Unit Test 2 Flashcards
Motor unit activation
First step in initiating action potential
Trigger zone
Site of action potential; AP initiated when cell body is depolarized past AP threshold
Action potential threshold
Critical level to which a membrane potential must be depolarized to initiate AP
Excitatory neurons
Cause depolarization of motor nerve; membrane potential becomes more positive
Inhibitory neurons
Cause hyperpolarization of motor nerve; membrane potential becomes more negative
Spatial summation
When three excitatory neurons fire with their graded potentials being separate and below the threshold, the graded potentials arrive at trigger zone together and sum to create a supra threshold signal, generating AP
What happens if there is an inhibitory neuron present in spatial summation?
The sum of one inhibitory and two excitatory will not be enough to generate an AP
Temporal summation
When multiple excitatory neurons cause a depolarization that reaches the trigger zone at the same time, and sum to cause a depolarization that triggers AP
Spatial vs temporal summation
Spatial: several weak signals from different locations converted to a single one
Temporal: converts a rapid series of weak pulses from a single source of into one large signal
Depolarization
Opening of voltage gates Na+ channels
Repolarization
Closure of Na+ and opening of K+ voltage-gated channels
Hyperpolarization
Voltage gated K+ channels remain open after potential reaches resting level (refractory period)
- necessary for system to rest Na+ and K+ concentrations for next AP
Acetylcholine release
- AP depolarizes axon terminal
- Opening of voltage gates Ca+ channels and
Ca+ enters the cell - Triggers exocytosis of acetylcholine in the
synaptic cleft and binds with receptors on
the postsynaptic cell - ACh diffuses across the synaptic cleft and
binds with receptors on the postsynaptic cell - Response initiated in the postsynaptic cell
ACh breakdown
- ACh made from choline and acetyl CoA
- ACh broken down by AChesterase in synaptic
cleft - Choline transported back into axon terminal
and is used to make more ACh
Excitation of muscle membrane
Initiated by ACh in NMJ and triggers contraction by releasing Ca2+ from SR into muscle’s cytosol
ACh breakdown
- ACh made from choline and acetyl CoA
- ACh broken down by AChesterase in synaptic
cleft - Choline transported back into axon terminal
and is used to make more ACh
Ca2+ release
- Somatic motor neuron releases ACh into NMJ
- Entry of Na+ through ACh receptor channel
initiates AP - AP activates DHPR
- DHPR activates RYR which triggers the release
of Ca2+ from SR into cytosol
Contraction
Release of Ca2+ into cytosol
Relaxation
A muscle will continue to contract until Ca2+ is pumped out of cytosol back into SR by SERCA pumps
Contraction cycle
- Calcium binds to troponin exposing myosin
binding sites on actin - Myosin head forms cross-bridge w actin
- Pi released from myosin head
- Power stroke
- ATP replaces ADP on myosin head
- Myosin releases actin and moves into cocked
position
Sliding filament theory of muscle contraction
- Ap arrives at the axon terminal of a somatic
motor neuron; axon terminal of the motor
neuron connects to muscle fibre via
neuromuscular junction - Stimulates opening of voltage-gated ca2+
channels and ca2+ enters the axon terminal
3 Increased ca2+ stimulates exocytosis of
synaptic vesicles which release Ach into
synaptic cleft - Ach binds to Ach receptors on postsynaptic
cell (motor end plate of sarcolemmal) - Ligand-gated Na+/K+ channels open; Na+
moves into cell, K+ moves out - Depolarization of Sarcolemma causes voltage
gated Na+ channels to open causing an Ap
across sarcolemma and T-tubules - DHP channel causes RyR to open and allows
Ca2+ to leave sarcoplasmic reticulum +
diffuse into the sarcoplasm - Calcium ions bind to troponin, moving t
tropomyosin off of the active actin sites - Myosin can bind to actin, forming a cross-
bridges … then the contraction cycle
Resting membrane potential
Negative inside, positive outside
Central fatigue
A decrease in the ability of motor neurons to be excited and conduct APs; results in decreased ACh release into NMJ, less excitation and contraction of muscle, decreased force production
Mechanisms of central fatigue
- Decreased motor outflow
- Increased inhibitory nerve activity
- Decreased excitability of motor neurons
Decreased motor outflow
- Decreased excitatory nerves stimulating motor
stimulating motor neurons - Fewer AP
