Overload
Training effect occurs when a physiological system is exercised at a level beyond which it is normally accustomed
Specificity
Training effect is specific to:
- Muscle fibers recruited during exercise
- Energy system involved (aerobic vs. anaerobic)
- Velocity of contraction
- Type of contraction (eccentric, concentric, isometric)
Reversibility
Gains are lost when overload is removed
Endurance Training to Increase VO2 max:
Large muscle groups, dynamic activity
20-60 min, ?3 times/week, ?50% VO2 max
Expected Increases in VO2 max With Endurance Training
Average = 15-20%
2-3% in those with high initial VO2 max
- Requires intensity of >70% VO2 max
Up to 50% in those with low initial VO2 max
- Training intensity of 40-50% VO2 max
Genetic Predisposition for VO2 max
Accounts for about 50% of VO2 max
Prerequisite for very high VO2 max
Impact of Genetics on VO2 Max and Exercise Training Responses
Genetics plays an important role in determining VO2 max
- Heritability determines ~50% of VO2 max in untrained subjects
- Genetics also plays a key role in determining how individuals respond to exercise training
1. Average training improvement of VO2 max
Fick Equation
VO2 max = HR max x SV max x a-vO2 difference max
Product of maximal cardiac output and arteriovenous difference
Differences in VO2 max in Different Populations
Primarily due to differences in SV max
Exercise-induced improvements in VO2 max
Short duration training (~4 months); 26% increase in VO2 max
- SV > a-vO2 (10% increase in SV; 2% improvement in a-vO2 )
Longer duration training (~28 months); 42% increase in VO2 max
- a-vO2 > SV (15% increase in SV; 25% improvement in a-vO2)
Training-induced increased maximal stroke volume
Preload (EDV) increased
- Plasma volume increased
- Venous return increased
- Ventricular volume increased
Afterload (TPR) increased
- Arterial constriction decreased
- Maximal muscle blood flow with no change in mean arterial pressure increased
Contracti
Training-induced changes in stroke volume occur rapidly
11% increase in plasma volume, 7% increase VO2 max, and 10% increase in stroke volume with six days of training
Training Induced Arteriovenous 02 difference
Increased blood flow to the muscles
- Decreased SNS vasoconstriction
Improved ability of the muscle to extract oxygen from the blood
- Increased Capillary density (Slows blood flow through muscle)
- Increased Mitochondrial number
The ability to perform prolonged, submaximal exercise is...
...dependent on the maintenance of homeostasis
Endurance exercise training results in:
1. More rapid transition from rest to steady-state
2. Reduced reliance on glycogen stores
3. Cardiovascular and thermoregulatory adaptations
4. Neural and hormonal adaptations
5. Biochemical changes in muscle
Endurance Training-Induced Changes in Fibre Type
Fast-to-slow shift in muscle fiber type
- Reduction in fast myosin
- Increase in slow myosin
- Extent of fiber type change determined by type of training and genetics
Endurance Training-Induced Changes in Capillarity
Increased number of capillaries
- Enhanced diffusion of oxygen
- Increased removal of wastes
Two Populations of Mitochondria Exist in Muscle Fibres
Subsarcolemmal are located below sarcolemma
Intermyofibrillar are located around contractile proteins
Endurance Training Increases Mitochondrial Volume and Turnover in Skeletal Muscle Fibres
Mitochondrial content increases quickly
- Depends on intensity and duration of training
- Can increase 50-100% within first 6 weeks
Increased mitochondrial volume results in increased endurance performance due to improved bioenergetics homeostasis, decrea
Increased Mitochondrial Volume and Exercise Performance - details
[ADP] stimulates mitochondrial ATP production
Increased mitochondrial volume following training
- Lower [ADP] needed to increase ATP production and VO2
Oxygen deficit is lower following training
- Same VO2 at lower [ADP]
- Energy requirement can be met by
Role of Exercise Intensity and Duration on Mitochondrial Adaptations
Citrate synthase (CS)
- Marker of mitochondrial oxidative capacity
Effect of exercise intensity
- 55%, 65%, or 75% VO2 max
- Increased CS in oxidative (IIa) fibers with all training intensities
Effect of exercise duration
- 30, 60, or 90 minutes
- No diff
Exercise Training-induced Changes in Muscle Fuel Utilization
Increased utilization of fat and sparing of plasma glucose and muscle glycogen
Transport of FFA into the muscle
- Increased capillary density
- Increased fatty acid binding protein and fatty acid translocase
Transport of FFA from the cytoplasm to the mito
Free Radicals
