Midterm: ch 6, 7, 21, 15-17 Flashcards

1
Q

Discuss two contributions of high-energy phosphates for energizing biologic work

A
  1. Conserve energy from food in ATP bonds, 2. extract and transfer chemical energy in ATP to power work
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List 2 important functions of carbohydrate in energy metabolism

A
  1. Provide the only macro substrate for anaerobic glycolysis, 2. Creates intermediates needed for fat catabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Discuss dynamics of lactate formation and accumulation during increasing exercise intensity

A
  • At <50% of aerobic capacity, blood lactate production = blood lactate clearance. Rapid and large accumulation occurs during max PA of 60-180 sec.
  • Some lactate produced at low PA/rest, thru metabolism of RBCs and limitations by enzyme activity in muscle fibers.
  • When it forms, it diffuses into interstitial space and blood for removal, or provides gluconeogenic substrate for glycolysis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Discuss the role of the citric acid cycle (aerobic) in energy metabolism

A
  • Releases last 95% of energy in glucose, happens when pyruvate converts to acetyl CoA. The CAC degrades acetyl CoA to Co2 and hydrogen atoms. ATP formed when hydrogen oxidizes during electron transport oxidative phosphorylation.
  • 34 ATP is total yield
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Contrast ATP yield from catabolism of a molecule of carbohydrate, fat, and protein.

A
  • Fat: 460 ATP, plentiful source of energy. Becomes primary energy fuel for exercise and recovery when intense, long duration exercise depletes both blood glucose and muscle glycogen. Aerobic.
  • Protein: After deamination, the remaining carbon skeleton produces ATP aerobically.
  • Carb: only anaerobic! Supplies about ⅓ of bodys energy requirement during light and moderate physical activity. 32 ATP.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain the meaning of: “fats burn in a carbohydrate flame”

A

FAs require intermediates generated in carb breakdown for continual catabolism to produce energy in the metabolic mill → fats burn in carb flame. Acetyl Coa enters CAC by combining with oxaloacetate to form citrat (key step). Oxaloacetate then reforms from pyruvate from carb breakdown. Conversion is under enzymatic control of pyruvate carboxylase which adds a carboxyl group to the pyruvate molecule. Only continues if theres sufficient oxaloacetate to combine w the acetyl CoA formed during beta oxi.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Outline the interconversions among carbohydrate, fat, and proteins

A

Carbs → fats or nonessential AAs
Fats → nonessential AAs
Proteins → carbs or fats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe lactate threshold.

A

occurs when muscle cells can neither meet energy demands aerobically nor oxidize lactate at its rate of formation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe lactate threshold differences between sedentary and endurance-trained individuals.

A
  • Untrained: lactate accumulation starts at 50-55% of max aerobic capacity.
  • Trained persons perform SR aerobic exercise at 80-90% of max aerobic capacity due to: genetics, local training adaptations, more rapid lactate removal at any intensity.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the pattern of oxygen uptake during progressive increments of exercise intensities to maximum.

A

O2 uptake initially rises exponentially before plateau, then remains in SR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Differentiate between type 1 and type 2 muscle fibers.

A
  • Fast twitch: rapid contraction speed and high capacity for anaerobic ATP production in glycolysis, highly active in change of pace and stop and go activities. Type IIA - high aerobic capacity.
  • Slow twitch: generates energy thru aerobic pathways, slower contraction speed than fast twitch fibers, active in continuous activities requiring steady rate aerobic energy transfer.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Discuss differences in recovery oxygen uptake from light, moderate, and intense exercise.

A

Recovery VO2 follows a logarithmic curve, decreasing by 50% over each subsequent 30 sec period until reaching pre exercise levels. Light activity with rapid steady state VO2 attainment produced a small O2 deficit with rapid recovery VO2. moderate to intense aerobic activity requires a longer time to achieve steady rate VO2. this creates a larger O2 deficit with a longer recovery time for the VO2 to restore resting levels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List three factors that account for excess post-exercise oxygen consumption.

A

Body temperature, blood returning to lungs from active muscles, restoring oxygen dissolved in bodily fluids and bound to myoglobin within muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Discuss the rationale for intermittent exercise applied to interval training

A

•Produces rapid recovery and enables subsequent intense exercise to begin following a brief recovery.
•Manipulating the duration of exercise and rest intervals can effectively overload an energy system of choice.
- Relative balance between energy requirements during PA and aerobic energy transfer within muscles.
- Rapid recovery in O2 uptake, because high energy phosphates supply most energy, minimal reliance on glycolysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Discuss and provide examples of the exercise training principles of overload, specificity, individual differences, and reversibility.

