topic 10

Topic 10: Effects of disuse on NM system

→ e.g., being on crutches.

Effects of Changes in Activity on Neuromuscular System: Decreased use.

In humans, muscle unloading causes rapid loss of strength that is related to duration of unloading.

14 d of unloading results in 25% ↓ in strength, 7d of unloading results in 20% ↓ in strength

• *rapid loss not associated with significant difference in muscle mass or myofiber size, but highly correlated to ↓ EMG activity + neural activation of muscle ↓ by 30–50%

• more severe in soleus than EDL EMG activities.
  → Posture, extensor fibers (condensed) vs locomotors (ankle flexor)

• Loss of muscle mass dependent upon fiber type composition & function of muscle.

• Fastest shock within first week (loss of muscular strength)

• unilateral lower limb suspension, electromyography, superimposed electrical stimulation

Hindlimb suspension model used to mimic unloading

• By 4 weeks of unloading in humans, see atrophy at whole muscle & myofiber level (most pronounced in postural muscles)

• At 4 weeks of unloading, whole muscle CSA ↓ by 9%, but in 10d CSA (cross-sectional area) smaller by 5%
  → Type II fibers show greatest atrophy (36% in type IIx, 23% in Type IIa, 11% in Type I)
  → Unloading results in ↓ in specific tension (mainly due to decreased myofiber density)
  → Unloading results in shift from Type I to Type II fibers (increases power, rate of contraction)

**The type of fiber (in terms of function) is shifting toward fast-twitch.

But those fibers are also the ones most prone to atrophy (shrinking) during unloading.

Effects of aging on unloading-related myofiber atrophy:

• In soleus of aged rats, 4 wks of unloading

  • Type I: 45% atrophy, Type IIa: 28% atrophy, Type IIx: 32% atrophy.

• With fiber types combined, aged soleus show 48% atrophy vs 29% in young fibers as a result of unloading.

• In young rats, 4 wks of unloading causes NO fiber atrophy in EDL muscles.

• In aged rats, 4 wks of unloading causes significant atrophy only in Type IIb/X fibers (28%) of EDL.

• In aged men, 7d of ULLS results in greater decline in strength than young men, but only at faster rates of isokinetic contraction.

  • Isokinetic = contraction at a constant speed (velocity), typically measured with a machine like a dynamometer.

  • Faster isokinetic contractions = contractions at high movement speeds (e.g., kicking out the leg quickly).

  • older men show a greater drop in strength specifically at higher movement speeds.

• Muscle endurance unaffected by unloading both in young & aged men.

• 4 wks of unloading causes no morphological change in NMJ’s of young rats, but in aged rats see signs of degeneration (expansion of pre- & post-synaptic areas, increases in presynaptic branching, increased NCAM expression).

  • NCAM = neural cell adhesion molecule

    High levels of NCAM are often seen during development, regeneration, or denervation

    So ↑ NCAM suggests the NMJ is undergoing stress or attempting to repair or reinnervate muscle fibers

Gender effects of unloading - induced adaptations:

• In humans, ULLS causes greater decline in strength in women than men (29% vs. 16%), (23% vs. 13%) *Different Studies

• Associated with greater EMG decreases in women than men

• neither 7 nor 14 days of ULLS results in significant changes in myofiber size or thigh muscle mass

• Gender differences also not due to differences in neuromuscular transmission efficiency

Effects of exercise training on NMJ structure:

• Both endurance training & resistance training result in ↑ size at post-synaptic endplate (increased # of ACh receptors, no change in density) *adaptations of endurence training greater than those to resistance training

• Training increases nerve terminal branching (more branches, same length)

  • The nerve terminal is the part of the motor neuron that connects to the muscle.

  • Still one nerve per fiber

    But that one nerve’s terminal is more branched and complex

• ↑ branching associated with greater # of ACh vesicles

• No change in pre- or post-synaptic coupling

  • Coupling refers to the alignment and communication efficiency between the nerve terminal and the muscle membrane.

Neurophysiological Effects of Endurance Training:

• Endurance training ↑ quantal content (~30%)

  • Quantal content = the number of vesicles of acetylcholine (ACh) released per nerve impulse.

• No change in quantal size → single vesicle

  • Quantal size = the amount of ACh per vesicle

• Endurance training decreases rate of EPP “rundown” during train of stimuli (increased resistance to fatigue)

  • When a nerve fires rapidly (a "train of stimuli"), the EPP (endplate potential) can weaken over time — this is called rundown.

  • Endurance training reduces this effect, meaning EPP stays stronger for longer, even with repeated use.

• Training ↓ incidence of spontaneous release of ACh (MEPP) mini endplate potential → have much control nerve terminals have over release -70mV

  • MEPPs (Miniature Endplate Potentials) = tiny, random releases of ACh that happen without stimulation.

• Training results in hyperpolarization of resting nerve terminals & sarcolemma (more Na⁺/K⁺ pump)

  • Hyperpolarized cells are less likely to fire spontaneously.

Effects of Resistance Training on Neuromuscular Physiology (also weight lifting):

• Resistance training ↑ motor drive to trained muscle (primary movers)

• Resistance training ↓ motor drive to antagonist

• Resistance training ↑ synchronization in motor unit firing (affects power, not strength)

• Resistance training ↑ conduction velocity in trained muscles

• Resistance training causes greater myofiber hypertrophy in young vs. aged men (aged still show 30–40% myofiber hypertrophy)