Week 2 Flashcards
Bioenergetics definition?
The flow and exchange of energy within a living system, primarily the conversion of foodstuffs (fats, proteins, carbohydrates) into usable energy for cellular work.
How this relates to performance - energy systems etc. Chemical > Mechanical
Key Components of the Cell?
Cell Membrane (Sarcolemma): Semipermeable, separates the cell from its environment.
Nucleus: Houses genes for protein synthesis.
Cytoplasm (Sarcoplasm in muscle): Fluid portion containing organelles.
Mitochondria: Site of oxidative phosphorylation.
Metabolism definition and types?
Sum of all chemical reactions in the body.
Anabolic Reactions: Synthesis of molecules (e.g., glucose stored as glycogen).
Catabolic Reactions: Breakdown of molecules (e.g., glycogen into glucose).
Types of Reactions?
Endergonic: Require energy input to be added to reactants
Exergonic: Release energy.
Coupled Reactions: Energy from exergonic reactions drives endergonic reactions (e.g., ATP hydrolysis).
Oxidation-Reduction Reactions:
Oxidation: Electron removal.
Reduction: Electron addition.
Nicotinamide adenine dinucleotide (NAD) and Flavin adenine dinuceotide (FAD) act as carrier molecules in bioenergetic reactions.
First Law of Thermodynamics?
Energy cannot be created or destroyed, only transformed.
Enzymes role and characteristics ?
Role: Catalysts that lower activation energy, increasing reaction speed/product formation
Key Characteristics:
Enzymes remain unchanged after reactions.
Influenced bytemperatureandpH(e.g., intense exercise lowers pH due to increased H+).
Enzyme classifications?
Kinases: Add phosphate groups.
Dehydrogenases: Remove hydrogen atoms.
Oxidases: Facilitate oxidation-reduction.
Isomerases: Rearrange molecular structures.
ATP Structure, Processes and Storage?
Structure: High-energy phosphate molecule.
Processes:
- Synthesis: ADP + Pi → ATP.
- Breakdown: ATP → ADP + Pi + Energy.
Storage: Limited intramuscular stores; sufficient for <2 seconds of all-out exercise.
Anaerobic ATP Production Pathways?
Anaerobic Pathways (Do not require oxygen):
ATP-PC System:
Rapid, single-enzyme reaction.
Dominates in activities <10–15 seconds.
PC + ADP → ATP + Creatine (via creatine kinase).
Glycolysis:
Increase in by-products of ATP hydrolysis = ^ activation of energy flux through reactions
Breakdown of glucose/glycogen.
Produces 2 ATP (glucose substrate) or 3 ATP (glycogen substrate).
Ends in 2 NADH and either 2 pyruvate or 2 lactate (anaerobic condition).
Aerobic ATP Production Pathways?
(Requires oxygen):
Involves oxidative phosphorylation.
Citric Acid Cycle (Krebs Cycle) and Electron Transport Chain (ETC) are key components
Citric Acid Cycle (Krebs Cycle)?
Pyruvate (from glycolysis) → Acetyl-CoA → Citrate
Net gain = - 1 ATP per cycle, 3 NADH and 1 FADH2 for the ETC, CO2 as a byproduct.
Process
1. Glycolysis generates 2 molecules of
pyruvate
2. Pyruvic acid (3-C) enters the mitochondria
and is converted to acetyl-CoA (2-C), losing
a carbon (generating CO2)
3. Acetyl-CoA combines with oxaloacetate (4-
C) to form citrate (6-C)
4. Series of reactions to regenerate
oxaloacetate (generating 2 CO2 molecules).
5. Each turn of the cycle, 1 ATP molecule is
synthesized from guanosine triphosphate
(GTP: high-energy compound) with the
release of high-energy electrons (3 NADH
and 1 FADH2)
Interactions between metabolic fuels ?
Beta Oxidation: Process of oxidizing fatty acids to Acetyl-CoA
No focus on proteins as not major fuel - only 2%
Electron Transport Chain (ETC)?
- NADH and FADH2 donate electrons Which are passed along series of carriers (cytochromes).
