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KIN 3600
midterm 2
| Question | Answer |
|---|---|
| Short duration – high intensity: springing 8-10 seconds | ^ 25% ATP & 40% CP stores ^ duration - top speed stays same Enzymes: ^ ATPase 30%, MK 20%, CPK 36% ^ top speed increase |
| Short duration – high intensity: springing 20-60 seconds | ^ glycogen ^ duration - top seed remains same Enzymes: Glycolytic = ^ PFK 83% ^ top speed increase |
| Endurance training – adaptations | • ^ myoglobin 26% • ^ number 120% & size 40% of mitochondria • Enzymes: ^ TCA & ETC 40% • ^ glycogen storage 2.5x • ^ fatty acid utilization • Greatest ^ Type IIa & Type IIx |
| High resistance strength training – adaptations | • ^ strength 28% • ^ CP concentration 5.1% • ^ Creatine concentration 35.2% • ^ ATP Concentration 17.8% • ^ Muscle Glycogen 32% |
| Why does ATP use increase with exercise? | • As activity levels increase, breathing rateincreases to supply more oxygen for increased ATP production • As the work of the muscle increases, more and more ATP get consumed and must be replaced in order for the muscle to keep moving. |
| What does it mean for aerobic metabolism to meet ATP demand? | • oxygen uptake correlates with increasing speed |
| what is aerobic metabolism? | • the oxidative process of the generation of ATP or energy that occurs in the body to provide the body with fuel during both resting and exercise states. |
| Incremental phase (O2 Deficit) | •Energy is mostly supplied by the hydrolysis of ATP, CP, and anaerobic glycogenolysis (lactate) • Utilization of storage oxygen o O2 in Capillary blood & interstitual fluid o O2 present in sarcoplasm with myoglobin o O2 present in mitochondria |
| what is O2 deficit | Difference between oxygen demand and supply during exercise bout |
| Steady state phase (Plateau Phase) | • Energy demand of the exercise is completely met by the aerobic phosphorylation. (O2 demand – O2 Supply) |
| EPOC (recovery phase) | • Excessive Post-Exercise Oxygen Consumption instead of “oxygen debt” |
| Factors responsible for “oxygen debt | o resynthesize ATP & CP form ADP & Pi o replenish the O2 stores of the body o resynthesis of glycogen from lactic acid in liver (gluconeogenesis) |
| why EPOC is than bigger O2 deficit | • Extra oxygen consumed by Heart, respiratory muscles, hormonal, Q10 effect |
| Difference in VO2 kinetics during a maximal (heavy) and light exercise | • Higher (heavier) the intensity of the exercise the higher the oxygen deficit and EPOC – vice versa |
| Difference in training vs untrained who has bigger oxygen deficit and or EPOC and WHY... | •Trained person will develop smaller O2 deficit and EPOC, due to faster response of aerobic energy transformation system ^ rate-limiting enzymes: Isocitrate, Cytochrome oxidase ^ TCA intermediary synthesis |
| Single stage | single, supra-maximal workload. Warm up before testing. |
| Multiple stage | Progressively incremental exercise testing (GXT). The warm up is built into the workout. |
| how do you test VO2 max? | Single vs multiple stage |
| Modes | • Cycle ergometer • Arm crank ergometer • Treadmill • Stair climb ergometer • Swimming flume • Rowing ergometer |
| What is VO2max | • maximum rate of oxygen consumption measured during incremental exercise; that is, exercise of increasing intensity. • "V" for volume, "O₂" for oxygen, and "max" for maximum |
| Relative Vo2 max | better predictor aerobic fitness, health-related fitness, and endurance performance in weight–bearing sports and activities. |
| Absolute Vo2 max | better predictor of performance in non-weight-bearing endurance sports and activities |
| Difference between relative and absolute VO2 max? | Relative takes size into account and is measured in ml/kg/min and Absolute doesn't and is measured in L/min |
| How do we use this for an index of exercise intensity? | • Objective expression of exercise intensity • Exercise intensity expressed relative to Vo2 max • Exercising Vo2= Vo2 max x intensity % / 100% |
| Who has higher Vo2max in different athletes or sex? | athletic males |
