6) Adaptations to Resistance Training Programs Flashcards
How do relative gains in strength compare between groups?
Relative gains in strength are similar when comparing different groups but the increase in absolute weight lifted varies between groups
Gains in muscle size (?) are often paralleled by gains in ?
Gains in muscle size (hypertrophy) are often paralleled by gains in strength
What is involved in muscle strength?
- Amount of force generated depends on the amount of actin and myosin and the number of cross-bridges formed within the sarcomere
- Involves neuroadaptations (increasing motor recruitment)
- and Size of muscle // amount of Actin/myosin cross-bridges possible
Are increases in strength always observed as increased MM size?
No, Early in training, neuroadaptations are seen 1st
- Leads to increased strength without increase in size (ie no visible change)
However, Increases in MM size will always result in Increased strength
? always accompany strength gains that result from resistance training but hypertrophy may or may not take place
Neural adaptations always accompany strength gains that result from resistance training but hypertrophy may or may not take place
What are four ways in which the nervous system adapts to resistance training?
- Synchronization and recruitment of additional motor units
- Increased Rate Coding of motor units
- Increased Neural Drive
- Autogenic Inhibition
i) Synchronization and recruitment of additional motor units:
* Strength gains may result from increased synchronicity of motor units resulting in greater number of motor units firing at any one time, increasing force generation
* Controversy: does synchronicity increase force generated or rate of force development and capability to exert steady forces
ii) Increased rate coding of motor units:
* Increased neural drive to α-motor neurons increases frequency of discharge, or rate coding, of motor units
* Increases force or tension ie reach state of tetanic contraction
iii) Increased neural drive
* Neural drive is a combination of motor unit recruitment and rate coding of the units
* Neural drive starts in CNS and travels to muscles in peripheral nerves
iv) Autogenic inhibition
* Inhibitory mechanism to prevent muscles from exerting more force than bones and connective tissues can tolerate
* Golgi tendon organs: when the tension on a muscle’s tendons and internal connective tissue structures exceeds the threshold of Golgi tendon organs, motor neurons to that muscle are inhibited
* Resistance training can gradually reduce or counteract these inhibitory impulses; muscles can achieve a greater force production independent of increases in muscle mass
Neural Control of Strength Gains
How does the neural adaption increase strength?
~Synchronization and Recruitment of Additional Motor Units ~
Synchronization and recruitment of additional motor units:
* Strength gains may result from increased synchronicity of motor units resulting in greater number of motor units firing at any one time, increasing force generation
* “Training Neurons to fire synchronously”
* Controversy as to whether its because of actual increas in force or from increased rate of recruitment
i) Synchronization and recruitment of additional motor units:
* Strength gains may result from increased synchronicity of motor units resulting in greater number of motor units firing at any one time, increasing force generation
* Controversy: does synchronicity increase force generated or rate of force development and capability to exert steady forces
ii) Increased rate coding of motor units:
* Increased neural drive to α-motor neurons increases frequency of discharge, or rate coding, of motor units
* Increases force or tension ie reach state of tetanic contraction
iii) Increased neural drive
* Neural drive is a combination of motor unit recruitment and rate coding of the units
* Neural drive starts in CNS and travels to muscles in peripheral nerves
iv) Autogenic inhibition
* Inhibitory mechanism to prevent muscles from exerting more force than bones and connective tissues can tolerate
* Golgi tendon organs: when the tension on a muscle’s tendons and internal connective tissue structures exceeds the threshold of Golgi tendon organs, motor neurons to that muscle are inhibited
* Resistance training can gradually reduce or counteract these inhibitory impulses; muscles can achieve a greater force production independent of increases in muscle mass
How does the neural adaption increase strength?
Increased Rate Coding of Motor Units
Increased rate coding of motor units:
* Increased neural drive to α-motor neurons increases frequency of discharge, or rate coding, of motor units
* Increases force or tension ie reach state of tetanic contraction
i) Synchronization and recruitment of additional motor units:
* Strength gains may result from increased synchronicity of motor units resulting in greater number of motor units firing at any one time, increasing force generation
* Controversy: does synchronicity increase force generated or rate of force development and capability to exert steady forces
ii) Increased rate coding of motor units:
* Increased neural drive to α-motor neurons increases frequency of discharge, or rate coding, of motor units
* Increases force or tension ie reach state of tetanic contraction
iii) Increased neural drive
* Neural drive is a combination of motor unit recruitment and rate coding of the units
* Neural drive starts in CNS and travels to muscles in peripheral nerves
iv) Autogenic inhibition
* Inhibitory mechanism to prevent muscles from exerting more force than bones and connective tissues can tolerate
* Golgi tendon organs: when the tension on a muscle’s tendons and internal connective tissue structures exceeds the threshold of Golgi tendon organs, motor neurons to that muscle are inhibited
* Resistance training can gradually reduce or counteract these inhibitory impulses; muscles can achieve a greater force production independent of increases in muscle mass
How does the neural adaption increase strength?
