Comprehensive Exercise-Induced Adaptations (Ch. 13-14)

Principles of Training

• Overload

  • Definition: Application of an unaccustomed physiological stress to a system (muscle, cardiovascular, metabolic, etc.).

  • Manipulated through intensity, duration, frequency → summed as overall volume (how hard, how long, how often).

• Specificity

  • Adaptations mirror the exact muscles, energy systems, contraction velocities, and contraction types trained.

  • Example: Soccer involves repeated short sprints → training should bias anaerobic intervals rather than only long-slow jogging.

• Reversibility

  • Period in which stimulus is reduced or removed.

  • Short taper (few days before competition) ≠ detraining.

  • Extended removal (off-season) → loss of previously gained adaptations.

Minimal Effective Dose for Aerobic Capacity

• Generic “floor” for untrained adults to raise \dot{V}O_{2\,\text{max}}:

  • Duration: 20–60\;\text{min} per session.

  • Frequency: \ge 3 sessions·wk^{-1}.

  • Intensity: \approx 50\%\;\dot{V}O_{2\,\text{max}} (≈ light jog / brisk walk for most).

• Caveat: Already-fit individuals will not improve at this dosage; in them the same program behaves like reversibility.

VO₂max: Typical Values & Genetic Influence

• Average untrained college population:

  • Males ≈ 45\;\text{ml·kg}^{-1}·\text{min}^{-1} .

  • Females ≈ 38\;\text{ml·kg}^{-1}·\text{min}^{-1}.

• Average training response: 15\%–20\% ↑ from baseline (larger % in low-fit, smaller in high-fit).

• Heritability: ≈ 50\% of untrained VO₂max ceiling governed by parental genetics.

Fick Equation Refresher

VO2 MAX= HR MAX x SV MAX a-vO2MAX (difference)
At maximal work: the heart rate (HR) reaches its maximum capacity while stroke volume (SV) is optimized to ensure efficient oxygen delivery, resulting in a higher arteriovenous oxygen difference (a-vO2) that reflects enhanced muscular oxygen utilization. This interplay highlights the significance of both cardiovascular and muscular adaptations in improving overall exercise performance. Furthermore, regular training enhances both heart rate efficiency and stroke volume, leading to improved VO₂max values that can significantly elevate an individual's endurance capabilities. Additionally, these adaptations contribute to a more effective energy production system, allowing trained individuals to sustain higher intensities of exercise for longer periods.

Stroke Volume – Key Driver of Inter-Individual VO₂ Differences

• Stroke volume (SV) = blood ejected·beat^{-1} from LV.

• Largest single physiological factor explaining why people differ in VO₂max (training and genetics held constant).

Short-Term vs Long-Term Adaptations

Hemodynamic Adaptations

• Preload (End-Diastolic Volume) ↑ stoke volume by:

  • Plasma-volume expansion within 6 days of training.

  • Enhanced venous return (muscle pump, respiratory pump).

  • Ventricular volume Left Ventricular chamber dilation (eccentric hypertrophy).

• Afterload (Total Peripheral Resistance, TPR) ↓ stroke volume by:

  • Lower resting sympathetic tone, ↑ local vasodilation (↑ nitric oxide, ↓ catecholamine-induced constriction).

• Result: SV↑ → Cardiac output (Q)↑ even though HRmax is unchanged (age-limited).

Peripheral Adaptations

• Mitochondrial Biogenesis

  • ↑ number and size of mitochondria (especially with long-slow & HIIT).

• Angiogenesis

  • More capillaries per fiber ("capillary density").

  • Term: Angiogenesis / re-vascularization (heart) / sympatholysis (functional dilatation).

• Fiber-Type Shift

  • ↑ proportion of Type I and Type IIa myosin heavy chain; Type IIx ↓.

• Metabolic Enzymes

  • ↑ CPT-1, β-oxidation enzymes, citrate synthase, etc.

  • LDH isoform shifts to H₄ (lower pyruvate→lactate affinity).

O₂ Kinetics & Substrate Use

• Steady-state O₂ deficit reached faster → less early reliance on anaerobic glycolysis.

• Crossover shift: Trained muscle uses more fat at higher intensities → spares glycogen, lowers lactate/H⁺ accumulation.

