Bioenergetics

Question 1

metabolism defn

Answer 1

sum of all chemical reactions that occur within the body

Question 2

anabolic reaction

Answer 2

synthesis of molecules, requires energy

Question 3

catabolic reaction

Answer 3

breakdown of molecules, releases energy

Question 4

bioenergetics defn

Answer 4

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

Question 5

energy to perform work - ATP

Answer 5

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

Question 6

enzymes defn

Answer 6

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

Question 7

enzyme action - induced fit model

Answer 7

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

Question 8

kinases function

Answer 8

add phosphate group to the substrates, eg creatine kinase

Question 9

dehydrogenase function

Answer 9

removes hydrogen from the substrate eg lactate dehydrogenase

Question 10

factors that alter enzyme activity

Answer 10

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

Question 11

control of bioenergetics - rate limiting enzymes

Answer 11

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

Question 12

energy systems (fn and list)

Answer 12

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

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

Question 13

order of dominant energy systems

Answer 13

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

Question 14

ATP hydrolysis

Answer 14

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

Question 15

Phosphocreatine system (PC/CP)

Answer 15

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

Question 16

ATP-PC system

Answer 16

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)

Question 17

glucose and glycogen

Answer 17

glucose general formula = C6H12O6

glycogen is a more compact storage form of glucose

Question 18

glycogenesis

Answer 18

formation of glycogen from glucose (gluc –> glyc)

Question 19

glyconeogenesis

Answer 19

formation of glycogen from substrates other than glucose

Question 20

gluconeogenesis

Answer 20

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

Question 21

glycolysis

Answer 21

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

Question 22

glycolysis - energy investment phase

Answer 22

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

Question 23

glycolysis - energy generation phase

Answer 23

not added yet

Question 24

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

Answer 24

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

Question 25

conversion of pyruvic acid to lactic acid - NADH and mitochondria

Answer 25

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

Question 26

Lactic acid and reaction

Answer 26

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.

Question 27

glycolysis regulatory factors

Answer 27

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

Question 28

glycogen phosphorylase

Answer 28

converts glycogen --> glucose activation: inc ADP, Ca2+, adrenaline inhibition: inc ATP, inc FA

Question 29

hexokinase (HK)

Answer 29

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

Question 30

phosphofructokinase (PFK)

Answer 30

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

Question 31

pyruvate kinase

Answer 31

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

Question 32

lactate system and performance

Answer 32

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.

Question 33

removal of lactate and H+ following exercise

Answer 33

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 ```

Question 34

aerobic energy system

Answer 34

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

Question 35

krebs cycle

Answer 35

citric acid cycle/tricarboxylic acid cycle (TCA) | function: complete oxidation of CHO, fats (sometimes protein). Uses NAD+ and FAD+ as H+ carriers.

Question 36

oxidation

Answer 36

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

Question 37

reduction

Answer 37

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

Question 38

reduction/oxidation NAD, FADH and fuel

Answer 38

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

Question 39

krebs cycle products per glucose molecule

Answer 39

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

Question 40

ETC - e- function

Answer 40

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

Question 41

chemiosmotic hypothesis of ATP formation

Answer 41

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

Question 42

factors that stimulate & inhibit glycolysis, Krebs cycle and ETC

Answer 42

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

Question 43

ATP yield per 1 glucose

Answer 43

``` 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

Question 44

fat metabolism

Answer 44

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)

Question 45

beta (B) oxidation | - where from, activation and inhibition

Answer 45

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

Question 46

aerobic and anaerobic metabolism interaction (rest vs exercise)

Answer 46

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

Question 47

intensity continuum

Answer 47

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

Question 48

determining exercise intensity with tests

Answer 48

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

Question 49

VO2 max values

Answer 49

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

Question 50

steady state

Answer 50

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

Question 51

limitations during aerobic exercise

Answer 51

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

Question 52

blood lactate

Answer 52

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

Question 53

critical power (CP)

Answer 53

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

Question 54

CP power asymptote

Answer 54

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

Question 55

CP and W'

Answer 55

``` 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)

Question 56

blood concentration changes above CP

Answer 56

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

Question 57

fuel contributions aerobic to anaerobic

Answer 57

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

Question 58

fuel selection in exercise - CHO metabolism

Answer 58

``` 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

Question 59

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

Answer 59

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

Question 60

insulin

Answer 60

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

Question 61

glucagon

Answer 61

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

Question 62

adrenaline and noradrenaline hormonal control

Answer 62

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

Question 63

effect of SNS on substrate mobilisation during sub maximal exercise

Answer 63

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

Question 64

fat metabolism - lipolysis

Answer 64

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

Question 65

changes in plasma FFA due to lactic acid

Answer 65

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

Question 66

protein metabolism

Answer 66

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.