Week 13: Intro to Models of Skeletal Muscle Fatigue

Definitions of Fatigue

Fatigue is a complex physiological phenomenon that can be described through several definitions:

• Fatigue is a complex, multi-dimensional physiological phenomenon categorized by several specific criteria:

  • General Sensations: Subjective experiences of tiredness, lethargy, and an increased perception of effort for a given workload.

  • Scientific Definition: A transient decrease in the maximum capacity to generate force or power. Crucially, this impairment is reversible with rest, distinguishing it from clinical muscle damage or chronic weakness.

  • Electromyographic (EMG) Changes: A shift in the power spectrum of the EMG signal toward lower frequencies (spectral compression). This occurs due to a reduction in muscle fiber conduction velocity as fatiguing metabolites accumulate

Changes in Physical and Mental Capabilities

Fatigue involves changes in both physical and mental capabilities that lead to:

• An increase in the psychological or energy cost of exercising.

• A decrease in maximal strength or power output, which can alter the ability to sustain physical tasks.

Causes of Muscle Fatigue

The causes of muscle fatigue are multifaceted and can include:

• Task Specificity: Different exercises may target different muscle groups, resulting in unique fatigue profiles.

• Training Status: The individual's level of fitness can influence how fatigue manifests.

• Physiological Status: Factors such as hydration, carbohydrate loading, and stress levels also play a role.

• Environmental Conditions: Temperature, humidity, and altitude can affect endurance and strength.

Physiological Causes of Fatigue

Muscle fatigue has two primary physiological types:

1. Peripheral Fatigue: Originates directly in the muscles themselves.

2. Central Fatigue: Caused indirectly by changes within the central nervous system (CNS), particularly involving the brain.

Homeostatic Limitations and Theories of Muscle Fatigue

Muscle contraction induces physiological changes at multiple levels, affecting metabolism, energy supply, cardiovascular function, and body temperature. The failure to maintain homeostasis can result in:

• Peripheral Fatigue: Directly related to muscle-specific changes.

• Central Fatigue: Indirectly related to overall bodily changes and CNS responses.

Models to Explain Muscle Fatigue

Several models have been proposed to explain muscle fatigue and the physiological implications of training:

1. Energy Supply/Energy Depletion Model (Slides 7-23)

2. Metabolic Waste Model (Slides 24-33)

3. Central Fatigue Model (Slides 35-40)

4. Psychological Model (Slides 41-42)

5. Cardiovascular/Anaerobic Model (Part 2)

6. Central Governor Model (Part 2)

1. Energy Supply/Depletion Model

• Performance Determination: Performance is determined by the capacity to produce energy, specifically ATP, through various metabolic pathways including:

  • ATP-Phosphocreatine (ATP-PCr)

  • Anaerobic glycolysis (glucose from carbohydrates without oxygen)

  • Aerobic glycolysis (glucose from carbohydrates with oxygen)

  • Aerobic lipolysis (oxidation of fatty acids with oxygen)

• Superior Performance: Greater capacity to generate ATP in specific metabolic pathways correlates with superior exercise performance.

Depletion of Energy Substrates

• High-Intensity Exercise: Depletion of ATP and phosphocreatine (PCr) primarily affects performance.

• Glycogen Levels: Depletion of glycogen occurs during light to high intensity exercise and depletion of blood glucose happens during prolonged exercise.

ATP and PCr Dynamics

• During the onset of exercise, ATP levels slightly decrease, while PCr levels drop significantly.

• Eventually, both substrates reach low levels, contributing to fatigue, but they are not completely depleted.

• Muscle fatigue aligns with PCr depletion particularly during isometric and maximal exercise.

ATP Compartmentalization

• Total muscle ATP concentrations may only drop to 70% of baseline during exhaustive exercise. This indicates that ATP levels may support basic functions even in fatigue.

