Lecture 23 Flashcards
What 3x ways can you modulate the force of contraction?
Summation and Tetanus
Recruitment of Motor Units
Action of sympathetic Nervous system
Skeletal:
Shorter AP
Refractory period: short
Relaxation: when Ca taken back up to SR
Can stimulate multiple times before fully relaxed
-Single stimulas:150ms
Summation: Ca2+ is released with each stimulus, not removed rapidly, crossbridge cycle continues
Unfused Tetanus: some relaxation but not complete
Fused Tetanus: multiple stimulus, but multiple AP at N junction
-most contractions in body are due to sustained Tetani - Multiple burst of AP arriving at NJ
Modulate force of contraction by regulating interval between stimuli/AP
Weak contraction:
Fewer motor units recruited
Frequency of AP reduced
Isometric
NO external Shortening
Force weight = Force developed
Isotonic
contraction where Movement occurs
Mismatched Tension generated by the contracting muscle and the (constant) Load on the muscle (more tension than needed
a) Concentric- shortening muscle
b) Eccentric- produce force while lengthening
Concentric Isotonic contraction
Contracted Shortening
F.weight
Eccentric Contraction
F.weight > F.developed by muscle
-climbing down mountains, running down hilly, downward motion of pushups
-Muscle damage typically occurs DOMS
strengthening exercises
-growth aided due to eccentric m damage causes Cytokine release
Not all sarcomeres will legnthen evenly, the weaker sarcomeres will lengthen, and once stretched beyond optimal length will produce less force. Repetitive eccentric contraction, will lengthen and give way/pop first = Popping sarcomere theory and produce less work
DOMS
Delayed onset muscle soreness
Isolated force length Experiments
Electrodes applied to muscle to provide electrical stimulus
Force-length relationship
Stimulate muscle at different muscle lengths
Passive force
Nebulin and Titin
Sarcomeric Proteins -produce elastic properties of sarcomeres
Increased stretch = increase in passive force produced(not relying on cross bridge)
Force velocity
Rate of shortening = load vs velocity
heavier load= slower velocity of contraction
Load= max force produced by muscle = isometric(crossbirdge cycling but no shortening)
Continue to load with force- lengthen- Negative shortening (eccentric)
Force-velocity relationship is the most important contractile property of muscle that limits maximum sprinting speed
ATP breakdown
ATP breakdown varies in no other cell
Rest= ATP breakdown at BASAL level
Max activity= Basal 20-100 fold
Sustain contraction, need to produce ATP at same rate that they breakdown
3x sources of ATP in muscle
- Creatine Phosphate -give p to ADP. gets ATP from mitochondria to site of ATP consumption. Breatine phosphate smaller than ATP. Shuttle to ATP so more is generated
- Glycolysis. Glygocen.
- Oxidative Phosphorlylation
What are the 3x ATP sinks?
Myosin ATPase
Cerca ATPase
Na/K pump
Atp big molecule, simple diffusion too long
What are the 3x main consequences of different energy sources?
Immediate: Creatine phosphate
Short Term: Glycolytic/Glycolysis
Long Term: Aerobic/Oxidative (over few mins)
S fibres:
Type 1
Red - myoglobin
-lots of mitochondria (aerobic)
Posture and endurance muscles
type IIa
Fast Oxidative hybrid of ii fibres Red and lots of Mitochondira both aerobic and anareobic More prone than type 1
F fibres
Fast glycolytic White Anaerobic production of ATP slower Short, fast bursts of fibres --> can turn into Type IIa by Resistance training
What is the relationship transition between Type IIa and b fibres?
Type IIb fibres cans turn into type IIa by Resistance Training
What are 3x causes of muscle weakness?
- Muscle fatigue
- Muscular dystrophy
- Sarcopenia
Muscle fatigue
failure to maintain required/expected POWER output
- leads to reduced muscular performance
- motivation
- Potential sites between brain and contractile protein interactions
- Athletes Target pathways that are assumed to cause muscle fatigue - to enhance performance
- Carb loading
- high altitude:max O2 by increase Hb
- creatine supplementations
Central fatigue
Decreased motivation/activation
decreased MN recruitment
Peripheral fatigue
Cellular mechanisms
- Ca transient (amount of SR Ca delivery per AP= amount of crossbirdge cycling)
- less ca sensitivity of myofilaments
- Slower crossbridge cycling
1. accumulation of metabolites (ionic conc change)
2. depletion of energy supplies to muscle (glycogen)(rate of ATP production)
DMD Duchenne’s Muscular dystrophy
1/3500 Male live births
Normal at birth - diagnose at 4
abnormal gate
genetic mutation of Distrophin
Big stocky muscles- fewer muscle fibres
Increased Weakness and degeneration of skeletal muscle
10= wheelchair
20=respiratory failure -not if on ventilator
Die late 20s
Genetic technique cure
Cardiac involvement- Dilated Cardio myopathy
Distrofin gene = decreased distrophin in muscles
connected to proteins that link ECM to intracellular F.actin (actin Filaments)
when crossbridge cycling occurs/force produce, force is tranduced across membrane
Less Distrophin = Actin Filaments no longer Linked to membrane proteins
+ controls Channels/receptors (TripC channels- allow Ca2+ influx)
-High levels of Intracellular Calcium
-enzymes (creatine kinase) leaks out =leaky cell membranes
Increased membrane permeability = enzymes such as Creatine kinase leak out. And ions such a Ca2+ Leak in
Age related loss of Muscle function
early muscle mass and strength increase old age have little muscle mass= muscle deterioration =injury prone Sarcopenia: Poverty of flesh -Primary consequence of agying Muscle m: Body mass ratio decreased Significant loss of strength
Sarcopenia
Age related (intrinics changes) primary cause
-can be slowed
Immutable and Irreversible
Muscle mass: Body mass ratio decreases
More type 1, no change in mean XSA cross sectional area for Type I or Type II B
Decrease in capillary:fibre ratio - less o2 removal
Denervation fo FF fibres + Motor unit remodelling
Mice: Less NMJ proteins (decreased activation)
Less alpha MN numbers
New muscle formation ISNT impaired
Exercise and diet can SLOW progression
