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University at Buffalo
Exercise Science
ES 330

ES 330 Lifespan Physiology Exam 2 Skeletal Muscle Video Cross bridge cycle causes contraction. Functional unit of contraction is a sarcomere Myosin heads and thick myofilaments cross bridge with Actin and thin myofiliments Ca+ ions released from sarcoplasmic reticulum bind to troponin Troponin moves Tropomyosin away from myosin head so that actin can bind ATP binds to myosin head and it is hydrolyzed to ADP + IP  activating the myosin head to cocked position 1) Cross bridge formation: Myosin head on Actin  release of IP 2) Power Stroke: ADP released  Head Pivots 3) Cross bridge detachment: ATP binds to myosin head  head detaches 4) Reactivation of myosin head: ATP hydrolyzed to ADP + IP  energy reactivates myosin head to cocked position Thin myofiliments pulled toward each other and muscle contracts. Sarcomere shortens Process ends when Ca+ is actively transported back to sarcoplasmic reticulum Troponin returns to original shape and Tropomyosin covers myosin binding site on actin. Sarcomere Contraction: Sliding filaments (Myofilbril contraction) muscle contacts Actin filaments slide along myosin filaments pulling Z bands close shortening sarcomere Skeletal Muscle Lecture 1 3/4 Muscle  Fascicles  Muscle fibers  Myiofibril  Sarcomere Runners all have similar # of muscle fibers  sprinters just have larger muscle fibers.  performance =training Myofibers: 10-100micro meter diameter Larger the diameter/ CSA stronger the muscle Length: excursion, amount that it can shorten Hypertrophy: getting larger and Hyperplasia: not in skeletal muscle (divides and makes more muscle) Multiplefibrils within a fiber •  “String of sarcomeres” •  Ordered array of proteins •  Interconnected by intermediate filaments= protein Dystrophin: In the myotendinous junction connects myofibrils to connective tissue of the cell wall. Muscular Dystrophy cannot adequately connect the myofibrils to the cell walls. Connective Tissue •  Threesheaths of connective tissue surrounding the anatomical subdivisions. – Epimysium- whole muscle – Perimysium- muscle fascicle – Endomysium- muscle cell •  Blend at the myotendonous junction CT around fascicles become the tendon  impossible to pull muscle off Network of intermediate filaments so the muscle does not all contract at the same time. Muscle soreness is caused by intermediate filaments damaged and myofibrils done stay perfectly in formation. Intermediate filaments have to hold the muscle together. Myosin: head that hydrolysis ATP, two flexion points, polymerize to form thick filaments Core thin filaments= Actin which Myosin interacts with to contract .  No muscle Actively Lengthens. Titin: Large (3MD)protein spanning half a sarcomere •  Responsible for a portion of the passive tension in muscle •  Molecular “sticky spring” Clinical Correlation: Ruling out Myocardial Infarctions - when the cell wall is damaged Troponin is small so it escapes into the blood. Nuclei: Center in developing and regenerating fibers, migrate to the periphery. Vary in number depending on atrophy and hypertrophy. Skeletal mm. may have many nuclei Nuclear domain: specific area served by a single myonuclei Hypertrophy: size of the domain increases or the number of nuclei increases This is needed because a single nuclei can only make so much protein. - initially they make more protein and then more nuclei Satellite Cells: undifferentiated myoblast on periphery of skeletal muscle. Between Sarcolemma and basal lamina Divides and one cell mature into a myonucleus and one cell replaces the satellite cell.  activated by damage or hypertrophy but may have limited potential to divide. Synthetic machinery in myofibrils: poorly developed in ER, large # ribosomes, passive ROM keep from atrophying Deinervation: ATROPHY: 1 muscle fiber= 1 nerve ending Mitochondria: found throughout cell, varies with fiber type and training, endurance - Myoglobin: carries Oxygen hemoglobin, Glycogen, Lipid: can be good, Glycolytic enzymes: phosphocreatine Excitation/ Contraction Coupling Electrical signal from the brain (Ca+ and ATP) Dihydropyridine receptors (DHPR) Ryanodine receptors (RyR) Regulator of Ca+ release DHPR and RyR  mediate excitation (nerve stimulation) and contraction ( Ca+ Release) tell cell when to let Ca+ out DHPR pushes RyR to let all Ca+ out of sarcomere into myofiber  depolarization and turn into muscle shorten Sarcolemma Depolarization gets propagated down into T-Tubule and tells the sarcomere how much Ca+ to contract using the Excitation/ Contraction coupling method above. NMJ: voltage gated Ca+ channels activated by depolarization. Fusion of synaptic vesicles Binding of Ach to post synaptic membrane  AchE cleaves Ach to stop the depolarization.  contraction ends Sliding filament Theory: 1) Ca+ released in sarcoplasm  binds to troponin C changes shape  moves tropomyosin from actin binding site 2) Myosin binds to actin 3) Power stroke pulls actin drags Z line to M line  release ADP + IP from Myosin heavy Chain. Sarcomere short “rigor complex” myosin has to be forced to let go of actin. 