- Less ACh release into NMJ
Increased inhibitory nerve activity
- Increased effort required to stimulate motor
neurons - A variety of stimuli in exercise muscles can activate group III/IV afferent fibres
- Fibres inhibit the excitation of motor nerves by
causing hyperpolarization of motor nerve cell
bodies
Decreased excitability of motor neurons
- Axon membranes become depolarized
following repeated action potentials - Voltage-gated ion channels on motor nerve
axons can become dysfunctional - Decreased excitability
Peripheral fatigue
- Decrease in the ability of muscles to respond to increases in Ach
- The effect of peripheral is less excitation and or contraction of skeletal muscle, and decreased force production
Mechanisms of peripheral fatigue
- Neuromuscular junction failure
- Membrane depolarization
- Voltage-gated channel dysfunction
- DHPR voltage insensitivity
Neuromuscular junction and E-C coupling failure
- Membrane depolarization
- Voltage-gated channel dysfunctional
- DHPR voltage insensitivity
Membrane depolarization
- If the membrane becomes depolarized, action
potentials are no longer possible - Membrane depolarization decreases the
ability of muscle to respond to increased ACh - Resulting in fewer/less powerful contractions
Voltage gated channel dysfunction
-
DHPR voltage insensitivity
- DHPRs can also become dysfunctional during
intense or prolonged exercise - Dysfunctional DHPRs become insensitive to
changes in voltage across muscle membrane
Accumulation of fatigue inducing metabolites
↓ ATP
↓ PCr
↑ Pi
↑ H+
Decreases in ATP (and PCr)
- Less ATP = Less Ca2+ release
- Less ATP = less/slower Ca2+ uptake by SERCA
pump and slower relaxation
Pi
- Increased Pi contributes to the development of muscle fatigue in 4 ways
1. Slowed release of Pi from myosin head and
decreased rate of cross-bridge cycling
2. Decreased sensitivity of Troponin C for Ca2+
3. Inhibition of DHPR and RYR complex
4. Binding of free Ca2+ in the cytosol
H+
Increased H+ contributes to the development of muscle fatigue in 2 ways
1. Decreased sensitivity of Troponin C for Ca2+
2. Competes with Ca2+ at the binding site on SERCA
Creatine kinase reaction
- Providing an energy reserve in a muscle
- Highest rate of ATP resynthesis
Anaerobic Glycolysis
- The transformation of glucose to lactate when
limited amounts of oxygen (O2) are available - High rate of ATP resynthesis
Oxidative phosphorylation (aerobic metabolism)
- Moderate, sustainable rate of ATP resynthesis
Key determinant of lactate production
- Pyruvate
- More substrate = more lactate production
- The balance of inflow and outflow to acetyl
CoA and the accumulation of Pyruvate
determines the rate of production of lactate
Hyperoxia
A state of excess supply of O2 in tissues and organs
Hypoxia
Low levels of oxygen in your body tissues
Determinants of strength, power and speed
- Fibre distribution
- Muscle size
- Metabolic capacity
Fibre distribution
- Type IIx superior at producing power
- Type IIa powerful and resist fatigue
Fatigue resistance of muscle fibres
- I > IIa > IIx
- Type I are more fatigue resistant than IIa
- Type IIa are more fatigue resistant than IIx
Muscle size
- Larger muscles (by CSA) produce greater force
- Type II fibres are larger than type I
Metabolic capacity
- Phosphagen system (PCr) power and capacity
are important for very brief, very high intensity
contraction - Anaerobic glycolytic power and capacity are important for longer duration sprints
Determinants of speed and endurance
- VO2 max
- Lactate threshold
- Critical power
- Efficiency
- Metabolic capacity
VO2 max
Sets the upper limit for speed/endurance performance
Lactate threshold
Highest sustainable intensity without significant lactate accumulation
Critical power (MLSS)
Highest sustainable intensity
Which muscle fibres have the highest efficiency?
- Type I are more efficient than type II
Efficiency
The amount of work that can be performed for a given energy expenditure
What impacts efficiency?
- Work rate
- Speed of movement
- Fibre type composition
Factors that determine metabolic capacity?
- Fibre type distribution
- Glycogen stores
- Fatty acid oxidative capacity
Performance
- Endurance performance is greater when muscle glycogen stores are high
- Increased ability to metabolize fatty acids improves endurance performance because reliance on glycogen is decreased
Force of muscle fibres
- IIx >IIa > I
- Type IIx produce more force than IIa
- Type IIa produce more force than I
