492 Final Exam Complete Study Guide PDF

**Exam I Content** **Chapter 1:** - [Exercise responses to constant load/work rate:] no change in intensity level over time - Plateau at steady-state / positive or negative drift **Chapter 2:** - [Exercise-induced hormesis:] low/moderate dose of a...

**Exam I Content** **Chapter 1:** - [Exercise responses to constant load/work rate:] no change in intensity level over time - Plateau at steady-state / positive or negative drift **Chapter 2:** - [Exercise-induced hormesis:] low/moderate dose of a harmful stressor (exercise), results in an adaptive response -- defines what we know about exercise adaptations - [Homeostasis:] maintenance of relatively constant internal environment during resting conditions - Variables vary around a "set point" - Used to describe "resting values" or a "resting state" - [Steady-State]: constant internal environment during sub-maximal constant-load exercise, different than resting values - Variable unchanging but not normal - [Biological control systems:] series of interconnected components that maintain a parameter at a near "constant value" -- how training adaptations manifest - Components: - Sensor/receptor: detects change in variable - Control center: assesses input from sensor & initiates response - Effector: changes internal environment back to normal - Gain: degree to which a control system maintains homeostasis -- larger gain = more control (major systems) - [Negative feedback systems:] response reverses the initial disturbance in homeostasis (most control systems) -- ex. Bringing down HR after exercise - [Positive feedback systems:] response increases initial stimulus -- ex. Nitric oxide as a vasodilator - [Exercise as a test of homeostatic control:] body doesn't maintain homeostasis during exercise -- changes in pH, O2, CO2, & temperature - Sub-maximal: most systems reach & maintain steady-state - Maximal: cannot maintain steady-state, results in fatigue or cessation of exercise **Chapter 7:** - [CNS:] brain & spinal cord - [PNS:] afferent & efferent divisions - Afferent: sensory -- receptors \> CNS - Somatic sensory - Visceral sensory - Special sensory - Efferent: motor -- CNS \> effector organs - Somatic motor (voluntary) - Autonomic motor (involuntary) - [Synaptic Transmission:] how impulses are transmitted via neurotransmitters along axons via "excitable tissue" - \*\* only with EPSPs - [Resting membrane potential:] the negative charge inside cells (-40mV - -75mV) - [Depolarization:] when the membrane potential becomes less negative than the RMP -- marked by an influx of sodium ions making the inside of the cell more positive, increases the likelihood of an action potential - [Repolarization:] the process of restoring the membrane potential back to its resting state -- marked by the efflux of potassium ions making the inside of the cell more negative, prepares cell for the next action potential - [Hyperpolarization:] when the membrane potential becomes more negative than the RMP -- marked by potassium leaving the cell, results in a refractory period - [EPSP:] causes depolarization -- stimulates muscle contraction - Increase permeability of calcium, leads to release of Ach - Ach binds to nicotinic receptors - Sodium ion channels open - [IPSP:] cause hyperpolarization -- inhibits muscle contraction - Prevents depolarization - More polarized neurons "resist" depolarization - [Joint proprioceptors]: provide CNS with body position information 1. Free nerve endings: most abundant, sensitive to touch and pressure, initially strong then adapt to stimulus 2. Golgi-type receptors: in ligaments & joints, cause relaxation during exercise 3. Pacinian corpuscles: around joints, detect rate of joint rotation - [Muscle proprioceptors]: (mechanoreceptors) provide info about movement 1. Muscle spindles: responds to changes in length and maintain posture -- consist of intrafusal fibers & gamma motor