Fatigue: Central vs Peripheral, Anaerobic vs Aerobic

Defining Fatigue

• Exercise physiology construct: Inability to maintain power output or force during repeated muscle contractions, reversible with rest.
• Causes vary and are specific to the type of physical activity.

Central Fatigue Theory (A. V. Hill Model, 1923)

• Initial theory: Lactic acid interferes with voluntary muscular contraction.
• Factors: Heart, muscle, mitochondria, lactic acid accumulation, coronary blood flow.
• Limitations: Doesn't account for the brain's role.

Central Governor (Brain)

• The brain regulates muscle recruitment and maintains homeostasis during exercise.
• Regulates muscle fibres recruited and stimulus received.
• The brain receives afferent input, integrates it, and produces an efferent outcome.

Sites of Fatigue: Central vs. Peripheral

• Central fatigue: Originates in the central nervous system (brain, spinal cord, motor neurons).
• Peripheral fatigue: Originates outside the CNS (peripheral nervous system, skeletal muscle fibre).

Central Fatigue Mechanisms

• Exercise begins and ends with the central nervous system.
• Early research: Decreases in motor unit functioning and firing frequency.
• Voluntary vs. electrically induced maximal contraction: Early studies showed no difference, suggesting the CNS isn't a limiter.
• Later research: Psychological elements (shout) can increase maximal strength, suggesting CNS impact.
• Other factors: Serotonin and dopamine release, motor neuron depression and arousal.
• Accounts for roughly 10% of physiological fatigue.

Peripheral Fatigue Mechanisms

• Originate outside the central nervous system (neural, mechanical, bioenergetic).
• Far more significant contributor than central fatigue.

Neural Elements

• Sarcolemma and T tubules: Inability to maintain Na+/K+ concentrations, reduction in action potential amplitude, diminished calcium release, decreased muscle contractility.
• Occur past the neuromuscular junction.

Mechanical Elements

• Crossbridge cycling: Altered actin and myosin arrangement, diminished calcium availability, decreased ATP use.
• Increased hydrogen concentration impairs force per crossbridge, inhibits calcium release.
• Radical-induced fatigue: Free radicals damage contractile proteins, limit myosin crossbridge binding, depress Na+/K+ pump activity.
• Antioxidant supplementation: Potential to delay fatigue, but high doses can impair muscular adaptation.

Bioenergetic Elements

• Fatigue as a result of imbalance between ATP required and ATP generated.
• ATP demand exceeds supply, signals muscle cell to slow down energy utilization.
• Phosphate accumulation impairs force production.
• Cells typically maintain ATP concentrations around 70%.

Anaerobic vs. Aerobic Fatigue

• Muscle fibre recruitment shifts as exercise intensity increases (Type I → Type IIa → Type IIx).
• Fatigue is specific to the task and muscle fibre type recruited.

Depletion vs. Accumulation

• Depletion: Decrease in metabolites (e.g., ATP) impairs force generation.
• Accumulation: Increase in metabolites (e.g., phosphate, hydrogen) impairs force generation.
• Primary site of fatigue is within the muscle (peripheral fatigue).

Anaerobic Fatigue (Short Duration Activities)

Ultra Short Term Performance ( < 10 seconds)

• Targets ATP-PC system.
• Factors: Motivation, arousal, practice, skill, technique.
• Neuromuscular drive fuels PC and glycolysis.
• Utilizes Type II muscle fibres.

Short Term Performance (10 - 180 seconds)

• Targets anaerobic glycolytic pathway.
• Fatigue profile: Increase in muscle and blood hydrogen.
• Breakdown of ATP produces low oxygen environment and lactate.
• Accumulation of hydrogen is a primary contributor to fatigue.

Aerobic Fatigue (Longer Duration Activities)

Moderate Length (3 - 20 minutes)

• VO2 max is the biggest contributor to fatigue.
• Factors limiting VO2 max: Arterial oxygen content, muscle fibre typing, mitochondrial content, cardiac output.

Intermediate Length (21 - 60 minutes)

• VO2 max remains a significant contributor.
• Running economy.
• Lactate threshold:
  • Key predictor of race performance.
  • Influenced by muscle fibre distribution.

Long Term Performance (1 - 4 hours)

• VO2 max, fuel utilization, environmental conditions (heat, dehydration).
• Diet and supplementation become crucial.

Delayed Onset Muscle Soreness (DOMS)

• Mechanism of resistance training, related to muscle damage.
• Mechanical force → Structural damage → Increased intracellular calcium → Degradation of Z discs and regulatory proteins → Inflammation.
• Changes in tissue osmolarity, accumulation of hydrogen ions → Pain.
• Inflammation → Swelling → Local ischaemia → Exacerbates pain.
• Typically peaks 24-48 hours after high-intensity resistance training.

Applying Understanding of Fatigue to Exercise and Sport

• Managing fatigue can improve performance.
• Overlap between maximizing performance and minimizing fatigue.
• Key factors: Energy production, diet, CNS function, strength, skill/technique, environment.

Training to Improve Aerobic Power (VO2 max)

• Methods: Interval training, long slow distance training, high-intensity circuit training.
• Highly specific to the sport or individual.

Training to Improve Anaerobic Power

• ATP-PC system: 5-10 seconds work, 30-60 seconds rest (replenishes ATP-PC).
• Glycolytic system: 20-60 seconds work, extended recovery (flush out lactate).
• Mimic sporting activity.

Training Principles and Fatigue

Individuality

• Genetic predisposition: Influences aerobic performance improvement.
• Running economy: Improvements possible despite VO2 max plateau.
• Lactate threshold: Improvements in pace and lactate tolerance influence performance.

Overload

• Disrupts homeostasis, allowing adaptation.
• Acute responses: Changes in mood, testosterone/cortisol ratio, increased creatine kinase, glycogen depletion.
• Recovery within two weeks.

Overtraining

• Under-recovery or excessive training.
• Signs/symptoms: Altered mood, disrupted sleep, loss of appetite, weight loss, frequent infections.
• Doesn't dissipate with short rest/recovery.
• Clinically diagnosed.

Rest and Recovery

• General Adaptation Syndrome: Training stimulus, fatigue, rest, recovery → super compensation.
• Balance: Stress/recuperation = performance, Stress > Recuperation = Reduced capacity
• Need for: Systemic monitoring (Performance, Cardiovascular variables, Strength based variables), Collaboration and Multidisciplinary approach