Lec 7 Factors Affecting Human Performance
Chapter 19: Factors Affecting Human Performance
General Overview
Focus on performance factors for the remainder of the semester, exploring:
- Limiting factors
- Training
- Nutrition and body composition
- Assessments
- Special populations
- Ergogenic aids
Lecture Outline
Topics to be covered include:
- Fatigue:
- Definition
- Sites of Fatigue
- Central
- Peripheral
- Factors limiting performance based on activity duration:
- All-out anaerobic performances
- All-out aerobic performances
- Concept of Athlete as Machine
Fatigue
Definition: Fatigue is defined as an inability to maintain power output or force during repeated muscle contractions.
Two primary types of fatigue:
- Central Fatigue: Central nervous system (CNS).
- Peripheral Fatigue: Neural factors, Mechanical factors, Energetics of contraction
Central Fatigue
What is Central Fatigue?
Reduction in motor units activated
Reduction in motor unit firing frequency
Central nervous system arousal can alter the state of fatigue
By facilitating motor unit recruitment
Increasing motivation
Physical or mental diversion
Excessive endurance training (overtraining) is associated with:
Reduced performance, prolonged fatigue, etc.
Related to brain serotonin levels, but also, dopamine and norepinephrine.
Central Fatigue
“Central Governor” model
Conscious and subconscious brain, not spinal cord or motor unit
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While central fatigue is certainly a factor it is estimated to only contribute about 10% to total fatigue
Peripheral Fatigue: Neural Factors
Neuromuscular junction
Not the site of fatigue
Sarcolemma and transverse tubules
Altered ability of muscle membrane to conduct an action potential
Inability of Na+/K+ pump to maintain action potential amplitude and frequency
This doesn’t seem to cause fatigue
Can be improved by training
An action potential block in the T-tubules
Can happen under certain conditions
Reduction in Ca++ release from sarcoplasmic reticulum leads to reduced force production
Peripheral Fatigue: Mechanical Factors
Cross-bridge cycling and tension development depends on:
Arrangement of actin and myosin
Ca++ binding to troponin
ATP availability
High H+ concentration may contribute to fatigue
Reduce the force per cross-bridge
Reduce the force generated at a given Ca++ concentration
Inhibit Ca++ release from SR
Longer “relaxation time” is a sign of fatigue
Due to slower cross-bridge cycling
Peripheral Fatigue: Energetics of contraction
Imbalance between ATP requirements and ATP generating capacity
Accumulation of Pi
Inhibits maximal force
Reduces cross-bridge binding to actin
Inhibits Ca++ release from SR
Rate of ATP utilization declines faster than the rate of ATP generation
Maintains ATP concentration
The cell does not run out of ATP
Summary Sites of Fatigue § The cross-bridge's ability to “cycle” is important in continued tension development. § Fatigue may be related, in part, to the effect of a high H+ concentration and the inability of the sarcoplasmic reticulum to rapidly take up Ca++. § The end result may be a longer relaxation time, which affects the rate of muscle contraction.– Extends the time it takes for the muscle to return to resting length § Fatigue is directly associated with a mismatch between the rate at which the muscle uses ATP and the rate at which ATP can be supplied. § Cellular fatigue mechanisms slow down the rate of ATP utilization faster than the rate of ATP generation to preserve the ATP concentration and cellular homeostasis
Peripheral Fatigue: Energetics of contraction
Muscle fiber recruitment in increasing intensities of exercise
Type I → Type IIa → Type IIx
Up to 40% VO2 max type I fibers recruited
Least fatigable because they’re highly aerobic
Type IIa fibers recruited at 40–75% VO2 max
These can do Aerobic & Anaerobic pretty well
Exercise >75% VO2 max requires IIx fibers
These are predominantly anaerobic
Results in increased lactate and H+ production
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Radical Production During Exercise Contributes to Muscle Fatigue During Prolonged Exercise
Exercise promotes free radical production in muscles
Radicals are molecules that contain an unpaired electron in outer orbital
Capable of damaging proteins and lipids in muscle
Can contribute to fatigue during exercise > 30 minutes long
Damage contractile proteins (myosin and troponin)
Limits the number of cross-bridges in strong binding state
Depress sodium/potassium pump activity
Supplementation with most antioxidants does not prevent fatigue and high antioxidant doses can impair muscle performance
Summary of fatiguing issues § Central fatigue (≤10% of fatigue) § Sarcolemma conduction and t-tubule block § Accumulation of H+ and Pi § Inability to produce ATP at a rate equal to its utilization during heavy exercise § Reactive oxidative species production during prolonged exercise
Factors Limiting Performance
Several factors contribute to performance limitations, which can be categorized into:
1. Diet:
- Carbohydrate intake
- Water intake
2. Environment:
- Altitude
- Heat
- Humidity
3. Strength/Skill:
- Practice
- Natural endowment
- Body type
- Muscle fiber type
4. CNS Function:
- Arousal
- Motivation
5. Energy Production:
- Anaerobic sources (Phosphocreatine, Glycolysis)
- Aerobic sources (VO2 max, Cardiac output, O2 delivery)
- Related metrics include hemoglobin content, partial pressure of O2 (PO2), O2 extraction, and mitochondrial function.
