Muscles pt. 2 Flashcards
(107 cards)
Describe how muscle function gets complicated in life-like scenarios in terms of residual force enhancement (rFE)
Experimental setup: Isometric contraction
1. Muscle is set up at peak length -> force ramps up due to latency, and then plateaus at a consistent level of peak force.
2. Take the same muscle and shorten it. Force ramps up due to latency, but then plateaus at a smaller force (due to force-length curve)
3. Take muscle and stretch it back to peak length.
Expectation: same force as trial 1
Real result: Increase in force (rFE)
Mechanism: maybe titin? But we don’t really know what’s going on which this
Describe how muscle function gets complicated in life-like scenarios in terms of tendon/latch mechanisms
The frog ankle illustrates how tendon/latch mechanisms bypass muscle’s force-velocity relationship (explains how a frog jumps - generates a lot of force and quickly)
- There is a mechanism in frogs that is locking the ankle in place (the ankle can’t rotate) -> mechanics of leg act as the latch
- Muscle shortens but ankle can’t rotate, so applying force to stretch a tendon (tendon=elastic like a rubber band; energy stored as stretched)
- Tendon snap back when latch released and we get high force and velocity at the same time (at some point, the mechanics of the leg are going to change and release the latch)
- Stored energy released all at once
- Rapid ankle rotation and high force delivered to ground for hopping
Work general definition, formula and units
Energy used to do stuff, or force (F) applied to move something a distance (d)
- W = Fxd (if direction of force and movement are aligned)
- Units: Nm = Joules (J)
Are you doing mechanical work if you’re pushing on a heavy box that’s not moving?
No
What kind of contraction are you performing while holding a plank? Are you doing work?
Isometric, no
Power definition, formula and units
The rate energy is used to do stuff, or work (W) over time
P=W/t=(Fxd)/t=Fxv where v=shortening velocity
Units: Watts (W) = J/t = (Nxm)/t
Draw the force-velocity curve and the power-velocity curve for a single myofibril, a single fiber and a constant number of fibers. Where is peak power?
Peak power: 20-40% of Vmax
Assume you are operating at peak power on flat ground. Describe what happens to force and power once you hit a hill and you don’t shift gears
Pedaling is harder at the hill, so need more force. Power decreases because we’re moving at a slower velocity (P=F x v) and as force increases, power decreases
If you were to bike up a hill at a lower gear than before, is your leg moving slower or faster than before? is your muscle shortening slower or faster?
You’re moving faster cause it’s easier to pedal
If you were to bike up a hill at a lower gear than before, is your muscle producing as much force as before? How does power change?
Less force is being produced (because legs are moving faster - force-velocity relationship)
Power increase compared to before because velocity is greater
A muscle fiber has enough ATP for ~3 sec of activity at max power. What are the 3 energy sources for contraction
- Phosphocreatine-creatine system
- Oxidative phosphorylation
- Glycolysis-lactic acid system
Describe how the phosphocreatine-creatine system replenishes the muscle fiber’s energy for contraction
Phosphocreatine reacts with ADP to form Cr + ATP
- Fast: 4 mol ATP/min, but Cr-Pi is depleted in 5-8 sec
Describe how oxidative phosphorylation replenishes the muscle fiber’s energy for contraction
- Replenishes muscle’s energy at <70% of muscle’s max intensity
- Supplies 95% of all long-term contraction energy
- Muscle glycogen supplies glucose for 5-10 mins for oxidative phosphorylation
- To sustain energy for hours: up to 1/2 of fuel is glucose from the blood for 2-4 hours. Then, fatty acids (less efficient fuel source)
- Slow to start, and slow ATP supply (1 mol ATP/min)
Why do runners “hit the wall” when running?
There is a fuel change from blood glucose to fatty acids. Since fatty acids are a less efficient fuel source, runners experience exhaustion and pain.
Describe how the glycolysis-lactic acid system replenishes the muscle fiber’s energy for contraction
- Fills time between the phosphocreatine-creatine system and oxidative phosphorylation when <70% of muscle’s max intensity is being used
- primary energy source at >70% max
- intermediate speed - 2.5 mol ATP/min
- uses muscle glycogen to make ATP faster than oxidative phosphorylation
- consumed supply in ~1.5 mins (much faster than oxidative phosphorylation, makes ATP much faster)
- End products (lactic acid) may impact contraction?
What are two ATP uses in muscle?
- Myosin head (Cross-bridges)
- Ca2+ pumps on the SR
Only the ATP use at the myosin head can count toward…
Useful, mechanical work
- the myosin head is the only thing that’s tagging on something and moving a certain distance in the muscle
Max energetic efficiency of human muscle and what this means
25%
- that means, at max, 25% of muscle energy goes to useful mechanical work.
- The rest is converted to heat (Ca2+ pump is counted as heat)
True or false: the muscle is usually much less efficient than 25% (max energetic efficiency of human muscle)
True
- we don’t use muscle optimally
How efficient is an isometric contraction?
0% efficient because work isn’t being done at all (no energy is going to useful mechanical work)
Why do your muscles get warm during use?
Our muscles are poorly efficient -> a lot of our energy ends up producing heat.
Some individuals have genetic mutations affecting DHPRs and RyRs. When exposed to certain anesthetics, these abnormal receptors stop regulating Ca2+ release, leading to constant, high levels of Ca2+ in the cytoplasm.
- how might this affect the cross-bridge cycle?
Cross-bridge cycle just keeps going
Some individuals have genetic mutations affecting DHPRs and RyRs. When exposed to certain anesthetics, these abnormal receptors stop regulating Ca2+ release, leading to constant, high levels of Ca2+ in the cytoplasm.
-What impact does this have on muscle energy use?
Use lots of energy
Some individuals have genetic mutations affecting DHPRs and RyRs. When exposed to certain anesthetics, these abnormal receptors stop regulating Ca2+ release, leading to constant, high levels of Ca2+ in the cytoplasm.
- What symptoms do you think you would see in an affected individual? (4)
- Muscle rigidity (due to continuous contractions)
- Stop breathing (all muscles are tensed up)
- Heat up
- Depleted glycogen stores