neurons a. Response: myotatic reflex: rapid lengthening causes contraction 2. Golgi tendon organs: monitors tension during excessive force generation, extension of extrafusal fibers b. Response: inverse stretch reflex: relaxation to reduce tension via IPSPs - [Somatic motor neurons]: carries message from spinal cord to muscles, axon splits into collateral branches - Motor unit: motor neuron and all it innervates - Innervation ratio: number of fibers innervated by alpha motor neuron - [Types of motor units]: 1. Type I: greater glycolytic, less oxidative, small (less contractile proteins) 2. Type IIa: intermediate, fast, fatigue resistant 3. Type IIx: largest, fast, fatigable - [Size principle]: smallest motor units recruited first to connect with external demands - Incremental: I \> IIa \> IIx **Chapter 8:** - [Microstructure of muscle fibers: ] 1. Sarcoplasm: cytoplasm of muscle cell 2. Myofibrils: protein myofilaments & contractile proteins 3. Sarcomere: contractile unit 4. Sarcoplasmic reticulum: storage for calcium 5. Transverse-tubules: extend from sarcolemma to SR, spreads action potentials - [Myonuclear domain]: volume of sarcoplasm around each nucleus - [Satellite cells]: facilitate growth & repair damaged tissue (hypertrophy), typically dormant but donate nucleus for repair - [Neuromuscular junction]: space between neurons - [Muscle contraction]: excitation-contraction coupling - Excitation: 1. Excitatory signal arrives at terminal axon 2. Motor neuron releases Ach into synaptic cleft, sodium channels open a. Calcium released via exocytosis, Ach binds to nicotinic receptors 3. Wave of depolarization spreads via t-tubules - Contraction-coupling: 4. Depolarization causes SR to release calcium (CICR & non-CICR) 5. Calcium enters sarcoplasm & binds to tropomyosin 6. Positional shift causes tropomyosin to expose actin's active site 7. Activated myosin head binds to actin b. "cross-bridge" release stored energy, releases ADP & Pi 8. Fresh ATP binds and breaks cross-bridge c. ATP hydrolysis via Myosin ATPase - Relaxation: 9. Stimulation ends, Ach release stops, fiber repolarizes 10. Calcium removed & pumped back into SR - [Muscle fiber types ] 1. IIx: low mitochondrial density, fastest ATPase, low oxidative, high glycolytic 2. IIa: anaerobic & aerobic, moderate efficiency, high oxidative & glycolytic 3. I: high mitochondrial density, slow ATPase, aerobic, high efficiency, high oxidative, low glycolytic - [Biochemical properties of muscle fibers]: 1. Oxidative capacity: oxidative enzymes, number of capillaries & mitochondria, amount of myoglobin 2. Type of ATPase isoform: speed of degradation 3. Abundance of contractile proteins - [Contractile properties of muscle fibers]: 1. Max specific force production: force per unit CSA 2. Speed of contraction (Vmax): regulated by Myosin ATPase 3. Max power output: amount of work accomplished per unit of time (II\>I) 4. Fatigue resistance: ability to sustain contraction 5. Efficiency: lower amount of ATP to generate force - [Speed of muscle action and relaxation]: muscle twitch -- result of a single stimulus, three phases 1. Latent period: short, corresponds to depolarization of fiber 2. Contraction: calcium released from SR, cross-bridge formation 3. Relaxation: (50ms) cross-bridge detachment, reuptake of calcium - [Determinants of force regulation in muscle] 1. Number/type of motor units recruited 2. Muscle length 3. Firing rate of neurons 4. Contractile history - [Force-velocity relationship]: inverse, Vmax of shortening is greatest at lowest force - [Force-power relationship]: direct, peak power proportional to velocity until 200-300s - [Muscle fatigue]: decline in power output, causes depend on intensity & duration - Central fatigue: occurs in CNS, decreased units activated and firing frequency - Peripheral fatigue: neural and mechanical factors, energetics of contraction - Neural factors: NMJ (unlikely), altered