Increased neural drive
* Neural drive is a combination of ? and ?
* Neural drive starts in ? and travels to muscles in ?
Increased neural drive
* Neural drive is a combination of motor unit recruitment and rate coding of the units
* Neural drive starts in CNS and travels to muscles in peripheral nerves
* Results in stronger contraction
* Higher centres trained to stimulate faster and Recruit more
i) Synchronization and recruitment of additional motor units:
* Strength gains may result from increased synchronicity of motor units resulting in greater number of motor units firing at any one time, increasing force generation
* Controversy: does synchronicity increase force generated or rate of force development and capability to exert steady forces
ii) Increased rate coding of motor units:
* Increased neural drive to α-motor neurons increases frequency of discharge, or rate coding, of motor units
* Increases force or tension ie reach state of tetanic contraction
iii) Increased neural drive
* Neural drive is a combination of motor unit recruitment and rate coding of the units
* Neural drive starts in CNS and travels to muscles in peripheral nerves
iv) Autogenic inhibition
* Inhibitory mechanism to prevent muscles from exerting more force than bones and connective tissues can tolerate
* Golgi tendon organs: when the tension on a muscle’s tendons and internal connective tissue structures exceeds the threshold of Golgi tendon organs, motor neurons to that muscle are inhibited
* Resistance training can gradually reduce or counteract these inhibitory impulses; muscles can achieve a greater force production independent of increases in muscle mass
How does the neural adaption increase strength?
Autogenic inhibition
Autogenic inhibition
* Inhibitory mechanism to prevent muscles from exerting more force than bones and connective tissues can tolerate
* Golgi tendon organs: when the tension on a muscle’s tendons and internal connective tissue structures exceeds the threshold of Golgi tendon organs, motor neurons to that muscle are inhibited
* Resistance training can gradually reduce or counteract these inhibitory impulses; muscles can achieve a greater force production independent of increases in muscle mass
i) Synchronization and recruitment of additional motor units:
* Strength gains may result from increased synchronicity of motor units resulting in greater number of motor units firing at any one time, increasing force generation
* Controversy: does synchronicity increase force generated or rate of force development and capability to exert steady forces
ii) Increased rate coding of motor units:
* Increased neural drive to α-motor neurons increases frequency of discharge, or rate coding, of motor units
* Increases force or tension ie reach state of tetanic contraction
iii) Increased neural drive
* Neural drive is a combination of motor unit recruitment and rate coding of the units
* Neural drive starts in CNS and travels to muscles in peripheral nerves
iv) Autogenic inhibition
* Inhibitory mechanism to prevent muscles from exerting more force than bones and connective tissues can tolerate
* Golgi tendon organs: when the tension on a muscle’s tendons and internal connective tissue structures exceeds the threshold of Golgi tendon organs, motor neurons to that muscle are inhibited
* Resistance training can gradually reduce or counteract these inhibitory impulses; muscles can achieve a greater force production independent of increases in muscle mass
What are three factors affecting rate and total amount of gains of lean muscle mass?
Genetics
Age
Gender
What is the Principle of Specificity?
Idea that there are certain training programs best-suited to individual goals
- “pick a program that benefits your goal”
Hypertrophy vs Hyperplasia
Compare Hypertrophy and Hyperplasia:
Similarities // Differences
Both enlarge axial cross-sectional area of a muscle (Muscle gets bigger)
Fiber Hyperplasia:
- Increase in axial cross-sectional area of MM due to increases in number of muscle fibers (cells) per fascicle
- “Add more muscle cells (fibers) = bigger muscle”
- DEBATED - “it happens, we don’t know how”
Fiber Hypertrophy:
- Increase in axial-cross-sectional area of MM due to increases in size of pre-existing muscle fibers (cells)
- Make muscle bigger by increases the size of the muscle fibers that are already present
Hypertrophy vs Hyperplasia
What is Hypertrophy
Fiber Hypertrophy:
- Increase in axial-cross-sectional area of MM due to increases in size of pre-existing muscle fibers (cells)
- Make muscle bigger by increases the size of the muscle fibers that are already present
Hypertrophy vs Hyperplasia
What is Hyperplasia?