- Coupled with Proton (H+) pumping into intermembrane space, this pump creates an electrochemical gradient.
- ATP is produced as protons diffuse back across the membrane, through ATP synthase channel, energy from this channel drives production of ATP.
- Oxygen is the final electron acceptor, combining with hydrogen forming water. This is vital as without OP is not possible.
Aerobic ATP Yield?
32 ATP per glucose molecule (textbook standard). Total with all process combined = 38 ATP (32 = OP, 4 = G (2 net as 2 used), 2 = Krebs)
2.5 ATP per NADH, 1.5 per FADH, Historically = 3, 2
Efficiency: 34% of energy from glucose is converted into ATP.
Equation: 32 moles ATP/mole glucose 7.3 kcal/mole ATP / 686 kcal/mole glucose x 100 = 34%
Biochemical pathways are regulated by very precise control systems?
Rate-Limiting Enzymes:
- Early-stage control in pathways.
- Regulated by ATP availability and modulators.
Exercise Metabolism with Intensity and Duration influences?
Short-term, High-Intensity Exercise (<5s):
- ATP-PC system dominates.
Moderate-Intensity Exercise (5–45s):
- Shift to glycolysis.
Longer Duration (>45s):
- Mix of anaerobic and aerobic systems.
Prolonged Exercise (>10 mins):
- Predominantly aerobic metabolism.
Hormonal Control of Substrate Mobilization?
Hormones regulate the mobilization of:
Glucose from liver glycogen.
Free Fatty Acids (FFA) from adipose tissue.
Key hormone types:
Slow-acting (Permissive) hormones: Thyroxine, cortisol, and growth hormone.
Fast-acting hormones: Epinephrine, norepinephrine, insulin, and glucagon.
4 Key processes to maintain blood Glucose Homeostasis During Exercise ?
- Liver glycogen mobilization→ Releases glucose.
- FFA mobilization from adipose tissue→ Spares blood glucose.
- Gluconeogenesis→ Formation of glucose from non-carbohydrate sources.
- Blocking glucose entry into cells→ Encourages fat metabolism
Key Hormonal Regulators?
Thyroid hormones (T3 & T4): Enhance other hormones’ effects.
Growth hormone (GH): Promotes fat utilization, protein synthesis, and reduces glucose use.
Cortisol: Supports glucose maintenance, increases with exercise intensity.
Functions of Catecholamines (Epinephrine & Norepinephrine)?
- Released from the adrenal medulla.
- Increase HR, BP, and metabolic rate.
- Bind toalpha (α) and beta (β) adrenergic receptorsto stimulate different responses.
Catecholamines (Epinephrine & Norepinephrine) Effects during exercise?
- Increase with intensity.
- Stimulate glycogenolysis and lipolysis.
- Reduce response after endurance training.
Catecholamines affects on insulin & glucagon?
Epinephrine suppresses insulinandenhances glucagon, leading to increased blood glucose.
Insulin & Glucagon?
Insulin (from β-cells in the pancreas):
- Promotes glucose uptake & storage.
- Decreases during exerciseto allow glucose mobilization.
Glucagon (from α-cells in the pancreas:
- Promotes glucose release & gluconeogenesis.
- Increases during exercise(except in trained individuals).
Hormone-Substrate Interaction & FFA Utilization?
- Exercise stimulates fat mobilization, but FFA oxidationdecreases at high intensitydue to:
- Increased**lactate levels.
- ElevatedH+ concentration(lowers fat breakdown).
- Reduced blood flow to adipose tissue
- Limited**albumin transport of FFAin the plasma.
- Endurance training reduces lactate levels, allowing greater fat oxidation.
Energy Requirements at Rest?
Almost100% of ATPis produced byaerobic metabolism.
Blood lactate levels remain low(<1.0 mmol/L).
Restingoxygen consumption (VO₂):
- 0.25 L/min(absolute)
- 3.5 mL/kg/min (relative) →1 MET (Metabolic Equivalent of Task.
Rest-to-Exercise Transitions?
- ATP production increases immediatelywhen exercise begins.