ability of sarcolemma and t-tubules - Mechanical factors: cross-bridge & tension development needs lots of calcium, inability of SR to take up calcium, longer relaxation time - \*\* most probable - Energetics of contraction: slowed rate of ATP utilization, accumulation of Pi **Chapter 3:** - [Endergonic]: requires energy, ATP \> ADP -- drives exergonic reactions - [Exergonic:] energy released, ADP \> ATP - [Oxidation-reduction reactions (redox]): always coupled, transfer of energy via electrons - Oxidation: removal of electron - Reduction: addition of electron - [Hydrogen carriers:] - NAD: nicotinamide adenine dinucleotide - Oxidized: NAD+ - Reduced: NADH + H+ - FAD: flavin adenine dinucleotide - Oxidized: FAD - Reduced: FADH2 - High energy products of metabolism for energy production - 1 NADH = 2.5 ATP - 1 FADH2 = 1.5 ATP - [Rate-limiting enzymes]: regulate metabolic pathways, stimulated/inhibited by metabolic product - [Anaerobic ATP Production]: - ATP-PC: - Starting substrate: phosphocreatine - End products: ADP, Pi, energy - 1 PC = 1 ATP - \# of steps/pathways involved: single enzyme reaction - Replenishment time: 10-15s - When it provides bulk of ATP: single reaction - Location: sarcoplasm - RLE: creatine kinase - Rapid Glycolysis: - Starting substrate: glucose/glycogen - End products: ATP, lactate - 1 glucose = 2 ATP - 1 glycogen = 3 ATP - \# of steps/pathways involved: ? - Replenishment time: 30-60 min - When it provides bulk of ATP: generation phase - Location: sarcoplasm - RLE: PFK-1 - [Aerobic ATP Production:] - Oxidative phosphorylation: - Starting substrate: FFA, glucose, glycogen - End products: ATP, water - 1 FFA = 106 ATP (depends on length) - 1 glucose = 32 ATP - 1 glycogen = 33 ATP - \# of steps/pathways involved: Krebs Cycle, ETC - Replenishment time: 2-4 hours - When it provides bulk of ATP: ETC - Location: mitochondria - RLE: cytochrome c oxidase - [Krebs Cycle:] oxidation of substrates for redox reactions, so NAD & FAD can be shuttled in ETC - [ETC:] consists of 4 cytochromes, 3 are pumps - [Interaction between anaerobic and aerobic pathway]s: work together for ATP production, fats burn in a carbohydrate flame - [RLE stimulators/inhibitors]: - Universal stimulator: ADP - Others: Pi, calcium, NAD+/NADH - Universal inhibitor: ATP - Others: PC, citrate **Exam II Content** **[Values during Rest-to-Exercise Transition: ]** **[Values during Incremental Exercise:] ** **[Values during Submaximal Constant Workload Exercise: ]** 1\. Lactate removal: small portion of EPOC (happens all the time)  **DURING EPOC:** fuel switches to mainly FFAs to generate ATP, lower RER EPOC (happens at end of exercise) is directly related to O2 deficit (happens on the onset) \- Fats & CHO differ in amount of O2 used and CO2 produced during oxidation  \- Crossover concept": RER = 0.85, shift from fat as intensity increases  **[Exercise Duration & Fuel Selection: ]** - \- Intramuscular Triglycerides: primary source during [short duration, high intensity] **[AP in Cardiac vs Skeletal Muscle:]  ** ▪ Isovolumetric contraction: ventricles are full of blood but no   contraction yet, pressure to propel blood into circulation 2\. Chemoreceptors: located in carotid & aorta, important during exercise a. Detect changes in O2 & CO2 levels  b\. \*\* most important, can't eject what you don't have  a\. Inversely related to SV (inc in MAP \> dec in SV)  1\. Venoconstriction: via increased SNS stimulation  2\. Skeletal muscle pump: skeletal muscle contractions force blood from extremities,  one-way valves prevent back flow  3\. Respiratory pump: changes in thoracic pressure pull blood towards heartA close-up of a label Description automatically generated **[Average Aortic Pressure (MAP): ]** - MAP increases with exercise because of Up in CO (TPR decrease but not enough) \- Determinants of resistance: blood viscosity, vessel radius (greatest influence)  **[Changes in Peripheral Factors