Fiber Hyperplasia:
- Increase in axial cross-sectional area of MM due to increases in number of muscle fibers (cells) per fascicle
- “Add more muscle cells (fibers) = bigger muscle”
- DEBATED - “it happens, we don’t know how”
What is currently believed about Hypertrophy and Hyperplasia in humans?
Increased MM cross-sectional area primarily due to individual fiber hypertrophy
Hyperplasia is believed to be possible in humans
- Only very high intensity resistance training can result in fiber hyperplasia
- Percentage of total MM size increase due to hyperplasia is only ~ 5-10%
What are two primary mechanisms of MM hyperplasia?
i) Fiber splitting
ii) Activation and Proliferation of satellite cells which fuse with each other to form new fiber
i) Fiber splitting
- observed in Cats; longitudinal split in muscle fibers in response to High resistance, Low Repititions (Performed wrist flexion against resistance for reward)
ii) Activation and Proliferation of satellite cells which fuse with each other to form new fiber
- Satellite cells are Myogenic stem cells
- Activated with sufficient mechanical stimulus (during injuring or increased mm loading/stretch)
- New Myoblastic Cells can
1) Fuse with existing MM fiber causing that fiber to get bigger (hypertrophy)
2) Fuse with each other to form a new fiber (hyperplasia)
How does Fiber splitting result in hyperplasia?
Fiber splitting
- observed in Cats;
- longitudinal split in muscle fibers in response to High resistance, Low Repititions (Performed wrist flexion against resistance for reward)
- Unsure if this happens in humans
i) Fiber splitting
- observed in Cats; longitudinal split in muscle fibers in response to High resistance, Low Repititions (Performed wrist flexion against resistance for reward)
ii) Activation and Proliferation of satellite cells which fuse with each other to form new fiber
- Satellite cells are Myogenic stem cells
- Activated with sufficient mechanical stimulus (during injuring or increased mm loading/stretch)
- New Myoblastic Cells can
1) Fuse with existing MM fiber causing that fiber to get bigger (hypertrophy)
2) Fuse with each other to form a new fiber (hyperplasia)
What is the role of Satellite cells in Hyperplasia?
Activation and Proliferation of satellite cells which fuse with each other to form new fiber (hyperplasia)
- Satellite cells are Myogenic stem cells
- Activated with sufficient mechanical stimulus (during injuring or increased mm loading/stretch)
- New Myoblastic Cells can
1) Fuse with each other to form a new fiber (hyperplasia)
2) Fuse with existing MM fiber causing that fiber to get bigger (hypertrophy)
Satellite cells are ? stem cells
- Activated with sufficient ? stimulus
- New Myoblastic Cells can
1) Fuse with ? to ? (hyperplasia)
2) Fuse with ? to ? (hypertrophy)
- Satellite cells are Myogenic stem cells
- Activated with sufficient mechanical stimulus (during injuring or increased mm loading/stretch)
- New Myoblastic Cells can
1) Fuse with each other to form a new fiber (hyperplasia)
2) Fuse with existing MM fiber to increase size of that fiber (hypertrophy)
Define:
i) Transient Hypertrophy
ii) Chronic Hypertrophy
iii) Sarcoplasmic Hypertrophy (SH)
iv) Myofibrillar Hypertrophy (MH)
Define:
i) Transient Hypertrophy
- Fluid accumulation (edema) in interstitial and EC spaces of mm immediately following a single bout of exercise
- Short // MM appear bigger for few hours MAX
ii) Chronic Hypertrophy
- Increase in MM size (axial-cross-sectional area) that occurs with long-term Resistance Training
- Eccentric Contraction results in greater hypertrophy and strength
- Two types: Sarcoplasmic and Myofibrillar
iii) Sarcoplasmic Hypertrophy (SH)
- type of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resitance (Low weight; High Rep)
iv) Myofibrillar Hypertrophy (MH)
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance (High weight; Low rep)
What type of Hypertrophy involves:
- Fluid accumulation (edema) in interstitial and EC spaces of mm immediately following a single bout of exercise
- Short // MM appear bigger for few hours MAX
Transient Hypertrophy
- Fluid accumulation (edema) in interstitial and EC spaces of mm immediately following a single bout of exercise
- Short // MM appear bigger for few hours MAX
ii) Chronic Hypertrophy
- Increase in MM size (axial-cross-sectional area) that occurs with long-term Resistance Training
- Eccentric Contraction results in greater hypertrophy and strength
- Two types: Sarcoplasmic and Myofibrillar
iii) Sarcoplasmic Hypertrophy (SH)
- type of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resitance (Low weight; High Rep)
iv) Myofibrillar Hypertrophy (MH)
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance (High weight; Low rep)
Transient Hypertrophy
- ? in interstitial and EC spaces of mm immediately following ?
