Week 9 - Physiology of Training Flashcards
What are the key things to consider when training
Source of energy and muscle fibre recruitment used for force production
What are the principles of training
Overload: Training effect occurs when a phyisological system is exercised at a level beyond which it is normally accustomed
Specificity: Training effect is specific to:
1. Muscle fibres
2. Energy system involved
3. Velocity of contraction
4. Type of contraction
Reversibility: Gains are lost when training ceases
What effects does endurance training have on VO2 max
Increases VO2 max
Average increase = 15-20%
Smaller increases in individuals with high VO2
Up to 50% in low VO2 max
Difference between short and long adaptations of exercise-induced improvements of VO2 max
Short: Increase in SV and cardiac output
Long: Increase in SV, and a-vO2
How does endurance training increase stroke volume
Increases preload (plasma volume and venous return)
Decreases afterload (aterial constriction)
Increases contractility (greater force from each contraction)
Why is heart rate lower following training
Increased stroke volume compensates for it
Resting HR lower after training because of vagal tone increased, allowing for greater filling time
How does training increases arteriovenous O2 difference
- Muscle blood flow increases (Decreases sns vasoconstriction and increase diameter of arteries)
- Improved ability of muscle fibres to extract and utilise O2 from the blood (increased capillary density and mitochondrial number)
- Increased capillary supply and oxygen delivery in trained muscle
What difference do vascular remodelling and muscle metabolic changes make to muscle blood flow in exercise
Blood flow is lower during submaximal exercise because the a-V difference is greater
Blood flow is higher during maximal exercise
What adaptations in muscle fibre occurs in maintaining homeostasis from training
- Shift in muscle fibre type and increased number of capillaries
- Increased mitochondrial volume
- Training-induced changes in fuel utilisation
- Increased antioxidant capacity
- Improved acid-base regulation
How does endurance training promote a shift in muscle fibre type and capillary density
Reduction in fast fibres and increase in slow fibres
Increased number of capillaries surrounding muscle fibres
How does endurance training increase mitochondrial volume and turnover
Increases volume of both subsarcolemmal and intermyofibrillar mitochondria (80%)
Increases in number of ADP transporters in mitochondria membrane = faster ADP uptake into mitochondria and lower cytosolic
How does endurance training induce changes in fuel utilisation
Increased utilisation of fat and sparing plasma glucose and muscle glycogen
Increased transport of FFA into muscle, from cytoplasm to mitochondria, and mitochondrial oxidation of FFA
How does endurance training improve antioxidant capacity of muscle
Contracting muscle produces free radicals = Training increases endogenous antioxidants enzymes
How does endurance training improve acid-base balance during exercise
- Increased in mitochondria leads to increased FFA oxidation and decreased PDK activity and increased mitochondrial uptake of pyruvate and NADH
- Increased FFA oxidation and decreased PFK activity lead to decreased pyruvate formation
- Increased mitochondrial uptake of pyruvate and NADH, decreased pyruvate formation, and increased H4 form of LDH leads to decreased lactate and hydrogen ion formation which ensures that blood pH is maintained
When do mRNA levels typically peak from training-induced muscle adaptation
4-8 hours, back to baseline within 24 hours.
Daily exercise required for training-induced adaptation
What are some secondary messengers in skeletal muscle
AMPK (glucose uptake)
p38 (Important signalling)
PGC-1a (mitochondrial biogenesis, promotes angiogenesis, synthesis of antioxidant enzymes)
CaMK (activation of PGC-1a)
Phosphatase (muscle fibre regeneration and shift)
NFxB (synthesis of antioxidant enzymes)
mTOR (protein synthesis and muscle size)
What are some primary signals to intracellular signalling in response to exercise
Resistance: Mechanical stretch
Endurance: Calcium, AMP/ATP, Free radicals
What biochemical changes in HR and ventilation occur due to endurance training
HR and ventilation reduced due to reduced feedback to cardiovascular control centre and number of motor units recruited
What adaptations occur with detraining on VO2 max
Rapid decrease in VO2 max
Decrease stroke volume, maximal a-v O2 difference
50% of Mitochondrial adaptations lost in 1 week of detraining
Requires 3-4 weeks to regain mitochondrial adaptations
What muscle adaptations occur during anaerobic training
Improves muscle buffering capacity by increasing both intracellular buffers and hydrogen ion transporters
Results in hypertrophy of type 2 muscle fibres and elevates enzymes involved in both ATP-PC system and glycolysis
Promotes mitochondrial biogenesis
Define Musclsr Strength and Muscular Endurance
Muscular strength: maximal force (1 rep max)
Muscular endurance: ability to make repeated contractions
Strength training: High (6-10 reps) and low (35-40 reps) resistance training
What neural adaptations occur during early gains of resistance training
Increased neural drive, number of motor units, firing rate, unit synchronisation, and transmission across neuromuscular junction
Define the terms hyperplasia and hypertrophy
Hyperplasia - increased number of fibres
Hypertrophy - increased cross-sectional area of muscle fibres
What signalling events occur after resistance training
Activation of mTOR for protein synthesis
Molecules that stimulate mTOR activation are PA and Rheb
What is the role of satellite cells in hypertrophy
Satellite cells are stem cells located between the sarcolemma and basal lamina (divide and fuse with adjacent muscle fibres to increase myonuclei)
Resistance training results in parallel increases in muscle fibre size and number of myonuclei
What is the magnitude of genetic influence on hypertrophy
80% of difference in muscle mass between individuals is due to genetic variation
The affect of detraining on strength muscle adaptations
Cessation of resistance training results in muscle atrophy and loss of strength (20-30%) from 20-30 days
Individuals can make rapid recovery during retraining from detraining (muscle memory)
What is the key mechanism responsible for inactivity induced muscle atrophy
Increased radical production promotes muscle atrophy during prolonged inactivity by depressing protein synthesis and increasing degradation
What effects do concurrent strength and endurance training have
Potential for interference of training adaptations.
