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EPHE 441 > Neuromuscular responses > Flashcards

Neuromuscular responses Flashcards

1
Q

What does 1-RM represent?

A

Muscular strength/maximum force a muscle can generate

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2
Q

What is muscular endurance?

A

The ability of a muscle to make repeated contractions at submaximal load

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3
Q

What is cross education?

A

If one limb engages in resistance training the contralateral limb experiences an increase in musculoskeletal strength

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4
Q

What is neural drive?

A

The magnitude of efferent neural output from the CNS to the activated muscle fibers

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5
Q

What factors contribute to neural drive?

A

1) The total number of neurons firing
2) the firing rate of a motor neuron
3) motor unit synchronization
4) neural transmission across the neuromuscular junction

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6
Q

Why is force directly proportional to the to the amount of actin and myosin in a muscle fiber?

A

The more myosin cross-bridges that are attached to actin and engaged in the power stroke, the more power that is produced

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7
Q

What muscle fiber types have the greatest specific force production?

A

Type IIa and IIx

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8
Q

Why does muscle strength increase more than muscle size with resistance training?

A

Resistance training increases the specific force production of type I fibers, without changing the specific force production of type IIa or IIx

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9
Q

How does training increase the specific force of type I fibers?

A

By increasing calcium sensitivity. Increased calcium sensitivity results in a greater number of myosin cross-bridges binding to actin which results in greater force production.

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10
Q

What is hyperplasia?

A

Increase in the total number of muscle fibers within a specific muscle

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11
Q

What are two mechanisms that explain exercise-induced hyperplasia?

A

1) Muscle fiber splitting in response to intense resistance training (lots of supporting evidence)
2) Satellite cells are activated to form new and independent muscle fibers (likely not the primary mechanism)

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12
Q

Why is there an increase of actin/myosin fibers with resistance training?

A

Due to an addition of sarcomeres in parallel to existing sarcomeres resulting in hypertrophy.

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13
Q

How does an increase in contractile filaments influence force production?

A

Additional contractile elements increases the number of myosin cross-bridges in the fibers which increases the muscle fibers ability to produce force

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14
Q

What are the two primary influences on resistance training induced increases in strength?

A

1) Neural adaptations

2) Increase in fiber specific force production

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15
Q

What causes short term (2-8 weeks) increases in strength?

A

Nervous system adaptations

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16
Q

What causes strength gains in long term training programs?

A

1) Nervous system adaptations
2) Increase in muscle mass
3) Increases in type I muscle fiber specific force production

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17
Q

What is the relationship between muscle growth and protein synthesis?

A

Muscle growth occurs when the exercise induced muscle protein synthesis exceeds the rate of protein breakdown

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18
Q

Why does muscle hypertrophy occur more rapidly in an untrained individiual?

A

The percent increase in untrained individuals is greater than in trained because post exercise protein synthesis remains elevated for a longer period in untrained individuals

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19
Q

What are the steps of protein synthesis?

A

1) Cell signaling events stimulate transcriptional activators in the sarcoplasm
2) Activated transcription activator moves from the cytosol to the nucleus and binds to the gene promoter
3) Transcription results in the formation of mRNA which contains the genetic information for a specific protein’s amino acid sequence
4) mRNA leaves nucleus, travels through sarcoplasm to ribosome which is the site of protein synthesis
5) At ribosome, mRNA translated into specific protein

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20
Q

How are ribosomes influenced by resistance training?

A

Ribosomal abundance increases rapidly in the first few weeks of resistance training. Increase precedes hypertrophy. Increased ribosome numbers leads to increased efficiency of translation which allows for increased protein synthesis

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21
Q

What protein kinase is the regulator of protein synthesis and muscle size?

A

The mechanistic target of rapamycin (mTOR)

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22
Q

How does mTOR regulate protein synthesis?

A

Activation of mTOR increases translation leading to increased protein synthesis

23
Q

What signaling molecules are responsible for the activation of mTOR?

A

Insulin-like growth factor 1 (IGF-1), phosphatidic acid (PA), and Rheb (Ras homolog enriched in brain)

24
Q

What events need to occur to activate mTOR?

A

1) Muscle levels of PA must increase and/or

2) TSC2 blockade of Rheb must be eliminated

25
Q

During rest, what molecule stops Rheb from activating?

A

Tuberous sclerosis complex 2

26
Q

How does resistance exercise increase muscle PA levels and remove Rheb inhibition?

A

1) Muscle contractions activate a mechanoreceptor on the sarcolemma that stimulates the production of PA
2) Increased PA binds to mTOR leading to mTOR activation
3) Activation of mechanoreceptor also activates enzyme called extracellular signal-regulated kinase (Erk) that phosphorylates and inhibits TSC2
4) Rheb is uninhibited and can activate mTOR

27
Q

What is the main activator of muscle protein synthesis?

A

mTOR

28
Q

What endogenous hormones can influence muscle protein synthesis?

A

Testosterone, insulin-like growth factor 1 (IGF-1), and growth hormone

29
Q

Is ibuprofen beneficial for strength training?

A

Potentially. Ibuprofen can inhibit cyclooxygenase which can increase inflammatory factors and works to regulate muscle protein content

30
Q

What cells are responsible for an increase of myonuclei as an adaptation of resistance training?

A

Satellite cells

31
Q

Why are additional myonuclei important for achieving maximum hypertrophy?