- ?-lived
Transient Hypertrophy
- Fluid accumulation (edema) in interstitial and EC spaces of mm immediately following a single bout of exercise
- Short-lived // MM appear bigger for few hours MAX
ii) Chronic Hypertrophy
- Increase in MM size (axial-cross-sectional area) that occurs with long-term Resistance Training
- Eccentric Contraction results in greater hypertrophy and strength
- Two types: Sarcoplasmic and Myofibrillar
iii) Sarcoplasmic Hypertrophy (SH)
- type of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resitance (Low weight; High Rep)
iv) Myofibrillar Hypertrophy (MH)
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance (High weight; Low rep)
What type of Hypertrophy is being described?
- Increase in MM size (axial-cross-sectional area) that occurs with long-term Resistance Training
- Eccentric Contraction results in greater hypertrophy and strength
- Two types: Sarcoplasmic and Myofibrillar
Chronic Hypertrophy
- Increase in MM size (axial-cross-sectional area) that occurs with long-term Resistance Training
- Eccentric Contraction results in greater hypertrophy and strength
- Two types: Sarcoplasmic and Myofibrillar
Define:
i) Transient Hypertrophy
- Fluid accumulation (edema) in interstitial and EC spaces of mm immediately following a single bout of exercise
- Short // MM appear bigger for few hours MAX
iii) Sarcoplasmic Hypertrophy (SH)
- type of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resitance (Low weight; High Rep)
iv) Myofibrillar Hypertrophy (MH)
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance (High weight; Low rep)
Chronic Hypertrophy
- Increase in MM size that occurs with ? Training
- What type of Contraction results in greater hypertrophy and strength
- Two types: ? and ?
Chronic Hypertrophy
- Increase in MM size (axial-cross-sectional area) that occurs with long-term Resistance Training
- Eccentric Contraction results in greater hypertrophy and strength
- Two types: Sarcoplasmic and Myofibrillar
Define:
i) Transient Hypertrophy
- Fluid accumulation (edema) in interstitial and EC spaces of mm immediately following a single bout of exercise
- Short // MM appear bigger for few hours MAX
iii) Sarcoplasmic Hypertrophy (SH)
- type of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resitance (Low weight; High Rep)
iv) Myofibrillar Hypertrophy (MH)
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance (High weight; Low rep)
What are the two types of Chronic Hypertrophy?
i) Sarcoplasmic Hypertrophy (SH)
- type of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resistance (Low weight; High Rep)
ii) Myofibrillar Hypertrophy (MH)
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance (High weight; Low rep)
Define:
i) Transient Hypertrophy
- Fluid accumulation (edema) in interstitial and EC spaces of mm immediately following a single bout of exercise
- Short // MM appear bigger for few hours MAX
ii) Chronic Hypertrophy
- Increase in MM size (axial-cross-sectional area) that occurs with long-term Resistance Training
- Eccentric Contraction results in greater hypertrophy and strength
- Two types: Sarcoplasmic and Myofibrillar
iii) Sarcoplasmic Hypertrophy (SH)
- type of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resistance (Low weight; High Rep)
iv) Myofibrillar Hypertrophy (MH)
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance (High weight; Low rep)
What type of Hypertrophy is being described?
- Is a subtype of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resistance Training (Low weight; High Rep)
Sarcoplasmic Hypertrophy (SH)
- type of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resistance (Low weight; High Rep)
Define:
i) Transient Hypertrophy
- Fluid accumulation (edema) in interstitial and EC spaces of mm immediately following a single bout of exercise
- Short // MM appear bigger for few hours MAX
ii) Chronic Hypertrophy
- Increase in MM size (axial-cross-sectional area) that occurs with long-term Resistance Training
- Eccentric Contraction results in greater hypertrophy and strength
- Two types: Sarcoplasmic and Myofibrillar
iv) Myofibrillar Hypertrophy (MH)
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance (High weight; Low rep)
Sarcoplasmic Hypertrophy (SH)
- subtype of ?
