Untitled Quiz

Physiology of Training: Effects of Aerobic and Anaerobic Training

• Principles of Training:
  • Overload: For a system or tissue to improve, it must be challenged with an intensity, duration, or frequency of exercise that it is not accustomed to. Over time, the system or tissue adapts to this increased load.
  • Specificity: The training effect is specific. The training effect is limited to the muscle fibers involved and specific energy systems (aerobic or anaerobic) used. The velocity and type of contraction (eccentric, concentric, isometric) also matter.
  • Reversibility: Gains are lost when overload is removed.

Endurance Training and VO2 Max

• VO2 max: Maximal oxygen uptake, also called maximal aerobic power, is the body's maximum capacity to transport and use oxygen during exercise using large muscle groups (e.g., legs).
• Training to increase VO2 max: This involves large muscle groups, dynamic activity, and at least 20-60 minutes of exercise, at least 3 times per week, and at an intensity of at least 50% of VO2 max.
• Expected Increases: Improvements in VO2 max following 2-3 months of endurance training generally range from 15-20%, though improvements in individuals with high initial VO2 max may be lower (2-3%). High initial VO2 max individuals require higher training intensities (>70% VO2 max) while individuals with low initial VO2 max may benefit from lower training intensities (40-50% VO2 max).

Impact of Genetics on VO2 Max and Training Response

• Heritability: Genetics determines approximately 50% of VO2 max in sedentary adults.
• Training Response: Genetics significantly influences the training response. Average improvement in VO2 max is 15-20%, but this can vary considerably among individuals, with low responders reaching a 2-3% improvement and high responders potentially reaching a 50% increase with rigorous training. Heritability of training adaptations is approximately 47%.

Range of VO2 Max Values

• Values presented in a table show typical VO2 max values in various healthy and diseased populations (expressed in ml · kg⁻¹ · min⁻¹). Values for cross-country skiers and distance runners were significantly higher than sedentary individuals.

Why Does Training Improve VO2 Max?

• Fick Equation: VO2 max = maximal cardiac output × a-vO2 difference.
• Differences in VO2 max: Primarily due to differences in stroke volume.
• Short-term training (~4 months): The increase in stroke volume is the primary factor enhancing VO2 max.
• Long-term training (~32 months): Both stroke volume and a-vO2 difference contribute to improve VO2 max.

Factors Influencing Stroke Volume with Training

• Preload (EDV): Increased preload, meaning a larger end-diastolic volume, is largely due to an increase in plasma volume.
• Afterload (total peripheral resistance): A decrease in afterload, reducing total peripheral resistance. This usually means a reduction in sympathetic vasoconstriction and an increase in maximal muscle blood flow.
• Contractility: Changes related to contractility occur rapidly.

Arteriovenous O2 Difference (a-vO2 max)

• Endurance Training: Increased a-vO2 difference is a result of adaptations enhancing oxygen extraction from blood.
• Capillary Density: Increased capillary density, slower blood flow, and reduced diffusion distance to the mitochondria contribute to the increased oxygen extraction ability of the muscles.
• Mitochondrial Number: Increased mitochondrial number within the muscles further enhances oxygen's extraction from the blood.

Factors Causing Increased VO2 Max

• Maximal Cardiac Output: Increased maximal cardiac output is a crucial driver of increased VO2 max, as this correlates with a higher stroke volume.
• a-v O2 difference: An increase in arteriovenous oxygen difference. Increased oxygen extraction by the muscles occurs due to improvements in capillary density, mitochondrial number, and metabolic rate.
• Muscle Blood Flow: Also, an increase in muscle blood flow.
• Capillaries and Mitochondria: An increase in the number and density of capillaries and mitochondria within the muscles aids in oxygen delivery and utilization.
• Neural Response: The sympathetic nervous system influences muscle activity.

Endurance Training: Effects on Performance and Homeostasis

• Homeostasis: Prolonged, submaximal work capability depends on homeostasis maintenance.
• Adaptation: Endurance training leads to:
  • Faster transition from rest to steady state.
  • Reduced reliance on liver and muscle glycogen stores.
  • Cardiovascular and thermoregulatory adaptations. Adaptations are due to structural and biochemical changes.
  • Early metabolic changes are from neural and hormonal changes.

Endurance Training-Induced Changes in Fiber Type and Capillarity

• Fast-to-slow shift in muscle fiber type: Reduced fast myosin and increased slow myosin activity translate to improved work performance requiring comparatively less ATP.
• Increased number of capillaries: Enhanced oxygen and nutrient delivery to muscles, combined with increased waste removal.

