Review 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 threshold
The graded potentials arrive at trigger zone together and sum to create a supra threshold signal and an AP is generated
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 reach trigger zone at same time and sum to cause a depolarization that triggers AP
Spatial vs temporal summation
Spatial: several weak signals from diff locations converted to a single one
Temporal: converts a rapid series of weak pulses from a single source 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 reset Na+ and K+ concentrations for next AP
Acetylcholine release
- AP depolarizes axon terminal
- Opening of voltage gates Ca+ channels and Ca+ enters cell
- Triggers exocytosis of acetylcholine in synaptic vesicle
- Ach diffuses across synaptic cleft and binds w receptors on postsynaptic cell
- Response initiated in postsynaptic cell
ACh breakdown
- ACh made from choline and acetyl CoA
- ACh broken down by AChesterase in synaptic cleft
- Choline transported back intro 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 intro 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
① Ap arrives at axon terminal of a somatic motor neuron; axon terminal of motor neuron connects to muscle fibre via neuromuscular junction
② stimulates opening of voltage gated ca2+ channels and ca2+ enters axon terminal
3 Increased ca2+ stimulates exocytosis of synaptic vesicles which releases Ach into synaptic cleft
④ Ach binds to Ach receptors on postsynaptic cell (motor end plate of sarcolemmal)
③ Ligand gated Na+/K+ channels open; Na+ moves into cell, K+ moves out
⑥ Depolarization of Sarcolemma causes voltage gated Na+ channels to open causing an Ap across sarcolemma and T-tubules
⑦ DHP channel causes RyR to open and allows Ca2+ to leave sarcoplasmic reticulum + diffuse into sarcoplasm
⑧ calcium ions bind to troponin, moving tropomyosin off of the active actin sites
⑨ Myosin can bind to actin, forming cross bridges … then contraction cycle
Resting membrane potential
Negative inside, positive outside
Central fatigue
Decrease in the ability of motor neurons to be excited and conduct APs; everything upstream Ach being released at NMJ
Effect of central fatigue
Decreased Ach release into NMJ, less excitation and contraction of skeletal muscle and 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 neurons
- Fewer AP
- less ACh release into NMJ
Increased inhibitory nerve activity
- increased effort required to stimulate motor neurons
- results from activation of group III/IV afferent nerves bc they cause hyperpolarization rather than depolarization
- hyperpolarization requires more effort to excite
Decreased excitability of motor neurons
- voltage gated ion channels dysfunctional
- axon membrane depolarized following repeated AP
- axons can’t conduct AP= decreased ACh release into NMJ
Peripheral fatigue
Decrease in the ability of a muscle to respond to increases in ACh
Mechanisms of peripheral fatigue
- NMJ failure
- Accumulation of fatigue inducing metabolites
Neuromuscular junction failure
Decreased function of muscle membrane and DHPR/RYR)
Accumulation of fatigue inducing metabolites
- Decreases in ATP and PCr
- Pi
- H+
Decreases in ATP (and PCr)
ATP stimulates RYR mediated Ca2+ release which stimulates contraction
Required for rapid uptake of Ca2+
Phosphocreatine system is first defence against decrease in ATP which increases breakdown of PCr
Pi
- slowed release of Pi from myosin head and decreased rate of cross bridge cycling
- decreased sensitivity of troponin C fore Ca2+ (decreases number of crossbridges formed)
- inhibition of DHPR and RYR complex
- Binding of free Ca2+ in cytosol (less Ca2+ in cytosol =less force)
H+
Decreased sensitivity of troponin C for Ca2+
Competes w Ca2+ binding site on SERCA
Decreased ATP stmulates glycolysis which increases lactate and H+ accumulation
Creatine kinase reaction
PCr + ADP = ATP + Cr
- generates greatest sustainable max power, fatigues fast
- sprinting and powerlifting
Anaerobic Glycolysis
Negative relationship with ATP
Positive relationship with ADP
- high power, more fatigue resistant
Oxidative phosphorylation (aerobic metabolism)
- lowest power output, high maximal capacity
Key determinant of lactate production
The balance in activation btwn the conductances for inflow and outflow of pyruvate
- Inflow to pyruvate: ADP and AMP
- Outflow to pyruvate: PFK- PDH activity
*More pyruvate = more lactate
Hyperoxia
- excess O2
- increases aerobic ATP production bc system is better able to match ATP inflow to outflow
- Don’t require the activation of PCr or glycolysis and therefore reduce fatigue inducing metabolites
- less of an increase in ADP and Pi
Hypoxia
- low O2
- decreases production of ATP
- drives breakdown of PCr
- activates glycolysis = accumulation of H+
- increased ADP and Pi
How does higher intensity exercise use more ATP?
Increases activity of ATPases which increases outflow from the ATP pool
Determinants of strength, power and speed
- Fibre distribution
- Muscle size
- Metabolic capacity
Fibre distribution
- Slow twitch: oxidative type I
- most fatigue resistant
- lowest force output
- endurance athletes - Fast twitch
a) Type IIa oxidative glycolysis (longer sprints, lifting weights with higher reps)
x) Type IIx fast glycolytic (100m sprints, heavy weight 1-3 reps) *PCr
Force of muscle fibres
Type IIx>Type IIa>Type I
Fatigue resistance of muscle fibres
Type I>Type IIa>Type IIx
Muscle size
Bigger muscles= more force production
Cross sectional area: Type IIx>Type IIa>Type I
Inflows to ATP pool
Three 3 metabolic pathways
Outflow from ATP pool
ATP hydrolysis
Metabolic capacity
PCr power and capacity imp for brief, high intensity contraction
Anaerobic glycolytic power and capacity imp for longer duration sprints
Determinants of speed and endurance
- VO2 max
- Lactate threshold/ critical power
- Efficiency
- Metabolic capacity
VO2 max
Sets upper limit for speed/endurance performance
Higher relative max = greater absolute performance
Lactate threshold
Highest sustainable intensity without significant lactate accumulation
Higher the threshold, the higher sustainable work rate
Critical power (MLSS)
Highest sustainable intensity
Once you go over critical power threshold, you go from performing a sustainable work rate to fatiguing very quickly
Past the critical threshold, PCr and anareboic glycolysis kick in whereas before you would have been using aerobic metabolism
Which muscle fibres have the highest efficiency?
Type I
Efficiency
Amount of work you do that can be performed for a given energy expenditure
Work/energy expenditure
- highest power output for the same VO2
What impacts efficiency?
- Work rate: efficiency decreases at higher intensities
- Speed: everyone has a most optimal and most efficient speed; if you work above or below this speed it decreases efficiency
- Fibre composition: type I more efficient than type II
Factors that determine metabolic capacity?
- Fibre type distribution: type I for endurance
- Glycogen stores: when stores are high, endurance performance high (Type I preserves longer than Type II)
- Fatty acid oxidative capacity: increased ability to metabolize fatty acids improved endurance performance bc reliance on glycogen is decreased
Performance
Impacted by body weight