BIOL 252 1st Edition Lecture 13 Outline of Last Lecture I. RelaxationII. Muscle StrengthIII. Tension in muscle fibersIV. Length-tension relationshipV. Poll EverywhereVI. Whole-Muscle ContractionsVII. Muscle MetabolismOutline of Current LectureI. Modes of ATP Synthesis During ExerciseII. FatigueIII. Classes of Muscle FibersIV. Cardiac MuscleV. Smooth MuscleVI. Intercellular communicationVII. Principles of hormone communicationVIII. Classes of HormonesIX. Hormone Receptors and effectsX. Endocrine disordersXI. Hypothalamus and PituitaryCurrent LectureXII. Modes of ATP Synthesis During Exercisea. At start (0 seconds)i. Aerobic respiration using oxygen held by myoglobinb. In short time, our heart/lungs/cardiovascular system lag behindi. Move to phosphagen systemii. Quick way to create ATP (from ADP build up)iii. Does not last long1. 5-10 secondsc. If we run out of oxygen and ability to use phosphagen system, use glycolysisi. Not as efficient – 2 net ATPd. Aerobic respiration supported by cardiopulmonary function (once lungs/cardiovascular system catches up)These notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.e. Must consider what we’ve losti. Used up elements of phosphagen system 1. Consume ADPii. From glycolysis – consume glucose and glycogeniii. Put cell in state of debt, must put resources backiv. Oxygen debt: debt due to lack of oxygen1. Extra O2 needed following exercise for:2. Replacing body’s oxygen reserves3. Replenishing phosphagen system4. Oxidizing lactic acid converting it to glucose5. Serving elevated metabolic rate XIII. Fatiguea. Muscle fatigue – progressive weakness and loss of contractility from prolonged use of the musclesb. Causes:i. Glycogen depleted (decrease ATP)ii. Decrease ATP reduces Na+/K+ pump activityiii. Low pH (from lactic acid and other metabolic processes)iv. Reduced ACh (junctional fatigue)v. CNS fatigueXIV. Classes of Muscle Fibersa. Type Ii. Slow twitch fibers (slow to respond)1. Longer latency periodii. Red fibers (contain myoglobin)iii. Oxidative fibers (prefer aerobic metabolism)iv. [Slow red ox]b. Type IIi. Fast twitch (quick to respond)ii. White fibers (contain little myoglobin)iii. Glycolytic fibers (optimized for glycolysis)1. Use glycolysis alone (whereas the others don’t)2. Need lots of glycogen – giving white coloriv. Tend to be big – increase in muscle size = increase in glycogenXV. Cardiac Musclea. Striatedb. Intercalated discsi. To fill voids – on end of one cell, wavy edgeii. On the other cell – fills valleys => interlockingiii. Ions can flow from one cell to next and link cells; AP can propagate to next celliv. Gap junctions unite cell membranesc. Desmosomesi. Mechanical linkages between cellsii. Without these, one cell contracts and it tears away from neighbor d. Cell membrane admits calciumi. Dual source of calcium – SR and extracellular fluid e. Limited mitosisf. Contains autorhythmic cells that produce APsi. “Pacemaker” cellsg. ANS can adjust heart rate and strengthh. Very slow twitches – no summation or tetanusXVI. Smooth Musclea. No visible striationsb. Dense bodies similar to Z discsc. No T tubulesd. Calcium comes from extracellular fluide. Capable of mitosis and hyperplasia (growth of tissue through cell production)i. Uterus enlargementEndocrine SystemXVII. Intercellular communicationa. Gap junctions: through cytoplasmb. Neurotransmitters: through synaptic clefc. Paracrines: through interstitial fluid (to neighbors)i. If picked up by the blood = HORMONEd. Autocrines: through interstitial fluid (on itself) XVIII. Principles of hormone communicationa. Released by endocrine glands (endocrine cells, neuroendocrine glands)b. Picked up by bloodc. Travel throughout bodyd. “Diffuse” out of capillariese. Stimulate “target cells”XIX. Classes of Hormonesa. Steroid hormonesi. Derived from cholesterolii. Secreted by gonads and adrenal cortexb. Monoamines (biogenic amines)i. Derived from tyrosine and tryptophanii. Secreted by adrenal medulla, pineal, thyroid glands iii. NE and epinephrine c. Peptides and glycoproteinsi. Secreted by pituitary, hypothalamus, and othersXX. Hormone Receptors and effectsa. Target cells are those cells that have receptors for the hormoneb. Hydrophobic hormonesi. Steroid hormones and THii. Require transport proteinsiii. Penetrate plasma membrane and bind intracellular receptors1. Receptor is inside the cell2. The hormone + receptor => go to nucleus =>iv. Affect gene transcription1. Turn on genes that were previously off or turn off what was onc. Hydrophilic hormonesi. Do not require transport proteinsii. Do not pass into cellsiii. Stimulate cells (2nd messengers)iv. Peptides and catecholamines1. Hormone-receptor binding activates G protein2. G protein activates adenylate cyclase3. Adenylate cyclase produces cAMP (second messenger)4. cAMP activates protein kinases5. Protein kinases phosphorylate enzymes – activates some enzymes and deactivates others6. Activated enzymes catalyze metabolic reactions w/ wide range of possible effects on the cell7. => Ultimately changes behavior of target cellv. Other second messengers (besides cAMP)vi. How do hydrophobic hormones know which cells to enter?XXI. Endocrine disordersa. Abnormal signals w/in endocrine systemb. Hyper/hypo secretionc. Hyper/hypo sensitivityd. How? Tumors, lesion, autoimmune disordersXXII. Hypothalamus and Pituitarya. Form floor and walls of third ventricle of the brainb. Controls water balance, thermoregulation, sex drive, childbirth and various autonomic functionsc. Many of its functions executed by pituitary glandd. Nervous system structure/tissue but also produces hormonese. Anatomy of pituitary glandi. Anterior lobe (adenogypophysis [adeno means epithelial])1. Arises from pharynx during development2. Made of glandular epitheliumii. Posterior lobe (neurohypophysis)1. Outgrowth of brain2. Nervous tissue3. Makes NO HORMONESa. Releases 2b. ADH and oxytocin 4. Neuro-endocrine cells – nervous tissue that produces hormones5. ADHa. Produced in hypothalamusb. Transported by hypothalamo-hypophyseal tract to posterior lobec. Diuretic – causes you to make more urined. ADH = produce less urinee. Effects = raise amount of water in your bodyf. Two targets – kidneys, braini. Increase water retention, increase thirstg. Stimulants:i. High osmolality (salt concentration)h. Under which conditions would cause elevated ADH