Advanced strength + conditioning (Exam 1)

what is strength?

the ability to produce force or torque agains an external stimulus.

• shows up in our daily life

Strength = survival

• 50% higher likelihood of early death among older adults classified as “weak”

How does muscle weakness affect health-care costs?

Adults with muscle weakness (low grip strength) have higher annual health-care costs.

Muscle weakness is associated with increased costs for:

• Primary care

• Secondary/inpatient care

• Prescriptions

• Formal care

• Informal care

What are the 3 functional types of neurons?

1. Afferent (sensory) neurons

• Receptors → CNS

• Cell body located in PNS

• Bring sensory information IN to CNS

2. Efferent (motor) neurons

• CNS → muscles/glands/other neurons

• Cell body located in CNS

• Carry commands OUT from CNS

3. Interneurons

• Located in CNS

• 
  

99% of all neurons

• Integrate/connect afferent and efferent neurons

Memory: Afferent = Arrives at CNS; Efferent = Exits CNS.

What are the basic components of a neuron and their functions?

Dendrites → receive information

Cell body (soma) → processes/integrates information; contains the nucleus → “command module”

Axon → sends information away from the cell body to other neurons or target cells (e.g., muscle fibers)

Memory: Dendrites IN → Soma PROCESSES → Axon OUT

How does the axon conduct an action potential?

Axon → conducts the action potential (AP) away from the cell body, beginning at the axon hillock.

Myelin sheath → fatty insulating layer covering the axon that increases conduction speed.

Nodes of Ranvier → gaps between sections of myelin along the axon.

Saltatory conduction → AP “jumps” from one Node of Ranvier → the next.

Result → increases conduction velocity without increasing axon diameter.

Memory: Myelin = insulation → AP jumps node-to-node → faster conduction.

What is a motor unit?

Motor unit = 1 alpha-motor neuron + ALL muscle fibers it innervates

• One motor neuron can innervate 100s–1000s of muscle fibers

• Each muscle fiber has only ONE neuromuscular junction (NMJ)

• All muscle fibers within a motor unit contract together when stimulated

Memory: 1 motor neuron → many muscle fibers → all contract together

What is the innervation ratio, and how does it relate to movement precision?

Innervation ratio = # of muscle fibers ÷ # of α-motor axons innervating them

It represents the average motor unit (MU) size.

Large innervation ratio → many fibers per motor unit → large/gross movements

• Ex: Gastrocnemius ≈ 1,934 fibers/MU

Small innervation ratio → few fibers per motor unit → small/precise movements

• Ex: Rectus lateralis (eye) ≈ 5 fibers/MU

Memory: More fibers = more force, less precision; fewer fibers = more precision.

What is an action potential (AP), and what are its main phases?

Action potential = a rapid, large change in membrane potential used for fast, long-distance communication.

Occurs in excitable cells → nerves, muscles, glands.

Resting membrane potential ≈ −70 mV

1. Depolarization → voltage-gated Na⁺ channels open → Na⁺ enters → membrane becomes more positive

2. Repolarization → voltage-gated K⁺ channels open → K⁺ exits → membrane becomes more negative again

May briefly hyperpolarize before returning to resting potential.

Memory: Na⁺ IN = Depolarize → K⁺ OUT = Repolarize

How does an action potential (AP) propagate through a neuron?

1. AP is initiated at the axon hillock (trigger zone).

2. AP propagates along the axon → axon terminals.

3. Propagation occurs through activation of voltage-gated ion channels along the axon.

Memory: Axon hillock → Axon → Axon terminals

What is the all-or-none principle for motor units?

Motor unit (MU) activation depends on reaching a voltage threshold.

Threshold reached → ALL muscle fibers in that motor unit contract

Threshold NOT reached → NONE of the muscle fibers contract

• You cannot activate only some fibers within a single motor unit.

• A “larger” action potential does NOT cause a stronger contraction; APs are all-or-none.