A
  • Overload: manipulating frequency, intensity and/or duration
  • Specificity: Specificity of local changes - definition, greater BF in active tissue - results from incr microcirculation, more effective redistribution of CO, combined effect of both. Only happens in muscle being trained
    specificity of vo2max: aerobic overload requirements: engage appropriate muscles required by activity, provide exercise a level sufficient to stress the cardiovascular system. Little improvement is noted when measuring aerobic capacity with dissimilar exercise.
  • Individual differences
  • Reversibility: detraining rapidly occurs when terminating a training program. Only 1-2 wks of detraining reduces metabolic and exercise capacity. Beneficial effects of prior training remain transient and reversible.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Outline the metabolic adaptations to anaerobic exercise.

A

1) Incr. levels of anaerobic substrates.
2) Incr quantity and activity of key enzymes that control the anaerobic phase of glucose catabolism.
3) Incr capacity to generate high levels of blood lactate during all-out exercise:-Increased levels of glycogen and glycolytic enzymes-Improved motivation and tolerance to “pain”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Metabolic adaptations to aerobic exercise training

A

•Aerobic training improves capacity for respiratory control in skeletal muscle.
•Endurance-trained skeletal muscle fibers contain larger and more numerous mitochondria than less active fibers.
•Mitochondrial enzyme activity increases by 50%.
• Increased intramuscular fatty acid oxidation via:
1)Greater blood flow within trained muscle.
2)More fat-mobilizing and fat-metabolizing enzymes.
3)Enhanced muscle mitochondrial respiratory capacity.
4)Decreased catecholamine release for the same absolute power output.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cardiovascular adaptations to aerobic exercise training

A

Cardiac hypertrophy, incr plasma volume, decr RHR, incr SV → incr max CO, incr O2 extraction, greater BF distribution, incr in capillaries, decr BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pulmonary adaptations to aerobic exercise training

A

Incr VE, incr tidal volume, lower % Total exercise O2 cost → incr exercise endurance, decr breathing frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ATP - limited energy source

A

ATP, a limited currency: cells have to constantly resynthesize ATP (at its rate of usage) because they only contain a small amount. ATP levels in muscle only decrease in extreme conditions.
Major energy transforming activities: extract potential energy from food and conserve it within the ATP bonds, extract and transfer the chemical energy in ATP to power biological work.
ADP forms when ATP joins with water, catalyzed by the enzyme adenosine triphosphate (ATPase).
Body stores 80-100g of ATP at any time under normal rest, enough to power ⅔ sec of max exercise.

21
Q

PCr - energy reservoir

A

Fat and glycogen are the main energy source for ATP resynthesis. Some energy also comes from anaerobically splitting a phosphate from phosphocreatine (PCr) → also an intracellular high energy phosphate compound. ATP and PCr provide anaerobic sources of phosphate-bond energy. The energy freed from hydrolysis of PCr rebonds the ADP and Pi to form ATP. training increases the muscles’ quantity of high energy phosphates. P + Cr = PCr. ADP + P = ATP. PCr hydrolysis catalyzed by creatine kinase derives ADP phosphorylation to ATP. cells store 4-6x more PCr than ATP. PCr is a reservoir of high energy phosphate bonds. ADP phosphorylation > energy transfer for stored muscle glycogen ← because of high activity rate of creatine kinase.
Cells store 4-6x more PCr than ATP, PCr reaches max energy yield in 10 sec. The adenylate kinase reaction represents another single enzyme mediated reaction for ATP regeneration.

22
Q

Cellular oxidation

A
Most energy for phosphorylation comes from oxidation of dietary carbs, lipid and protein macros. Molecule accepts electrons from a donor → becomes reduced, the donor becomes oxidized. Provides hydrogen atoms from the catabolism of stored macros. Mitochondria carrier molecules remove electron from hydrogen (oxidation) and pass them to oxygen (reduction). 
Oxidation reactions (those that donate electrons) and reduction reactions (those that accept electrons) are coupled and constitute the biochemical mechanism that underlies energy metabolism. This process continually provides hydrogen atoms from the catabolism of stored macronutrients. 
The mitochondria contain carrier molecules that remove electrons from hydrogen (oxidation) and eventually pass them to oxygen atoms (reduction), ATP synthesis occurs during redox reactions. 
During cellular oxidation, hydrogen atoms are not merely turned loose in intracellular fluids. Substrate specific dehydrogenase enzymes catalyze hydrogens release from the nutrient substrate. The coenzyme component of the dehydrogenase accepts pairs of electrons from hydrogen. Nicotinamide adenine dinucleotide (NAD+)gains hydrogen and two electrons and reduces to NADH;the other hydrogen appears as H+ in the cell fluid. Flavin adenine dinucleotide (FAD) serves as another electron acceptor and becomes FADH2 by accepting two hydrogens.
23
Q

