Muscle Part 2 Flashcards
A muscle fiber generates force called
tension
Twitch
Mechanical response of a muscle fiber to a single AP.
Only in lab setting
Simplest contraction observable in lab (recorded as myogram)
Muscle contracts faster than it relaxes.
Latent period
The delay between the beginning of the AP and the initial increase in tension
E-C coupling is occurring
No muscle tension
Period of contraction
Cross bridge formation
Tension increases
Period of relaxation
Ca2+ reentry into SR
Tension declines to zero
Concentric contractions
Cross-bridges bound to actin= shortening of sarcomere
Eccentric contractions
The load pulls cross-bridges, while they are still bounded to actin, backwards towards the Z lines
Isotonic Contractions
Muscle changes in length and moves load. Thin filaments slide.
-Concentric
-Eccentric
Isometric Contractions
Load greater than tension muscle can develop
Tension increases to muscle’s capacity, but muscle neither shortens nor lengthens
Cross bridges generate force but do not move actin filaments
Load Velocity Relation
Muscles contract fastest when no load added
increased load =
increased latent period (Time needed for E-C coupling and for enough cross- bridges to attach to enable the muscle to lift the load )
decreased distance shortened
decreased velocity of shortening
decreased duration twitch
Graded muscle responses
- Varying strength of contraction for different demands
- Required for proper control of skeletal movement
Summation
Increased stimulus frequency= second contraction of greater force
Muscle (does not completely relax) between stimuli
Additional Ca2+ release with second stimulus stimulates more tension
Further increase in stimulus frequency
unfused tetanus
If stimuli are given quickly enough, muscle reaches maximal tension
fused tetanus
-Too long
-(No muscle relaxation)= Persistent elevation of cytosolic Ca2+
-Muscle cannot contract = zero tension
-Muscle fatigue
Length-Tension Relation
Passive tension due to titin proteins (Helps recoil after stretch).
Active tension during tetanic stimulation (stimulation
of a muscle or nerve at a high frequency)
Optimal Length - L0 (normal resting length)
– The greatest number of cross bridges when muscle fibers around 100% normal resting length
– Most force
Too short
– at <80%of L0 (normal resting length)= Actin fibers block other actin
binding sites= Decrease cross bridge access to thin filaments
– Z discs hit myosin
– Less force
– <60% of L0 - no force
Too long
– Actin fibers pulled off myosin at >120% normal resting
length Decrease cross bridge access to thin filaments
– Less force
– >175% - no force
Muscle Metabolism: Energy for Contraction
ATP only source used directly for contractile activities
- Move and detach cross bridges
- Calcium pumps in SR
- Return of Na+ & K+ after excitation-contraction coupling
ATP regenerated by:
1. Direct phosphorylation of ADP by creatine phosphate (CP)
2. Aerobic respiration
3. Anaerobic pathway (glycolysis= lactic acid)
Direct phosphorylation
CP + ADP= C + ATP
Creatine phosphate + ADP= Creatine and ATP
* Reversible
* At rest - CP 5X > ATP
* Short burst of ATP allows other
sources to catch up
Aerobic Pathway
- Produces 95% of ATP during
rest and light to moderate
exercise - Slow
- Efficient
- Series of chemical reactions that require oxygen
- Occur in mitochondria
- Breaks glucose into CO2, H2O, and large amount ATP
Fuels (in order of use)
1. Stored glycogen
2. Blood-borne glucose
3. Free fatty acids
Anaerobic Pathway
Glycolysis –
– Does not require oxygen
– Used when ATP breakdown
> 70%
– Glucose degraded to 2
pyruvic acid molecules
* Normally enter mitochondria= aerobic respiration
-Pyruvic acid converted to lactic acid
-Lactic acid is converted back into pyruvic acid or glucose by liver
Yields only 5% of ATP of aerobic but 2.5 times faster
Oxygen Debt
Breathing deeply and rapidly after exercise= repays the oxygen dept
- To return muscle to resting state:
1. Oxygen reserves replenished
2. Lactic acid converted to pyruvic acid
3. ATP and creatine phosphate reserves replenished
4. Glycogen stores replaced
Muscle Fatigue
Physiological inability to contract despite continued stimulation.
Acute metabolic changes:
– Decrease in ATP
– Increase in ADP, Pi, Mg2+, H+ (from lactic acid) & oxygen free radicals
Consequences:
1. Rate of Ca2+release, reuptake & storage by SR
2. Ability of Ca2+ activate thin filament proteins
3. Inhibit binding & power-stroke of myosin cross-bridges
* Decreased shortening velocity
* Slower relaxation rate
Long-term fatigue
– Ryanodine Ca2+ channels become leaky
– Activate proteases that break down
contractile proteins
– Depletion of glycogen
– Low blood glucose
– Dehydration
Central command fatigue:
– CNS stops sending APs to motor neurons
– No AP in motor neuron = no AP in muscle cell
– No contraction even though muscle is not truly fatigued