Produced by contracting skeletal muscles
- can contribute to muscle fatigue
Training Increases Endogenous Antioxidants
Protects against exercise-induced oxidative damage and muscle fatigue
Lactate Production During Exercise
Pyruvate + NADH --LDH--> Lactate + NAD
Training Adaptations to Acid-Base Balance
Increased mitochondrial number
- Less carbohydrate utilization = less pyruvate formed
Increased NADH shuttles
- Less NADH available for lactic acid formation
Change in LDH type
M4 --> M3H --> M2H2 --> MH3 --> H4
- Heart form (H4) has lower affinity for py
Endurance and resistance exercise increases specific muscle proteins
Exercise "stress" activates gene transcription
Process of training-induced muscle adaptation
Muscle contraction activates primary and secondary messengers
Results in expression of genes and synthesis of new proteins
- mRNA levels typically peak in 4-8 hours, back to baseline within 24 hours
- Hence, daily exercise is needed to continue training-i
Primary Signals for Muscle Adaptation
Mechanical stretch
Calcium
- Via calmodulin-dependent kinase
Free radicals
Phosphate/muscle energy levels
- AMP/ATP ratio activates AMPK
Primary and Secondary Signals Lead to Adaptations
Increased protein synthesis
Effect of Signals Depends on Exercise Stimulus
Intensity and duration
Resistance vs. endurance training
Secondary Messengers in Skeletal Muscle
- AMPK
- PGC-1a
- Calcineurin
- mTOR
- NFkB
AMPK
Glucose uptake, fatty acid oxidation, and mitochondrial biogenesis
PGC-1a
Increases in capillaries, mitochondria, antioxidant enzymes
Activated by p38, AMPK and CaMK
Calcineurin
Fiber growth, fast-to-slow fiber type change
mTOR
Protein kinase-major regulator of protein synthesis and muscle size
NFkB
Antioxidant enzymes
Primary Signals
Increases in cellular free calcium, elevated free radicals, and decreases in muscle phosphate/energy levels
What do primary signals do?
Activate one or more of the downstream secondary signalling pathways to promote gene expression
Responses to Endurance Exercise-induced Signaling Events
Fast-to-slow fiber type shift
Mitochondrial biogenesis
Antioxidant enzyme synthesis
Fast to Slow Fibre Transformations
Both active calcineurin and PGC-1a play important roles in endurance exercise-induced fast-to-slow fiber transformations
Activation of PGC-1a
Collectively, active CaMK, AMPK, and p38 all participate in activation of PGC-1a
Active PGC-1a
The master regulator for mitochondrial biogenesis
Active PGC-1a and NFkB
Contribute to the exercise-induced increase in muscle antioxidants
Biochemical Adaptations to Training
Influence the physiological response to exercise:
- Sympathetic nervous system ( decreases E/NE)
- Cardiorespiratory system (decreases HR, decreases ventilation)
Bichemical Adaptations Are Due To
Reduction in "feedback" from muscle chemoreceptors
Reduced number of motor units recruited
One-leg Training Studies
Lack of transfer of training effect to untrained leg
Demonstrates Links Between Muscle and Systemic Physiology
Peripheral Feedback from Working Muscles
Group III and group IV nerve fibers
- Responsive to tension, temperature, and chemical changes
- Feed into cardiovascular control center
Central Control of Cardiorespiratory Responses
Motor cortex, cerebellum, basal ganglia
- Recruitment of muscle fibres
- Stimulates cardiorespiratory control centre
Detraining and VO2 max
Rapid decrease in VO2 max
Decreases ~8% within 12 days
Decreases ~20% after 84 days
Decrease and SV max
Decreased SV max
- Rapid loss of plasma volume
Detraining and Maximal a-v O2 Difference
Decreased maximal a-v O2 difference
- Decreased mitochondria
- Decreased oxidative capacity of muscle
decreased type IIa fibres and increased type IIx fibres
Retraining and Muscle Mitochondria
Muscle mitochondria adapt quickly to training
- Double within 5 weeks of training
Requires 3-4 weeks of retraining to regain mitochondrial adaptations
Loss of Mitochondrial Adaptations
Mitochondrial adaptations lost quickly with detraining
- Loss of 50% of training gain within 1 week of detraining
- Majority of adaptation lost in two weeks
Muscular strength
Maximal force a muscle or muscle group can generate
- 1 repetition maximum (1-RM)
Muscular endurance
Ability to make repeated contractions against a submaximal load
Strength training
Percent gain inversely proportional to initial strength
- Genetic limitations exist to gains in strength
High-resistance (2-10 RM) training
- Gains in strength
Low-resistance training (20+ RM)
- Gains in endurance
Ageing and Strength
Decline in strength after age 50
- Loss of muscle mass (sarcopenia)
Loss of both type I and II fibers