Electron transport

A

During cellular oxidation, NAD+ (in dehydrogenase enzyme) accepts pairs of electrons from hydrogen, when the enzyme catalysez hydrogen’s release from nutrient substrate.
→ NAD+ gains hydrogen + 2 electrons and reduces to NADH (the other hydrogen is H+ in the cell fluid)
→ FAD is another electron acceptor (to oxidize food fragments) - it catalyzes dehydrogenation and accepts electron pairs. FAD becomes FADH2 by accepting both hydrogens.
The cytochromes, a series of iron protein electron carriers dispersed on the inner membranes of the mitochondrion, then pass in bucket brigade fashion pairs of electrons carried by NADH and FADH2.
Electron transport represents the final common pathway where electrons extracted from hydrogen pass to oxygen. Mitochondrial oxygen levels drive the respiratory chain by serving as the final electron acceptor to combine with hydrogen to form water. For each pair of hydrogen atoms, two electrons flow down the chain and reduce one atom of oxygen to form one water molecule. During the passage of electrons down the chain, enough energy is released to phosphorylate ADP to ATP.

24
Q

Macronutrient fuel sources

A

Energy release in macro catabolism aims to phosphorylate ADP to reform the energy rich compound ATP. 3 stages: 1. Digestion, absorption and assimilation of large food macromolecules into smaller subunits for use in cellular metabolism. 2. Degrades amino acid, glucose, fatty acid and glycerol units within the cytosol into acetyl-coenzyme A, with limited ATP and NADH production. 3. Within the mitochondrion, acetyl-coenzyme A degrades to CO2 and H2O with considerable ATP production.
6 fuel courses that supply substrate for ATP production:
- Triacylglycerol and glycogen molecules stored within muscle cells
- Blood glucose (derived from liver glycogen)
- Free fatty acids *derived from triacylglycerols in liver and adipocytes)
- Intramuscular and liver derived carbon skeletons of amino acids
- Anaerobic reactions in the cytosol in the initial phase of glucose or glycogen breakdown (small amount of ATP)
- Phosphorylation of ADP by PCr under enzymatic control by creatine kinase and adenylate kinase

25
Q

Energy release from carbs

A

Carbs provide the only macro substrate whose stored energy generates ATP without oxygen (anaerobically),important in activities requiring rapid energy release above levels supplied by aerobic metabolism - intramuscular glycogen supplies most of the energy for ATP resynthesis. Supplies about ⅓ of bodys energy requirement during light and moderate physical activity. Processing a large quantity of fat for energy requires minimal carb catabolism. Aerobic breakdown of carbs for energy occurs more rapidly than energy generation from FA breakdown. The CNS requires carbs to function - the brain uses blood glucose as fuel. Complete breakdown of one mole of glucose to carbon dioxide and water yields a max of 686 kcal of chemical free energy available for work.

26
Q

Anaerobic vs aerobic glycolysis

A

Glycolysis - a series of fermentation reactions, with two forms of carb breakdown: lactate, formed from pyruvate, becomes end product. In the other, pyruvate remains the end product. W pyruvate as the end substrate, carb catabolism proceeds and couples to further break down in the citric acid cycle with subsequent electron transport production of ATP. Carb breakdown of this form is a slow process resulting in substantial ATP formation (aerobic glycolysis). Rapid but limited ATP production comes from glycolysis that results in lactate formation (anaerobic). Need for ATP production speed determines the form of glycolysis! The glycolytic process itself does not involve oxygen.
Rapid: pyruvate to lactate formation with the release of about 5% of energy within the original glucose molecule. Slow: results in pyruvate to acetyl coenzyme A to CAC and electron transport of the remaining energy within the original glucose molecule.
Glucose degradation occurs in two stages: 1. Glucose breaks down rapidly into two molecules of pyruvate. Energy transfer for phosphorylation is anaerobic. 2. Pyruvate degrades further to carbon dioxide and water. energy transfers from these reactions require electron transport and accompanying oxidative phosphorylation (aerobic).
Anaerobic energy release from glucose: rapid glycolysis
Occurs in the watery medium of the cell outside the mitochondrion. More primitive form of rapid energy transfer - in humans, the cell capacity for glycolysis is crucial during max effort phys act for up to 90 sec. Glycolysis = a series of 10 enzymatically controlled chemical reactions create two molecules of pyruvate from the anaerobic breakdown of glucose. Lactate forms when NADH oxidation does not keep pace with its formation in glycolysis.

