HSC 308, Exam 1 Notes
HSC 308, Exam 1 Notes HSC 308
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This 29 page Class Notes was uploaded by Taylor Vermaat on Tuesday February 16, 2016. The Class Notes belongs to HSC 308 at Central Michigan University taught by Micah Zuhl in Summer 2015. Since its upload, it has received 43 views. For similar materials see Physiology of Sport and Exercise in Nursing and Health Sciences at Central Michigan University.
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Date Created: 02/16/16
1 HSC 308: Physiology of Sport and Exercise Chapter 3 Nervous System and Exercise Why to humans fatigue? Fatigue results: failure to maintain homeostasis either directly in the active muscles or indirectly in the CNS. Muscles: peripheral fatigue CNS: central fatigue Nervous System: regulated power output CNS PNS Sensory (afferent nerves), Motor (efferent nerves) Motor Autonomic, Somatic Autonomic Sympathetic, Parasympathetic CNS: brain and spinal cord PNS: sensory (afferent), incoming Response (efferent), outgoing Somatic: voluntary, to skeletal muscles Autonomic: involuntary, to viscera Sympathetic Parasympathetic Brain cerebellum, diencephalon, cerebrum, brain stem Cerebrum lobes (4): Frontal: general intellect, motor control Temporal: auditory input, interpretation Parietal: general sensory input, interpretation Occipital: visual input, interpretation Deep lobe (1), Insular: emotion, self-perception What are the regions of interest for exercise physiology? 2 Primary Motor Cortex: impulse for execution of movement, conscious/voluntaty movement Premotor Cortex: initiation of movement and voluntary movement, learned skill for repetitive movement pattern Supplementary Motor Area (SMA): coordination of both sides (bimanual movement) Basal Ganglia: Repetitive movements, relay center, locomotion control, posture Primary Sensory Cortex: afferent sensory information Diencephalon: neural regulation of pituitary and brain stem, hormonal regulation, relay center for sensory information Thalamus: relay center for sensory information Hypothalamus: maintains homeostasis, regulates internal environment ie… food intake, fluid balance, sleep, blood pressure, heart rate, breathing, body temperature Cerebellum: controls rapid, complex movements, coordinates movements, body position, input from primary motor cortex, fine tuning movement Brain Stem: relays information between brain and spinal cord; the gate way! Beta endorphin release w/ exercise, analgesia system modulate pain, suppress pain, cardiac/ respiratory function and locomotion Midbrain: vision, hearing, motor control Pons: relay center for cerebellum, role in respiration Medulla Oblongata: cardiac, respiratory, vomiting, vasometer – autonomic regulation center BRAIN STEM LOCOMOTION: initiation locomotion Retlculospinal (RS) and Mesencephalic Locomotor Region (MLR): neurons of the brain stem RS and MLR: locomotion initiated or accelerated, receive input from basal ganglia (inhibitory, ie…running walking) or motor cortex (fine movement) for adjustments, minimal conscious effort Basal Ganglia MLR RS [ACCELERATE MOVEMENT] 3 PNS: Connects brain to spinal cord via cranial (brain) /spinal (spinal cord) nerves TWO MAJOR DIVISIONS: Sensory (afferent) What is going on? Sensory Receptors: Mechanoreceptors: physical forces Thermoreceptors: temperature Nociceptors: pain Photoreceptors: light Chemoreceptors: chemical stimuli Special Families of Sensory Receptors: two sensory receptors in skeletal muscle and function Muscle Spindles: has few action and myosin filaments, cannot contract Sensitive to muscle stretch/length and rate of length change o Sends stretch information to CNS response is for muscle (extrafusal fibers) to contract Action potential is much greater when muscle is being stretched SUDDEN STRECH IN MUSCLE RESULTS IN: 1. Muscle spidndles detect stretch of muscle 2. Sensory neurons conduct action potentials to the spinal cord 3. Sensory neurons synapse directly with alpha motor nuerons 4. Alpha motor neurons conduct action potentials to the muscle, causing it to contract and resist being stretched a. The muscle that contracts is the muscle that is stretched Golgi Tendon Organs Sensitive to muscle-tendon tension Sense strength of contraction Protective benefit Motor (efferent) What is the response? Transmits information from