Atrophy of type II fibers
Loss of intramuscular fat and connective tissue
- Loss of motor units
- Reorganisation of motor units
- Also associated with NS
Progressive Resistance Training
Causes muscle hypertrophy and strength gains
Important for activities of daily living, balance, and reduced risk of falls
Muscle Adaptations to Anaerobic Exercise Training
Refers to short-duration (i.e., 10-30 seconds) all-out effort which is also referred to as "sprint training"
- Recruits both type I and II muscle fibres to perform the exercise
- During exercise lasting 10 seconds or less, the energy is primarily supplied
Anaerobic Training Increases Performance
- 4-10 weeks of sprint training can increase peak anaerobic power by 3-28% across individuals
- Sprint training improves muscle buffering capacity by increasing both intracellular buffers and hydrogen ion transporters
- Sprint training also results in hyp
Resistance Training-Induced Changes in the Nervous System
Neural adaptations responsible for early gains in strength
- Initial 8-20 weeks
Adaptations include:
- Increased ability to recruit motor units
- Altered motor neuron firing rates
- Enhanced motor unit synchronisation
- Removal of neural inhibition
Hyperplasia
Increase in muscle fiber number
Limited evidence in human studies
Most evidence indicates that 90-95% of muscle enlargement due to hypertrophy
Hypertrophy
Enlargement of both type I and II fibers
- Greater degree of hypertrophy in type II fibres
Increase in myofibrillar proteins
Increases number of cross-bridges
Increased ability to generate force
Fast-to-slow Shift in Fibre Type
From type IIx to IIa
- 5-11% change following 20 weeks of training
- Small increases occur in type I fibres
Compared to endurance training, resistance training-induced fast-to-slow shifts in fiber type are less prominent
Can Resistance Training Improve Muscle Oxidative Capacity and Increase Capillary Number?
Conflicting results of studies
- Some studies report a decrease, small increase, or no change in mitochondrial content
- Some studies show small increases in capillary number whereas others report a small decrease in capillary number
Reasons for conflicti
Resistance training improves antioxidant capacity in trained muscles
Resistance training-induced increases in muscle antioxidant enzyme activity is similar to the changes observed following endurance exercise training
Primary Signals of Resistance Training
Increased Muscle stretch (mechanoreceptor activation) promotes synthesis of phosphatidic acid and activation of the mTOR activator, Ras homolog enrich in brain (Rheb)
Secondary Signals of Resistance Training
Increases in Phosphatidic acid and Rheb promotes mTOR activation
mTOR activation promotes protein synthesis
- A single bout can increase protein synthesis 50-100%
Responses to Resistance Training-Induced Signaling Events
Muscle hypertrophy due to increased myofibrillar proteins
Increased number of myonuclei in each fibre
- Derived from satellite cells
- Increases in myonuclei may be important to support increased muscle protein synthesis as fibre increases in size
Satellite Cells
The source for additional nuclei in muscle fibres, and the supplement of myonuclei to muscle fibres is likely required to achieve maximal fibre hypertrophy in response to resistance training
Detraining and Loss of Muscle Strength
31% decrease in strength following 30 weeks detraining
Associated with small changes in fiber size
- Type I fiber size -2%
- Type IIa fiber size: -10%
- Type IIx fiber size: -14%
Due primarily to nervous system changes
Retraining and Muscle Strength and Size
Retraining results in rapid regain of strength and muscle size
- Within 6 weeks after resuming training
- Can maintain strength with reduced training for up to 12 weeks
Potential for Interference of Adaptations from Concurrent Strength and Endurance Training
Strength training increases muscle fibre size whereas endurance training does not
Depends on intensity, volume, and frequency of training
Concurrent Strength and Endurance Training
Numerous studies report that combining strength and endurance training impairs strength gains compared to strength training alone
- How much interference occurs depends on intensity, volume, and frequency of endurance training
Mechanisms for the Impairment of Strength Development during Concurrent Training
Neural factors
- Impaired motor unit recruitment (Limited evidence exists to support this concept)
Low muscle glycogen content
- Due to successive bouts of endurance exercise (Could result in impaired ability to perform a subsequent resistance training bo