4) Release of Actin from myosin ATP dependent process 5) ATP hydrolyzed ADP + IP and Myosin Reset. Ca+ gone= stop ATP gone= stop 6) Ca++ removed from sarcoplasm, tropomyosin back on Myosin Motor unit: Axons end in multiple terminals  each terminal goes to 1 myofibril. A motor unit 2 fibers (fingers) 100 or more fibers.( postural) • Single motor neurons divide into multiple axon terminals • Each axon terminal innervates a single fiber • All fibers innervated by a single nerve share a phenotype o Large MU= fast, glycolytic o Medium= fast contracting, some oxidative properties o Small MU= slow, oxidative. Recruitment: stimulation more MU  increase strength by activating larger number of fibers. Isometric Contraction: no change in length Isotonic Contraction: concentric and eccentric. ROM = DOES NOT MEAN FELX AND EXT -Concentric: + shorten - Eccentric: - lengthen  energetically less demanding Factors affecting muscle contraction •  Frequency of stimulation •  Number of motor units recruited •  Degree of muscle stretch Twitch •  Single contraction/relaxation= 100msec – Activation= 5msec – Physical movement = 95msec •  Phases – Latentperiod (taking slack out of m) – Contraction – Relaxation  Tenanic contractions build up •  No refractory period in muscle Temporal summation (not a functional way to move)  same as rate coding. •  Multiple impulses result in: – Increased Ca+ exposure to myofilaments – Greater force development •  “Pre-tightening” of sarcomeres •  Twitch •  Unfused tetanus •  Fused tetanus •  Fatigue Spatial summation: (how we move) Contractions are fused tetany providing steady control •  Sequential recruitment of motor units from Small to large allows for fine control of muscle force Length Tension Curve. (1) Ascending Myosin bumps into Z dics only so much tension (2) Exact # of myosin and actin overlap to have MAX tension isometric sweet spot for length (3) Descending: stretch it out- less overlap myosin heavy chains with no actin. Can’t generate as much tension  only applied to isometric  passive tension= titin Passive tension unhealthy m: swelling, increase CT, spasticity., tight. Force Velocity Relationship. ISOTONIC O velocity= Isometric contraction MAX Concentric: increase speed= less force Eccentric: myosin is being ripped off of actin eccentrically and it can generate more force because the myosin heads are attached longer = damage. Muscle does not respond to loading, it responds to overloading. Must generate a lot of force. FIBER TYPES Most muscles are composed of a mixture of fiber types. Soleus mostly Slow Ox where Tib Ant is FAST GLY Virtually all skeletal muscle proteins exist in fast and slow isoforms. Most fiber type schemes are based on myosin heavy chain (MHC) Myosin – 11 Myosin genes – 4 commonly expressed in adult mammalian limb musculature – 1 slow isoform (Iβ) and 3 fast isoforms (IIA, IIX, IIB) – Fetal and embryonic isoforms in adult muscle indicate disease or damage Contractile speed increases from – Iβ → IIA →IIX •  Single fibers – May be relatively pure in MHC composition •  I, IIA, IIX – May contain combinations of MHC (Hybrid fibers) •  C fibers, IIAX Recruit smaller MU to Larger MU IIX is the biggest and recruited the last. Fiber type transitions •  Altered neuromuscular activity •  Loading and unloading •  Altered hormone concentration •  Aging – Sarcopenia Type 1 slow cannot turn into type 2 and the other way around. X Glycolytic and A Oxidative Training pushes IIX to IIA still have glycolytic enzymes If you stop training then IIA fibers migrate back to type Couch potato fibers are glycolytic don’t use a lot of energy rarely recruit them, not designed for sprinting. Adaptation •  All stimuli represent decreased activity or additional Activity •  Decreased activity – Loss of cross sectional area – Loss of endurance – Loss of fit fiber types •  Additional activity – Shift towards fitter fiber types •  Activity dependent – “Strength”  CSA and contractile protein – “Endurance”  aerobic capacity, mitochondria and capillaries Critical Illness •  Common in patients even after brief ICU stays 40% if on mechanical ventilation >7 days •  Results in protein catabolism, increased urinary nitrogen loss, and muscle wasting •  Protein loss in critical illness myopathy even fasterthan seen with inactivity •  Results partially form the stress response Catabolic  lose muscle weight  Starved patients lose 200- 300g of muscle tissue per day  Stressed pa5entslose 750 - 1000 g of muscle per day – Aminoaids consume for gluconeogenesis – High morbidity/mortality – Lengthens time for patient to return to ambulatory status Muscle Damage: Delayed onset Muscle Soreness: Pain/ discomfort for 24-72 hours, worse eccentric stiff/swell/ sore/ dec strength No effective treatment: NSAIDs don’t really work Rhamdomyolysis: Rapid breakdown of skeletal muscle after physical injury – Exercise induced (extreme activity) – Trauma •  Loss of cellular contents into bloodstream •  RBC and myoglobin in urine (myoglobinuria) Skeletal Muscle Lecture 2 3/6 Resistance Training is beneficial to all age groups. Peak bone density is in early 20’s  declines