brain to periphery Two Divisions: 4 Autonomic: regulates visceral activity Exercise-related autonomic regulation: hear rate, blood pressure, sweat, metabolism SYMPATHETIC: fight or flight: prepares body for exercise Increased…heart rate, blood pressure, blood flow to muscles, airway diameter, metabolic rate, glucose levels, mental activity PARASYPATHETIC: rest and digest Increased…digestion, urination Conservation of energy Decreased…heart rate, diameter of vessels and airways Active at rest Somatic: Motor, stimulates skeletal muscle activity EXAMPLE: Emesis Nausea Sympathetic (increased heart rate) Parasympathetic (mouthwatering) Motor: Somatic Nervous System Voluntary skeletal muscle response Response to sensory information NS Structure Specialized area of motor neurons: Myelin Sheath (Schwann cells): Fatty substance that insulates cell membrane Nodes of Ranvier: Gaps in myelination where action potential jumps from gap to gap… SUPER FAST! NS Communication 5 Electrical signal for communication between periphery and brain MUST be generated by a stimulus, propagated down an axon, and transmitted to next cell Communicates through action potentials: a rapid depolarization of cell membrane Resting potential = -70 mV electronegative (more positive on outside) WHY -70 mV? High Na+ outside cell, medium K+ inside cell. Inside more negative relative to outside K+ wants outside of the cell, leaks out offset by Na+ and K+ pumps NA+ wants to enter cell, but can’t Action Potential Phases Phase 1: resting membrane potential (RMP) Controlled by Na+/K+ pump Leakiness of K+ channels RMP = Na+/ K+ pump and leaky K+ channels (-70 mV) Phase 2: threshold Stimulus that causes cell to reach threshold potential = occurs at axon hillock Around -50 mV Phase 3: depolarization Opening of Na+ channels (influx, flowing in) Na+ enters cells 6 Occurs when inside of cell becomes less negative (-70 mV 0 mV) Required for nerve impulse to arise and travel Phase 4: repolarization Closing of NA+ channels Opening of slower K+ channels, (K+ efflux, flowing out) Phase 5: hyperpolarization Additional K+ leaves cells through leaky channels causing a refractory Refractory = occurs when inside of cell becomes more negative (-70 mV -90 mV) Makes it more difficult for nerve impulse to arise 7 WE ALWAYS NEED A STIMULUS! Graded Potential vs. Action Potential GP: localized changes in membrane potential Generated by incoming signals from dendrites Inhibitory signal = K+ efflux = hyperpolarization Excitatory signal = Na+ influx = depolarization Strong GP AP AP will be propagated down axon If GP reaches threshold, AP will occur AP: propagation down axon and transmitted to next cell Myelin: speeds up propagation Fatty sheath Insulation Axon diameter: larger=faster Synapse: Transmitting APS Junction or gap between neurons Site of neuron to neuron communication Communication occurs through synapses via neurotransmitters 8 Dendrite Axon Synapse Dendrite Axon Electrical to chemical back to electrical Need AP to occur of skeletal muscle Cell body of motor neuron located in spinal cord. Neurotransmitters: ACh and norepinephrine (NE) govern exercise ACh: acetylcholine Stimulates skeletal muscle contraction NE: norepinephrine Mediates sympathetic nervous system effects Neuromuscular Junction (NMJ) Neuron to muscle communication Uses ACh as its neurotransmitter, passes AP along to muscle How do we generate movement? 9 Step 1: initiation of movement in higher brain areas Modulated by brain stem Step 2: the action potential travels down the corticospinal tract through the spinal cord Synapse on motor neuron occurs here, cell bodies located in cortex Step 3: AP acts on motor neuron in spinal cord releasing glutamate (excitatory neurotransmitter) Step 4: Causes Na+ influx raising potential to threshold Step 5: motor neuron depolarizes and AP travels down axon Step 6: Once AP reaches nerve terminals, Ca++ channels open and Ca++ moves into the cell causing terminals to release neurotransmitter Ca++ releases vessels that then release ACh to contract muscle Reflexes: process of communication and interaction between sensory and motor systems in the spinal cord As level of control moves from spinal cord to cerebral cortex, movement complexity increases Can’t wait for higher brain for communication ie…putting your hand on a hot stove Locomotion: 1. Initiated