Memory: Hit threshold = ALL. Miss threshold = NONE.

How does the CNS increase muscle force?

Muscle force is primarily controlled by 2 mechanisms:

1. Motor unit recruitment → activate more motor units

2. Rate coding → increase the firing rate of active motor units

↑ Recruitment + ↑ firing rate → ↑ muscle force

Memory: More motor units + faster firing = more force.

What is the motor unit size principle?

Motor units are recruited in an orderly fashion as force demand increases:

Low-threshold Type I → high-threshold Type II

• Type I: recruited first → lower force demands

• Type II: recruited later → higher force demands

• At a given force, firing rate and recruitment threshold are inversely related → lower-threshold MUs tend to fire faster than higher-threshold MUs (“onion skin” phenomenon).

Memory: Small/slow first → large/fast last.

How does the size principle determine motor unit recruitment?

Motor units are recruited from low → high threshold as force demand increases:

Type I → Type IIa → Type IIx

• Low-threshold MUs: recruited first, lower force production

• High-threshold MUs: recruited later, greater force production

• To recruit high-threshold MUs, the lower-threshold MUs must already be recruited.

↑ force demand → ↑ number/size of motor units recruited

Memory: You must recruit the small ones before the big ones.

How does resistance training affect motor unit recruitment?

Resistance training causes a neural adaptation that allows:

• Faster recruitment of motor units

• Earlier recruitment of high-threshold MUs

• More complete recruitment of available MUs

This helps explain why strength can increase before significant muscle hypertrophy occurs.

To recruit high-threshold, high-force fibers → load/effort must be high enough to reach their activation threshold.

Memory: Training → faster + more complete recruitment → early strength gains.

How does firing frequency affect motor unit force?

As firing frequency increases → force increases:

Single twitch → twitch summation → unfused tetanus → fused tetanus

• Single twitch = one stimulus/contraction

• Summation = twitches overlap → ↑ force

• Unfused tetanus = repeated contractions with partial relaxation

• Fused tetanus = sustained contraction with no relaxation → maximal force

Overall muscle force is increased by:

1. Recruiting more motor units

2. Increasing firing rate (rate coding)

Memory: ↑ frequency → ↑ summation → ↑ force → tetanus.

Nueromuscular physicology (Part 2) …

What is a motor unit?

A motor unit = 1 alpha-motor neuron + ALL the muscle fibers it innervates (ON QUIZ)

• The α-motor neuron controls when its muscle fibers contract.

• When the motor neuron fires → all fibers in that motor unit contract (all-or-none).

• One motor neuron can innervate many muscle fibers.

Memory: 1 neuron → all of its fibers = 1 motor unit.

What is the neuromuscular junction (NMJ)?

The NMJ = the synapse/interface between an α-motor neuron and a muscle fiber.

• NMJ signaling is always excitatory → initiates muscle contraction, never inhibits.

• Each muscle fiber has only ONE NMJ.

• The NMJ allows the motor neuron's electrical signal to activate the muscle fiber → excitation-contraction coupling.

Think: Motor neuron → NMJ → muscle fiber → contraction.

What are the steps of excitation-contraction coupling at the NMJ?

1. AP travels down the motor neuron → reaches axon terminal

2. Voltage-gated Ca²⁺ channels open → Ca²⁺ enters axon terminal

3. Ca²⁺ triggers synaptic vesicles → ACh released into synaptic cleft

4. ACh binds receptors on the motor end plate → Na⁺ channels open → Na⁺ enters

5. Creates a large end-plate potential (EPP) → depolarizes the sarcolemma

Sequence:
AP → Ca²⁺ IN → ACh release → Na⁺ IN → EPP → muscle depolarization

What happens after the muscle fiber is depolarized during excitation-contraction coupling?