during Aerobic Exercise: ]** ▪ No plateau in trained because of improved ventricular filling  **[Airway Resistance:]** -Most important factor: diameter of airway  Rest: when standing, most blood flow is towards the base of the lungs - [Gravitational force]  \- Reversible, dependent on: PO2 of blood, affinity between Hb and O2 o Lungs: high PO2 (unloading)  **Exam III Content** [**Ch 10/23: Exercise and the Effects of Altitude ** − ] **What happens to partial pressures at altitude compared to sea level? ** - [Hypoxia] -- Low PO2 , [Hyperoxia] -- High PO2  - Decreases at higher altitude  - The [partial pressure] of gasses is lower at altitude (same percentage tho)  What effect does this have on performance in short/anaerobic vs. longer/aerobic events?   - **Short-term anaerobic performance ** - [Lower PO2 at altitude = no effect on performance], O2 transport to muscle does not limit performance  - [Lower air resistance may improve performance ] - **Long-term aerobic performance ** - Lower PO2 at altitude = poorer aerobic performance, dependent on O2 transport to muscle  **Effects of altitude on responses to [MAXIMAL] vs. [SUBMAXIMAL] aerobic exercise −** [SUBMAXIMAL]**:** Elicits [higher HR], Requires [higher ventilation] ** ** **Ch 12 (some Ch 23) -- Temperature Regulation at Rest, During Exercise; Hot/Humid *vs.* Cold Conditions** − Major Topics:  - - - ***Role of the hypothalamus** -- body's [thermostat]*  - *Responses to increases vs. decreases in core temperature? * **Overview of Heat Production/Heat Loss ** - **Heat Production -- Involuntary vs. Voluntary  ** -Involuntary: Shivering, Non-shivering thermogenesis (increase in thyroxine, catecholamines) -Voluntary: [Exercise] **\* Heat loss -- 4 mechanisms to dissipate heat (temperature gradient vs. vapor pressure gradient) ** 1. [Radiation]: temperature gradient, main method of heat loss at rest 2. [Conduction]: temperature gradient, physical contact 3. [Convection]: temperature gradient, heat transfer b/w air/water molecules 4. [Evaporation]: [vapor pressure gradient,] most important mechanism during exercise ***Heat Loss during Exercise -- Thermoneutral vs. Hot vs. Humid Environments*** - MOST IMPORTANT FACTOR= RELATIVE HUMIDITY, Hot Environment → less heat loss (gradients) **Exercise in the Heat*, Why is performance compromised prior to heat acclimation? *** - Decreased effectiveness in heat loss mechanisms due to changes in gradients (think sweating and ambient temperature) → Earlier Cardiovascular drift  **Physiologic Adaptations Following Heat Acclimation & time Course of adaptations ** - **[\ \ Ch 23: Factors that contribute to cold injury? Cold Adaptations]** - [Individual Factors]: Gender (women at a disadvantage), Age - [Environmental Factors]: temperature, vapor pressure, wind, water immersion (25x greater heat loss) - [Acclimation starts within a week], (up thyroxine, catecholamines(NOR/EPI), non-shivering thermogenesis, warmer peripheries) **Ch 13 -- Training Principles and Adaptations to Aerobic (Endurance) Training**\* **Principles of Training: Overload, Reversibility, Specificity ** - Stress is specific to: Motor units, Energy systems, contraction velocity, contraction type, load  - **Training--induced muscle adaptations occur by way of:**  Muscle contractions that activate primary and secondary messengers  **Ch 13 -- Physiological Effects ("Adaptations") of Endurance or Aerobic Exercise Training (AET)** -- **Training-Induced Changes in V̇O~2~ max ** - - - - - - - - **[V̇O~2~ max: Maximal Cardiac Output \[Q̇ max\]; Maximal Stroke Volume (SV max) & Maximal Mixed Arteriovenous ]**  **Blood Oxygen Content Difference \[(a-v̅)O~2~ diff max\] ** ***What factors increase SV max?*  ** [Increase in Preload and Decreased in Afterload, Increase in Contractility] A diagram of a flowchart Description automatically generated ***What factors increase (a-*̅*v)O~2~ diff max?