or accelerated from the RS and MLR 2. MLR and RS receive input from basal ganglia (inhibitory) or motor cortex (fine mvmt) for adjustment 3. Travels down spinal tract 4. Walking/running occurs. Minimal conscious effort Central Pattern Generators (CPG) Movement is generated without input Rhythmic activity Neural Adaptations faster axonal transport from sciatic nerve of trained improved recruitment patterns after training 10 Structure and Function of Exercising Muscle: Smooth Muscle: involuntary, hollow organs Contraction: very slow Cardiac Muscle: involuntary, heart Contraction: slow Skeletal Muscle: voluntary, skeleton Contraction: slow to fast Epimysium Perimysium (fascicle) Endomysium muscle fiber (contains myofibrils) Muscle Fiber: Nerve Innervation Structure: Sarcolemma: composed of plasmalemma and basement membrane Plasmalemma: cell membrane, fuses with tendon, conducts AP, maintains pH, transports nutrients Folded characteristics: allows for muscle fibers to be stretched/ contracted without damaging membrane Satellite: muscle growth, development, Response to: injury, immobilization, and training. Between plasmalemma and basement membrane Sarcoplasm: cytoplasm of muscle cell, stores myoglobin and glycogen Transverse Tubule (T-Tublue): extensions of plasmalemma Sarcoplasmic reticulum (SR): Ca+ storage Terminal cisternae: region of SR that surround T-Tubule UP OF SARCOMERE)le fasciculi muscle fiber myofibril(MADE Sarcomeres (functional unit of muscle fiber): basic contractile element of skeletal muscle, end to end or Z-line to Z-line of full myofibril Contractile Protiens: 11 Myosin: think filament (myosin head), makes up 2/3 of skeletal muscle protein Actin: thin filament, contains binding sites for myosin head, connected to Z-disk Titin: stabilizes the myosin protein with the Z-disk Nebulin: anchors Actin to Z-disk Regulatory Proteins: located on Actin filament Troponin: binding site for Ca++ Tropomyosin: regulates the actin binding site Complete Saromere: Key Areas: DRAW and LABEL PROTEINS (Regulatory and Contractile) Z disk: join consecutive sarcomeres together (Actin only) I band: contains Actin only, light strip A band: contains myosin and actin, dark stripe, contain H- zone and M line H zone: contains only myosin, middle of A band M line: middle of H zone 12 Contraction: Myosin pulling Actin in, A band does not move, H zone shrinks Contraction stops when z disk hits myosin Motor Units: motor neurons innervate muscle fibers Activates certain muscle Motor neuron: and all fibers it innervates More operating motor units = more contractile force Motor pool: all the motor neurons that innervate an entire muscle How does AP lead to muscle contraction? 13 Excitation = contraction coupling Skeletal Muscle Contraction: Transmission of AP through NMJ 1. AP arrives at axon terminal, releases ACh (neurotransmitter) 2. ACh moves across synaptic cleft, binds to nicotinic receptors on plasmalemma 3. ACh is REMOVED by acetylcholisternase 4. AP travels down plasmalemma, T-tubules (depolarization) 5. Ca++ release from SR (sarcoplasmic reticulum) 6. Ca++ binds to troponin causing action-myosin contraction Role of Ca++ in Muscle Contraction AP arrives at SR from T-tubule SR is sensitive to electrical charge Ca++ binds to troponin on thin filament Troponin- Ca++ complex moves tropomyosin Sliding Filament Therory! Process of actin-myosin contraction Ca++ triggers the actin-myosin interaction What is the energy source? ATP: adenosine triphosphate Binds to myosin head ATP ADP + Pi + H + energy Relaxed state: No actnin-myosin contraction Myosin is still in contact with actin Myofilaments overlap Contracted State: Myosin head pulls actin towards sarcomere center (power stroke) Process will continue until Ca++ becomes unavailable, AP stops, or Z disk reaches myosin filaments 14 The Cross Bridge Actions: (1) Ca++ binds to troponin causing tropomyosin to move to the myosin binding site (2) Myosin head forms a cross bridge with actin (3) Power stroke occurs releasing ADP, Pi, and H and myosin head remains attached (4) ATP attaches to myosin head and is hydrolyzed by ATPase, causing the myosin to detach and re-load (5) ADP and Pi remain bound to myosin head, ready for additional Ca++ release When someone dies, in a constant state of RIGOR: ATP cannot detach. Sarcomere and Muscle Contraction: Sarcomere is