5. AP travels along the sarcolemma → T-tubules

6. T-tubule DHP receptor (voltage sensor) activates the ryanodine receptor (RyR) on the sarcoplasmic reticulum

7. RyR opens → Ca²⁺ released from SR → sarcoplasm

8. Ca²⁺ is now available to bind troponin → initiate contraction

Sequence:
AP → T-tubule → DHP → RyR → Ca²⁺ out of SR → troponin → contraction

What are the 3 connective tissue layers of skeletal muscle?

Epimysium → surrounds the entire muscle (outer layer)

Perimysium → surrounds each fascicle (bundle of muscle fibers)

Endomysium → surrounds each individual muscle fiber

Outside → inside:
Epimysium → Perimysium → Endomysium

What are the major structural components of a muscle fiber?

Myofibrils → cylindrical bundles of thick + thin filaments within muscle fibers

Sarcomere → functional/contractile unit of muscle; extends Z-line → Z-line

Z-line → defines sarcomere boundaries; anchors thin filaments

Titin → connects myosin (thick filament) → Z-line

Cross-bridges → globular myosin heads that project toward/bind thin filaments

Thick filament → myosin

• 2 heavy chains + 4 light chains

Thin filament → actin + tropomyosin + troponin

High-yield:
Thick = myosin
Thin = actin + tropomyosin + troponin

What is the A band of a sarcomere?

A band → spans the entire length of the thick (myosin) filaments

• Includes areas where myosin overlaps with actin

• Centered around the M line

• Does NOT change length during contraction

High-yield: A band = All of the thick filament.

What is the I band of a sarcomere?

I band → lighter region containing only thin (actin) filaments

• No thick/myosin filaments

• Contains the Z-line

• Shortens during muscle contraction

High-yield: I band = thIn filaments only.

hat is the H zone of a sarcomere?

H zone → contains only thick (myosin) filaments

• No thin/actin filaments

• Located in the center of the A band

• Contains the M line

• Shortens/decreases during contraction

High-yield: H zone = tHick only.

What is the M line of a sarcomere?

M line → anchors thick (myosin) filaments together

• Located at the center of the sarcomere

• Located in the center of the H zone

• Helps keep thick filaments aligned

High-yield: M = Middle + Myosin.

What happens during the sliding filament theory of muscle contraction?

Myosin cross-bridges pull actin (thin filaments) toward the center/M-line → sarcomere shortens.

During contraction:

• I band ↓

• H zone ↓

• A band stays SAME

• Z-lines move closer together

• Actin and myosin do NOT shorten → they slide past each other

High-yield: A = Always same; I + H shrink.

only H and I change sizes during contraction…

NO CHANGE in sarcomere during isometric

eccentric is Active

What is the role of ATP in cross-bridge cycling?

ATP has 2 key roles:

1. ATP binds myosin → myosin DETACHES from actin

2. ATP hydrolysis → energizes/cocks the myosin head for the next contraction

⚠ No ATP → myosin cannot detach from actin → rigor mortis.

Memory: ATP = Detach + Recharge.

What happens in Step 1 of cross-bridge cycling?

ATP → ADP + Pi via myosin ATPase

→ ADP + Pi remain bound to myosin
→ Energy from ATP hydrolysis cocks/energizes the myosin head
→ Myosin is ready to bind actin

Step 1 = ATP hydrolysis → cock the myosin head.

What happens in Step 2 of cross-bridge cycling?

↑ Ca²⁺ released from SR → Ca²⁺ binds troponin → tropomyosin moves → exposes myosin-binding sites on actin → energized myosin binds actin → cross-bridge forms

Memory: Ca²⁺ → Troponin → Tropomyosin moves → Actin exposed → Myosin binds.

What happens in Step 3 of cross-bridge cycling (power stroke)?

Myosin head bends/pivots → pulls actin toward the center (M-line) of the sarcomere → ADP + Pi are released.

Step 3 = Power stroke → Pull actin → Release ADP + Pi.

⚠ Small correction to the slide: actin is pulled toward the M-line, not the Z-line.

What happens in Step 4 of cross-bridge cycling (detachment)?

