Comprehensive Notes on Fatigue and Skeletal System Responses

Fatigue

Definition of Fatigue

1. Muscular Performance: Fatigue refers to decrements in muscular performance during continued effort, often accompanied by sensations of tiredness.

2. Power Output: It is characterized by the inability to maintain the required power output to continue muscular work at a given intensity. Importantly, fatigue is reversible with rest.

Complex Phenomenon of Fatigue

Fatigue is influenced by several factors:

• Type and Intensity of Exercise: Different forms and intensities of exercise lead to fatigue in different ways.

• Muscle Fiber Type: For instance, Type 2 b fibers lack mitochondria and rely solely on anaerobic processes.

• Training Status and Diet: A more fit individual can sustain a higher fatigue threshold compared to an unfit one. Diet (fed vs. fasted state) also plays a role in energy availability.

Major Causes of Fatigue

1. Inadequate Energy Delivery/Metabolism: If the body can't deliver or produce ATP, fatigue results.

2. Accumulation of Metabolic Byproducts: Accumulation of H+ ions and other metabolites changes the energy status of cells and signals a need to slow down.

3. Neural Transmission: Involves both central and peripheral fatigue, affecting muscle contraction mechanisms.

Energy Systems

Fatigue occurs when energy systems cannot generate adequate ATP:

1. Phosphocreatine Depletion:

   • Reaction: ADP + PCr →←ATP + Cr

   • This provides energy very rapidly for 10-15 seconds and is swiftly depleted.

   • Supplementation: Creatine monohydrate can increase muscle creatine levels, enhancing phosphate binding.

   • Type 2 b fibers primarily rely on phosphocreatine, making them susceptible to fatigue as they have no mitochondria.

2. Glycogen Depletion:

   • Glycogen reserves in muscle (approximately 1600 kcal) and liver (about 400 kcal) are limited and can become depleted quickly during prolonged exercise.

   • Depletion correlates with fatigue and can result in the "hitting the wall" phenomenon in endurance athletes (e.g., marathon runners).

   • Muscle fibers types 1 and 2a use glycogen to produce ATP during prolonged activity, especially in high-intensity situations.

   • Low blood glucose due to muscle glycogen depletion can result in fatigue and decreased performance.

Factors Affecting Fatigue

Muscle Fiber Recruitment Patterns

• Type 2 fibers deplete faster under high intensity, whereas Type 1 fibers are used during low/moderate activities.

• Muscles used for the activity deplete fastest due to the demand placed on them.

Blood Glucose Levels

• Insufficient muscle glycogen leads to increased reliance on liver glycogen, which fuels glucose supply through glycogenolysis during prolonged exercise.

Metabolic Byproducts of Fatigue

• Phosphate (Pi): Accumulation can impede muscle function and reduce energy production. The reactions:

  • ADP + Pi →←ATP + Cr

  • ATP + H2O →←ADP + Pi + energy + H+

• Heat: An increase in core temperature from exercise stresses the body and can lead to faster carb usage and potential muscle function impairment.

• H+ Ions: Produced during glycolysis and ATP hydrolysis, they lower the pH in muscles causing acidosis, thus impeding enzyme function hence slowing metabolism. Buffers are employed to counteract this pH drop.

Neural Transmission Fatigue

Central Nervous System (CNS)

• The central fatigue signals related to muscle performance originate in the brain, where inhibitory feedback may result in reduced motor output.

Peripheral Nervous System (PNS)

• Peripheral fatigue can occur at the neuromuscular junction due to altered neurotransmitter dynamics and changes in membrane potentials affecting calcium release.

Ergogenic Effects of Caffeine

• If taken in low to moderate doses, caffeine can improve muscle contraction and influence central nervous system functions enhancing performance.

• Optimal timing for ingestion is approximately 60 minutes before activity; habitual users may not experience increased performance.

Skeletal System Responses

Bone Remodeling

• Bone Remodeling: A continuous cycle of bone resorption and formation, recycling about 5-7% of bone mass weekly.

• Wolff’s Law: States that bone adapts to stresses placed upon it, leading to increased bone mineral density (BMD) under load and decreased BMD in the absence of stress.

Calcium Regulation in Bones

• Bones act as a reservoir for calcium and phosphorus, regulating blood calcium levels alongside kidneys and intestines.

• Hormones such as parathyroid hormone (PTH) and calcitonin regulate calcium release, affecting bone resorption and density.

Bone Composition

• Trabecular Bone: More porous and spongy, found in areas like the epiphysis of long bones.

• Cortical Bone: Densely packed, comprises approximately 80% of the skeletal system.

Bone Development and Adaptation

1. Growth Types:

   • Appositional Growth: Increases thickness.

   • Longitudinal Growth: Lengthening of bones.

   • Modeling: Adjusts shape and strength through resorption and formation.

2. Remodeling: Ongoing process ensuring balance between bone resorption and deposition, typically driven by mechanical stress.

Hormones in Bone Remodeling

• Calcitonin: Facilitates calcium deposition in the bone, counteracting high blood calcium levels.

• PTH: Promotes bone resorption in response to low calcium levels.

• Vitamin D: Enhances intestinal calcium absorption.

Mechanotransduction in Bone Response

• Mechanotransduction: Refers to the bone's response to mechanical loading, leading to adaptations and increased BMD through processes like fluid movement triggered by exercise.

Adaptations to Bone with Exercise

• Mechanostat Theory: Indicates bones adapt to the minimal effective strain to maintain or enhance BMD.

• Progressive overload and adequate recovery are essential to stimulate bone growth and avoid injury.

Effects of Detraining

• Loss of bone mass occurs in individuals with reduced activity, such as astronauts in microgravity or individuals with paralysis, due to decreased mechanical loading.