Week 2 Flashcards

(43 cards)

1
Q

Bioenergetics definition?

A

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

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2
Q

Key Components of the Cell?

A

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.

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3
Q

Metabolism definition and types?

A

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).

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4
Q

Types of Cellular chemical Reactions?

A

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.

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5
Q

First Law of Thermodynamics?

A

Energy cannot be created or destroyed, only transformed.

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6
Q

Enzymes role, characteristics and classifications? ?

A

Role: Proteins that are Catalysts for reactions via lowering activation energy (by forming enzyme substrate complexes which alter shape), increasing reaction speed/product formation

Key Characteristics:
Enzymes remain unchanged after reactions.

Influenced by temperature and pH(e.g., intense exercise lowers pH due to increased H+).

Kinases: Add phosphate groups.

Dehydrogenases: Remove hydrogen atoms.

Oxidases: Facilitate oxidation-reduction.

Isomerases: Rearrange molecular structures.

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7
Q

ATP Structure, Processes and Storage?

A

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.

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8
Q

Anaerobic ATP Production Pathways?

A

Anaerobic Pathways (Do not require oxygen): Usually in cytoplasm, uses PCr, Glucose, Glycogen, Glycerol, Some delaminated, amino acids

ATP-PC System (Phosphagen System):

  • Fastest ATP production (single enzyme: creatine kinase).
  • Dominates <10–15 sec of high-intensity activity.
  • Reaction: PCr + ADP → ATP + Creatine

Glycolysis (Anaerobic):

Occurs in two phases:
- Energy investment phase
- Energy generation phase

  • Substrates: Glucose, Glycogen
    (Also minor contributions from glycerol, some amino acids)
  • Pathway Overview:
    Glycogen → Glucose-6-Phosphate → Pyruvate →

If anaerobic: → Lactate

If aerobic: → Enters mitochondria

Net ATP Yield:
- 2 ATP (from glucose)
- 3 ATP (from glycogen)

By-products:
- 2 NADH
- 2 Pyruvate or 2 Lactate

High ATP hydrolysis by-products (like ADP, Pi) stimulate glycolytic flux.

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9
Q

Aerobic ATP Production Pathways?

A

Requires oxygen and primarily occurs in the mitochondria.

Utilizes several fuel sources:

  • Fatty acids
  • Pyruvate (from glucose via glycolysis)
  • Some deaminated amino acids

Involves two main processes:

  • Citric Acid Cycle (Krebs Cycle) – generates high-energy electron carriers (NADH, FADH₂)
  • Electron Transport Chain (ETC) – uses those carriers to produce ATP through oxidative phosphorylation

This pathway is slower than anaerobic processes but produces much more ATP and supports sustained, long-duration exercise.

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10
Q

Citric Acid Cycle (Krebs Cycle)?

A

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)

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11
Q

Interactions between metabolic fuels ?

A

Beta Oxidation: Process of oxidizing fatty acids to Acetyl-CoA

No focus on proteins as not major fuel - only 2%

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12
Q

Electron Transport Chain (ETC)?

A
  • 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.
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13
Q

Aerobic ATP Yield??

A

Total ATP per Glucose (Textbook Standard):
- 32 ATP
- 2 from Glycolysis (net)
- 2 from Krebs Cycle
- 28 from Oxidative Phosphorylation (mostly NADH/FADH₂)

Alternative Historical Value:
- Up to 38 ATP per glucose (older textbooks)

ATP Yield per Electron Carrier:
- 2.5 ATP per NADH
- 1.5 ATP per FADH₂
- (Older values: 3 ATP/NADH, 2 ATP/FADH₂)

Efficiency of Energy Conversion:
- 34% of glucose’s energy is converted into ATP
- Based on:
(32 molATP × 7.3 kcal/mol / 686 kcal/molglucose)
× 100 ≈ 34 %

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14
Q

Control of bioenergetics? Examples?

A

Biochemical pathways are regulated by very precise control systems which are:
Rate-Limiting Enzymes:

  • Early-stage control in pathways.
  • Regulated by ATP availability and modulators.

Examples:

  • ATP-PC: Creatine kinase, ADP stimulates, ATP inhibits
  • Glycolysis: PFK, AMP,ADP, Pi and Increase pH stimulate, ATP, CP, Citrate and decrease pH Inhibit
  • Krebs: Isocitrate dehydrogenase, ADP, Ca+, NAD+ stimulate, ATP and NADH inhibit
  • ETC: Cytochrome oxidase, ADP,Pi stimulate, ATP inhibits
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15
Q

Intensity and Duration influences on systems contribution of energy metabolism?

A

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.

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16
Q

Hormonal Control of Substrate Mobilization?