- Increase in ? with constant ? (no change in protein)
- Increase in ? other than ? (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by ? Training (? weight; ? Rep)
Sarcoplasmic Hypertrophy (SH)
- subtype of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resistance Training (Low weight; High Rep)
Define:
i) Transient Hypertrophy
- Fluid accumulation (edema) in interstitial and EC spaces of mm immediately following a single bout of exercise
- Short // MM appear bigger for few hours MAX
ii) Chronic Hypertrophy
- Increase in MM size (axial-cross-sectional area) that occurs with long-term Resistance Training
- Eccentric Contraction results in greater hypertrophy and strength
- Two types: Sarcoplasmic and Myofibrillar
iii) Sarcoplasmic Hypertrophy (SH)
- type of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resistance (Low weight; High Rep)
iv) Myofibrillar Hypertrophy (MH)
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance (High weight; Low rep)
Active Recall:
Sarcoplasmic Hypertrophy
Sarcoplasmic Hypertrophy (SH)
- subtype of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resistance Training (Low weight; High Rep)
What type of Hypertrophy is being described:
- subtype of Chronic hypertrophy
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance (High weight; Low rep)
Myofibrillar Hypertrophy (MH)
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance (High weight; Low rep)
Define:
i) Transient Hypertrophy
- Fluid accumulation (edema) in interstitial and EC spaces of mm immediately following a single bout of exercise
- Short // MM appear bigger for few hours MAX
ii) Chronic Hypertrophy
- Increase in MM size (axial-cross-sectional area) that occurs with long-term Resistance Training
- Eccentric Contraction results in greater hypertrophy and strength
- Two types: Sarcoplasmic and Myofibrillar
iii) Sarcoplasmic Hypertrophy (SH)
- type of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resistance (Low weight; High Rep)
Myofibrillar Hypertrophy (MH)
- Increase in ? in ?parallel/series? at a constant ?
- More ?
- Favoured by ? Training (? weight; ? rep)
Myofibrillar Hypertrophy (MH)
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance Training (High weight; Low rep)
Define:
i) Transient Hypertrophy
- Fluid accumulation (edema) in interstitial and EC spaces of mm immediately following a single bout of exercise
- Short // MM appear bigger for few hours MAX
ii) Chronic Hypertrophy
- Increase in MM size (axial-cross-sectional area) that occurs with long-term Resistance Training
- Eccentric Contraction results in greater hypertrophy and strength
- Two types: Sarcoplasmic and Myofibrillar
iii) Sarcoplasmic Hypertrophy (SH)
- type of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resistance (Low weight; High Rep)
What is the role of Sarcoplasmic Hypertrophy in the hypertrophic response to Resistance training?
- Sarcoplasmic Hypertrophy has a limited role in the hypertrophic response to resistance training
- Myofibrillar hypertrophy accounts for majority of fiber growth
- Hypothesis is that SH occurs first to make room for MH to occur
Hypertrophic responses to standardized training program can vary widely (genetics)
iii) Sarcoplasmic Hypertrophy (SH)
- type of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resitance (Low weight; High Rep)
iv) Myofibrillar Hypertrophy (MH)
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance (High weight; Low rep)
What type of hypertrophy accounts for the majority of fiber growth?
- Myofibrillar hypertrophy accounts for majority of fiber growth
- Hypothesis is that SH occurs first to make room for MH to occur
iii) Sarcoplasmic Hypertrophy (SH)
- type of Chronic hypertrophy
- Increase in sarcoplasm volume with constant sarcomere count (no change in protein)
- Increase in cellular components other than myofibrils (vol of mito // SR // T-tubules // Sarcoplasmic enzymes/substrate content)
- Favoured by Endurance resitance (Low weight; High Rep)
iv) Myofibrillar Hypertrophy (MH)
- Increase in number of sarcomeres in parallel at a constant sarcoplasmic volume
- More contractile proteins (actin and myosin)
- Favoured by Heavy-Load Resistance (High weight; Low rep)
In Resistance Training:
- Hypertrophy primarily results from:
In Resistance Training:
- Hypertrophy primarily results from an increase in sarcomeres and myofibrils added in parallel (increase diameter rather than length)
4 Steps to increase the size of a MM fiber: Pathway to hypertrophy:
i) ? stimulus skeletal MM
ii) perturbations in ? and related ? // Microtrauma (damage to ?)
iii) ↑ size and amounts of ?, ↑ in total number of ? in ?
iv) ↑ ? of individual fibers and ↑ muscle ?
4 Steps to increase the size of a MM fiber: Pathway to hypertrophy:
i) overload stimulus skeletal MM
ii) perturbations in myofibers and related ECM // Microtrauma (damage to sarcomere)
iii) ↑ size and amounts of myofibrillar contractile proteins actin and myosin, ↑ in total number of sarcomeres in parallel
iv) ↑ diameter of individual fibers and ↑ muscle cross-sectional area
Muscle Hypertrophy
Muscle cell repair: mediated by a balance between ? and ?