Endurance Training Increases Mitochondrial Content in Skeletal Muscle

• Mitochondrial Volume: Endurance training enhances mitochondrial volume and improves the ability to utilize fats as fuel and increase metabolic rate.
• Mitochondrial Turnover: Increased turnover of mitochondria (breakdown and replacement of damaged ones) improves oxidative capacity.
• Training Time: Mitochondrial volume increases quickly (within first 5 days) and may increase by 50-100% within 6 weeks, dependent on the training intensity and duration.

Endurance Training Reduces the O₂ Deficit

• Oxidative ATP Production: Enhanced reliance on oxidative ATP production during exercise, resulting in a faster rise in oxygen uptake and a quicker reach of a steady state.
• Lower Oxygen Deficit: Lower oxygen deficit results in reduced lactate and H⁺ formation and less PC depletion. This also helps maintain homeostasis.

Biochemical Adaptations and the Plasma Glucose Concentration

• Plasma glucose: This is the primary fuel for the nervous system.
• Endurance Training: Endurance training leads to improved glucose regulation during prolonged submaximal exercise by maximizing fat utilization.

Endurance Training Increases Fat Metabolism During Exercise

• Transport of FFA into muscle: Improvements in capillary density and fatty acid binding protein and translocase enhance fatty acid uptake.
• FFA Transport: This process facilitates the transport of fatty acids from the cytoplasm to the mitochondria.
• Mitochondrial Enhancements: Increasing mitochondrial number, size, and membrane surface area results in higher oxidative capacity and more efficient utilization of fats as a fuel.
• Fat Transport Enzymes: Increased enzymes (like carnitine palmitoyltransferase I & fatty acid translocase) support efficient transport of fatty acids and enhanced mitochondrial oxidation of FAs.
• Beta-oxidation: Key enzymes involved in β-oxidation are boosted by training, further promoting fat utilization, and thus sparing glucose and muscle glycogen.
• Citrate Inhibition: When citrate levels rise high, there's reduced activity of PFK and glycolysis.

Endurance Training Improves Muscle Antioxidant Capacity

• Free Radicals: Chemical molecules with an unpaired electron that are highly reactive, and can damage cellular structures, proteins, membranes, DNA.
• Muscle Contraction: Contracting muscles produce free radicals. Free radical production is highly correlated to fatigue.
• Antioxidants: Cells contain molecules that neutralize them (antioxidants) – endogenous (produced by the body) and exogenous (from diet).
• Training Effect: Training increases endogenous antioxidants, reducing oxidative stress and preserving muscle function.

Exercise Training Improves Acid-Base Balance During Exercise

• FFA Oxidation: Increased fatty acid oxidation and reduced PFK activity mean less pyruvate formation, less lactate formation.
• Lactate Formation: Lower lactate formation leads to a decreased buildup of H+, and contributes to improved acid-base balance during exercise.
• LDH Activity: The form of lactate dehydrogenase that has a lower affinity for pyruvate (H⁺ form) is more dominant in trained individuals.
• Mitochondrial Uptake: Increased mitochondrial uptake of pyruvate and NADH.
• H⁺ Shuttles: The improved capacity of the muscles to buffer and move protons (H⁺) to the electron transport chain (ETC).

Detraining and VO2 Max

• Rapid Decrease: VO2 max decreases quickly, declining by about 8% within 12 days and by 20% in 84 days, from detraining.
• Initial Decrease: The initial phase of detraining (12 days) is primarily due to a reduction in stroke volume (SV).
• Plasma Volume: Rapid loss of plasma volume is associated with the decrease in stroke volume.
• a-vO2 max: The maximal difference in oxygen concentration between arterial and venous blood also decreases.
• Mitochondria: Mitochondrial structure may not change, contrasting with increased capillary density, and this is independent to whether training occurs or not.

Time Course of Training/Detraining Mitochondrial Changes

• Training Effects: Increase mitochondrial content doubles within 5 weeks of training.
• Detraining Effects: About 50% of increase in mitochondrial content diminishes within 1 week of cessation of training.
• Retraining: Adaptations can be regained within 3-4 weeks of retraining.

Muscle Adaptations to Anaerobic Exercise Training

• Anaerobic Exercise: Short-duration, high-intensity exercise (~10-30 seconds), often called "sprint training."
• Energy Systems: primarily relies on ATP-PC system initially, transitioning to more aerobic contribution during prolonged exertion (20-30 secs).
• Performance Increase: 4-10 weeks of sprint training can increase peak anaerobic power by 3-25%.
• Capacity Improvements: Adaptations focus on increasing muscle buffering capacity, increasing type II muscle fiber size, and increasing enzymes involved in ATP-PC system and glycolysis.