* ** Increase in Muscle bf and increase in Capillaries, Mitochondria\ **Endurance Training: Effects on Performance & Homeostasis   Structural & Biochemical Adaptations**  Aerobic [ ] Training: [Eccentric Hypertrophy (Heart)]   ***Muscle Fiber Type* (From Aerobic Training)** ***Capillaries, Mitochondria* (From Aerobic Training)** 1. Increased capillary density (more oxygen diffusion, more removal of wastes) 2. mitochondrial biogenesis (grows big, splits)  (more ETCs, folds for aerobic, increase in both types) - ***Lactate Removal, Blood pH, Oxygen Deficit* ** 1. 2. ***Fuel Utilization (FFA & Glucose) Concentration* Primary Endurance Exercise-Induced Signaling** Primary Signalers: ↑Calcium, ↑AMP/ATP, ↑and Free Radicals, elicit endurance-specific adaptations  **Events − *Time-course of signaling events? (Outcomes of signalers above)*** Shift in fiber type characteristics, Increased protein synthesis, Fiber-specific structural and biomechanical changes +-----------------------------------+-----------------------------------+ | ***Which training adaptations | | | decrease the most in the | | | short-term (i.e., which are lost | | | the fastest)? *** | | | | | | \*short gains are lost quickly | | | ([SV]), long gains | | | lost later [(a-vO2]) | | | | | | ***Which training adaptations | | | decrease most in the long-term | | | (i.e., which are lost the | | | slowest)?*** | | | | | | A graph of different colored | | | lines Description automatically | | | generated | | +===================================+===================================+ | | | +-----------------------------------+-----------------------------------+ **[SIT AND HIT]** - [SIT]: 10-30 seconds, all out - [HIT]: alternating high (\>30 seconds) (anaerobic, glycolytic) and low intensity (oxidative) bouts - - - - Estimated \~50% of anaerobic capacity determined by genetics [Anaerobic System Changes with Training (sprint training)] 1. Increase in anaerobic substrate levels (ATP, PCr, free creatine, glycogen) 2. Increase in quantity and activity of anaerobic enzymes (PFK) - 3. Increase capacity to generate and tolerate high blood lactate Sprint training outcomes: 3-28% up peak anaerobic power 1. Hypertrophy 2. Tolerance to lactate/ up buffering 3. Up enzymes in ATP-PC (phosphorylase, PFK, LDH) [HIT Training Outcomes] - Similar adaptations to aerobic training, VO2max increase more - Both anaerobic and aerobic adaptations 1. Hypertrophy of type 1 and type 2 fibers  2. Increased tolerance to lactate, buffering capacity, lactate shuttling 3. Increase in enzymes involved in glycolysis and Krebs **[Additional Notes]** [Chapter 23: ] Effects of altitude training vary due to the degree of saturation of hemoglobin Living at high altitude → increase in red blood cell mass (EPO) - [Live high, train low] [Chapter 12] ADP + P → ATP + [Heat] Human: 20-25% efficient, 75-80% lost as heat [Indirect Calorimetry (open-circuit spirometry)] Voluntary heat production: [exercise,] Involuntary heat production: [shivering/non-shivering thermogenesis (hormones)] Hypothalamus = thermostat of body Environmental Temperature→ convective Humidity  → evaporative Wind → rate of heat loss Eccrine: primary sweat gland  [As Exercise intensity increase: ] ↑heat production, body temperature (linearly), core temp. (proportional to muscle), reliance on evaporation heat loss [As ambient temperature increases:] \*exercise induced heat production stays constant, ↑evaporative heat loss , ↓convective, radiant heat loss [Why Cardiovascular Drift? ↓SV = ↑HR] 1. Dehydration → ↓EDV→ ↓Plasma Volume → [↓SV → ↑HR] 2. Increase in BFskin (↓Venous Return → ↓EDV) Acclimation: short-term (lost in a few days)  Acclimatization: longer term, longer word = longer term [Physiological Adaptations During Heat Acclimation] ↑ in plasma volume, Earlier sweating, higher sweat rate, ↓Sodium Chloride lost in sweat, ↓ in BFskin, ↑Cellular shock proteins The rate of heat loss during [water immersion] is [25x