shortened: Z lines move closer H zone reduced I band reduced A band does not change Characteristics of Skeletal Muscle: Type 1: 50% of fibers in an average muscle Peak tension in 110 ms, SLOW TWITCH Slow oxidative (SO) Lower force production Smaller motor neuron Less developed SR unit Low intensity and aerobic exercise Mitochondria supports aerobic metabolism (ie…long distance runner) Type 2: Peak tension in 50 ms, FAST TWITCH 15 Type 2A: fast oxidative glycolytic (FOG) In the middle fiber type Middle sized motor neuron May be the best? Type 2X: fast glycolytic, very large (FG) Very fast contraction, fatigue fast Larger motor neuron Highly developed SR- greater Ca++ release Summary: Skeletal Muscle Types, Fiber Type Comparison (KNOW 3 DETAILS) Type 1 Type 2: A Type 2: X Small Medium Large Slower Faster Faster Moderate levels of Mitochodria Oxidative metabolism/ Oxidative and glycolytic Glycolytic metabolism/ Aerobic metabolism Nonaerobic All muscles have all three types. In max exercise every fiber in that muscle are contracting. Motor Units: Type 1: smaller neuron, more refined, used for intricate movements (ie…violinist) Type 2: larger neuron Distribution for Fiber Types: Each person has different ratios Arm and Leg ratios are similar in one person Endurance athlete: type 1 predominates Power athlete: type 2 predominates Fiber Type Determinants: Genetic Factors: 16 Determine which motor neuron innervate fibers Fibers differentiate based on motor neuron Training Factors: Endurance vs. strength training, detraining Call induce small (10%) change in fiber type Aging: Muscles lose type 2 motor units Sedentary: Great expression of type 2X fibers Does exercise change fiber type expression? Debatable. Muscle may take on characteristics but do not change. Type 2X may develop more mitochondria. Running: I IIA IIX (take on characteristics of type IIA fiber type) Strength Training: I IIA IIX Sedentary: I IIA IIX Motor Unit Recruitment: How are muscles Recruited? Method for altering force production Less force = fewer or smaller motor units (size principle) More force production: more or larger motor units (frequency principle) Type I motor units smaller than II Recruitment Order: Type I first, IIA second, IIX last At PEAK tension all muscle types work together Size principle: order of recruitment of motor units directly related to size of motor neuron Within a single motor pool (muscle) the motor neurons will be recruited in order of ascending size, smallest largest Frequency Modulation: 17 Low force production there is an increase in recruitment At higher force there is an increase in frequency Increase in number of motor neuron units recruited: lower force Generation of Force: Two Ways Size principle of muscle recruitment Frequency of stimulation (rate coding) Twitch: single electrical stimulus Summation: series of stimuli causing greater force production Tetanus: activation of all fibers at peak force Types of Muscle Contraction: Statics (isometric) contraction: Muscle produces force but does not change length Concentric Contraction: Muscle shortens while producing force Most familiar type of contraction Sarcomeres shortens, filaments slide toward center Eccentric Contraction: Muscle lengthens while producing force 18 Cross bridges for but sarcomere lengthens Example: lowering heavy weight Which dynamic contraction generates the most force? Isolated muscle eccentric force is 40%-60% greater Untrained human: equal when performing max contractions Generation of Force: Length tension relationship: Optimal sarcomere length = optimal overlap Speed force relationship: Concentric: maximal force development decreases at higher speeds Eccentric: maximal force development increases at higher speeds Force Velocity Curve: As the speed increases, force decreases. Because there is less time for motor neurons to recruit. Force Velocity Curve: Can you explain this? 19 What Affects Muscle Force Production: Increase in muscle temperature Increase max isometric tension Increase nerve conduction speed Increase enzyme activity Increase in core temperature Reduces force during prolonged exercise LECTURE 3 Homeostasis: Ability to maintain internal stability, owing to the coordinated response of its parts to any situation or stimulus that would tend to disturb its normal condition or function Major concern of body: Maintain