Dr Lucas: Lecture 4-7 Flashcards
Concentric contraction:
- Generating force and length is getting shorter (sarcomere shrinking)
Eccentric contraction + ex (2)
Generating force and length is getting longer
Pulling on muscle so much that it is extending out, controlled release
Ex: Bicep contracting to keep elbow bent, tricep descend arm so bicep is going through eccentric.
Isometric contraction (3)
What + often happens + ex
- Generating force and no length change.
- Often happen when we fix both ends
- carrying the box
Contractions induced in the lab to study muscle function: Isometric
constant + set up + what happens
- Constant length
- In lab you use heavy weight or fixed ends. You fix the two ends of the muscle or hang a heavy weight off the end of the muscle so it cannot shorten.
- tension never exceeds load. The contracting muscle bulges but not as much as during cocentric contraction.
Contractions induced in the lab to study muscle function: Isotonic
- Constant force
- Can only occur in lab setting because force is a vector, has magnitude and direction. So even if we are doing a bicep curl, the weight in my hand is not changing but the force vector relative to my muscle is because my position of my hand is and thats not isotonic.
Whole muscle length tension relationship (3)
2 components/how they contribute + final result
- Sarcomere length-tension relatinship is smooth at corners because we have a whole bunch of sarcomere+myofibril in the whole muscle and they are not totally in sync. (half round shape)
- Theres a stretching/shortening force and like a rubber band, the more you pull (length) the more it pulls back increasing in force. When the muscle length is really short, the rubber band is not pulling back on fingers, hanging loose (no force).
- Overall the whole muscle length tension relationship is the addition of the two components.
Trade off between force and velocity:
- you get this curve shape for a single myofibril, a single fiber or a constant number of fibers
- The right hand side of the x-axis is froom crossbridge cycling so fast that the myosin head and actin dont unbind fast enough (higher prob of finding them) so crossbridge dont detach fast enough.
- Left hand side of x-axis is from the myosin head and actin having an elastic force being bound together and resisting the external force.
Exact shape of length-tension and force-velocity relationships vary across species because of:
- length of filaments (invertebrates only)
- speed of ATPase in the myosin head
- Affinity of tropnin for Ca2+
Shape of the relationship are consistent
Sarcomeres in series boost
speed
Longer myofibril, the ends of the myofibril are going to shorten close to eachother
Long muscle fibres are —-
very fast
Sarcomeres in parallel boost
- Force
- Muscle that produce more force have more myofibril packed in. Calf would have more myofibril packed to make more force
Explain strength training and how it works
- We dont change the number of fibres or the arrangement of fibers. We make each fibre bigger in diameter by adding more myofibrils.
- We have the same number of muscle fibers as the rock but he is stronger because his muscle cells are bigger
—— stretch muscles back to starting length
Opposing muscles
Frog ankle illustrates how tendon/latch mechanism bypass muscle’s force-velocity relationship:
- Mechanism in Frog’s leg that lock the ankle in place. Ankle cannot rotate when muscle shortens so it stretches the tendon at some point.
- Tendon snaps back when latch released (ankle joint released)
- Stored energy released at once, rapid ankle rotation and high force delivered to ground for hoping.
You get high force and velocity at the same time because we used this tendon latch mechanism
Explain the experiment used to describe residual force enhancement
Trial 1: Peak length set up isometric contraction (length doenst change)
Trial 2: Start at a shorter length and halfway thru stretch to peak length. You would expect same force as trial 1 as same length
Real result: rFR= increase in force
Resting length
Work
energy used to do stuff or force applied to move something a distance
Power
The rate energy is used to do work or stuff over time
+ shortening velocity
get shorter faster (concentric)
Negative shortening velocity
Get longer, eccentric
Power-velocity curve
The problem is that a muscle fiber has enough ATP for —- of activity at max power.
There is 3 energy sources for contraction (3):
- 3 sec
- Phosphocreatine-creatine system
- oxidative phosphorylation
- Glycolysis-lactic acid system
Phosphocreatine-creatine system
- Cr-Pi + ADP -> Cr + ATP
- Fast - 4 mol ATP/min
- But Cr-Pi depleted in 5-8 second
*GONE FROM 3 SEC TO ~10ISH SEC
Oxidative phosphorylation (4)
inetnsity + percentage + fuel from/time + drawback
- < 70% Max intensity
- Supplied 95% of all long term contraction energy (When at less then 70% of muscle max intensity this will supply ~95% of all long term energy for contraction)
- Muscle glycogen supplies for 5-10 minutes the hours form blood (1/2 fuel is glucose for 2-4 hours then fatty acids)
- Slow to start and slow ATP supply (1mol ATP/min): Can sustain us for very long time but drawback is it takes a while to start up.