-
Oxygen uptake increases rapidly:
- Steady-state reached within1–4 minutes.
- At steady-state,aerobic metabolismis the primary ATP producer.
-
Initial ATP productionis supplied byanaerobic pathways:
- ATP-PC system(phosphocreatine breakdown).
- Glycolysis(anaerobic breakdown of glucose).
- This creates anoxygen deficit(temporary imbalance between demand and supply).
Training Adaptations of endurance training?
-
Endurance-trained individualshave alower oxygen deficitbecause of:
- Better-developed aerobic capacity.
- Increased mitochondrial volume.
- More efficient blood supplyto active muscles.
Recovery from Exercise?
- Oxygen uptake remains elevatedpost-exercise.
-
Excess Post-Exercise Oxygen Consumption (EPOC)replaces the outdated concept of “oxygen debt”:
- Only ~20%of elevated O₂ consumption is used to repay the O₂ deficit.
EPOC Components?
-
Rapid Phase(occurs in the first 2 minutes):
- Re-synthesis of phosphocreatine (PCr). - Usually within 60-120s
- Replenishment of muscle (myoglobin) and blood (haemoglobin) O₂ stores.
-
Slow Phase:
- Elevated HR and breathing→ increased energy demand.
- Increased body temperature→ higher metabolic rate.
- Elevated levels of epinephrine & norepinephrine→ higher metabolism.
- Lactic acid conversion to glucose (gluconeogenesis).
Factors influencing EPOC?
- Exercise intensity→ Higher intensity = larger EPOC.
- Exercise duration→ Longer exercise = prolonged EPOC.
Fuels for Exercise? Source, Store, Breakdown process
Carbohydrate - Glucose (4 kcal/g), stored as glycogen in muscles and liver, glycogenolysis
Fats - Fatty acids (9 kcal/g), triglycerides in muscles and adipose tissue, lipolysis
Proteins - Amino acids (4kcal/g), not a primary source, Gluconeogenesis.
Estimation of Fuel Utilization?
Respiratory Exchange Ratio (RER)estimates fuel use.
RER = VCO₂ / VO₂
- Fat oxidation: RER ~0.70(16 CO₂ / 23 O₂).
- Carbohydrate oxidation: RER ~1.00(6 CO₂ / 6 O₂).
- Higher intensity exercise shiftsfuel use toward carbohydrates.
Factors Governing Fuel Selection?
Exercise Intensity:
- “Crossover Concept”: Shift fromfattocarbohydratemetabolism as intensity increases.
- Fast-twitch muscle fibers favorglycolysis(CHO metabolism).
- Increasedepinephrinelevels stimulate glycolysis and inhibit fat metabolism.
B. Exercise Duration:
- Prolonged exercise (>2 hours) shifts toward fat metabolismdue to glycogen depletion.
- Glycogen is necessary for Krebs cycle intermediates →“Fats burn in the flame of carbohydrates.”
- Consuming30–60 g of CHO/hourcanimprove endurance performance.
Lactate and Fatigue?
Lactate Threshold
- The point where bloodlactic acid rises systematicallyduring exercise.
- Untrained individuals: 50–60% VO₂max.
- Trained individuals: 65–80% VO₂max.
- Onset of Blood Lactate Accumulation (OBLA)occurs at>4 mmol/L.
Causes of Lactate Accumulation?
- Hypoxia (low muscle oxygen levels).
- Accelerated glycolysis(excess pyruvate → lactate).
- Fast-twitch fiber recruitment(prefer lactate production).
- Reduced lactate clearance(liver, kidneys, and heart use lactate as fuel).
Does Lactate Cause Muscle Soreness?
- NO!
- Lactate removal is rapid(~60 min post-exercise).
- Delayed Onset Muscle Soreness (DOMS)is caused bymicroscopic muscle damage, not lactate.
Lactate as a Fuel Source?
- Lactate Shuttle Hypothesis: Lactate is transported toother tissuesfor oxidation.
- Cori Cycle: Lactate is transported to theliver, converted intoglucose, and sent back to muscles.
