Week 14: Models of Skeletal Muscle Fatigue

Part 2

5. The Cardiovascular/Anaerobic Threshold (CVS/AT) Model

Overview of VO2 Plateau During Exercise

The concept presented is that during an incremental exercise test, the volume of oxygen uptake (VO2) reaches a plateau due to a restricted capacity for oxygen delivery, which is primarily dependent on the heart’s ability to deliver oxygen-rich blood. This plateau also signifies the initiation of muscle hypoxia, where the muscles are insufficiently oxygenated to sustain aerobic metabolism.

Background

1. Endurance Performance Determination:
   a. The endurance performance of an individual is fundamentally determined by the heart's ability to pump substantial volumes of blood and oxygen to the muscles.
   b. The relationship is expressed through the formula:
   $VO2 = Q imes (a - v)<em>{O2 ext{ diff}}$ where Q is cardiac output, and (a - v){O2 ext{ diff}} refers to the arteriovenous oxygen difference.
   c. Muscles continue to perform work until the delivery of oxygen becomes inadequate, which is evidenced by a plateau in VO2 during incremental exercise, resulting in hypoxia or anaerobiosis.

2. Impact of Training on Endurance:
   a. Training enhances cardiovascular fitness (VO2max) by increasing cardiac output (CO) and the extraction of oxygen.
   b. Consequently, these adaptations prolong the onset of skeletal muscle anaerobiosis during intense exercise by minimizing lactate levels ([La]) at exercise intensities exceeding the anaerobic threshold (AT).
   c. Enhanced ability to utilize fatty acids boosts endurance performance.

The Limitations of the CVS/AT Model

1. Hypothesis of Muscle Oxygenation:

   • The theory underpinning the anaerobic threshold (AT) suggests that before reaching a certain intensity, the heart provides enough oxygen to the active muscles to maintain aerobic metabolism effectively.

   • Post anaerobic threshold more specifically, there is inadequate oxygen delivery to the mitochondria, causing a shift towards anaerobic metabolism. The exercise intensity where VO2 plateaus should coincidently align with the anaerobic threshold; however, discrepancies exist in this thesis that require investigation.

2. Physiological Adaptations Through Training:

   • Support for the CVS/AT model correlates with physiological adaptations observed through training.

   • For example, VO2max improvement with training is noted alongside a rightward shift of the AT/Lactate Threshold (LT), indicating augmented oxygen delivery to the muscles and enhanced aerobic capacity.

Muscle and Cardiac Interdependencies

1. Consequences of Insufficient Blood Flow:

   • When blood flow to muscle fibers is restricted, anaerobiosis rises, preventing the oxidative removal of lactic acid, consequently leading to lactic acid accumulation that impedes skeletal muscle relaxation.

   • Furthermore, the heart, being a muscle itself, also requires sufficient blood and oxygen supply; thus, any impairment in the pump capacity of the heart, or its ability to perform work without enhancing CO and coronary flow, would limit the oxygen supply to the heart.

Assumptions and Observations in Maximal Exercise

1. Cardiac Output (CO) Limitations:

   • The assumption made is that CO exhibits a plateau or decrease during maximal exercise efforts; however, it is observed that this plateau is observed in only 50% of tests at a VO2max level.

   • In healthy athletes, the absence of myocardial ischemia (lack of blood flow to the heart muscle) arises, indicating that the observed plateau does not imply ischemic conditions, and exercise is halted before muscle anaerobiosis emerges.

Factors Limiting Cardiac Output

1. Reasons for Limited CO:

   • Potential causes of decreased CO include:

     • Limited venous return

     • Constraints on the heart's volume capacity

     • Limits concerning the cardiac contractility.

   • These factors are prevalent within patients suffering from cardiovascular diseases exhibiting restricted exercise capacity.

   • A question arises regarding the potential of these factors being purposefully controlled in healthy individuals to safeguard the heart against undue strain.

Evidence of Cardiac Self-Protection

1. Physiological Responses at Altitude:

   • At high altitudes, observations indicate that the maximum lactate concentration ({La}) is lower than at sea level, referred to as the lactate paradox.

   • The maximum heart rate, stroke volume, cardiac output, and VO2 also decrease at altitude when compared to sea level, which means that muscle recruitment is minimized under these conditions.

   • Despite higher stress, there is no accompanying change in myocardial function, allowing for aerobic muscle function even under fatigue conditions.

2. Continuous Heart Oxygenation:

   • PaO2 levels remain consistent during exercise, ensuring a substantial CO to the heart and active muscles, resulting in adequate oxygenation of heart tissue even at peak heart rates.

   • Furthermore, the heart is capable of metabolizing alternative fuels, including ketones and lactic acid.

   • Healthy individuals typically do not experience ischemia during physical exertion, showcasing protective mechanisms against potentially dangerous conditions arising from exercise.

6. The Central Governor Theory

1. Overview of the Central Governor Theory:

   • This theory utilizes classical control system terminology, including sensor, feedback, controller, and effector mechanisms.

   • It posits that the reason healthy individuals do not suffer ischemia during exercise stems from feedback from the heart or other oxygen-sensitive organs, signaling to a central governor within the brain.

   • This central governor reduces motor unit recruitment during exercise to protect vital organs and tissues from hypoxia or ischemia.

2. The Concept of Inputs Adjustments in Heat Exercise:

   • The heat exercise context serves as an illustrative example of homeostasis failure, where inputs vary from expected due to challenges imposed on the body.

   • The brain anticipates feedback from physiological conditions and modifies exercise effort accordingly.

Catastrophic vs. Anticipatory Regulation Model in Heat Fatigue

1. Catastrophic Model Overview:

   • This model postulates that fatigue in heat derives from the body's failure to regulate temperature. Specifically, an elevated body temperature leads to reduced brain activity, which in turn affects muscle activation.

   • Key studies revealed that at 40 degrees Celsius, athletes tend to halt or significantly reduce their activity, linking fatigue with critical temperature thresholds.

2. Critique of Previous Studies

   • Researchers succeeded in demonstrating that fixed trials led to premature exercise cessation disregarding the possibility that athletes could have previously chosen to slow down driven by various physiological inputs before reaching critical thresholds.

Anticipatory Regulation in Exercise Performance

1. Anticipatory Regulation Model:

   • This alternative model indicates that performance adjustments occur well before critical limits are met, suggesting athletes deliberately slow down to prevent excess heat accumulation rather than reactively.

   • There is compelling evidence indicating that power output reduction occurs even at sub-maximal temperatures, suggesting that cognitive factors aside from direct thermal effects dictate pacing strategies.

2. Factors Influencing Decisions:

   • Athletes slow down potentially influenced by perceived straining, experience, current physical conditions, which are continually interpreted by the brain to modulate performance output effectively.

   • The core premise is that fatigue is a cognitive construct rather than purely a physiological event.

Conclusion of the Theoretical Models

1. Classical Exercise Models Fallacy:

   • Traditional catastrophic models inadequately factor cognitive and psychological components, limiting their understanding of fatigue. They lack recognition of how the brain integrates environmental, motivational, and experiential data for performance outputs.

2. Cognitive Over Physically Driven Regulation:

   • The conclusion drawn is that fatigue is primarily managed through anticipatory regulation, suggesting an intricate interplay among physiological states, mental cues, and behavioral responses relevant to exertional capacities.