linear and sudden drop off at 60  Power is reduced more! UE is affected affect more than LE -> hand grip is a good indicator of whole body strength Strength and Power decline with age due to - loss of m. mass with age, Sarcopenia. Sarcopenia effects VE, LE, flex, ext in all mm. - increased intramuscular fat - Lack of testosterone and GH pulse after resistance training in the elderly - Reductions in strength are inevitable even with lifelong resistance training - loss of type II fibers  decrease force development - reduction CSA and fiber # - Nutrition, not the right kind of calories • Aniasson & Gustafsson(1982) - Low intensity resistance training produced limited strength gains in elderly • Moritani & DeVries(1980)  this study was right - High intensity resistance training in older men produced significant strength gains o Strength training hypertrophy in type I and type II fibers. Inc. % type IIA and Dec. % type IIx fibers o 80% 1RM= safe o UE BW low ½ lb upper extremity in elderly o 2-3 min between sets for recovery time, possibly more in the beginning o TEST flexibility, balance, cardiac health (HR, BP) Periodization: Cycling sets and reps to maximize strength and power gains. “Peaking”  low to high intensity Risk factors 1) having only one coronary risk factor = OK 2) possible cardiopulmonary or metabolic disease or 2 or more coronary risk factors = use judgment 3) Known cardiac, pulmonary or metabolic disease = Time up and Go Test: WATCH VIDEO - subject fully sits in chair with arms - place tape marker 3m away so subject can see it - on “go” subject rises, walks to tape and back and sits - do not use arm rest, walk normal speed, use only normal assisted devices (cane) - Give one practice before actually timing - Normal values 60’s- 8.1s 70’s- 9.2s 80 – 90’s- 11.3s - community frail adults >14s high fall risk -post hip fracture > 24s will fall within 6mo -frail adults >30 require assistive device for safe ambulation UE- elastic resistance or dumbbell <5lb - front shoulder raise, wall push up, curls, shoulder press, lat. Raise, BOR LE- elastic resistance –wall squat, hip flex, hip ad abs, tow raise, standing knee curls -walking, core, balance  home and gym programming will be similar depending on machinery General Characteristics of training elderly: 1) LE quads, ham, gluet UE tri, bi, pi, lat, shoulders 2) bands, free weights, stack plates 3) 2-3 set 4) work to concentric failure= not good discharge valsalva  coronary risk high BP - Large before small muscle groups - elastic resistance before free weights - 80% 1RM for 8 reps is safe Cardiovascular and pulmonary system 3/11 • Systole-contraction of right and left ventricles • Diastole- ventricular relaxation – Ventricles fill passively to about 70% of capacity • Heart rate 60-80 at rest • Stroke volume- volume of blood pumped out of ventricles 60-139 ml • Cardiac Output= stroke volume x heart rate • CO= SV x HR • Pre-load- volume and stretch on the Ventricular myocardium at the end of diastole • After-load- pressure the L ventricle must work against to open the aortic valve Parasympathetic input  dominant at rest, decreases HR and causes bronchoconstriction Sympathetic input  increases HR, contractility, BV dilation and bronchodilator Left Bronchi is longer and 45 degree angle Right Bronchi is wider and shorter and 24 degree angle (straighter) Alveoli is for gas exchange Neurotransmitter signals for the ANS Adrenergic- sympathetic – norepinephrine – Alpha receptors – Beta receptors Cholinergic- parasympathetic – Acetylcholine – Nicotinic receptors – Muscarinic receptors Adrenergic: Cholinergic Alpha 1- Peripheral BV, abdominal viscera Muscarinic- Reduce HR and Bronchoconstrict Beta 1- heart and coronary vessels Beta 2- lungs, other sympathetic target organs Prenatal cardiovascular system •  Heart is first organ to develop •  Heart “tube” by week 3 •  Heartbeat in week 3 •  4 chambered heart present by week 7 •  Vascular system developing by week 3 •  Connects fetal circulation to maternal placenta •  Umbilical vein and artery for nutrient/waste exchange Fetal Circulation •  Mother provides oxygenated blood •  Designed to allow blood to bypass lungs •  Patent Foramen Ovale, Ductus Artereosis, Ductus Venosis (closes Fetal pulmonary system •  Lungsbegin development by week 4 •  By 8 weeks bronchi and lobes are forming •  Weeks 24-40 Alveoli are developed •  Fetal lungs do not oxygenate fetus Cardiovascular changes at birth •  Shunting system of heart closes for normal circulation •  Ductus venosus closes with occluding umbilical cord •  PFO closes as L atrial pressure increases •  Ductus arteriosus closes in first 2 weeks New born may have an abnormal ECG, Heart Volume is 10ml/kg of body weight. Increase HR because small SV Resting HR and RR higher, BP is lower Adults RHR: 70-80 BP 120/80 and MAX HR 220-age Infant: RHR: 100-160 65/45 to 90/65  no normal max HR Decreased HR around 70 BPM by 18 years old. And Vascular resistance is lower in children. Congenital heart defects (born with it) •  Most common birth defect •  Can be simple or very co
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