27
Q

Glycolysis - process, what happens to pyruvate

A

Glycolysis = a series of 10 enzymatically controlled chemical reactions create two molecules of pyruvate from the anaerobic breakdown of glucose. Lactate forms when NADH oxidation does not keep pace with its formation in glycolysis.
Aerobic glycolysis (slow): the citric acid cycle. CAC is second stage of carb breakdown to produce co2 and hydrogen atoms within mitochondria.
CAC slows down if insufficient oxaloacetate. Where are we getting energy from carb? Electron transport is bang for buck.
Phase 1: pyruvate from glycolysis (get some ATP), need to have coenzyme A to produce acetyl CoA → CAC. rich source of hydrogen ions!
Complete breakdown of glucose yields 34 ATPs, net is 32 ATP. 28 are from oxidative phosphorylation. Best bang for buck but slowest when oxygen is present.
Lactate dehydrogenase catalyzes the reaction of pyruvate to lactate.
In cytosol, anaerobic; phosphocreatine, glycose/glycogen, glycerol, some deaminated AAs. citric acid cycle: in mitochondrion, aerobic; fatty acids, pyruvate from glucose, some deaminated AAs.
Three factors regulate glycolysis: levels of the substrate fructose 1,6-diphosphate, oxygen (when abundant, oxygen inhibits glycolysis), concentration of 4 key enzymes
Concentration of four key enzymes: hexokinase, phosphorylase, phosphofructokinase, pyruvate kinase
Pyruvate can irreversibly bind to acetyl CoA and enter the CAC when there is an abundance of oxygen present. During strenuous physical activity, when energy demands exceed oxygen supply or its rate of use, the respiratory chain cant process all the hydrogen joined to NADH. continued release of anaerobic energy requires NAD+ to oxidize 3-phosphoglyceraldehyde .
During anaerobic glycolysis, NAD+ regenerates when pairs of hydrogens combine with pyruvate to form lactate. Lactate formation requires one additional step, catalyzed by lactate dehydrogenase, in a reversible reaction

28
Q

Lactate vs lactic acid

A

Lactic acid is an acid formed during anerobic glycolysis that quickly dissociates to release a hydrogen ion (H+). the remaining compound binds with a positively charged sodium (or potassium) ion to form the acid salt called lactate.

29
Q

Citric acid cycle

A

CAC is second stage of carb breakdown to produce co2 and hydrogen atoms within mitochondria.
CAC slows down if insufficient oxaloacetate. Where are we getting energy from carb? Electron transport is bang for buck.
Phase 1: pyruvate from glycolysis (get some ATP), need to have coenzyme A to produce acetyl CoA → CAC. rich source of hydrogen ions!
Complete breakdown of glucose yields 34 ATPs, net is 32 ATP. 28 are from oxidative phosphorylation. Best bang for buck but slowest when oxygen is present.
The formation of acetyl CoA from pyruvate is irreversible, FAD is involved in only one operation in the cycle, an acetyl group joins with oxaloacetate to produce citrate.
Rapid glycolysis releases only about 5% of the total energy within glucose; the remaining energy releases when pyruvate converts to acetyl-CoA and enter the CAC.

30
Q

Energy release from fatty acids and glycerol

A

460 ATP, depends on the number of carbons. Stored fat is a plentiful source of energy. Becomes primary energy fuel for exercise and recovery when intense, long duration exercise depletes both blood glucose and muscle glycogen.
Beta oxidation: glucose forms pyruvate w acetyl coa, can go into CAC and produce ATP. if we have triglyceride molecule and combine w water (hydrolysis) we can separate glycerol fra FAs. glycerol can go over and into CAC eventually - its a carbon structure, and a precursor that can enter cycle. Three FAs enter Beta oxi, creates large number of hydrogens that can go to ETC.
For each 18 carbon FA molecule, 147 molecules of ADP phosphorylate to ATP during beta oxi and CAC metab. Each TCG molecule contains 3 FA molecules to form 441 ATP molecules from the FA components (3x147 ATP) . 19 ATP molecules form during glycerol breakdown to generate 460 molecules of ATP for each TCG molecule catabolized.

