytic energy production, allows glycolysis to continue, lactate is a good marker of internal cell environment.
accumulates as a result of: hypoxia (O2 deficiency), rapid rate of NADh production, recruitment of fast twitch muscle fibres, decreased removal of lactate.
lactate is maintained at relatively low levels, during intense exercise bouts of ~15mins - due to high level of aerobic fitness/training

53
Q

critical power (CP)

A

CP = closely correspond to highest metabolic power output for which constant [blood lactate] [PC] and VO2 are possible.
CP is a power output that can theoretically be maintained indefinitely on the basis of principally ‘aerobic’ metabolism

CP unlimited in capacity, but limited in rate - important predictor of endurance performance

54
Q

CP power asymptote

A

distance between the curve and the asymptote tends t zero as they head to infinity - power that can be maintained indefinitely

55
Q

CP and W’

A 
W' = finite work capacity (J) available to athlete when attempting power output above CP
W' = CP curvature constant

W’ is constant regardless of rate of discharge, does not reflect anaerobic capacity (changes with O2 availability)

56
Q

blood concentration changes above CP

A

above CP, steady state is unattainable, [PC] decreases and VO2 increases.
muscle pH decreases, due to increased anaerobic contribution to energy production, results in increased H+
carbonic anhydrase
CO2 + H2O H2CO3 H+ + HCO3-
Krebs cycle inc CO2, glycolysis inc H+, leads to dec pH, inc Ve and inc VO2

57
Q

fuel contributions aerobic to anaerobic

A

dependent on intensity: aerobic systems used first, if intensity is too high, anaerobic systems are increased

58
Q

fuel selection in exercise - CHO metabolism

A 
CHO: primary fuel source for short duration, incremental or high intensity exercise. major substrate used at the onset of low to moderate intensity exercise.
prolonged exercise (>30min), gradual shift from CHO metabolism to inc reliance on FA as a fuel substrate

factors regulating CHO metab
NAD+ availability, O2 availability, [H+] - inhibits PFK, inc ADP and Pi - stim glycolysis

adrenaline released during periods of high stress/heavy exercise - stim glycolysis and promotes CHO metab.
glycogen phosphorylase activated by Ca2+ release

59
Q

blood glucose homeostasis during exercise (4 processes and hormones that control)

A

plasma glucose concentration maintained through food processes

  1. mobilisation of glucose from liver glycogen
  2. mobilisation of FA from adipose tissue (spares glucose)
  3. gluconeogenesis from AA, lactic acid and glycerol
  4. blocking entry of glucose into cells (forces use of FFA as a fuel)

hormones:
fast acting: insulin, glucagon, adrenaline, noradrenaline
slow acting: cortisol, growth hormone

60
Q

insulin

A

inc cellular uptake of glucose, insulin declines during exercise of inc intensity and duration

FFA + glucose –> TG in adipose tissue
glucose –> glycogen + CO2 in muscle
glucose –> glycogen in liver

61
Q

glucagon

A

inc blood glucose levels, increases mobilisation of liver glycogen, inc liver glucose output, increased sensitivity of liver to adrenaline

adipose tissue TG –> inc FFA + glycerol available to convert to glucose
liver AA and glycerol –> glucose
liver glycogen –> glucose

62
Q

adrenaline and noradrenaline hormonal control

A

glucagon: chemoreceptors in alpha cells detect and inc glucagon release, inc liver glycogen to glucose
insulin: chemoreceptors in beta cells detect and dec insulin, inc liver glycogen to glucose

63
Q

effect of SNS on substrate mobilisation during sub maximal exercise

A

inc adrenaline/noradrenaline –> inc glucagon –> inc liver glycogen to gluc, maintains BGL

inc adrenaline/noradrenaline –> dec insulin –> inc adipose TG conversion to FFA –> inc plasma FFA

64
Q

fat metabolism - lipolysis

A

first fat (triglyceride) must be broken down via lipase into FFA, then metabolised via B-oxidation into 2C chains and oxidised in the Krebs cycle

regulation: adrenaline, noradrenaline and glucagon inc lipase activity promoting lipolysis. prolonged exercise: insulin levels decline and adrenaline inc - promote higher level of fat metabolism. lipolysis is a slow process, occurs only after several minutes of exercise.
inhibition: insulin - inhibits lipase activity, dec insulin during longer duration exercise = inc FFA and glycogen sparing. lactate - high levels promote recombination of FFA and glycerol to form fats, therefore decreasing available FFA for fuel

65
Q

changes in plasma FFA due to lactic acid

A

FFA mobilisation dependent on hormone sensitive lipase (HSL), FFA mobilisation decreased ruing heavy exercise (occurs in spite of persisting hormonal stimulation for FFA mobilisation). Due to high levels of lactic acid (promotes TG resynthesis), elevated [H+] inhibiting HSL and inadequate blood flow to adipose tissue

66
Q

protein metabolism

A

contribution to fuel supply may reach 15% depending on duration (2hr+) and diet. Skeletal muscle can directly metabolise some AA via protease function. Liver can convert AA alanine into glucose. Proteases may become active in prolonged exercise.

Ex Phys (7 decks)

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