blood pressure, Maintain blood glucose levels Endocrine System: a communication system Coordinates integration of physiological systems Nervous System = electrical communication Endocrine System = chemical communication Slower responding, longer lasting that nervous system (neurotransmission) Maintains homeostasis Hormone: Chemical that controls and regulates the activity __________________________. Can circulate free or bound to transport protein Binding Proteins: Provides reservoir or pool hormone, control levels Free Proteins: Fast acting 20 Roles in acute metabolic responses (catecholamines) Hormone Secretion: Secreted in bursts Plasma concentrations fluctuate over minutes/ hours Concentration also fluctuate over days/ weeks Plasma concentration can be poor indicator of hormone activity Cells change sensitivity to hormones Downregulation: decrease number of receptors during high plasma concentration = desensitization Upregulation: increase number of receptors during high plasma concertation = sensitization Receptors dictate hormone secretion. Intro: Classifying Hormones: Hormones may be peptide, amino acids, or steroids Steroid or non-steroidal Steroid Hormones: Derived from cholesterol Lipid soluble, diffuse through membranes Steroid receptors found inside cell Hormone- receptor complex enter nucleus Binds to DNA, direct gene activation Gene activation – nucleus Structural proteins – protein synthesis Regulatory proteins Nonsteroidal Hormones: No lipid soluble, cannot cross membranes Divided into two groups: Protein/ peptides 21 Amino Acid derived hormones Hormone Control of Metabolism in Blood Glucose Regulation: Hormones of Metabolism Blood glucose increase, must be brought down (insulin) Blood glucose decreases… Mobilize liver glucose production Fatty acid release from adipose tissue Block glucose entry into tissue Hormones: Insulin: Released in response to HYPERglycemia: promotes glucose uptake by most tissue, turns off fat oxidation Released from beta cells of pancreas Elevated glucose is key sensor for beta cells Insulin Regulation: Hyperglycemia = insulin levels to go up Parasympathetic (ACh) = insulin increase Sympathetic (NE) = insulin decreases Glucagon: (opposite of insulin) Released from pancreas, stimulates glycogenolysis, gluconeogenesis, and ketogenesis Acts on liver and skeletal muscle Causes release of liver glucose Increase glucose availability from liver Increase fat oxidation Increase protein breakdown in muscle Released form alpha cells Signal: decrease glucose, key is rising amino acids levels Epinephrine and Nonepinephrine: (Catecholamines) Released from Adrenal Medulla – 80% E, 20% NE 22 Release and Regulation: Metabolic Signals: mainly through sympathetic activation during exercise HYPOglycemia SNS (sympathetic nervous system) acts on the adrenal medulla causing E/NE release! Growth Hormone: Released from anterior pituitary Acute Effects: stimulates liplysis Inhibits glucose uptake by muscle Stimulates glyconeogensis Long Term Effects: protein synthesis (growth) IGF-1 release Tissue growth Metabolic Signals: drop in blood glucose, stress, exercise Cortisol: Released from adrenal cortex Assists in maintaining blood glucose levels Amino acid release from muscle Hepatic gluconeogenesis FFA release Metabolic Signals: falling blood glucose, prolonged exercise, stress Thyroid Hormone: Released from thyroid gland – 2 hormone complex T4: greater amounts released most is bound to binding proteins T3: active form of hormone Increase oxygen consumption Glycogenolysis 23 Lipolysis Metabolic Signals: increase CHO (carbohydrate) intake (metabolic rate), cold stress, any condition that increases body energy requirements Summary Slide: Resting Metabolism: Insulin and glucagon are the major regulators of resting metabolism Eat = increased insulin Fasted or amino acids ingestion = increased glucagon Greater PNS control: reduced catecholamine levels (E/NE) Growth Hormone: follows circadian rhythms as normal Cortisol: may be variable based on stress levels Thyroid Hormone: variable regulation based on energy needs and feeding Moderate Intensity Exercise: 50%-60% Increase of NE/E: glycogenolysis in skeletal muscle, lipolysis is adipose Decrease insulin/ increase glucagon Growth hormone levels increase: amino acid breakdown, decrease glucose uptake by muscle Increase in thyroid