| Muscle fiber types and Vo2max (%ST and max) | • Slow Twitch (ST) muscle fibers are highly aerobic fibers |
| What is anaerobic threshold (OBLA | • Power output or Vo2, during progressively incremental exercise, after which there is a systematic increase in blood lactate concentration. |
| Why does Dr. K like using OBLA | Descriptive term without a why or how, just what happens |
| Why does he NOT like anaerobic threshold | • Claims that it’s because anaerobic system as underlying mechanism |
| OBLA vs Ventilatory threshold | •OBLA – increased exercise leads to increase blood lactate •Ventilatory- refers to the point during exercise at which the intensity level increases, breathing becomes faster; more steadily first and then more rapid as the intensity increases |
| When does OBLA happen | |
| three ways lactate production increases | -Hormonal stimulating of glycolysis b/c during fight or flight you release a lot of stress hormones that ^ ET -Blood being shunt away from liver and kidney. B/c function of gluconeogenic organs need that blood to bring lactate to them. |
| How does the removal of lactate become difficult | |
| Where does vasodilation and constriction occur? | |
| What is lactate turnover rate | • Percentage of lactate leaving |
| What happens with endurance trained individuals vs untrained | |
| Why is OBLA a better predictor for performance | |
| How does training effect OBLA | |
| Difference in healthy person compared to McArdle’s | • McArdle's Metabolic myopathy caused by a deficiency in muscle glycogen phosphorylase |
| Direct Calorimetry | The rate of energy expenditure may be measured by measuring the rate of heat liberated by the body during rest or during various physical activities |
| Indirect Calorimetry | measurement of the amount of heat produced by a subject by determination of the amount of oxygen consumed and the amount of carbon dioxide eliminated. |
| What is the Atwater Rossa | • Insulated heat chamber o No heat in or out • Mesh tubing • Person push out CO2 • Take out the CO2 of the chamber & push in O2 to make O2 constant |
| What is the respiratory exchange ratio | CO2 expired : O2 consumed |
| What do we use R for | • calculate relative contributions (%) of fats and carbohydrates to energy transfor mation and the amounts (grams) of fat and carbohydrates utilized. • Unknown R - 4.82 or 5 Kcal∙LO2-1 |
| following ratio 1.0 | • C6H12O6 + 6O2 = 6CO2 + 6H2O R = 6CO2 / 6O2 |
| following ratio 0.696 | • C16H32O2 + 23O2 = 16CO2 + 16H2O R = 16CO2 / 23O2 |
| following ratio 0.818 | • C72H112N2O22S + 77O2 = 63CO2 + 38H2O + SO3 + 9CO(NH2)2 R = 63CO2 / 77O2 |
| how to calculate R | • R = Vco2 / Vo2 |
| what is energy equivalent of Oxygen? | |
| when do you use energy equivalent of Oxygen? | |
| Basal metabolic rates (BMR) | the rate of energy expenditure during absolute rest |
| Basal metabolic rates (BMR) test protocol | •Absolute rest •12 hours pos-absorptive state •12 hours post-exercise •Overnight restful sleep •Dimly lit room •Room temperature 68 to 80º F •In semi-recumbent position at least 30 to 60 minutes before the measurements of the energy expenditure |
| Resting metabolic rate (RMR) test protocol | • 2 hours post-pranidal • Sitting position |
| Factors Affecting BMR | • Weight • Body Surface Area • Age & Gender • Fitness level • Body composition • Genetics • Metabolic disease (hypothyroidism and hyperthyroidism) |
| What is a Metabolic Equivalent? | • 1 MET is the rate of resting energy expenditure or the rate of resting O2 consumption |
| When do we use a MET? | • Used to express the rate of energy expenditure or exercise intensity of various physical activities as multiples of BMR |
| calculate energy expenditure from METS | • Vo2 = weight kg × 1 MET (3.5 ml·kg-1·min-1) × Given MET |
| E.E. of O2 | = 5.0 Kcal·L-1 |
| Estimated rate of E.E | = Vo2 answer × 5 Kcal·LO2-1 |
| Actual Rate of E.E. | = Given Resting VO2 × Given MET × 1 E.E. (5 Kcal·LO2-1) |
| Know how to calculate mechanical Efficiency | • M.E.(gross) = Work output Energy input 100 % |
| Energy input | = given Vo2 × E.E. O2 (4.82 kcal·L-1 |
| Energy output | = Power Output x 60 sec·min-1 ÷ 1Kcal (4186.85 J·Kcal-1) |