Sites of Fatigue
Central Fatigue:
- Causes include:
- Decreased motor unit activation
- Reduced motor unit firing frequency
- Factors affecting CNS arousal which include motivation, physical or mental diversion, and effects of excessive training.Peripheral Fatigue: Factors here could be:
- Altered ability of muscle membranes (sarcolemma) to conduct action potentials.
- Mechanisms of fatigue include disruptions in ionic balance (K+, Na+) and reduction in calcium (Ca++) release.
Detailed Mechanisms of Fatigue
Potential Sites of Fatigue:
1. Spinal cord
2. Peripheral nerve
3. Muscle membranes (sarcolemma, transverse tubular system)
4. Calcium release from the sarcoplasmic reticulum (SR)
5. Actin-myosin interactions, leading to changes in cross-bridge tension and heat production.
Specific kinds of performance
Now we’ve talked about particular sources of fatigue which may limit performance
Central
Changes in motor recruitment
Due to afferent information, brain metabolism, changes in neurotransmitters, and motivation
Peripheral
Altered neuromuscular coupling
Changes in metabolites that interfere with muscle mechanics
Mismatched ATP requirement and ATP generation
These are the general points where fatigue seems to occur
However, the source of fatigue may differ based on the activity being performed (specificity)
Short-term High intensity
Long-term “high” intensity
Performance Factors Related to Fiber Type
Muscle fiber recruitment increases with intensity:
- Type I fibers recruited at lower intensities (~40% of VO2 max)
- Type IIa fibers between 40–75% of VO2 max
- Type IIx fibers for performances >75% of VO2 max, predominantly anaerobic, leading to increased lactate production.
Exercise Duration Categories
Ultra Short-Term Performances
Less than 10 seconds (e.g.,high power events 100-meter dash):
- Rely primarily on Type II muscle fibers and anaerobic energy sources (ATP-PC system and glycolysis).
- Motivation, skill, and arousal play key roles in force generation
- Creatine supplementation may enhance performance.
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Short-Term Performances
Lasting 10-180 seconds:
- Transition from anaerobic to aerobic metabolism.(~70% energy supplied anaerobically at 10s )
(60% supplied aerobically at 180s)
- Significant contributions from anaerobic glycolysis; H+ accumulationimpacts performance (interferes with Ca++ binding with toponin & Interferes with glycolytic ATP production )
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Short-Term Events: can vary based on their duration because this is a transitory period beyond the capacity of the ATP/PC system, but too short to reach beyond oxygen deficit.
About 50/50 at ~2 minutes of exercise
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Moderate-Duration Performances
3-20 Minutes (Moderate):
- Vo2 max is critical, with a reliance on aerobic metabolism.60% ATP generated aerobically at 3 min
90% ATP supplied aerobically at 20 min
High VO2 max is important
High maximal stroke volume
High arterial oxygen content
Hemoglobin content
Inspired oxygen
Moderate-Duration Performances
These activities require an energy expenditure near VO2 max, with type II fibers being recruited, in addition to type I fibers.
Any factor interfering with oxygen delivery (e.g., altitude or anemia) would decrease performance, since it is so dependent on aerobic energy production. High levels of H+ accompany these types of activities
Intermediate-Duration Performances
Events lasting 21–60 minutes
Predominantly aerobic
Usually conducted at <90% VO2 max
High VO2 max is important
Other important factors
Running economy or exercise efficiency
High percentage of type I muscle fibers
Environmental factors
Heat
Humidity
State of hydration
Lactate threshold
~7,400m → ~20:00 (est.) ~6m/s
~21,000m → ~60:00(est.) ~5.9m/s
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Long-Term Performances
1-4 Hours (Long-Term): clearly aerobic
- Carbohydrate availability and hydration become crucial. Environmental factors (heat/humidity) significantly impact performance.Maintaining rate of carbohydrate utilization
Muscle and liver glycogen stores decline
Ingestion of carbohydrate
Maintain carbohydrate oxidation by the muscle
Consumption of fluids and electrolytes
Diet also influences performance
Is Maximal Oxygen Uptake Important in Distance Running Performance?
VO2 max sets the upper limit for ATP production in endurance events
Even though race is not run at 100% VO2 max
A 2:15 marathon requires sustaining a VO2 of ~ 60 ml•kg-1•min-1
However they cannot perform at max for 135 min. So their maximal aerobic capacity must be higher
= At 80% VO2 max, this requires VO2 max of 75 ml•kg-1•min-1
Performance determined by:
%VO2 max at which runner can maintain performance
Estimated by the lactate threshold
Running economy
Factors Affecting Performance in Ultra-Endurance Events
Examples
166 km mountain run, Triple Iron Triathlon, 24 hour run
Most important variables
VO2 max
%VO2 max that can be sustained
Metabolic responses
Fat oxidation is 3.5x higher after event
Consistent with exercise at <60% VO2 max
50% reduction in muscle glycogen stores
Potential for hyponatremia
Only affects 4% athletes
Excessive sweating & fluid replacement without electrolytes
Athlete as Machine
Continuing goal to improve performance
Potential to treat elite athletes like machines
Collection of parts evaluated by specialists
Implementation of research to improve performance
May be exposing athletes to risk
In research or in implementation of techniques
Institutional Review Boards
Minimize risk to subjects being studied