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Vocabulary flashcards covering the physiological mechanisms of fatigue, factors influencing athletic performance across different event durations, and muscle recruitment concepts from the lecture.
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Muscle Fatigue
The decline in force or power output during repeated muscle contractions, where power is calculated as force multiplied by shortening velocity.

Sites of Fatigue Model
A physiological framework mapping candidate locations of fatigue from central motor recruitment in the brain down through peripheral excitation-contraction coupling to actin-myosin cross-bridge interaction.
Central Fatigue
Fatigue driven by the central nervous system, characterized by reductions in motor unit recruitment and motor unit firing frequency.
Brachioradialis Motor Unit Firing Rate Reduction
During sustained isometric contractions at 25–30% MVC, motor unit firing rates decrease by 20% at the midpoint of the contraction and by 30% at task failure (Calder et al., 2008).
Peripheral Fatigue: Neural Factors
Fatigue mechanisms occurring downstream of the central nervous system, including inability of the sarcolemma Na+/K+ pump to maintain action potential frequency or an action potential block in the T-tubules.
Peripheral Fatigue: Mechanical Factors
Impairments in cross-bridge cycling and tension development, often caused by high H+ concentration inhibiting Ca2+ release from the SR, impairing Ca2+ binding to troponin, or slowing Ca2+ re-uptake.
Peripheral Fatigue: Energetics of Contraction
Reductions in maximal force caused by high rates of ATP hydrolysis accumulating metabolites such as ADP, Pi, and H+, where Pi inhibits cross-bridge binding to actin (Nelson & Fitts, 2014).
Free Radicals
Highly reactive molecules containing unpaired electrons in their outer orbital produced during exercise; they damage proteins (myosin and troponin), limit strong cross-bridge binding, and disrupt potassium homeostasis (Reid, 2001).

Cellular Redox State vs. Isometric Force Curve
An inverted U-shaped relationship showing that optimal levels of reactive oxygen species maximize force output, whereas excessively reduced or oxidized states impair muscle performance.

Order of Muscle Fiber Type Recruitment
The progressive recruitment of muscle fiber types with increasing exercise intensity: Type I fibers up to ∼40%V˙O2max, Type IIa fibers at ∼40–75%V˙O2max, and Type IIx fibers above 75%V˙O2max.

Ultra Short-Term Performances
Athletic events lasting less than 10 seconds, limited primarily by Type II muscle fiber recruitment, motivation, skill, and phosphocreatine (PC) / anaerobic glycolysis energy systems.

Short-Term Performances
Athletic events lasting 10–180 seconds, shifting from 70% anaerobic at 10 s to 60% aerobic at 180 s, where high H+ accumulation limits performance and ingestion of buffers like bicarbonate (HCO3−) can improve performance.
Bicarbonate Buffering System
The chemical equilibrium CO2+H2O⇌H2CO3⇌HCO3−+H+ catalyzed by carbonic anhydrase to buffer excess hydrogen ions generated during high-intensity exercise.

Moderate-Length Performances
Aerobic events lasting 3–20 minutes, requiring energy expenditure near maximal oxygen uptake (V˙O2max) with aerobic ATP contribution rising from 60% at 3 min to 90% at 20 min.

Intermediate-Length Performances
Aerobic events lasting 21–60 minutes, typically run at less than 90%V˙O2max, where running economy, lactate threshold, and percentage of Type I muscle fibers are key determinants.
Sub 2-Hour Marathon Requirement
The physiological requirement for an elite distance runner to sustain a V˙O2 of 67ml⋅kg−1⋅min−1 over the marathon distance (Jones et al., 2021).

Long-Term Performances
Aerobic events lasting 1–4 hours, where liver and muscle glycogen stores decline, making carbohydrate intake during exercise and hydration critical for performance maintenance.
Hyponatremia
A condition of abnormally low blood sodium levels affecting approximately 4% of ultra-endurance athletes, caused by electrolyte loss from dehydration/vomiting or severe sodium dilution from excessive fluid intake.