Muscle cell repair: mediated by a balance between Muscle Protein Synthesis and degradation
Hypertrophy occurs when Protein Synthesis exceeds Protein Breakdown
? occurs when Protein Synthesis exceeds Protein Breakdown
Hypertrophy occurs when Protein Synthesis exceeds Protein Breakdown
What cell type mediates MM Hypertrophy?
MM: muscle
Satellite cells
- New myoblastic cells fuse with existing MM fiber causing that fiber to get bigger (Hypertrophy)
Role of satellite cells in hyperplasia: Satellite cells fuse with eachother to form a new fiber
How do Satellite cells facilitate muscle hypertrophy?
Satellite cells facilitate muscle hypertrophy by donating extra nuclei to mm fibers, increasing synthesis of contractile proteins
The role of Satellite cells in hypertrophy:
New ? cells can fuse with damaged but viable ? to promote ?
Add ? -> Increases synthesis of ?
- Myonuclear domains:
- ? regulates mRNA production for a finite ?
- Increases in fiber size must be accompanied by a proportional increase in ?
- Muscles have multiple ?
New myoblastic cells can fuse with damaged but viable myofibers to promote repair and regeneration
Add nuclei -> Increases synthesis of contractile proteins
- Myonuclear domains:
- Myonucleus regulates mRNA production for a finite sarcoplasmic volume
- Increases in fiber size must be accompanied by a proportional increase in myonuclei (increase number or increase size)
- Muscles have multiple myonuclear domains
Each Nuclei can handle only a finite cell volume; as MM fiber size increases, requires more nuclei
Three functions of satellite cell proliferation
- Repair damaged myofibrils (fuse with and repair via protein synthesis)
- Enlarge existing myofibers
- Increase total fiber number (can fuse together to form new fiber (hyperplasia))
Muscle Hypertrophy
Training → ? (at cellular level // damage to ? →? signaling → ? activation → muscle ?
Training → microtrauma (at cellular level // damage to sarcomere →hormonal signaling → satellite cell activation → muscle protein synthesis
3 primary factors responsible for initiating the hypertrophic response to resistance exercise
3 primary factors responsible for initiating the hypertrophic response to resistance exercise:
1. Mechanical tension
2. Muscle damage
3. Metabolic stress
Training must have a combination of these three to cause mm hypertrophy
Factors such as genetics, age and gender will affect rate and total amount of gains of lean mm mass
What is Mechanical Tension?
- Mechanically induced tension produced by both force generation and stretch
- Essential to muscle growth
- Additive
- One of the three factors responsible for initiating the hypertrophic response to resistance exercise
What is the impact of eccentric contractions on Mechanical Tension?
Eccentric Contractions cause passive muscular tension due to lengthening of extramyofibrillar elements (eg collagen content in ECM and titin)
- Adds to active (contraction) tension developed by contractile elements (Actin and myosin) → ↑ Damage → ↑ Hypertrophy
- Enhances hypertrophic response
Mechanical Tension
- One of the three factors responsible for initiating the hypertrophic response to resistance exercise
- Mechanical overload increases mm mass
- tension associated with resistance training* disturbs the integrity of skeletal mm* leading to mechano-chemically transduced molecular and cellular responses in myofibers and satellite cells
Mechanical tension
- Mechanical overload increases ?
- tension associated with ? training disturbs the integrity of skeletal mm leading to ? transduced molecular and cellular responses in ? and ?
- Mechanical overload increases mm mass
- tension associated with resistance training disturbs the integrity of skeletal mm leading to mechano-chemically transduced molecular and cellular responses in myofibers and satellite cells
What type(s) of contraction(s) cause MM damage resulting in hypertrophy?
- Caused by eccentric, concentric, and isometric contractions
- Eccentric: cause the most damage to MM fibers -> activates satellite cells
Muscle Damage - Hypertrophy
- Resistance training can cause localized damage to MM tissue
How does MM damage contribute to hypertrophy?
Repeated process of injuring fibers followed by regeneration may result in an overcompensation of protein synthesis resulting in a net anabolic effect
MM damage is one of the three factors required for Hypertrophy
Microtrauma (localized damage to MM tissue) → neutrophils migrate to damage → agents released (eg cytokines) attract macrophages and lymphocytes
Macrophages
- Remove cellular debris
- Release cytokines → activate myoblasts, macrophages, lymphocytes
- Growth factors are released that regulate satellite cell proliferation and differentiation
How does MM damage contribute to hypertrophy?