A

During exercise or periods of energy demand, the body must rapidly access fuel sources to supply muscles and organs. Hormones act as chemical messengers that regulate this process

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.
    — Prepare tissues to respond by upregulating enzymes and receptors
  • Fast-acting hormones: Epinephrine, norepinephrine, insulin, and glucagon.
    — Rapidly adjust metabolism during stress or exercise by promoting glycogen breakdown, fat release, or glucose uptake
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17
Q

4 Key processes to maintain blood Glucose Homeostasis During Exercise ?

A
  1. Liver glycogen mobilization→ Releases glucose.
  2. FFA mobilization from adipose tissue→ Spares blood glucose.
  3. Gluconeogenesis→ Formation of glucose from non-carbohydrate sources.
  4. Blocking glucose entry into cells→ Encourages fat metabolism
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18
Q

Key Hormonal Regulators? Role?

A

• Thyroid Hormones (T3 & T4): Enhance effects of other hormones by increasing receptor number and affinity. T3 boosts epinephrine’s ability to mobilize fatty acids from fat stores (ineffective without T3). Levels remain stable during exercise, but hypothyroidism impairs hormone-driven fuel mobilization and lowers metabolic rate.

• Growth Hormone (GH): Promotes fat use, protein synthesis, and long bone growth, while reducing glucose use—helping preserve blood glucose during exercise. GH rises with intensity; e.g., after 60 mins at 60% VO₂max, levels are 5–6× higher than at rest. Used medically (e.g., childhood dwarfism), but high doses have adverse effects. No solid evidence it boosts strength or has anti-aging benefits; use is hard to detect in athletes.

• Cortisol: A steroid hormone from the adrenal cortex that helps maintain blood glucose. Stimulated by stress (via ACTH) and exercise. Levels rise with intensity and vary by time of day (highest in the morning). Effects are slow, acting through gene expression, likely contributing more to post-exercise tissue repair than immediate fuel mobilization

19
Q

Functions of Catecholamines (Epinephrine & Norepinephrine)?

A

Released from the adrenal medulla as part of the “fight or flight” response

Fast-acting hormones that:

  • Increase heart rate (HR)
  • Elevate blood pressure (BP)
  • Boost metabolic rate

Act on alpha (α) and beta (β) adrenergic receptors

  • Specific effects vary depending on the hormone and receptor type
20
Q

Catecholamines (Epinephrine & Norepinephrine) during exercise? Actions? Adaptations?

A

Catecholamines (epinephrine & norepinephrine) rise with exercise intensity and activate the sympathetic nervous system (SNS).

Key Actions:

  • Act via cyclic AMP/adenylate cyclase pathway.
  • β1 receptors → stimulate glycogenolysis & lipolysis.
  • β3 receptors → stimulate lipolysis.
  • Increase heart rate, blood pressure, and vascular tone.

Training Adaptations:

  • Trained individuals have ~35% greater catecholamine capacity.
  • Chronic endurance training reduces SNS response to a fixed workload.
  • Plasma glucose remains more stable in trained individuals; SNS fine-tunes hormone secretion instead.
21
Q

Catecholamines Links to glycogen depletion?

A
  1. Glycogenolysis and Exercise Intensity
  • Higher exercise intensity → faster & greater glycogen depletion.
  • Glycogenolysis is strongly linked to how hard you’re working.
  1. Role of Epinephrine (a catecholamine)
  • Stimulates glycogen breakdown:
  • Inhibits insulin (reduces glucose uptake/storage)
  • Enhances glucagon (promotes glucose release)
  • Result: Increased blood glucose to fuel activity.
  1. Plasma Epinephrine & Exercise
  • Intense exercise → higher levels of plasma epinephrine.
  • Correlates with increased glycogen breakdown.
  1. Control of Muscle Glycogen Breakdown

Redundant control system:

  • Both local (muscle-based) and systemic (hormonal, e.g., epinephrine) pathways exist.
  • Glycogenolysis can occur without epinephrine, but epinephrine still enhances it.
22
Q

Role of Pancreas?

A

The pancreas has both exocrine (via ducts) and endocrine (directly into the blood) functions.

Its endocrine role involves secretion of key counter-regulatory hormones from the islets of Langerhans:

Insulin (from β-cells):

  • Promotes glucose uptake and storage in tissues.
  • Decreases during exercise to allow glucose mobilization for energy.
  • Drives uptake and storage of substrates (e.g., glucose, fatty acids), lowering their levels in the plasma.

Glucagon (from α-cells):

  • Promotes glucose release (from glycogen) and gluconeogenesis (glucose formation from non-carb sources).
  • Increases during exercise, though this response may be blunted in trained individuals.

The glucagon-to-insulin ratio is crucial in regulating the mobilization of glucose and free fatty acids (FFA) during exercise and fasting.

23
Q

Energy Requirements at Rest?

A

At rest, almost 100% of ATP is produced via aerobic metabolism.

