Physiology of Training: VO₂ max, Performance & Resistance Adaptations (Ch. 13–14)

Principles of Training

• Overload
  • Training adaptations occur when a physiological system is exercised at a level beyond its habitual load.
  • Manipulated via intensity, duration, frequency.
• Specificity
  • Adaptations are specific to:
  • Recruited muscle‐fiber types
  • Primary energy system (aerobic vs. anaerobic)
  • Contraction velocity
  • Contraction mode (eccentric, concentric, isometric)
• Reversibility
  • Training gains are lost once the overload stimulus is removed.

Endurance Training & VO₂ max

Standard Prescription

• Dynamic exercise, large muscle groups
• 20–60 min/session, ≥ 3× week, ≥ 50 % VO₂ max
• Expected mean ↑ in VO₂ max = 15–20 %
  • High initial VO₂ max → 2–3 % gain (need > 70 % VO₂ max stimulus)
  • Low initial VO₂ max → up to 50 % gain (40–50 % VO₂ max stimulus sufficient)

Genetic Contribution

• Heritability ≈ 50 % of baseline VO₂ max; ≈ 47 % of training response (≈ 21 genes identified).
• “Low responders” ≈ 2–3 % gain; “high responders” ≈ 50 % gain.

Population VO₂ max Ranges (mL·kg⁻¹·min⁻¹)

• Cross-country skiers ♂ 84, ♀ 72
• Distance runners ♂ 83, ♀ 62
• Sedentary young ♂ 45, ♀ 38
• Sedentary middle-aged ♂ 35, ♀ 30
• Post-MI pts ♂ 22, ♀ 18
• Severe pulmonary dz ♂ 13, ♀ 13

Mechanistic Basis (Fick Equation)

• \dot V{O2\,max}=HR{max}\times SV{max}\times (a\text{-}v\,O2)_{max}
• Short-term training (~4 mo):
  • 26 % ↑ VO₂ max (≈ 10 % ↑ SV, 2 % ↑ a-vO₂)
• Long-term (~28 mo):
  • 42 % ↑ VO₂ max (≈ 15 % ↑ SV, 25 % ↑ a-vO₂)

Stroke-Volume Adaptations

• ↑ Preload (↑ plasma volume, venous return, ventricular volume)
• ↓ Afterload (↓ TPR via ↓ arterial constriction; ↑ maximal muscle blood flow at unchanged MAP)
• ↑ Contractility
• Rapid changes within 6 days: +11 % plasma volume, +7 % VO₂ max, +10 % SV

a-vO₂ Difference Adaptations

• ↑ Muscle blood flow (↓ SNS vasoconstriction)
• ↑ Capillary density → slower transit time↑O₂ extraction
• ↑ Mitochondrial number (biogenesis)

Performance & Homeostasis Improvements

• Faster transition rest→steady-state; ↓ O₂ deficit
• ↓ Reliance on muscle glycogen & blood glucose (↑ fat use)
• Improved cardiovascular & thermoregulatory control (↓ HR, ↓ ventilation for given workload)
• Neural & hormonal adaptations (↓ catecholamine spillover)

Muscle Fiber, Capillary & Mitochondrial Adaptations

• Fast-to-slow MHC shift (↓ IIx, ↑ IIa/Type I; magnitude = training type × genetics)
• ↑ Capillary number (angiogenesis) → ↑ O₂ & metabolite exchange
• Two mitochondrial pools: subsarcolemmal & intermyofibrillar
  • Content ↑ 50–100 % within 6 wk (intensity × duration dependent)
  • ↑ Turnover (mitophagy) removes damaged organelles

Autophagy / Mitophagy

• Autophagy = non-/selective removal of organelles & misfolded proteins; energy balance role.
• Mitophagy = selective clearance of dysfunctional mitochondria (limits ROS, apoptotic signaling).

Intensity & Duration Effects (Citrate Synthase, CS)

• Intensity (55, 65, 75 % VO₂ max): ↑ CS in IIa at all; IIx only at 75 % w/ longer bouts.
• Duration (30, 60, 90 min): similar IIa response; IIx needs longer-higher load.

Fuel Utilization Shifts

• ↑ Fat oxidation, glycogen sparing via:
  • ↑ Capillary density, FABP/FAT/CD36 transporters
  • ↑ CPT-I, FAT → better cytosol→mitochondria FFA transport
  • ↑ β-oxidation enzymes → ↑ acetyl-CoA; high citrate ↓ PFK → ↓ glycolysis
• Consequence: lower [ADP] needed for oxidative ATP → ↓ lactate, ↓ H⁺, ↓ PCr depletion

Antioxidant & Acid-Base Improvements

• Contracting muscle generates ROS; training ↑ endogenous enzymatic (SOD, CAT, GPx) & non-enzymatic defences.
• Mechanisms reducing exercise lactate/H⁺:
  • ↑ Mitochondria → ↓ glycolytic flux (less pyruvate), ↑ NADH shuttling
  • LDH isoform shift toward H₄ (lower pyruvate affinity)

Molecular Signaling for Endurance Adaptation

• Primary sensors: ↑ [Ca²⁺], ↑ AMP/ATP, ↑ ROS.
• Secondary messengers:
  • CaMK, Calcineurin → fiber type shift
  • AMPK, p38, PGC-1α → mitochondrial biogenesis, angiogenesis
  • NFκB → antioxidant enzymes
• mRNA peaks 4–8 h post-exercise; returns by 24 h → need daily stimulus.
• Training ↓ multiple miRNAs that normally repress protein translation → facilitates adaptation.