New ATP binds myosin → myosin DETACHES from actin.

Then ATP is hydrolyzed → myosin head re-cocks/energizes → cycle repeats if Ca²⁺ remains present.

Memory: New ATP = LET GO of actin.

What happens during muscle relaxation?

Nerve stimulation stops → Ca²⁺ pumped back into SR → Ca²⁺ leaves troponin → tropomyosin re-covers actin binding sites → cross-bridge cycling stops → muscle relaxes.

Memory: ↓ Ca²⁺ → actin sites covered → no myosin binding → relaxation.

Why does rigor mortis occur?

After death → ATP runs out → myosin cannot detach from actin → actin-myosin cross-bridges remain locked → muscle becomes rigid.

Memory: No ATP = No detachment = Rigor mortis.

Bioenergetics…

Why is bioenergetics important for human movement?

• Food (carbohydrates, fats, proteins) provides chemical energy

• Chemical energy is used to produce ATP

• ATP provides energy for cellular activity and mechanical work (movement)

• ATP → ADP + Pi releases energy

• Some energy is released as heat

• Energy = capacity to do work

What is bioenergetics, and how does the first law of thermodynamics apply to it?

• Bioenergetics = flow of energy in a living system; conversion of macronutrients into biologically usable energy

• First law of thermodynamics = energy cannot be created or destroyed, only transformed

• Chemical energy from food can be converted into:

  • Work

  • Heat

  • Stored energy molecules

What are catabolism and anabolism?

Catabolism = breakdown of larger molecules → smaller molecules + releases energy

Anabolism = synthesis of smaller molecules → larger molecules + requires energy

Key distinction:
Catabolism = breaks down, releases energy
Anabolism = builds up, requires energy

What are exergonic vs. endergonic reactions, and how do they relate to metabolism?

Exergonic = releases energy → generally catabolic
Example: glycolysis

Endergonic = requires energy → generally anabolic
Example: protein synthesis

Energy released by exergonic reactions is used to drive endergonic reactions.

Metabolism = total sum of all chemical reactions occurring in the body’s cells.

Why is bioenergetics important when designing training programs?

Identify the predominant energy system for the activity → design an effective, individualized training program.

Energy system determines:

• Intensity

• Duration

• Work-to-rest ratio

• Exercise mode

As maximal exercise duration increases:
Phosphocreatine → dominates first, rapidly decreases
Glycolytic → increases early, then decreases
Aerobic → gradually increases and becomes predominant

Key idea: Train the specific energy pathways required by the sport/activity.

What is the role of ATP in the body?

ATP (adenosine triphosphate) = universal energy currency of cells

• Directly provides energy for cellular processes

• All energy systems ultimately function to resynthesize ATP

• ATP → ADP + Pi releases usable energy

• ATP must continually be resynthesized because cellular activities constantly use it

Key idea: Food fuels cannot directly power cellular work → their energy is transferred to ATP → ATP powers cellular work.

How does ATP provide energy for muscle contraction?

• ATP fuels the actomyosin cross-bridge cycle

• Energy is associated with the bond involving the terminal (3rd) phosphate

• ATPase breaks down ATP

ATP → ADP + Pi + energy

Released energy is used for muscle contraction.

What occurs during ATP hydrolysis, and why must ATP be continually resynthesized?

ATP hydrolysis = breakdown of ATP to release energy

ATP + H₂O → ADP + Pi + H⁺ + energy

• Catalyzed by ATPase

• Energy released fuels muscle contraction and other cellular processes

• Body stores only ~80–100 g of ATP

• Because ATP stores are limited but demand is constant → ATP must be continually resynthesized

How do the energy systems contribute during exercise, and what is the rate vs. capacity tradeoff?

All energy systems are always active → exercise demand determines which dominates.

• Phosphocreatine (PCr) = fastest ATP production, lowest capacity → dominates first

• Glycolytic = intermediate rate and capacity → contributes most during short-duration exercise

• Aerobic/oxidative = slowest ATP production, highest capacity → dominates prolonged exercise

Key idea: Faster ATP production = lower capacity; greater capacity = slower ATP production.