| Net O2 consumption | = given Vo2 – MBR in L |
| Net energy input | = Net o2 consumption × E.E. O2 (4.82 kcal·L-1 ) |
| M.E. (Net) | = Energy output÷ Net energy input x 100 % |
| Three Main functions of nervous system | • Sensory • Integratory • Motor |
| Central Nervous System (CNS) | Brain and Spinal cord |
| Peripheral Nervous System (PNS) | Afferent and Efferent neurons |
| SOMA (CELL BODY) | proteins produced to build new dendrites |
| Dendrites | transmit impulses towards the cell body |
| Axon | transmit impulses away from cell body |
| Nucleus | contains genetic material |
| Cytoplasm | synthesis of proteins |
| Myelin | protective covering that surrounds fibers called axons, the long thin projections that extend from the main body of a nerve cell or neuron |
| characteristics of neurons | Neuron is electrically charged, polarized Excitability – ability to respond stimuli - altering its polarization. Conductivity–ability to transmit electrical impulses. B/c of these characteristics’ neurons can generate and conduct electrical impulses |
| Electrical & chemical gradients are responsible for what | |
| influx of Na+ means what? | Inside cell turns positive |
| Outflux of K+ means what? | Exits the cell to try and keep electrochemical equilibrium |
| What are voltage regulated Na+ and K+ responsible for? | |
| Na+/K+ pumps do what? | . The process of moving sodium and potassium ions across the cell membrance is an active transport process involving the hydrolysis of ATP to provide the necessary energy |
| Relative refractory | cell may be stimulated if stronger than normal stimulation will trigger a reaction |
| Absolute refractory | - Time elapsed from beginning of stimulation during which another action potential cannot be generated in the cell regardless if stimulus strength. |
| What is the all or non-principle | The size of A.P is independent of the stimulus intensity (strength). No matter the size of the stimulation the AP is ALWAYS be the same. Under stimulation, nothing happens. |
| When does AP actually occur? | When it passes the simulation threshold |
| Eddie currents are responsible for what? | heating tissue heating or peripheral nerve stimulation. |
| What does diameter and length do to the propagation velocity | • The larger is the diameter of an axon the greater is the propagation velocity |
| Why is myelination important? | • helps prevent the electric current from leaving the axon |
| What does Saltatory conduction do? | Propagation of A.P. trough myelinated axons |
| What does it mean to be frequency coded? | • the stronger is the stimulus intensity the higher is the frequency of action potentials propagated. |
| What is a synapse? | • functional connections between neurons, between neurons and other cells – muscles and glands, or between muscle cells |
| the components of a synapse | i. Presynaptic terminal ii. Motor end plate iii. Synaptic cleft iv. Basal Lamina v. Quanta |
| What is the motor end plate | specialized chemical synapses formed at the sites where the terminal branches of the axon of a motor neuron contact a target muscle cell. |
| What do vesicles hold | liquid |
| Quanta | number of neurotransmitter vesicles released per Action Potential. |
| What is the basal lamina | is a layer of extracellular matrix secreted by the epithelial cells, on which the epithelium sits |
| Starting from AP reaching axon button, release of what neurotransmitter? How do we release this neurotransmitter? | voltages which cause depolarization of skeletal muscle fibers caused by neurotransmitters binding to the postsynaptic membrane in the neuromuscular junction |
| What is the neurotransmitter responsible for activation of the muscle and what does it exactly do | Acetylcholine is excitatory at the neuromuscular junction in skeletal muscle, causing the muscle to contract. When a nerve signal, reaches the end of the axon, the vesicles release a neurotransmitter into the synaptic gap. |
| How do we stop activation? | • Acetylcholinesterase |
| Why is this Acetylcholinesterase important? | • stops the signal between a nerve cell and a muscle cell. |