Systemic Links & Neural Feedback

• Biochemical muscle changes dampen afferent feedback (Grp III/IV) → ↓ SNS drive, HR, VE for same workload.
• Unilateral training: adaptations local; untrained limb shows none (evidence from one-leg studies).

Detraining & Retraining (Endurance)

• VO₂ max ↓ ≈ 8 % in 12 d, 20 % in 84 d.
  • Early loss = ↓ SV (plasma volume);
  • Later loss = ↓ a-vO₂ (mitochondria, fast fiber rebound).
• Mitochondrial content halves within 1 wk off; majority lost by 2 wk.
• Retraining: 3–4 wk to regain mitochondrial gains; rapid due to residual transcriptional capacity.

Anaerobic (Sprint) Training Adaptations

• 10–30 s all-out bouts recruit I & II fibers; energy from ATP-PCr (≤10 s) and anaerobic glycolysis (20–30 s, 80 %).
• 4–10 wk → +3–28 % peak anaerobic power.
• ↑ Muscle buffering (↑ carnosine, H⁺ exporters), ↑ II fiber hypertrophy, ↑ glycolytic & ATP-PCr enzymes.
• HIIT ≥ 30 s intervals at/above VO₂ max also stimulates mitochondrial biogenesis.

Resistance (Strength) Training

Strength & Endurance Definitions

• Muscular strength = 1-RM; endurance = repeated submaximal contractions.
• Percent improvement inversely related to initial strength; genetic ceiling exists.
• Loading continuum:
  • 1–5 reps @ 80–100 % 1-RM → maximal strength
  • 8–12 reps @ 60–80 % 1-RM → hypertrophy
  • 15+ reps @ < 60 % 1-RM → muscular endurance

Neural Adaptations (0–8 wk)

• ↑ Neural drive:
  • ↑ MU recruitment number, firing rate, synchronization
  • Improved NMJ transmission (larger endplates, ↑ AChR dispersion)
• Possible ↓ antagonist co-activation.

Hypertrophy (≥ 3 wk)

• Primarily fiber hypertrophy (90–95 % of size gains):
  • ↑ Myofibrillar proteins (actin, myosin) → ↑ cross-bridge number
  • Greater in Type II fibers but occurs in Type I as well; ↑ specific tension in Type I via ↑ Ca²⁺ sensitivity.
• Human hyperplasia evidence minimal; seen mainly in animal models.

Muscle Architecture Changes

• ↑ Pennation angle alters force transmission; aponeuroses remodel.
• Possible radial & longitudinal fascicle growth.

Substrate & Enzymatic Adaptations

• ↑ PCr & ATP stores (augmented by creatine); mixed evidence for enzyme activity ↑.
• Resistance training may ↓ mitochondrial density (dilution), mixed capillary adaptations (depends on volume/intensity).

Antioxidant Capacity

• 12 wk RT can ↑ muscle antioxidant enzymes ~100 %, similar to endurance training.

Endocrine Responses

• Acute RT (high intensity, volume, short rest) transiently ↑ Testosterone, GH, IGF-1, catecholamines, cortisol.
• Chronic basal levels little-changed; chronic adaptation not dependent on large hormonal surges.

Molecular Signaling for Hypertrophy

• Primary stimulus: mechanical load → mechanoreceptors → phosphatidic acid (PA) synthesis & Rheb activation.
• Secondary: PA & Rheb activate mTORC1 → ↑ translation initiation (p70 S6K, 4E-BP1) → MPS ↑ 50–100 % within hrs.
• Satellite cells may donate myonuclei, but recent data suggest hypertrophy can occur without SC fusion, esp. in older adults.
• Leucine can acutely trigger mTORC1 but cannot replace RT for growth.

Genetic Variability

• ≈ 80 % inter-individual hypertrophy potential genetically determined (≥ 47 genes, many mTOR-linked).
• High, moderate, non-responders documented across ages/sexes.

Detraining (RT)

• Strength ↓ ~31 % over 30 wk off; fiber CSA losses: Type I −2 %, IIa −10 %, IIx −14 % (neural loss prominent).
• Retraining restores strength & size within 6 wk; “muscle memory” likely via retained myonuclei & epigenetic marks.

Concurrent Strength + Endurance Training

• Possible “interference” on strength gains; depends on endurance intensity/volume/frequency & glycogen status.
• Mechanism: endurance-induced AMPK activation may inhibit mTORC1; overtraining, MU recruitment interference less supported.
• Proper scheduling (separate bouts, adequate nutrition) minimizes interference.

Comparative Summary of Chronic Adaptations (Endurance vs Resistance)

• Endurance: ↑ Mitochondrial density, capillarization, VO₂ max, lactate tolerance, fat metabolism; modest strength/power gains.
• Resistance: ↑ Muscle CSA, strength/power, myofibrillar protein synthesis, bone density; modest mitochondrial or capillary changes unless high-volume.
• Both improve insulin sensitivity, body composition, antioxidant capacity, basal metabolic rate, and reduce cardiovascular risk.

Practical Implications & Health

• Progressive overload with attention to specificity and recovery essential for sustained adaptations.
• Regular exercise prevents detraining losses and maintains favorable gene expression/epigenetic profiles.
• Combining modalities yields complementary health benefits when programmed correctly.