greater] than air of the same temperature Fat is a primary fuel for shivering, shivering can lead to muscle glycogen depletion [Cold Acclimatization] Higher non-shivering thermogenesis, later onset of shivering, Maintain higher hand and foot temp, Higher ability to sleep in cold **[The Physiology of Training: Effect on the Cardiovascular System, VO2max, & Performance]** Central Adaptations: heart  better at O2 delivery Peripheral Adaptations: vasculature/muscle better at O2 extraction High Initial VO2max, need \>70%max training for response Low initial VO2max, need 40-50%max training for response \*Heritability explain \~50% of VO2max Exercise Volume = (Frequency\***Intensity\***Time) **[Review]** - Lose most heat via radiation at rest, evaporation during exercise During exercise: increased temperature gradient which increases skin BF and SR **Ch 14 -- ("Adaptations") of Strength Training (ST)/ Resistance Training (RT)** **− Key Terms/ Definitions ▪ Muscle Fitness -- strength vs. endurance vs. power** Muscular Strength: max force a muscle can generate (GS = 1RM) Muscular Endurance: ability to make repeated contractions against submax load Muscular Power: amt of work (force) generate per unit of time Muscular Fitness: collectively describes all of the above **− Neuromuscular Adaptations to ST/RT: For each of the following define/explain the adaptation, describe what happens at the neuromuscular level and the time course of these changes (when applicable), and whether this is a plausible mechanism for increased muscular strength in humans:** **▪ Hyperplasia vs. Hypertrophy vs. Neural Changes** Hyperplasia: increase in number of muscle fibers (myogenesis) NOT HAPPENING IN HUMANS Hypertrophy: increase in muscle cross-sectional area (main driver of late strength gains) - 'increase in size and number of myofibrils (width) - Increase in contractile proteins and sarcomeres - Increase in connective tissues around muscle fiber Neural Changes: increase in neural drive - Increase ability to recruit motor neurons - Select and recruit higher threshold motor units (type 2s) - Altered motor neuron firing rate - Increase motor unit synchronization - Removal of neural inhibition (lower GTO action) **− RT-induced changes/shift in muscle fiber types (biochemical changes that occur) − - Primary & Resistance Exercise-Induced Signaling Events** **▪ Primary signal? Skeletal muscle responses? mTOR -- significance?** - Muscle Stretch/Sarcolemma Mechanoreceptor Activation - mTOR activation promotes protein synthesis\* **− Cellular Mechanisms of Muscle Remodeling Underlying RT-Induced Increases in Strength & CSA** - Increase in myofibrillar proteins, increase myonuclei in each fiber (bc of satellite cells), **▪ Protein synthesis vs. degradation** **▪ Key Hormones + time course of action?** - Cortisol: PRO catabolism when muscle glycogen is low, inhibits PRO synthesis (SLOW) - Testosterone: main steroid hormone, directly influence increase in PRO synthesis, counters cortisol, fast, acute from RT - Growth Hormone (GH): slow release, enhances amino acid uptake (indirect) - Insulin-Like Growth Factor (IGF-1): 8-29hrs post RT, protein hormone (from liver) enhances amino acid uptake (indirect) **− Detraining vs. Retraining -- Effects on Muscular Strength?** **▪ Neural changes vs. Muscle Fiber changes + time course of changes? Time-course for re-training?** - Detraining: slow loss \~30% 7-8 months of detraining, [primarily due to loss of neural adapts] - Retraining: rapid regain (6wks) of strength and muscle size **Ch 14 -- Physiological Effects ("Adaptations") of Concurrent Exercise Training (CET) − \-\-\-- -Define concurrent exercise training.** - Concurrent Training: combining RT and endurance training in a single bout of exercise - Main Evidence: Depressed Protein Synthesis: endurance training adaptations interfere with RT protein synthesis (AMPK inhibits mTOR), [Lift before running if do]