How does the phosphagen (PCr) system rapidly resynthesize ATP?

Phosphagen system = fastest ATP-producing system

Creatine phosphate (CP/PCr) donates a phosphate to ADP → rapidly reforms ATP

ADP + PCr → ATP + creatine
Enzyme = creatine kinase (CK)

• Very high rate of ATP production

• Very low capacity because PCr stores are small

• CK highest in Type IIx muscle fibers

• Important for short, high-intensity strength/power activities

Key idea: PCr acts as an immediate energy reserve to rapidly replenish ATP.

What happens to ATP and PCr during maximal sprinting?

• ATP is continuously broken down but rapidly resynthesized → levels initially remain relatively stable

• PCr rapidly donates phosphate to regenerate ATP → PCr levels fall quickly

• PCr stores are limited → PCr depletion becomes a limiting factor during maximal sprinting

• As PCr becomes depleted → ATP eventually declines → contributes to fatigue/exhaustion

Key idea: PCr drops much faster than ATP because PCr is being used to maintain ATP levels.

What is glycolysis?

Glycolysis = breakdown of carbohydrates to resynthesize ATP

Fuel sources:

• Muscle glycogen

• Blood glucose

• Does NOT require O₂ → anaerobic

• Occurs in the sarcoplasm

Key idea: Glycolysis breaks down glucose/glycogen to rapidly produce ATP without

What is the ATP investment and payoff of glycolysis?

Glucose:

• Investment = 2 ATP used

• Payoff = 4 ATP produced

• Net gain = 2 ATP

• Produces 2 pyruvate

Muscle glycogen:

• Net gain = 3 ATP per glycogen-derived glucose

Key idea: Glycolysis from glycogen yields 1 extra ATP because it bypasses the first ATP-requiring step.

What determines the fate of pyruvate after glycolysis?

Depends on O₂ availability and ability of mitochondria to metabolize pyruvate.

Fast (anaerobic) glycolysis:

• Glycolysis exceeds aerobic metabolism

• Pyruvate → lactate

• Associated H⁺ accumulation → ↓ pH → contributes to fatigue

Slow (aerobic) glycolysis:

• Glycolysis matches aerobic metabolism

• Pyruvate + NADH enter mitochondria

• Pyruvate proceeds through Krebs/TCA cycle and ETC

Key idea: Fast glycolysis → lactate; slow glycolysis → mitochondrial oxidation.

What happens to lactate produced during glycolysis?

• Pyruvate → lactate via lactate dehydrogenase (LDH)

• Lactate is associated with fatigue but is not necessarily the cause

• Highest lactate concentrations occur in Type II muscle fibers

• Blood lactate = balance between lactate production and clearance

• Greatest accumulation occurs with high-intensity, intermittent exercise

Cori cycle:
Lactate → bloodstream → liver → converted back to glucose via gluconeogenesis

Key idea: Lactate is not simply a waste product; it can be recycled into glucose.

How does H⁺ accumulation contribute to muscle fatigue?

↑ H⁺ from ATP hydrolysis → ↓ pH (acidosis)

Muscle pH:

• Resting ≈ 7.1

• Exercise can ↓ to 6.4–6.6

H⁺ contributes to fatigue by:

• ↓ enzyme activity

• ↓ actin-myosin binding affinity

• ↓ O₂-carrying capacity of hemoglobin

Key idea: H⁺ accumulation, rather than lactate itself, contributes to fatigue during high-intensity exercise.

What are lactate threshold (LT) and onset of blood lactate accumulation (OBLA)?

Lactate Threshold (LT) = exercise intensity where blood lactate begins to abruptly rise above baseline

• Indicates increased reliance on anaerobic metabolism

OBLA = point where blood lactate reaches 4 mmol/L

• Lactate production > lactate clearance

Training effect:

• Trained individuals reach LT at a higher exercise intensity

• Higher LT = can sustain greater intensity before rapid lactate accumulation

Key distinction: LT = initial abrupt rise; OBLA = 4 mmol/L.

