Resistance-Training Physiology & Adaptations

Terminology & Repetition-Range “Continuum”

• Instructor prefers the term Resistance Training (RT) over “strength training.”
• Classic repetition ranges (widely cited since the 1980s) form a continuum:
  • \le 6 reps → predominantly “strength.”
  • \approx 6–12 reps → hypertrophy.
  • \ge 15 reps → muscular endurance.
• Reality = gray zone; adaptations overlap:
  • 6-rep work can still produce hypertrophy.
  • 13-rep work can still increase strength.
• Principle of Specificity remains: train in the zone most aligned with the desired outcome but expect spill-over.

Intensity Recommendations for Hypertrophy

• Textbook guideline: \sim70\% 1-RM for optimal hypertrophy.
• Practical issue: most trainees & clinicians never directly test 1-RM, so true %-based loading is rare.
• Research updates:
  • Hypertrophy achievable at low loads (≈30\% 1-RM) when sets are carried close to failure.
  • Blood-flow–restriction (BFR) can further enhance low-load hypertrophy.
  • Heavy lifting is not mandatory for muscle growth—contradicts older dogma.

Timeline of Adaptations

• Weeks 0–2 (familiarisation): technical learning, minor neural change.
• Weeks 2–8: rapid strength gains primarily neural.
• Weeks 8 +: hypertrophy becomes the dominant contributor to further strength increases.
• Strength curve: neural gains plateau; muscle cross-section continues to rise (up to individual/genetic ceiling).

Neural Adaptations: “Neural Drive”

• 4 key components (all improve within first 2–8 wk):
  • Motor-unit recruitment ↑ (more α-motoneurons + fibres activated).
  • Rate coding ↑ (faster firing frequency).
  • Synchronization ↑ (units fire more simultaneously → summation of force).
  • NMJ transmission efficacy ↑ (enhanced ACh release & receptor density).
• Additional neural points:
  • Golgi Tendon Organ (GTO) inhibition diminishes → higher force tolerance.
  • NMJ morphology: terminal branching increases, expanding the end-plate.

Age-Related & Pathological Muscle Loss

• Sarcopenia = age-related loss of muscle mass/function (inevitable but modifiable).
• Cachexia (cancer, cardiac, etc.) = disease-driven atrophy.
• Preferential loss of Type II fibres with aging.
• Sarcopenic obesity: simultaneous high fat mass + low muscle mass (MRI examples: normal → obese → sarcopenic → sarcopenic-obese).

Types of Muscle Growth

• Myofibrillar Hypertrophy
  • ↑ number & diameter of contractile proteins (actin–myosin); denser cross-section; greater force.
• Sarcoplasmic Hypertrophy
  • ↑ non-contractile volume (glycogen, water, enzymes); size ↑, force less affected.
• Hyperplasia (↑ fibre number)
  • Robust in animal overload models (quail, cats); evidence in humans limited—if present, likely via myofibre splitting.

Structural & Architectural Changes

• Cross-sectional area (CSA) ↑ in recruited fibres; type II gains > type I gains.
• Pennation angle ↑ in pennate muscles → allows more fibres in given volume → force advantage.
• Possible lengthening of fibres with eccentric-biased training.

Enzymatic & Metabolic Adaptations to RT

• ↑ content/activity of anaerobic enzymes (e.g., CK, ATPase, PFK).
• Slight ↑ in intramuscular PCr & creatine stores (greater if supplementing).
• Minimal change in capillary density, myoglobin, mitochondria—unless very high-volume, endurance-style RT.

Hormonal Responses

• Acute RT bout ↑ testosterone, GH, IGF-1, cortisol, catecholamines.
• Chronic training → blunted acute peaks; long-term hypertrophy not strongly correlated with basal or acute hormone levels.

Protein Turnover & Muscle Protein Synthesis (MPS)

• Net protein balance (NPB) =MPS – MPB
  • \text{NPB}=0 → maintenance.
  • \text{NPB}>0 → hypertrophy.
  • \text{NPB}<0 → atrophy.
• One RT session ❯ MPS ↑ up to 100 % for ≈48\text{ h} (greater & longer in untrained).
• Untrained ↑ MPS longer due to higher damage/repair demand.

Molecular Signalling: Mechanotransduction & mTOR

• Mechanical load = dominant stimulus; gravity removal (spaceflight, bed-rest) → rapid atrophy.
• mTOR (mechanistic Target Of Rapamycin)
  • Central secondary messenger for RT.
  • Activated within minutes post-exercise.
  • Drives translation initiation → protein synthesis.
• AMPK (energy sensor) can inhibit mTOR—important for concurrent training interference.
• Leucine spikes mTOR but full MPS requires all 20 AA. Leucine-only supplements offer little benefit.

NSAIDs & Training

• Standard OTC doses of NSAIDs (e.g., ibuprofen) do not blunt hypertrophy/strength if used prudently for soreness.

Individual Response Variability

• High-, moderate-, non-responders documented for strength & size.
• Influencers: genetics, nutrition, sleep, stress, programme design.
• Bell-curves in studies: most gain 5–15 % CSA & 15–25 % strength; some gain ⩾40 % strength; a few lose mass.

Detraining & Muscle Memory

• Order of loss: neural strength ↓ first, CSA ↓ later.
• Loss rates slower than aerobic detraining.
• Re-training restores strength rapidly (neural memory) and CSA thereafter.
• Epigenetic signatures (e.g., retained DNA methylation patterns) may underpin “muscle memory.”

Concurrent Training (Endurance + RT)

• Potential interference effect:
  • Endurance → ↑ AMPK, glycogen use → can dampen mTOR signalling if poorly sequenced.
  • Practical tips:
  • Prioritise goal-specific modality first.
  • Separate RT & endurance sessions by ≥6 h (ideally >24 h) when maximal strength/hypertrophy is the goal.
  • Neural interference minimal; energy substrate & molecular signalling are bigger issues.

Over-Training Concept

• Term loosely applied; no single definition.
• Symptoms = persistent fatigue, performance drop, mood disturbance; multifactorial.

Comparative Snapshot: Aerobic vs Resistance Training

Key Exam Review Prompts (as emphasised by lecturer)

• Define Neural Drive and list its 4 sub-components.
• NMJ adaptation: ↑ branching / end-plate area.
• Explain mechanotransduction → mTOR → protein synthesis.
• Distinguish myofibrillar vs sarcoplasmic hypertrophy; know which yields more force.
• Recall sarcopenia vs cachexia vs sarcopenic obesity.
• Recognise \sim70\% 1-RM guideline yet appreciate low-load hypertrophy evidence.
• Be able to comment on concurrent training interference (AMPK ↔ mTOR).
• Understand detraining order: neural first, muscle mass second.
• Chapters highlighted as “heavy” for the exam: 13 & 14 (RT physiology), with supportive knowledge from Ch. 9 (CV), 10 (pulmonary), 11 (acid–base) but at lighter emphasis.