| What will occur if higher frequency of activation occurs? | • The larger is the frequency of APs arriving to the presynaptic terminal, the higher is the frequency of neurotransmitter vesicle released in the synaptic cleft, the larger is the EPP |
| Nerve gas | inactivates Acetylcholinesterase - Spastic Paralysis – post-synaptic blockade |
| Curare | competitively binds to Ach receptors of Post synaptic membrane - Flaccid Paralysis – post-synaptic neuromuscular blockade |
| How are we graded at the end plate | the larger is the amount of the transmitter released the larger is the size of the EPP) |
| How do we stop stimulation of end plate? | Botulinum Toxin??? |
| Characteristics of EPP | • No overshoot and may go only up to 0 mv • EPPs are Graded • Conducted decrementally along the end plate • very long duration • no refractory periods |
| What are the four principals’ characteristics of muscle | • Excitability, Contractility, Extensibility, Elasticity |
| Excitability | ability to respond to stimuli |
| Contractility | ability to contract and produce a force |
| Extensibility | ability to be stretched without rupture |
| Elasticity | ability to return to its original shape after shortening or extension |
| What does the connective tissue do for the structure and force | • Structural support • Force transmission |
| What are the three connective tissue | • Epimysium • Perimysium • Endomysium |
| Epimysium | envelops individual muscles from outside providing structural integrity for the whole muscle |
| Perimysium | envelops several hundred muscle fibers forming Fascicles |
| Endomysium | envelopes each muscle fiber individually |
| What is the tendon and what does it do? | • fusion of all three connective tissues together at the two distal end of the muscle forms tendons • capable of resisting high tensile forces while transmitting forces from muscle to bone |
| What is a muscle fiber? | • Structural unit of the muscle • Multinucleated |
| Structure component of a muscle fiber? | i. Sarcosol ii. Saroclemma iii. Sarcoplasm |
| Sarcosol | aqueous solution containing electrolytes, glucose, aminoacids, peptides, proteins, enzymes, fat droplets, glycogen granules, ATP, & CP. |
| Saroclemma | Phospholipid bilayer with imbedded proteins |
| Sarcoplasm | Cytosol + organelles (nuclei, mitochondria, filaments, endoplasmic reticulum, etc.). |
| What are Myofibrils made of? | • Thick (myosin) and thin (actin) myofilaments |
| How do these changes when contractions occur | • I-bands progressively narrow and eventually disappear. • A-bands remain at the same length • H-zone progressively narrows, disappears, and then reappears as a darker zone becoming progressively wider |
| What is a sarcomere and why is it important? | • a segment of a muscle fiber or myofibril located between two adjacent Z-disks. |
| What happened when sarcomeres are arranged in series vs parallel? | • in-series (increased range and velocity of contraction) and in-parallel (increased force of contraction) |
| Why do sarcomeres have striations? | • Under light microscope muscle fibers demonstrate alternating light (Isotropic) and dark (Anisotropic) regions called I-band and A-band |
| The sarcomeres has two myofilaments | Thick and Thin filaments |
| What is the key function of T-tubules | muscle contraction |
| Where are they in skeletal muscle vs cardiac | sarcolemma |
| What is the Sarcoplasmic reticulum (SR) | - is a membrane-bound structure found within muscle cells that is similar to the endoplasmic reticulum in other cells. |
| What are the dilated parts of Sarcoplasmic reticulum called? | Triads |
| What is the SR mechanically coupled with? | t-tubules |
| What is the mechanism for muscular contraction? | • Sliding Filament Theory of Muscular Contraction |
| How does the sliding filament theory occur | • the actin and myosin filaments within the sarcomeres of muscle fibers bind to create cross-bridges and slide past one another, creating a contraction. |
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rmart11
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