Glycolysis-lactic acid system (4)
sequence + primary at + speed + uses/time consumption
- Fills time between the other two
- Primary energy source at >70% max High intensity
- Intermediate speed - 2.5 mol ATP/min
- Uses muscle glycogen and consumes it in 1.5 min (faster then oxidative phosphorylation so provides ATP faster)
Only the ATP use at the —– can count towards useful mechanical work
myosin head
The one at the Ca2+ pump is not becauseit is not associated with a force
Mac energetic efficieny of human muscle is —- which means —–
- 25%
- 25% of muscle energy goes to useful mechanical work, rest to heat (Ca2+ pump is counted as heat)
How efficient is an isometric contraction?
0% efficient we are not doing work at all.
Why do your muscles get warm during use?
- Poorly efficient, alot of energy produced as heat
Maglignant Hyperthermia
How might this effect cross-bridge
Symptoms?
Treatment?
Vertebrate Fiber types
Slow oxidative (7)
- Slow
- Good (red)
- oxidative (aerobic)
- High: Supply good blood supply to bring in O2 + lots of myoglobin
- Low (Use oxidative metabolism and that runs slower ans we can supply fuel from liver so glycogen in muscle decrease)
- Fatigue resistant (use oxidative metabolism so can run for hours)
- Posture, slow walk (Dont need as much power)
Fast oxidative glycolytic (7)
- Fast
- High
- Can perform glycolytic (anaerobic) but mostly rely on oxidative metabolism
- Good (pink) Because oxidatice metabolism have decent aerobic support
- Medium (support glycolytic)
- Fatigue resistant (use oxidative metabolism so can run for hours)
- Rapid but sustained (fast walks, slow jogs)
Fast Glycolytic (7)
- Fast
- Very high
- Glycolytic (anaerobic)
- Low (white) No aerobic support because no oxidative phosp.
- High Support glycolysis lactic acid
- Rapidly fatigued
- Sprint
Fiber types have different force and power-velocity curves explain the differences:
FG achieve more force at slow velocities
Fibre type location differs across vertebrate muscle. Explain:
- FG fibers make up most of the muscle blocks and seperated from SO fibers. Different fiber types are physically seperated in space and individual muscle have 1 fiber type (diff muscle used for fast swimming and slow swimming)
- Other vertebrates: fiber are mixed within a muscle, instead of using different muscles to achieve faster speed, you use more of diff types of fiber within the same muscle
Talk about the bicycle gear and muscle force/power relationship
- You are at optimal force and power (middle of both graph, part B)
- You reach a hill and to pedal upwards you need to increase force so the velocity decrease and everything shifts left. Power also decreases.
- You have to shift gears to get back to B
Fast-twitch fibers produce force at ——– than slow-twitch fibers.
higher maximum shortening velocities
SO fibers has a higher peak power at —- velocity than FG fibers so it is more effective at —–.
- slow
- slow speed
Fast-twitch fibers produce
—— power
higher
The same isometric contraction (no shortening of the muscle)
over an equal time interval, costs fast-twitch fibers three times
more energy compared to slow-twitch fibers, as their power
stroke goes faster and they need to ——
perform 3 power strokes in the time that 1 power stroke is performed in slow-twitch fibers
Slow-twitch fibers are more energy efficient!
What is the arrangement of motor control neurons?
- Motor cortex has axon that originate and goes to spinal cord (descending pathway)
- Interneurons in spinal cord
- Alpha motor neurons (connected to interneuron) out of SC to muscle (NMJ). Interneuron in spinal cord synapses onto alpha motor neuron which synapses to a muscle.
- Ascending axons are also present, bringing sensory info to the brain.
Summation lets us modulate the level of force produced by a muscle.
