Adaptations to Aerobic Endurance Training Programs

What does periodization mean?

A structured, sequential plan that organizes training phases to create specific physiological adaptations and peak performance.

What is cardiac output (Q)?

Amount of blood pumped per minute = Stroke Volume × Heart Rate.

How does cardiac output change during steady-state exercise?

Increases rapidly at onset, then plateaus at about 4 × resting Q.

What increases stroke volume?

Greater end-diastolic volume (Frank-Starling Mechanism) and increased sympathetic input (catecholamines).

How does heart rate respond to intensity?

Increases linearly with exercise intensity.

What are two common HRmax prediction formulas?

220 - age (± 10-12 bpm) and Tanaka formula 208 - 0.7 × age.

What is oxygen uptake (VO₂)?

The amount of oxygen consumed by tissues per minute; rises with exercise intensity.

What is the Fick equation?

VO₂ = Q × (a-vO₂ difference).

What is resting VO₂ in METs?

1 MET = 3.5 ml O₂ · kg⁻¹ · min⁻¹.

How does blood pressure change acutely?

SBP ↑ with intensity; DBP ≈ same or slightly ↓.

What is the rate-pressure product (RPP)?

HR × SBP → reflects myocardial workload.

How is local circulation controlled?

Arterioles vasodilate to active muscle and vasoconstrict to inactive tissue.

What summary changes occur during aerobic exercise?

↑ Q, ↑ SV, ↑ HR, ↑ VO₂, ↑ SBP, ↓ DBP, ↑ blood flow to active muscles.

What increases during aerobic exercise?

O₂ delivery, CO₂ removal, and minute ventilation.

What is the ventilatory equivalent?

Volume of air breathed per L O₂ consumed (≈ 20-25 L air · L⁻¹ O₂).

What is tidal volume?

Air moved per breath; increases via deeper breathing.

What is anatomical dead space?

Airways where no gas exchange occurs (nose, mouth, trachea).

What is physiological dead space?

Alveoli not functioning properly or poor blood flow.

Why is deeper breathing better?

Improves ventilation efficiency vs. shallow, fast breathing.

What happens to gas exchange at high intensity?

Larger O₂/CO₂ pressure gradients → greater diffusion capacity.

How is O₂ transported?

98% bound to hemoglobin.

How is CO₂ removed?

70% as bicarbonate (HCO₃⁻) via carbonic acid dissociation.

When does lactate accumulate?

During high-intensity exercise when production > removal (lactate threshold ≈ 4 mmol/L).

What happens to VO₂max after training?

Increases due to greater Q and SV.

How does resting HR change?

Decreases from enhanced parasympathetic tone.

What structural change occurs in muscle capillaries?

Increased density → better O₂ delivery and waste removal.

What key adaptations improve VO₂max?

↑ Q, ↑ SV, ↑ capillary density, ↑ mitochondria, ↑ oxidative enzymes.

Does ventilation limit performance?

Generally no.

How do ventilatory patterns change?

Max exercise → ↑ tidal volume and rate; submax → ↑ tidal volume, ↓ rate.

Are these adaptations activity-specific?

Yes — specific to trained movement patterns.

What neural improvements occur?

↑ motor unit efficiency and coordination, ↓ fatigue of contractile mechanisms.

How does the nervous system reduce energy cost?

Synergists alternate activity to lower energy expenditure.

What happens to aerobic capacity of muscle?

Increases significantly.

What metabolic changes occur?

↑ glycogen storage, ↑ fat utilization, ↑ mitochondria, ↑ myoglobin, ↑ oxidative enzymes (LDH, PFK, CS, SDH).

What happens to lactate handling after aerobic training?

Improved clearance and higher threshold.

What fiber type shifts occur?

Type IIx → Type IIa (more fatigue-resistant).

What enzyme change supports less lactate build-up?

↑ H₄ form of LDH (lower pyruvate affinity).

What happens to NADH shuttles with aerobic training?

Increase → better redox balance and aerobic metabolism.

How do bones, tendons, and ligaments adapt?

Become stronger proportionally to weight-bearing load intensity.

Why is bone stimulation limited over time?

Bone adapts to habitual loads and requires progressive stress for continued growth.

What hormones increase with aerobic training?

Testosterone, IGF-1, GH, cortisol, epinephrine, norepinephrine.

How do trained vs untrained responses differ?

Trained athletes show larger maximal hormone release but blunted responses to submax work.

What are cytokine responses to training?

↑ IL-6 and ↑ TNF-α → enhanced recovery and metabolism.

What structural muscle adaptation is seen with running?

↑ mitochondrial protein synthesis (rather than myofibrillar hypertrophy).

What are the key benefits of aerobic endurance training?

Reduced body fat, increased VO₂max, improved running economy, greater respiratory capacity, lower blood lactate during submaximal exercise, increased mitochondrial and capillary density, and improved oxidative enzyme activity.

At what altitude do adaptations begin?

> 1,200 m (≈ 3,900 ft).

Why does altitude affect performance?

↓ partial pressure of O₂ → less diffusion → less ATP production.

What are acute pulmonary responses to hypoxia?

Hyperventilation ↑ breathing rate → ↑ alveolar PO₂ ↓ CO₂.

What acid-base change occurs at altitude?

Body fluids become more alkaline from CO₂ loss.

What are acute CV responses to altitude?

↑ HR and Q at rest and submax exercise, ↑ BP from sympathetic activity (↑ NE).

How long until HR and Q normalize at altitude?

≈ 10-14 days as EPO stimulates RBC production.

What is hyperoxic breathing?

Inhaling O₂-enriched gas to theoretically enhance performance (limited evidence).

What is blood doping?

Artificially raising RBC count to improve O₂ delivery — banned and dangerous.

What are benefits of blood doping?

↑ aerobic capacity, better thermoregulation, greater submax tolerance.

What is genetic potential in training?

As you approach biological limits, gains diminish.

How does age affect aerobic power?

VO₂max declines with age due to ↓ muscle mass and ↑ fat mass.

How does sex influence aerobic capacity?

Women average 73-85% of men's VO₂max due to smaller heart size and lower hemoglobin.

What is overtraining?

Excessive training without adequate recovery → performance decline.

What are two stages before OTS?

Functional and Nonfunctional Overreaching.

Define functional overreaching.

Short-term fatigue followed by supercompensation after rest.

Define nonfunctional overreaching.

Performance stagnation or decline lasting weeks to months.

What percentage of endurance athletes experience NFOR/OTS?

≈ 7-21%.

What happens to heart rate with overtraining?

RHR may ↑ or ↓; HRV ↓; HR at submax ↑.

What happens to blood pressure?

DBP may ↑ slightly with high intensity.

What biochemical marker increases?

Creatine Kinase (CK) — muscle damage indicator.

What happens to muscle glycogen with OTS?

Decreases.

What endocrine marker signals OTS?

↓ testosterone:cortisol ratio (> 30% drop).

What other endocrine changes occur?

↓ GH release, ↓ dopamine, ↓ catecholamine sensitivity.

How to prevent OTS?

Good nutrition, adequate sleep, recovery time, stress management, and support system (coach, physician, nutritionist, psychologist).

What is detraining?

Loss of training adaptations from insufficient stimulus.

What principle does this illustrate?

Reversibility — "use it or lose it."

How quickly does VO₂max decline after inactivity?

≈ 8% in 12 days; ≈ 20% after 84 days.

What causes the initial drop in VO₂max?

↓ max stroke volume and plasma volume.

What causes later declines?

↓ mitochondria, ↓ oxidative enzymes, ↓ a-vO₂ diff, ↑ Type IIx fibers.