Blood lactate levels remain low, typically below 1.0 mmol/L, indicating minimal anaerobic activity.

Resting oxygen consumption (VO₂):

  • Absolute VO₂: ~0.25 L/min
  • Relative VO₂: ~3.5 mL/kg/min → defined as 1 MET (Metabolic Equivalent of Task)
24
Q

Rest-to-Exercise Transitions?

A

ATP production increases immediately when exercise begins to meet rising energy demands.

Oxygen uptake (VO₂) rises rapidly, with steady-state typically reached within 1–4 minutes depending on intensity and fitness level.

Once steady-state is achieved, aerobic metabolism becomes the primary source of ATP.

However, during the initial moments of exercise, anaerobic pathways provide most of the ATP:

  • ATP-PC system (phosphocreatine breakdown)
  • Glycolysis (anaerobic breakdown of glucose)

This early reliance on anaerobic systems creates an oxygen deficit—a temporary mismatch between oxygen demand and oxygen supply.

25
Training Adaptations of endurance training?
Endurance-trained individuals experience a lower oxygen deficit at the onset of exercise due to several key adaptations: - Improved aerobic capacity – better ability to produce ATP aerobically. - Increased mitochondrial volume – enhances oxidative metabolism. - More efficient blood supply to active muscles – improved oxygen delivery and waste removal. These adaptations lead to faster transitions to steady-state exercise and reduced reliance on anaerobic energy systems early in exercise.
26
Recovery from Exercise?
- **Oxygen uptake remains elevated** post-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.
27
EPOC Components?
1. **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**. 2. **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)**.
28
Factors influencing EPOC?
- **Exercise intensity** → Higher intensity = larger EPOC. - **Exercise duration** → Longer exercise = prolonged EPOC.
29
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.
30
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 shifts **fuel use toward carbohydrates**.
31
Factors Governing Fuel Selection?
A. Exercise Intensity - Crossover Concept: As exercise intensity increases, the body shifts from primarily fat metabolism to carbohydrate metabolism. - Fast-twitch muscle fibers favor glycolysis (carbohydrate use) over fat metabolism. - Increased epinephrine levels during high-intensity exercise: - Stimulate glycolysis - Inhibit fat metabolism B. Exercise Duration - During prolonged exercise (>2 hours), the body gradually shifts toward greater fat metabolism due to glycogen depletion. - Glycogen is essential for maintaining Krebs cycle intermediates: → “Fats burn in the flame of carbohydrates.” - Consuming 30–60 g of carbohydrates per hour during prolonged exercise can help sustain performance and delay fatigue.
32
Lactate and Fatigue?
**Lactate Threshold** - The point where blood **lactic acid rises systematically** during exercise. - **Untrained individuals**: 50–60% VO₂max. - **Trained individuals**: 65–80% VO₂max. - **Onset of Blood Lactate Accumulation (OBLA)** occurs at **>4 mmol/L**.
33
Causes of Lactate Accumulation?
1. **Hypoxia (low muscle oxygen levels)**. 2. **Accelerated glycolysis** (excess pyruvate → lactate). 3. **Fast-twitch fiber recruitment** (prefer lactate production). 4. **Reduced lactate clearance** (liver, kidneys, and heart use lactate as fuel).
34
Does Lactate Cause Muscle Soreness?
- **NO!** - **Lactate removal is rapid** (~60 min post-exercise). - **Delayed Onset Muscle Soreness (DOMS)** is caused by **microscopic muscle damage**, not lactate.
35
Lactate as a Fuel Source?
- **Lactate Shuttle Hypothesis**: Lactate is transported to **other tissues** for oxidation. - **Cori Cycle**: Lactate is transported to the **liver**, converted into **glucose**, and sent back to muscles.
36
Electron carrier molecules?
For glycolysis to continue, sufficient NAD⁺ must be available to accept hydrogen ions (H⁺). This means NAD⁺ must be rapidly regenerated from NADH to sustain ATP production. Two Main Pathways to Regenerate NAD⁺: 1. Aerobic Conditions (with sufficient O₂): - H⁺ from NADH is shuttled into the mitochondria, where it enters the Electron Transport Chain (ETC) to produce ATP. - NAD⁺ is regenerated during this process. 2. Anaerobic Conditions (lack of O₂): - Pyruvate accepts the H⁺ from NADH to form lactate. - This reaction is catalyzed by lactate dehydrogenase. - This process allows continued recycling of NAD⁺ so glycolysis can proceed even without oxygen. Key point: Lactate formation enables glycolysis to continue under anaerobic conditions by regenerating NAD⁺.
37
Interaction of fat/CHO metabolism?