1. At slow stimulation:
2. Stimulate bit faster:
3. Moderate lebel of summation:
4. High stimulation:
- Trigger the NMJ that let out some Ca2+ and little bit of force (twitches)
- Ca2+ left over + new Ca2+ come in so more CB
- Summation/incomplete tetanus
- Fused tetanus Stimulate so much you use all Ca2_ reach mac CB
Motor unit
Alpha motor neuron and all fibers it connects to; only have 1 type of fiber within the unit (SO, FG or FOg)
How is the problem that there is too many motor units for brain to individually control (6)?
ESPS + SO + FG + FOG + increase stimul + slow stimul
- Bigger cells require more EPSP to get to AP threshold
- Alpha motor neurons with smallest cell bodies = innervates SO fibers
- Alpha motor neurons with largest cell bodies = innervates FG fibers
- FOG fiber in between
- Increase stimulation rate of brain on alpha motor neuron recruit faster fibers
- Slow stimulating send to all alpha neurons only SO fibre depolarize, rest doesnt hit threshild. Faster and faster will hit threshold for the remaining.
Pull limb back in response to pain
Explain the withdrawal reflex (5)
- Pain on left arm activates sensory neuron to send AP to left hand side of spinal cord.
- Excites IN1 and sends signal to brain
- The interneuron branch 1.1 send excitatory signal to alpha motor neuron to NMJ to flexor muscle for bending.
- The interneuron branch 1.2 also send a excitatory signal to IN2 for inhibitory synapse.
- IN2 inhibits the alpha motor neuron to the extensor muscle
Withdrawal reflex + keep the other leg straight
Cross-extensor reflex:
- Signal to spinal cord
- Excites 1st interneuron and signal to brain
- Finish withdrawal reflex with reciprocal innervation in pain leg (IN branch 1.1 and 1.2)
- Branch 1.3 cross to the other side of the spinal cord and excite a 3rd IN
- 3.1 excites alpha motor neuron of extensor
- 3.2 excites 4th interneuron which inhibits alpha motor neuron to flexor
Muscle responses to changes in neural tone
Increase tone:
Decrease tone:
stimulation-signal-contract
Muscle spindle (2)
what + always
- Special muscle fiber wrapped by stretch-sensitive neuron
- Stretch neuron has tone, it is always firing but squish (decrease) or stretch increases the tone
Contract in response to sudden stretch
Stretch myotactic reflex cycle (4)
- When muscle is stretched it carry the spindle with it and also stretch. That is the stimulus and cause increase in tone, fire more = bring to threshold.
- It synapse directly on alpha motor neuron in SC and that comes back to the same muscle.
- The muscle contracts and shortens (squish spindle, decrease in tone), spindle length is reduced
- This causes reduce firing rate of stretch neuron.
Gamma motor neuron effect on muscle spindle
If the muscle is shortened, we now have slack. We cannot detect small length changes. Gamma motor neuron control spindle length (change set point for spindle) to let stretch neuron work effectively.
(gamma motor neurons fire on the ends of the spindle and do contraction-coupling to lengthen it out)
Describe how sliding filaments are arranged in smooth muscle
Filaments in lattice arrangement throughout cell, and are held together by dense bodies on the cytoskeleton.
Describe how ATPase is switched off, decreasing contraction (control at the thick filament) (4 steps)
- Ca2+ is removed from cytoplasm through several pumps
- Low Ca2+ concentration promotes unbinding of Ca2+ from CaM, so MLCK deactivated
- MLCP dephosphorylates MLC, ATPase switched off
- Cross-bridge cycle stops = relaxation
Describe how ATPase is switched on, increasing contraction (control at the thick filament) (4 steps)
- Ca2+ binds to a protein called calmodulin (CaM)
- Ca2+-CaM complex activates MLCK
- MLCK phosphorylates MLC, which swithces the ATPase on
- Cross-bridge cycle runs = contraction
What are the 3 pathways that can connect excitation to an increase in cytoplasmic Ca2+ in smooth muscle?
- Sarcolemma, voltage-gated Ca2+ channels opened by AP
- SR, triggered by second messenger
- Sarcolemma, Ca2+ channel opened by second messenger
Group single and multiunit in terms of :
phsic, tonic, myogenic, neurogenic
So you can see that the neuron is not touching every single cell in —— unit, because we have these electrical synapses. And so we don’t need to stimulate every single cell individually, whereas in —- unit there is the neuron will touch every single cell individually in order to be able to control every single cell individually.
- single
- multi