Mechanisms responsible:
1. Neural factors
2. Overtraining
3. Depressed protein synthesis via AMPK activation and inhibiting mTOR
Possible sites of central and peripheral fatigue
Fatigue: Inability to maintain power output or force during repeated muscle contraction, which is reversible with rest
Central fatigue: CNS
Peripheral fatigue: Neural, mechanical factors, energetics of contraction
What are the sites of central fatigue
Motor units activated & motor unit firing frequency
CNS arousal can alter fatigue (motivation or mental diversion)
Overtraining (Reduced performance, prolonged fatigue)
What are the neural factors in peripheral fatigue
Sarcolemma and transverse tubules:
1. Altered muscle membrane to conduction and action potentials (Na/K pump)
2. An action potential block in the T-tubules (Ca release)
What are the mechanical factors in peripheral fatigue
High H+ concentration may contribute to fatigue:
1. reduce force per cross-bridge
2. Reduce force generated given Ca concentration
3. Inhibit Ca release from SR
End result is longer (relaxation time)
What are the energetics of contraction factors in peripheral fatigue
- Imbalance between ATP requirements and ATP generating capacity (accumulation of Pi)
- Rate of ATP utilisation is slowed faster than rate of ATP generation (Maintain ATP concentration)
What muscle types are recruited based on VO2 max
Type 1 = 40% VO2 max
Type 2a = 40-75% VO2 max
Type 2x fibres = >75% VO2 max
How does radical production affect muscle fatigue during exercise
Exercise promotes muscle free radical production.
Free radical production can:
1. Damage contractile proteins
2. Depress sodium/potassium pump activity
Antioxidant supplements do not prevent fatigue (only delay)
Factors limiting ultra short-term performances (<10 secs)
Motivation, skill, arousal.
Primary energy system is anaerobic
Type 2 muscle fibres
Factors limiting short-term performances (10-180 secs)
Shift from anaerobic to aerobic metabolism
Fuelled primarily by anaerobic glycolysis
Ingestion of buffers may improve performance
Factors limiting moderate-duration performances (3-20mins)
Requires energy expenditure near VO2 max (high maximal stroke volume & arterial oxygen content)
High VO2 max is advantageous (type 2x fibres recruited)
Factors limiting intermediate-duration performances (20-60mins)
Predominantly aerobic
Running economy (type 1 fibres)
Environmental factors
State of hydration
Lactate threshold
Factors limiting long performances (1-4 hours)
Environmental factors
Maintaining rate of carbohydrate utilisation
Mainly aerobic (VO2 max and economy)
Consumption of fluid and electrolytes (diet)
Factors limiting ultra-long performances (>4 hours)
VO2 max, and % it can be sustained
Environmental conditions
Metabolic responses
Potential for hyponatremia
Non-physiological factors can end performance too (injury or foot management)
What is the process of acid-base regulation
- Increase in mitochondria leads to increased FFA oxidation and decreased PFK activity along with increased mitochondrial uptake of pyruvate and NADH.
- Increased FFA oxidation and decreased PFK activity lead to decreased pyruvate formation.
3.Increased mitochondrial uptake of pyruvate and NADH, decreased pyruvate formation, and increased H4 form of LDH leads to decreased lactate and hydrogen ion formation which ensures that blood pH is maintained.
Why does endurance training reduce HR and ventilation
Training results in greater homeostasis during exercise and thus less feedback to cardiovascular control centre
Less feedback of temperature and biochemical changes to cardiovascular control centre
Thus less motor units recruited
Post resistance training molecular responses
Activation of PA & Rheb
Activation of mTOR
Protein synthesis
What occurs to VO2 max with detraining
Initial decrease from decreased stroke volume due to decreased plasma volume
Later decrease due to max a-vO2 difference due to decreased mitochondria