• Functional ATP sets aside for activities beyond basal metabolic needs may become depleted, implying a 'governor' mechanism controlling ATP usage during exercise.

Conclusion from This Model

It's noted that muscle fatigue is closely associated with PCr depletion but not necessarily with ATP depletion. Negative down-regulation of functions, such as enzyme activity and muscle contraction, occur when ATP levels drop, leading to fatigue.

Muscle Glycogen Use During Prolonged Exercise

• Prolonged submaximal exercise (beyond 2 hours) leads to muscle glycogen depletion. The exhaustion point correlates with glycogen stores running out, affected by exercise intensity and muscle fiber types.

• Glycogen in specific muscle fibers can be mobilized during rising epinephrine levels, facilitating glycogenolysis and glycolysis, resulting in lactate production.

Evidence for Glycogen Depletion

• Fatigue during prolonged exercise has been associated with decreased liver glycogen stores (leading to hypoglycemia) and muscle glycogen depletion.

• CHO supplementation can alleviate hypoglycemia and prolong exercise capacity, hence, carbohydrate loading enhances endurance.

2. Metabolic Waste Model

• Classical Theory: High-intensity exercises result in oxygen deficit, requiring anaerobic metabolism and increasing lactic acid concentration, leading to fatigue.

Lactic Acid Accumulation and pH Changes

• Free H+ ions from lactic acid cause a decrease in intracellular pH.

• ATP catabolism additionally produces H+, contributing to metabolic acidosis and generally leading to fatigue.

Consequences of Low pH Levels

• Low pH inhibits the activity of phosphofructokinase (PFK), which slows glycolysis.

• It can stimulate pain receptors, replace Ca2+ on troponin-C disrupting muscle contraction, and negatively affect oxygen binding to hemoglobin in the lungs.

Evidence Against Lactate Accumulation Theory

• McArdle’s Disease: Absence of lactate production does not result in muscle fatigue.

• Eccentric Exercise: Muscle soreness can occur despite low lactate levels, indicating that lactate is not the sole cause of delayed onset muscle soreness (DOMS).

• High Altitude Exercise: Elevated lactate levels do not always correlate with fatigue.

Conclusion of Metabolic Waste Model

• There is no definitive cause-and-effect between lactate levels and fatigue, but metabolic acidosis is acknowledged as a contributor.

Accumulation of Phosphates

• ATP and PCr depletion leads to phosphate accumulation, which can inhibit glycolytic pathways and impede Ca2+ binding to troponin-C.

3. Central Fatigue Model

• Central fatigue occurs when muscle performance is limited by factors related to skeletal muscle recruitment, excitation, and contraction influenced by the central nervous system.

Hypotheses:

• Increased levels of serotonin (and possibly dopamine and acetylcholine) may reduce nerve impulses reaching muscles.

• Inhibitory reflexes from working muscles can feedback to the spinal cord, consequently reducing α-motor neuron recruitment.

Research Evidence Supporting Central Fatigue

• Serotonin: Levels rise during prolonged exercise, coinciding with exhaustion; serotonin agonists impair endurance, whereas antagonists enhance performance.

• Motor Unit Recruitment: During extreme conditions (altitude, heat), motor unit recruitment decreases, suggesting CNS protects muscles from damage.

Conclusion:

Central fatigue may serve as a protective mechanism to prevent harm to bodily systems.

4. Psychological Model

• This model suggests that the ability to sustain exercise stems from conscious effort, wherein discomfort tolerance dictates performance.

• There exists a conflict with the central fatigue model, which posits that CNS involuntary control prevents overexertion to mitigate risk of injury.

Summary of the Models

Conclusion

Each model presents unique aspects of muscle fatigue. While metabolic depletion and waste accumulation models focus on the muscle, the central fatigue model highlights the brain's role, suggesting fatigue also has an involuntary component governed by the CNS. Overall, understanding muscle fatigue requires a holistic view incorporating both peripheral and central mechanisms.