31
Q

Steps to break down fat

A

Lipid mobilization (steps to break down fat) - 7 steps:
Breakdown of TCG to FFAs - liberate the carbon chain from its attachment
Transport of FFA in the blood
Uptake of FFAs from blood to muscle (where it’ll be oxidized)
Prep of FAs for catabolism
Entry of activated FAs into muscle mitochondria
Breakdown of FAs into acetyl-CoA via beta oxidation (breakdown of fat) and prod of NADH and FADH2 - yields a nr of hydrogen NAD, FADH that can go to electron transport
Couples oxidation in CAC And electron transport chain (ETC)

32
Q

Hormonal effects on fat breakdown

A

Epinephrine, norepinephrine, glucagon and GH augment lipase activity. The metabolism of lipid is complicated , endocrine effort. Hormonal release triggered by exercise stimulates adipose tissue lipolysis to further augment FFA delivery to active muscle.

33
Q

Protein breakdown

A

When used for energy metabl, AA must convert to a form that can enter energy pathways - requires removal of nitrogen from the AA. after deamination, the remaining carbon skeleton can enter metabolic pathways to produce ATP aerobically. Glucogenic AAs: when deaminated, they yield intermediates for glucose synthesis. Ketogenic AA: when deaminated, they yield intermediates acetyl COa fro TAG formation.

34
Q

ATP-PCr energy system

A

High intensity exercise of short duration (10 sec) requires immediate energy from intramuscular ATP and PCr
Each kg of skeletal muscle contains 3-8 mmol of ATP and 4-6x more PCr

35
Q

Short term glycolytic energy system - anaerobic

A

energy to phosphorylate ADP during intense, short duration exercise comes mainly from stored muscle glycogen breakdown via anaerobic glycolysis with resulting lactate formation. Rapid and large accumulation of blood lactate occurs during max exercise of 60-180 sec. Decr exercise intensity is one way to lower lactate accumulation.
One molecule of glucose will have a net production of 2 moles of ATP when degraded in anaerobic glycolysis.

36
Q

Lactate producing capacity

A

High blood lactate levels during max exercise incr w specific sporting power anaerobic training and decr when training ceases due to improved motivation, inct intramuscular glycogen stores, training induced incr in glycolytic related enzymes.

37
Q

Long term energy: aerobic system

A

aerobic metabolism provides nearly all energy transfer when exercise is beyond a few min. O2 uptake initially rises exponentially before plateau, then remains in SR. ST aerobic metabolism reflects balance between energy required by working muscles and ATP production in aerobic reactions - no appreciable lactate accumulates under SR metabolic conditions.

38
Q

Limits of steady rate aerobic metabolism

A

SR could theoretically progress indefinitely , assuming that AR aerobic metabolism determines capacity to sustain submax exercise. Two limiting factors: fluid loss and electrolyte depletion, maintaining adequate reserves of liver glycogen and muscle glycogen. Individuals possess many SR levels during exercise depending on training level.

39
Q

Many levels of steady rate

A

Two factors can help explain high SR levels: high capacity of the central circulation to deliver oxygen to working muscles, and high capacity of the active muscle to use oxygen.

40
Q

Maximal oxygen consumption

A

Vo2max occur when o2 uptake plateaus, provided quantitative measure of ap persons capacity for sustained aerobic ATP resynthesis, indicated ability to maintain intense exercise for longer than 4-5 min.
High vo2 max required high level responses of hemoglobin concentration, pulmonary ventilation, aerobic metabl, peripheral blood flow, blood volume and CO.
Four factors determine vo2max: arterial o2 saturation (how much o2 bound to hemoglobin), mixed venous saturation (extraction), o2 capacity of the blood (how much hemoglobin), circulation rate (CO). ventilation, central BF, active muscle metabl, peripheral BF → improvement in these will improve o2 uptake.

41
Q

Energy spectrum of physical activity

A

Energy for PA from each energy transfer form progresses along a continuum. In intense brief exercise the intramuscular high energy phosphates supply almost all of the energy for exercise. The ATP-PCr and lactic acid systems supply about half the energy for intense exercise lasting 2 min with aerobic reactions supplying the remainder. Long duration endurance exercise requires a constant aerobic energy supply with little reliance on energy transfer from anaerobic sources.