hormone: mobilization of fuels, increase in metabolic rate Cortisol levels decline Blood glucose levels maintained Summary: E/NE increase Insulin decrease GH increase Glucagon increase Cortisol decrease Blood glucose levels maintained High Intensity Exercise: >70%-80% 24 Large increase of NE/E GH large increase Increase in cortisol o Maintain blood glucose Increase in Thyroid hormone o Increase metabolic rate Summary: NE/E large increase GH large increase Cortisol increase Thyroid hormone increase Glucagon increase Blood glucose level maintained Prolonged Exercise: >60 minutes Summary: GH large increase NE/E large increase Insulin decrease Glucagon increase Cortisol increase Thyroid Hormone increase Blood glucose maintained during exercise 5 hormones increase (NE/E, GH, TH, Cortisol, Glucagon), 1 hormone decreases (insulin) with EXERCISE: 6 (all) preserve blood glucose Response to chronic training: Glucagon lower release GH lowers E/NE lowers Dehydration has enormous effect on exercise performance! 25 Losses of 5% BW decrease the capacity to work (lower intensity by 30% Losses of 2.5% decrease the ability to perform high intensity exercise by 45% Why? Decrease in blood V Decrease skin blood flow Decrease sweat rate Decrease heat dissipation Increase core temperature Increase rate of muscle glycogen use What happens when we start to sweat during exercise? We MUST preserve cardiac output and blood pressure! Must release heat from body through skin (sweat) Two most important things to regulate blood glucose levels and blood pressure. Hormonal Regulation of Fluid and Electrolytes during Exercise: During exercise: Plasma volume decrease, causing increase osmolality – decrease in plasma water content via sweating = increase heart strain and decrease blood pressure Osmolality: measure of concentration of dissolved particles Values: > 300 mOsm/kg dehydration 26 Hormones to correct fluid balance: Posterior pituitary gland: ADH (Anti Diuretic Hormone) Increase in water reabsorption at kidneys Less water in urine, antidiuretic Also called vasopressin or arginine vasopressin Stimulus for release of ADH: Decrease in plasma V = hemoconcentration = increase osmolality = (mechanism for ADH release) Minimizes water loss, severe dehydration Release of ADH: 1. Workout 2. Sweating, decrease BP, increase in plasma osmolality 3. Hypothalamus is stimulated increase thirst 4. ADH secreted vasoconstriction increase BP 5. ADH acts on kidneys water reabsorption increase plasma volume 6. Water reabsorption increase plasma volume Adrenal cortex Increase Na retention in kidneys Increase water retention 27 Increase K+ excretion Stimuli: Decrease in plasma Na+ Decrease in bV, BP Increase sympathetic activation Increase in plasma K+ Stimulus release of aldosterone: Na+ moves, water follows 1. Decrease in bV/ BP, SNS discharge 2. Renin release from kidney 3. Renin coverts angiotensinogen to ANG1 4. ANG I coverts to ANG II by ACE 5. ANG II major vasoconstrictor 6. Aldosterone release (adrenal cortex) 7. Na+ retention/ K+ excretion increase blood plasma V Prolonged Na+ retention abnormally high Na+ after exercise Prolonged rehydration effects Stimulus for renin release: decrease volume, increase BP Atrial Natriuretic Peptide (ANP) Release from atria Causes Na+ excretion Increases natriuresis ACTIVATED by increased stretch or plasma volume Kidneys Target tissue for ADH, aldosterone Secrete renin Secrete EPO Na+ depletion will cause water to move to a higher concentration, causing damage to cells. Hormones included in glucose homeostasis: 28 Hormones involved in blood pressure and electrolyte homeostasis: Review for Exam One: Nervous System… Region of the brain Initiation of movement Muscle spindles feedback from muscle Neural adaptations Two neurotransmitters that regulate exercise Motor neurons Mechanoreceptors Skeletal Muscle… Sarcomere Steps of contraction (brain to molecular level/sliding filaments) Motor unit recruitment Contraction coupling, ACh release to Ca++ binding to troponin Properties of muscles Characteristics of muscle fiber types, how they change Hormone control… 6 hormones that regulate metabolism and glucose levels Plasma volume and blood pressure Hormone control of glucose at high/moderate/and resting 29 ADH, aldosterone, and ANP release and mechanisms
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