Does lactate cause DOMS, and how is lactate cleared after exercise?

Lactate does NOT cause DOMS.

Lactate fate:

• ~70% oxidized → used as fuel by heart/skeletal muscle

• ~20% → converted back to glucose

• ~10% → converted to amino acids

Lactate clearance:

• Light exercise clears lactate faster than complete rest

• Optimal active recovery ≈ 30–40% VO₂ max

Key idea: Lactate is rapidly cleared/reused after exercise and does not cause delayed-onset muscle soreness.

What is the oxidative energy system and how does it produce ATP?

Oxidative system = primary ATP source at rest and during low-intensity/prolonged activity

Fuel:

• Carbohydrates + fats

• Protein = minimal contribution

Fat pathway:
Triglycerides → free fatty acids → mitochondria → β-oxidation → acetyl-CoA

Then:
Acetyl-CoA → Krebs cycle → NADH/FADH₂ → ETC → ATP

Key idea: Oxidative system = slow ATP production but very high capacity; requires mitochondria and O₂.

What determines oxidative capacity?

3 main factors:

• Oxidative enzyme levels → ↑ enzyme activity = faster Krebs cycle + ETC

• Fiber-type composition → Type I fibers have high oxidative capacity

• Oxygen availability → depends on cardiac output, capillary density, and hemoglobin

Key idea: Oxidative capacity depends on the muscle’s ability to use O₂ and the body’s ability to deliver O₂.

What is cardiorespiratory endurance and VO₂ max?

Cardiorespiratory endurance = ability of the whole body to sustain prolonged aerobic exercise

VO₂ max = highest rate of O₂ consumption during maximal exercise

• Major measure of aerobic fitness

• Important for exercise performance + cardiovascular health

• Assessed using a graded exercise test (GXT)

Key idea: Higher VO₂ max = greater capacity to take in, transport, and use oxygen during maximal exercise.

What are the major requirements for endurance success?

• High VO₂ max

• High economy of effort

• High lactate threshold

• High percentage of slow-twitch (Type I) muscle fibers

Key idea: Endurance success requires high aerobic capacity + efficient movement + ability to sustain high intensity aerobically.

What is the relationship between the rate and capacity of ATP production?

Rate = how fast ATP can be produced
Capacity = total amount of ATP that can be produced

Inverse relationship: ↑ rate → ↓ capacity

Fastest rate → slowest:
Phosphagen > fast glycolysis > slow glycolysis > carbohydrate oxidation > fat/protein oxidation

Capacity is the opposite order.

Key idea: Phosphagen = fastest but lowest capacity; fat oxidation = slowest but highest capacity.

What is the relationship between the rate and capacity of ATP production?

Rate = how fast ATP can be produced
Capacity = total amount of ATP that can be produced

Inverse relationship: ↑ rate → ↓ capacity

Fastest rate → slowest:
Phosphagen > fast glycolysis > slow glycolysis > carbohydrate oxidation > fat/protein oxidation

Capacity is the opposite order.

Key idea: Phosphagen = fastest but lowest capacity; fat oxidation = slowest but highest capacity.

How do exercise duration and intensity determine the primary energy system used?

All energy systems are always active, but intensity + duration determine which predominates.

• 0–6 sec, extremely high intensity → Phosphagen

• 6–30 sec, very high → Phosphagen + fast glycolysis

• 30 sec–2 min, high → Fast glycolysis

• 2–3 min, moderate → Fast glycolysis + oxidative

• 
  

3 min, lower intensity → Oxidative

Key idea: Shorter + higher intensity → anaerobic systems; longer + lower intensity → oxidative system.

How are phosphagen and glycogen stores depleted and replenished during exercise?