42
Q

Implications of EPOC for exercise and recovery

A

resynthesize ATP and PCr, resynthesize lactate to glycogen oxidize lactate, resort o2 to myoglobin and blood, restore thermogenic effects of elevated temp, thermogenic effects of hormones, restored elevated heart rate, ventilation and other functions.
No appreciable lactate accumulates w SR aerobic exercise or brief 10-15 second bouts of all out effort. Recovery progresses rapidly and exercise can begin again with only a brief rest period and passive recovery. Lactate buildup occurs during prolonged anaerobic exercise so recovery VO2 takes longer to return to baseline. Athletes attaining a high level of anaerobic metabolism during exercise may not fully recover during brief intermittent rest intervals of less intense exercise.
Active recovery: incl submax exercise may prevent muscle cramps and stiffness and facilitate overall recovery. Passive recovery: individual lies down w minimal energy expenditure, which is believes to reduce the recovery energy requirements and thus “Free” oxygen to fuel the recovery process.

43
Q

Relationship between %HRmax and %VO2max

A
% HRmax - % Vo2max
50 - 28
60 - 40
70 - 58
80 - 70
90 - 83
100  - 100
44
Q

Blood lactate concentration

A

Endurance training lowers blood lactate levels and extends exercise duration before onset of blood lactate accumulation during exercise of increasing intensity by:
Decr rate of lactate formation during exercise
Incr rate of lactate clearance during exercise
Combined effects of both

45
Q

Clamping and infusing lactate - what happens to the rate of glucose oxidation?

A

Decreased glucose oxidation by exercising muscle resulted in a decreased demand for blood glucose and consequently decreased glucose production to maintain blood glucose homeostasis. With exogenous lactate infusion, lactate incorporation into glucose increased and the contribution of glycogenolysis to glucose production decreased.

46
Q

Oxidative phosphorylation

A

OP synthesizes ATP by transferring electrons from NAD:H and FADH2 to oxygen. More than 90% of ATP synthesis takes place in the respiratory chain by oxidative reactions coupled with phosphorylation. Energy transfer from NADH to ADP to reform ATP happens at 3 coupling sites during electron transport. If FADH2 originally donates hydrogen, only 2 ATP molecules form for each hydrogen pair oxidized. This occurs because FADH2 enters the respiratory chain at a lower energy level at appoint beyond the site of the first ATP synthesis. On average, oxidation of one NAD:H produced 2.5 molecules of ATP and oxidation of FADH2 produces 1.5 molecules of ATP.
3 prerequisites exist for continual resynthesis of ATP during couples oxidative phosphorylation:
Tissue availability of the reducing agent NADH or FADH2
Presence of the oxidizing agent oxygen in tissues
Sufficient concentration of enzymes and mitochondria to ensure that energy transfer reactions proceed at the appropriate rate

47
Q

Glucose → glycogen and glycogen → glucose conversion

A

Glycogenesis (glycogen synthesis): surplus glucose forms glycogen in low cellular activity. The enzyme glycogen synthase facilitates the linking of glucose molecules into large glycogen molecules.
Glycogenolysis (glycogen breakdown): glycogen reserves breakdown to produce glucose in high cellular activity with glucose depletion. The enzyme glycogen phosphorylase removes a glucose form the glycogen chain.

48
Q

HIIT for disease

A

Exercise stimulates cardiorespiratory function and substrate mobilization and oxidation. Exercise training improves glycaemic control in individuals w type II diabetes, but the precise training regimen that confers the most beneficial metabolic adaptations in this population is unknown.
Resistance training promotes hyupertrophy allowing for more powerful contractions fuelled by glycolysis and supported by higher lactate dehydrogenase content. All training types improve skeletal muscle glucose transport and glycogen synthesis capacity, expanding glycogen stores and improving glycaemic control.
Glycemic effects of different training intensity: HIIT confers superior glycaemic improvement
Training with low carbohydrate availability: training in a low carb state is achieved by several methods:
Fasting overnight before exercise bout, depletes liver glycogen content and lowers carb availability
Training twice a day depletes skeletal muscle glycogen content during the first exercise bout, allowing the second bout to be initiated with low carb availability
The sleep low strategy encompasses both, by depleting skeletal muscle glycogen through an evening bout of exercise and liver glycogen by fasting, before the second bout of exercise in the morning
In individuals with type 2 diabetes, superior glycaemic improvements can be achieved through high intensity exercise in postprandially or low intensity exercise under fasted conditions