During prolonged (>2 hours) high-intensity exercise, muscle glycogen becomes depleted. This leads to: - Decreased glycolysis and reduced pyruvate production — a key precursor for Krebs cycle intermediates. - Reduced Krebs cycle activity, which slows down the rate of aerobic ATP production. Since fats are oxidized within the Krebs cycle, this reduction in intermediates also lowers the rate of fat oxidation. "Fats burn in the flame of carbohydrates" → Fat metabolism depends on carbohydrate availability to maintain Krebs cycle function. As muscle and blood CHO stores decline, the body’s ability to maintain energy output drops, contributing to fatigue. Consuming 30–60 g of carbohydrate per hour (e.g., sports drinks) during prolonged exercise can help: - Maintain CHO availability - Support fat oxidation - Delay fatigue and improve endurance performance
38
Impact of exercise intensity on fat metabolism? What intensity is best for burning fat?
Fat metabolism is influenced by both the percentage of energy coming from fat and the total energy expended. At low exercise intensities (around 20% of VO₂ max), a high percentage (~66%) of the energy comes from fat. However, because total energy expenditure is low (about 3 kcal/min), the actual amount of fat burned is also low (about 2 kcal/min). At moderate intensities (around 60% of VO₂ max), a lower percentage (~33%) of the energy comes from fat, but overall energy expenditure is much higher (around 9 kcal/min). This results in a greater total amount of fat burned (about 3 kcal/min), despite the lower percentage. FATmax: - FATmax is the point at which your body burns fat at its highest absolute rate. - It usually occurs just below the lactate threshold. - This makes it the most effective intensity for fat burning, especially during prolonged, steady-state exercise.
39
Sources of fuel supply during exercise? And influences?
Carbohydrate Storage: Liver glycogen: - Mixed diet: 60 g (240 kcal or 1005 kJ) - High-CHO diet: 90 g (360 kcal or 1507 kJ) - Low-CHO diet: <30 g (120 kcal or 502 kJ) Glucose in blood and extracellular fluid: - All diets: 10 g (40 kcal or 167 kJ) Muscle glycogen: - Mixed diet: 350 g (1400 kcal or 5860 kJ) - High-CHO diet: 600 g (2400 kcal or 10,046 kJ) - Low-CHO diet: 300 g (1200 kcal or 5023 kJ) Fat Storage (Fat Mixed Diet): - Adipocytes: 14 kg (107,800 kcal or 451,251 kJ) - Muscle triglycerides: 0.5 kg (3850 kcal or 16,116 kJ)
40
Influences of intensity and duration on fuel source?
The relative contribution of muscle glycogen and blood glucose changes depending on both the intensity and duration of exercise. At higher intensities: - There is an increased rate of glycogenolysis (breakdown of glycogen) due to: - Greater recruitment of fast-twitch muscle fibers - Elevated blood epinephrine levels, which stimulate glycogen breakdown During prolonged submaximal exercise (around 65% to 75% VO₂ max): - Immediate energy sources stored in the muscle become depleted over time. - This leads to an increased reliance on blood-borne substrates (like glucose and free fatty acids) to maintain energy supply.
41
Changes in plasma insulin during exercise?
During moderate-intensity exercise, plasma insulin concentrations can decrease by approximately 50%. This decline helps to favor the mobilization of glucose from the liver and free fatty acids (FFA) from adipose tissue, making more fuel available for working muscles. After an endurance training program, the glucagon response during exercise is often diminished, sometimes showing little to no increase, reflecting improved metabolic efficiency.
42
Summary of the hormonal responses to exercise?
Maintaining adequate fuel supply for exercising muscles while preserving plasma glucose concentration—especially for the brain’s needs—is a complex process. Multiple hormones coordinate this task by mobilizing fats and carbohydrates to meet energy demands. All key hormones involved, except insulin, act to increase blood glucose availability and promote fuel mobilization. Insulin decreases during exercise, reducing glucose uptake by non-essential tissues and allowing more glucose to remain in the blood for active muscles and the brain.
43
Hormone-substrate interaction?
During exercise, several hormones rise that promote mobilization of free fatty acids (FFA) from adipose tissue. However, despite this hormonal stimulation, FFA oxidation actually decreases during heavy exercise. Possible reasons for this paradox include: - High levels of lactic acid produced during intense exercise. - Increased H⁺ concentration inhibits hormone-sensitive lipase (HSL), reducing fat breakdown. - Reduced blood flow to adipose tissue, limiting FFA release. - Insufficient albumin in plasma to transport FFAs effectively. - As a result, there is a decrease in FFA use and a compensatory increase in glucose utilization during heavy exercise. Impact of Endurance Training: Endurance training lowers lactate concentrations at any given exercise intensity, reducing the inhibitory effects on FFA mobilization. Combined with a training-induced increase in mitochondrial volume, trained individuals can: - Use more fat as fuel - Spare limited carbohydrate stores - Improve endurance performance