Phosphagens:

• CP ↓ ~50–70% within first 5–30 sec of high-intensity exercise

• Can be nearly depleted during maximal exercise

• ATP fully resynthesized within ~3–5 min

• CP fully resynthesized within ~8 min

Muscle/liver glycogen:

• Glycogen depletion ↑ as exercise intensity ↑

• Above ~60% VO₂ max → muscle glycogen becomes increasingly important

• Glycogen stores can become depleted during prolonged exercise

Key idea: Phosphagens deplete rapidly but recover quickly; glycogen depletion depends largely on exercise intensity.

Where is glycogen stored in the body and approximately how much is stored?

Glycogen is stored as granules in the cytoplasm of muscle and liver cells.

• Muscle glycogen ≈ 400 g

• Liver glycogen ≈ 100 g

Key idea: Most of the body’s glycogen is stored in skeletal muscle.

What is oxygen deficit during the beginning of exercise?

Oxygen deficit = initial period when aerobic ATP production cannot yet meet ATP demand.

At exercise onset:

• O₂ uptake gradually increases

• ATP demand initially met by anaerobic pathways → phosphagen + glycolysis

• O₂ reaches steady state within ~1–4 min during light-moderate exercise

• At steady state → ATP demand is primarily met aerobically

Key idea: Oxygen deficit = gap between ATP demand and aerobic ATP production before steady state is reached.

what causes the lag that produces an oxygen deficit at the start of exercise?

Oxidative phosphorylation does not immediately reach full activity.

• ADP + Pi stimulate oxidative phosphorylation in the ETC

• ADP and Pi take time to accumulate to sufficient levels

• This delays full activation of aerobic ATP production

Key idea: The oxidative system needs time to “turn on,” so anaerobic systems initially help meet ATP demand.

How does aerobic training affect oxygen deficit?

Trained individuals:

• Reach steady-state VO₂ faster

• Have a smaller O₂ deficit

• Activate aerobic ATP production earlier

• Rely less on anaerobic pathways

• Produce less lactate and H⁺ at exercise onset

Key idea: Training → faster aerobic response → smaller O₂ deficit + less anaerobic reliance.

What is EPOC during recovery from exercise?

EPOC = excess post-exercise oxygen consumption

After exercise stops:

• VO₂ does NOT immediately return to resting levels

• O₂ consumption remains elevated during recovery

Two components:

• Rapid component = first ~2–3 min

• Slow component = >3 min

Key idea: EPOC = elevated O₂ consumption after exercise as the body recovers toward resting conditions.

Why does oxygen consumption remain elevated during EPOC?

Rapid component (first 2–3 min):

• Resynthesize ATP + creatine phosphate

• Replenish muscle + blood O₂ stores

Slow component (>3 min):

• HR + breathing remain elevated

• Body temperature remains elevated

• Gluconeogenesis → converts lactate back to glucose

Key idea: EPOC provides the extra O₂ needed to restore the body to its pre-exercise state.

How does exercise intensity affect EPOC?

Higher exercise intensity → greater and longer EPOC

Why?

• Higher body temperature

• Greater phosphocreatine (PCr) depletion

• Greater blood lactate accumulation

Key idea: High-intensity exercise creates greater recovery demands → more post-exercise O₂ consumption.

What is metabolic specificity of training (SAID principle)?

Training should match the specific metabolic demands of the activity.

• Exercise intensity + rest intervals determine which energy systems are emphasized

• Training a specific energy system → specific adaptations

• Sprinters → train sprinting/high-intensity energy systems

• Distance runners → train prolonged aerobic energy systems

Key idea: The body adapts specifically to how it is trained.

What is interval training and what is its purpose?

Interval training = alternating predetermined periods of exercise and rest.

• Promotes bioenergetic adaptations → more efficient energy transfer

• Allows more training to be performed at higher intensities

• Work-to-rest ratios can be manipulated to target specific energy systems

Key idea: Alternating work + recovery allows repeated bouts of higher-intensity exercise.