Quiz 2 Material Flashcards
ATP
Energy of the cell
Requires as much ATP to relax muscle as to contract
Addition of ATP allows myosin to interact with actin
Muscle movement = continuous breakdown and reconstitution of ATP
Aerobic Pathway
Type I Muscles Prefer
Location: Mitochondria
More Efficient, Slower
Uses Fatty Acids to make ATP
Fatty Acids
Stored in fat cells
Must be released into blood stream (triglycerides) during exercise for aerobic pathway
Anaerobic Pathway
Creatine Phosphate- used first- allows muscle to immediately contract (always small amount stored)
Glycogen- used second- produces ATP via glycolysis
Lactic Acid- by product of glycolysis
Brain can only produce ATP anaerobically!!!
Exercise (Metabolic View)
Phase 1- first few min, creatine phosphate and glycogen primary fuel source
**want to shift to phase 2 quickly
Phase 2- aerobic metabolism & use of fatty acids to produce ATP
**want to stay in phase 2 as long as possible
Phase 3- back to anaerobic (use remaining stored glycogen in muscle fibers and liver cells); lactic acid accumulates
Carb Loading
Only for endurance
Goal: Increase storage of glycogen in muscle fibers (Prevent using glycogen from liver during Phase 3- save for NS)
Doesn’t increase strength/run faster
Side effects: hypoglycemia, weight gain (3 grams water:1 gram glycogen)
Caffeine
1 hr before event: ingestion may help burn fatty acids more efficiently & increase Ca permeability
Delay glycogen utilization (Phase 1 to Phase 2 faster)
1000mg threshold for competition (only supplement with threshold)
Blood Doping / Induced Erythrocythemia
Affects any phase (oxygen always needed)
-increase O2 carrying capacity of RBCs
(Increase concentration of RBCs = increase endurance= exercise longer)
Risks of Blood Doping
- Rashes/fever
- Acute hemolysis (breakdown of RBC’s)
- Transmission of viruses
- Fluid overload (kidney damage, intravascular clotting)
Erythropoietin (EPO)
Natural hormone produced by kidneys
Travels to bone marrow to produce RBC
Synthetic EPO
Used to increase RBC concentration
Thickens blood -> cardiac problems and death
Anabolic Steroids
Synthetic form of testosterone
“Minimal” androgenic effects and “more” androgenic
Anabolic
Stimulation of protein synthesis
Androgenic
Development of secondary sexual characteristics
Oil Based
Injected
Fewer side effects, detectable longer
Water Based
Pill form
More side effect, cleared from body faster
Stacking
Take several forms of drug
Pyramiding
Start with low dosage, raise to a peak, then taper down amount taken
Short term side effects of Anabolic Steroids
Acne (esp. back) Shrinkage of testes Increased aggressiveness Gynecomastia Tendon damage
Why is tendon damage a short term side effect of steroids?
Tendons respond slowly to strength regimes
Steroids my inhibit formation of collagen (main constituent of tendons and ligaments)
Long term side effects
CVS
Digestive system
Reproductive System
Endocrine System
Adolescent use of steroids
Premature closing of growth plates
Anabolic steroids work by
- Increasing secretion of growth hormone
2. Activates protein synthesis and prevents protein breakdown
Chemical composition of muscle
75% water
20% Protein (mostly myosin)
5% Other
Nerve Supply of Skeletal Muscle
Motor Nerve Fiber (efferent/motor impulse)
Sensory Nerve Fiber
Motor Unit
Single motor neuron (nerve fiber) and the group of muscles fibers it supplies
Strength of muscle contraction depends on…
Number of motor units begin activated/ recruited at same time
Size of motor unit (number of fibers in unit) indication of…
How much fine control (precision) muscle carries out
More Precision a muscle has means…
Fewer fibers
Neuromuscular Junction
Presynaptic portion
Postsynaptic portion
Synaptic cleft
Presynaptic portion
Nerve ending
Postsynaptic portion
Sarcolemma of muscle fiber
Synaptic cleft
Space between pre and post synaptic portions
How a nerve impulse makes its way from presynaptic to postsynaptic portion of neuromuscular junction (Steps)
- Neve impulse reaches presynaptic portion of NMJ
- NT ACH is released
- ACH will diffuse across synaptic cleft and bind to specific receptor site on sarcolemma of muscle fiber
- Binding will result in setting off an action potential down transverse tubule
- Actin and myosin interact, causing muscle contraction
- Acetylcholinesterase destroys ACH when task is completed
Myasthenia Gravis
Most common neuromuscular junction disorder Autoimmune Disorder (ABS damage/destroy ACH receptor sites on sarcolemma of muscle fibers)
Co-morbidities with Myasthenia Gravis
Hyperplasia of thymus gland
Thymoma
Gland probably giving incorrect information to immune system about ACH receptor sites
Transitional neonatal myasthenia Gravis
25% pregnant women will transmit condition to infant
Condition eventually passes once maternal ABS are passed from infant’s system
Nicotine
Competitive inhibitor with ACH
Action is much more prolonged than ACH (no enzyme to break it down)
Snake Venom
Competitive Inhibitor
Cytotoxin- destroys tissue
Neurotoxin- makes way to NMJ and competes with ACH to bind at receptor- No action potential produced
Organophosphates
Inactivate ACHe
Accumulation of ACH at postsynaptic portion of junction- muscles remain contracted
Botulin Toxin
Blocks release of ACH from presynaptic portion of NMJ
