Neuromuscular physiology:
1. Action potential (AP) transmitted along axon from brain or spinal cord
2. AP reaches axon terminal
3. Voltage-dependent calcium gates open
4. Stimulates release of acetylcholine (Ach)
5. Ach binds to receptors on sarcolemma
6. Causes ion channels to open, Na in K out generates AP
7. AP stimulates sarcoplasmic reticulum to release calcium into the muscle
cell
8. Calcium binds and troponin allowing actin and myosin to bind > contract
using ATP
9. Sarcomeres create tension (shorten), muscle generates force
10. Force applied to tendon, which elongates before applying force to bone
11. Some deformation of bone, but mainly force transmitted into movement
Determinants of musculoskeletal function:
1. Nerve: neural drive, maximal activity, excitability, neural inhibition (limit
block), motor unit (MU) firing rates
2. Muscle: size, fiber type, fiber number, specific tension, shortening velocity,
fatigability
3. Tendon: stiffness, energy storage, size, material properties
4. Bone: size, shape material properties
a. A high bone mineral density is one where the bone mineral density
(BMD) is usually greater than two standard deviations above what is expected for age. This can sometimes be seen
on routine DXA scan assessment.
Acute muscle-tendon response to exercise:
- Clear change in muscle and tendon metabolism
- Changes in tendon may be more subtle and prolonged, in line with lower blood supply and turnover
- Blood supply is very weak to tendons, hence why they take a long time to recover if ruptured
, Assessment of exercise effects:
a. Easier to assess relationships between ex. Metabolic a. Difficult to examine effects of long term exercise in an
changes and ‘whole-organ’ changes in size, function, interventional model
etc. b. Athletes or other cross-sectional studies are one approach, but
b. Ability to detect time course of adaptation may be affected by self-selection bias
c. Ability to manipulate exercise parameters to c. More effective for systems ex. Bone size change which take
investigate their effects months or years
Acute-chronic muscle remodelling in response to exercise:
- Increases in muscle protein synthesis (MPS) from increased
translational efficiency (protein per unit RNA) and translational
capacity (number of ribosomes)
- Initially, MPS elevated to repair structural and contractile material
damage
- Progressively, focus on contractile material
- With more exercise, there’s no new addition of muscle fibers, the size
of the muscle fiber changes instead
Neural adaptation to exercise:
- Motor patterns and motor unit recruitment become more efficient with
exposure to regular exercise
- EMG activity
- Inconsistent results with nerve conduction velocities
- Maybe increase in power and decrease in endurance but small
magnitude
- Potential to reduce motor nerve impairment in clinic conditions
- Exercise in older age may improve reinnervation of orphaned fibers
following MU loss in order to preserve muscle
Time Course of adaptation to exercise:
- Early strength adaptation to resistance exercise mainly due to neural
changes
- With increased training duration, muscle hypertrophy also contributes
- Quick increase in muscle strength (25% over 10 days), without any result in muscle, it’s
just being used more efficiently.
- Muscles can’t act at full capacity, there’s a neural protective system, to protect from
injury
1. Action potential (AP) transmitted along axon from brain or spinal cord
2. AP reaches axon terminal
3. Voltage-dependent calcium gates open
4. Stimulates release of acetylcholine (Ach)
5. Ach binds to receptors on sarcolemma
6. Causes ion channels to open, Na in K out generates AP
7. AP stimulates sarcoplasmic reticulum to release calcium into the muscle
cell
8. Calcium binds and troponin allowing actin and myosin to bind > contract
using ATP
9. Sarcomeres create tension (shorten), muscle generates force
10. Force applied to tendon, which elongates before applying force to bone
11. Some deformation of bone, but mainly force transmitted into movement
Determinants of musculoskeletal function:
1. Nerve: neural drive, maximal activity, excitability, neural inhibition (limit
block), motor unit (MU) firing rates
2. Muscle: size, fiber type, fiber number, specific tension, shortening velocity,
fatigability
3. Tendon: stiffness, energy storage, size, material properties
4. Bone: size, shape material properties
a. A high bone mineral density is one where the bone mineral density
(BMD) is usually greater than two standard deviations above what is expected for age. This can sometimes be seen
on routine DXA scan assessment.
Acute muscle-tendon response to exercise:
- Clear change in muscle and tendon metabolism
- Changes in tendon may be more subtle and prolonged, in line with lower blood supply and turnover
- Blood supply is very weak to tendons, hence why they take a long time to recover if ruptured
, Assessment of exercise effects:
a. Easier to assess relationships between ex. Metabolic a. Difficult to examine effects of long term exercise in an
changes and ‘whole-organ’ changes in size, function, interventional model
etc. b. Athletes or other cross-sectional studies are one approach, but
b. Ability to detect time course of adaptation may be affected by self-selection bias
c. Ability to manipulate exercise parameters to c. More effective for systems ex. Bone size change which take
investigate their effects months or years
Acute-chronic muscle remodelling in response to exercise:
- Increases in muscle protein synthesis (MPS) from increased
translational efficiency (protein per unit RNA) and translational
capacity (number of ribosomes)
- Initially, MPS elevated to repair structural and contractile material
damage
- Progressively, focus on contractile material
- With more exercise, there’s no new addition of muscle fibers, the size
of the muscle fiber changes instead
Neural adaptation to exercise:
- Motor patterns and motor unit recruitment become more efficient with
exposure to regular exercise
- EMG activity
- Inconsistent results with nerve conduction velocities
- Maybe increase in power and decrease in endurance but small
magnitude
- Potential to reduce motor nerve impairment in clinic conditions
- Exercise in older age may improve reinnervation of orphaned fibers
following MU loss in order to preserve muscle
Time Course of adaptation to exercise:
- Early strength adaptation to resistance exercise mainly due to neural
changes
- With increased training duration, muscle hypertrophy also contributes
- Quick increase in muscle strength (25% over 10 days), without any result in muscle, it’s
just being used more efficiently.
- Muscles can’t act at full capacity, there’s a neural protective system, to protect from
injury