Microtrauma (localized damage to MM tissue) → ? migrate to damage → agents released by ? (eg cytokines / Growth factors) attract ? and ?
Microtrauma (localized damage to MM tissue) → neutrophils migrate to damage → agents released by damaged fibres (eg cytokines) attract macrophages and lymphocytes
Macrophages
- Remove cellular debris
- Release cytokines → activate myoblasts, macrophages, lymphocytes
- Growth factors are released that regulate satellite cell proliferation and differentiation
Repeated process of injuring fibers followed by regeneration may result in an overcompensation of protein synthesis resulting in a net anabolic effect
What is the role of macrophages in muscle hypertrophy resulting from muscle damage?
1) Remove ?
2) Release ?
3) Activate ?
Macrophages
1) Remove cellular debris
2) Release cytokines → activate myoblasts, macrophages, lymphocytes
Microtrauma → neutrophils migrate to damage → agents released by damaged fibers attract macrophages and lymphocytes
Macrophages
- Remove cellular debris
- Release cytokines → activate myoblasts, macrophages, lymphocytes
- Growth factors are released that regulate satellite cell proliferation and differentiation
Repeated process of injuring fibers followed by regeneration may result in an overcompensation of protein synthesis resulting in a net anabolic effect
What is the role of growth factors released during Muscle Damage?
Growth factors regulate Satellite cell proliferation and differentiation
What type of training causes build-up of metabolites resulting in Metabolic Stress?
High repetitions, low weight, low rest
- Metabolite accumulation in muscle cells
- Muscle Ischemia (↓ BF → ↑CO2 / ↑H+ / ↓O2)
Metabolic stress
* High repetitions, low weight training, low rest
- Metabolite (ie. lactate, inorganic phosphate, ADP, hydrogen ions) accumulation in muscle
cells
Muscle ischemia:
* Produces substantial metabolic stress and potentially additive to the hypertrophic effect when combined with glycolytic training
* Induces alterations in hormonal milieu, cell swelling, free radical production, increased activity of growth-orientated transcription factors
Effective hypertrophy-orientated resistance training should consist of a combination of ? and ?
Effective hypertrophy-orientated resistance training should consist of a combination of mechanical tension (Stress) and metabolic stress (environment changes)
muscle damage
How does Metabolic stress contribute to MM hypertrophy?
Metabolic stress
?type of exercise? (rep/weight/rest) exercise causes build up of Metabolites (ie. ?, ?, ?, ? ions) in muscle cells
Metabolic stress
High Rep, low weight, low rest exercise causes build up of Metabolites (ie. lactate, inorganic phosphate, ADP, hydrogen ions) in muscle cells
Muscle ischemia: (↓ BF → ↑CO2 / ↑H+ / ↓O2)
- Produces substantial metabolic stress and potentially additive to the hypertrophic effect when combined with glycolytic training
- Induces alterations in hormonal milieu, cell swelling, free radical production, increased activity of growth-orientated transcription factors → Trigger Satellite cells
Metabolic stress and muscle hypertrophy
Muscle ischemia: (↓ BF → ↑? / ↑? / ↓?)
- Produces substantial metabolic stress and potentially additive to the hypertrophic effect when combined with ? training
Muscle ischemia: (↓ BF → ↑CO2 / ↑H+ / ↓O2)
- Produces substantial metabolic stress and potentially additive to the hypertrophic effect when combined with glycolytic training
Metabolic stress induces alterations in
* ?,
* cell ?,
* ? production,
* increased activity of ? transcription factors → Trigger ?
Metabolic stress induces alterations in
* hormonal milieu,
* cell swelling,
* free radical production,
* increased activity of growth-orientated transcription factors → Trigger Satellite cells
? and ?
- upstream regulators of anabolic processes
- Facilitate protein metabolism and subsequent muscle growth
- Involved in satellite cell proliferation and differentiation
- Facilitate binding of satellite cells to damaged fibers to aid in muscular repair
Hormones and cytokines
- upstream regulators of anabolic processes
- Facilitate protein metabolism and subsequent muscle growth
- Involved in satellite cell proliferation and differentiation
- Facilitate binding of satellite cells to damaged fibers to aid in muscular repair
Hormones and cytokines
- upstream regulators of ? processes
- Facilitate ? metabolism and subsequent ?
- Involved in ? cell proliferation and differentiation
- Facilitate binding of satellite cells to damaged fibers to aid in ?