A

Additional of myonuclei to growing fibers is required to maintain the high level of transcriptional capacity needed to synthesize muscle proteins at an increased rate following a strength training workout

32
Q

Why can older persons not reach the same level of muscle hypertrophy as a younger person?

A

Due to depressed protein synthesis as a result of age-related suppression of satellite cell number and function

33
Q

What is responsible for the difference in muscle hypertrophy levels between persons?

A

Largely due to genetic variation, up to 80%. 47 genes are major contributors to muscle mass. Many are directly linked to mTOR signaling pathway and are activated during resistance training

34
Q

What are the classifications of different responses to resistance training?

A

High responders, moderate responders, low responders

35
Q

What is muscle atrophy?

A

A reduction in cross-sectional area of muscle fibers resulting in a decrease of muscle mass

36
Q

How quickly do muscles begin to atrophy following inactivity?

A

6-12 hours. Result of increased protein degradation and decreased protein synthesis

37
Q

What mechanisms are responsible for inactivity-induced increases in muscle protein breakdown and decreases in muscle protein synthesis?

A

1) Production of free radicals in the inactive muscle fibers, results in oxidative damage of muscle fibers aka oxidative stress
2) Oxidative stress activates cell signaling pathways that control proteolysis and protein synthesis in muscle fibers. Specifically proteases that breakdown muscle proteins

38
Q

How is muscle hypertrophy affected if a person does both resistance training and high-intensity resistance training simultaneously?

A

They experience impaired strength in comparison to someone only doing strength training

39
Q

What are the three mechanisms responsible for the impairment of strength development during concurrent strength and endurance training?

A

1) Neural factors
2) Overtraining
3) Depressed protein synthesis

40
Q

How does depressed protein synthesis contribute to the impairment of strength development during concurrent strength and endurance training?

A

Resistance training increases muscle contractile protein synthesis through activation of mTOR. Endurance training increases AMPK activation and increases mitochondrial biogenesis. AMPK can also activate TSC2 which inhibits mTOR activity limiting protein synthesis.

41
Q

What is fatigue?

A

An inability to maintain power output or force during repeated muscle contraction

42
Q

What are the nine potential sites of fatigue?

A

Brain, spinal cord, peripheral nerve, muscle sarcolemma, transverse tubular system, calcium release, actin-myosin interaction, cross-bridge tension and heat, force/power output

43
Q

What are some of the factors that influence performance?

A

Energy production: Anaerobic (PC, glycolysis). Aerobic (VO2max, cardiac output, O2 delivery[Hb]/PO2, O2 extraction, mitochondria
Environment: altitude, heat, humidity
Diet: Carbs, water
CNS function: Arousal, motivation
Strength/Skill: Practice, natural environment (body type, muscle fiber type)

44
Q

What is central fatigue?

A

a) When there is a reduction in the number of functioning motor units involved in the activity
b) a reduction in motor unit firing frequency

45
Q

What are the peripheral factors of fatigue?

A

Neural factors( neuromuscular junction, sarcolemma and transverse tubules), mechanical factors, energetics of contraction

46
Q

How do neuromuscular junctions contribute to fatigue?

A

They don’t

47
Q

How does the sarcolemma contribute to muscular fatigue?

A

When Na/K pump can’t keep up, depolarization of cell occurs and the amplitude of action potential reduces. Gradual depolarization can alter t-tubule action potential causing calcium release form the sarcoplasmic reticulum to be diminished

48
Q

What is the primary mechanical factor related to fatigue?

A

Cycling. Cross bridging relies on the functional arrangement of actin and myosin, the availability of calcium, and ATP which is needed for the activation of cross-bridging

49
Q

How do high H+ levels contribute to fatigue?

A

1) Reduce the force per cross-bridge
2) Reduce the force generated at a given calcium concentration
3) Inhibits SR calcium release

50
Q

What is a sign of fatigue during isometric contractions?

A

A longer “relaxation time” aka the time from peak tension development to baseline relaxation, especially important in fast-twitch fibers

51
Q

How do radicals contribute to muscle fatigue?

A

1) Radicals can damage key contractile proteins including actin and myosin
2) High radical production can depress sodium/potassium pump activity leading to problems achieving excitation-contraction coupling

52
Q

What is the series of events that occurs when exercise begins and an increase in ATP production is needed?

A

1) As the cross-bridges use ATP and generate ADP, phosphocreatine provides for the immediate resynthesis of the ATP
2) As the phosphocreatine becomes depleted, ADP begins to accumulate and the myokinase reaction occurs to generate ATP
3) The accumulation of all these products stimulates glycolysis to generate additional ATP, which may result in an H+ accumulation

53
Q

What is the relationship between fatigue and ATP?

A

Fatigue is associated with a mismatch between the rate at which the muscle uses ATP and the rate at which ATP can be supplied. Accumulation of Pi and ADP as a result of ATP breakdown contributes to fatigue. Cellular fatigue mechanisms slow down the use of ATP more than the rate of generation in order to preserve ATP concentration and cellular homeostasis

54
Q

How do metabolites like Pi and H+ affect neural control/fatigue?

A

When they reach enough level, H+ and Pi can reflexively reduce motor unit recruitment and cause fatigue through the action of type III/IV afferent nerve fibers

EPHE 441 (6 decks)

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