Acid–Base & Oxidative Stress

• ↑ Intramuscular carnosine + ↑ MCT (monocarboxylate) transporters → better H⁺ buffering & lactate efflux.

• Training ↑ endogenous antioxidants (e.g., SOD, glutathione peroxidase) to cope with exercise-derived reactive oxygen species (ROS).

Cell Turnover Concepts

• Autophagy: Normal self-degradation/recycling of cellular components.

• Mitophagy: Selective removal of damaged mitochondria; stimulated by endurance training → maintains “high-quality” mitochondrial pool.

Molecular Signaling Cascade

Primary Signals During Contraction

• Mechanical stress on sarcolemma / cytoskeleton.

• ↑ [Ca^{2+}]_{cyto} (from SR).

• Energy status: ↑ AMP/ATP, ↑ ADP/ATP.

• ↑ ROS.

Key Secondary Messengers

• AMP-activated protein kinase (AMPK)

  • “Gas gauge” for low ATP.

  • ↑ Glucose uptake, ↑ fat oxidation, starts mitochondrial biogenesis signaling.

• PGC-1α (Peroxisome-Proliferator-Activated Receptor-γ Co-Activator-1α)

  • Master regulator of endurance adaptations.

  • Drives mitochondrial biogenesis + angiogenesis gene programs.

Time Course

• Seconds: Metabolite changes.

• Minutes: AMPK activation.

• Hours (≈6–8 h): Burst of mRNA transcription for mitochondrial proteins.

• Days–Weeks: Translation → measurable ↑ mitochondrial content & capillaries.

Training Modalities & Mitochondrial Outcomes

Detraining & “Muscle Memory”

• 12 days off: ≈ 8 % ↓ VO₂max → driven mainly by ↓ plasma volume → ↓ SV.

• 84 days off: ≈ 20 % ↓ VO₂max. Later losses due to ↓ mitochondria & capillaries → ↓ (a-v)O₂.

• Heart Rate: Resting & submax HR ↑ as compensation for SV decline.

• Retraining: VO₂max and performance recover faster than original learning curve (popularized as “muscle memory”).

Anaerobic / Sprint Training Adaptations

• 30 s Wingate-style sprints recruit Type I and II fibers; enormous glycolytic demand.

• Adaptations:

  • ↑ Peak & mean power output.

  • ↑ Glycolytic & ATP-PCr enzyme activity.

  • Hypertrophy of Type II fibers.

  • ↑ Carnosine, ↑ MCT transporters → superior H⁺ buffering.

• HIIT merges some of these with endurance benefits → common public prescription.

Example Exam-Style Prompts (Self-Check)

• List and define the three overarching principles of training.

• State the minimal weekly FIT (frequency-intensity-time) to raise VO₂max in an untrained adult.

• Average percent increase in VO₂max after a standard endurance program?

  • Answer: 15–20\%.

• Identify the two signaling molecules most closely linked to mitochondrial biogenesis and describe their trigger.

  • AMPK: Low ATP (high AMP/ADP).

  • PGC-1α: Downstream “master switch” initiating biogenesis & angiogenesis.

• During the first 4 months of training VO₂max rises chiefly because increases; after 2+ years the rise is mainly due to .

  • Answer: Stroke volume; (a-v)O₂ difference via mitochondrial/capillary gains.

Quick-Look Flowchart (Text Version)

1. Endurance bout → ↓ATP, ↑Ca²⁺, ↑ROS.

2. Activate AMPK & other kinases.

3. ↑ PGC-1α transcription.

4. Up-regulate nuclear & mitochondrial genes.

5. Weeks-Months → ↑ mitochondria, ↑ capillaries, ↑ fatty-acid transport, ↓ glycolytic reliance.

6. Functional impact → Faster steady state, lower lactate, higher sustained work.

Equations & Numerical Reminders

• Fick: \dot{V}O{2} = HR \times SV \times (a-v)O2.

• Plasma-volume expansion can occur in ≤6 days; VO₂max gain appears alongside.

• Detraining VO₂max losses: −8\% (12 d), −20\% (84 d).

• Resting Q at sea level ≈ 5\;\text{L·min}^{-1}; elite max Q up to 30\;\text{L·min}^{-1}.

These bullet-point notes consolidate all major and minor points, mechanisms, numbers, examples, and exam cues shared in the lecture transcript. They are intended to fully substitute for the original recording while serving as concise study material.