Hormones and cytokines
- upstream regulators of anabolic processes
- Facilitate protein metabolism and subsequent muscle growth
- Involved in satellite cell proliferation and differentiation
- Facilitate binding of satellite cells to damaged fibers to aid in muscular repair
What are three training methods to maximize muscle hypertrophy?
- Agonist/Antagonist
- High load Resistance training + low load blood flow restriction training
- Accentuated eccentric training
3 training methods to maximize muscle hypertrophy:
1 Agonist/antagonist
* Or upper/lower body supersets
* Short rest periods and higher metabolic stress
2 High load resistance training + low load blood flow restriction training * Occlude venous return of blood from an extremity when training
* Increases metabolic stress even at low loads
3 Accentuated eccentric training
* Use a higher load on the eccentric portion of the exercise than on the concentric portion of the exercise
* During eccentric contractions, passive muscular tension develops because of lengthening of extramyofibrillar elements ie collagen content in ECM and titin
3 training methods to maximize muscle hypertrophy:
What is Agonist/antagonist Training
* ?
* Short ?
* higher ?
1 Agonist/antagonist
* Or upper/lower body supersets
* Short rest periods
* higher metabolic stress
3 training methods to maximize muscle hypertrophy:
1 Agonist/antagonist
* Or upper/lower body supersets
* Short rest periods and higher metabolic stress
2 High load resistance training + low load blood flow restriction training * Occlude venous return of blood from an extremity when training
* Increases metabolic stress even at low loads
3 Accentuated eccentric training
* Use a higher load on the eccentric portion of the exercise than on the concentric portion of the exercise
* During eccentric contractions, passive muscular tension develops because of lengthening of extramyofibrillar elements ie collagen content in ECM and titin
3 training methods to maximize muscle hypertrophy:
What is “High load resistance training + low load blood flow restriction” training
* Occlude ? from an extremity when training
* Which serves to Increase ? even at low loads
High load resistance training + low load blood flow restriction” training
* Occlude venous return of blood (BF) from an extremity when training
* Which serves to Increase metabolic stress even at low loads
3 training methods to maximize muscle hypertrophy:
1 Agonist/antagonist
* Or upper/lower body supersets
* Short rest periods and higher metabolic stress
2 High load resistance training + low load blood flow restriction training * Occlude venous return of blood from an extremity when training
* Increases metabolic stress even at low loads
3 Accentuated eccentric training
* Use a higher load on the eccentric portion of the exercise than on the concentric portion of the exercise
* During eccentric contractions, passive muscular tension develops because of lengthening of extramyofibrillar elements ie collagen content in ECM and titin
3 training methods to maximize muscle hypertrophy:
What is Agonist/antagonist Training
* ?
* Short ?
* higher ?
3 training methods to maximize muscle hypertrophy:
1 Agonist/antagonist
* Or upper/lower body supersets
* Short rest periods
* higher metabolic stress
3 training methods to maximize muscle hypertrophy:
1 Agonist/antagonist
* Or upper/lower body supersets
* Short rest periods and higher metabolic stress
2 High load resistance training + low load blood flow restriction training * Occlude venous return of blood from an extremity when training
* Increases metabolic stress even at low loads
3 Accentuated eccentric training
* Use a higher load on the eccentric portion of the exercise than on the concentric portion of the exercise
* During eccentric contractions, passive muscular tension develops because of lengthening of extramyofibrillar elements ie collagen content in ECM and titin
3 training methods to maximize muscle hypertrophy:
What is Accentuated eccentric training
* Use a ? on the eccentric portion of the exercise than on the concentric portion of the exercise
* ? eccentric contraction
* During eccentric contractions, ? develops because of lengthening of extramyofibrillar elements ie collagen content in ECM and titin
Accentuated eccentric training
* Use a higher load on the eccentric portion of the exercise than on the concentric portion of the exercise
* Slower eccentric contraction
* During eccentric contractions, passive muscular tension develops because of lengthening of extramyofibrillar elements ie collagen content in ECM and titin
3 training methods to maximize muscle hypertrophy:
1 Agonist/antagonist
* Or upper/lower body supersets
* Short rest periods and higher metabolic stress
2 High load resistance training + low load blood flow restriction training * Occlude venous return of blood from an extremity when training
* Increases metabolic stress even at low loads
3 Accentuated eccentric training
* Use a higher load on the eccentric portion of the exercise than on the concentric portion of the exercise
* During eccentric contractions, passive muscular tension develops because of lengthening of extramyofibrillar elements ie collagen content in ECM and titin
