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Tissue and organ metabolism- Muscle and Exercise

Tissue and organ metabolism- Muscle and Exercise ط      Classification of muscle Tissues ,Types of muscle fibers ط      Metabolism during exercise: Sprinting and Marathon running

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Tissue and organ metabolism- Muscle and Exercise

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  1. Tissue and organ metabolism- Muscle and Exercise ط     Classification of muscle Tissues ,Types of muscle fibers ط     Metabolism during exercise: Sprinting and Marathon running ط     Sprinting: Fiber composition, Fuels used, Control of Phosphocreatine and  Glycogen utilization, Fatigue and Training ط     Marathon running : Fiber composition, Fuels used, Control of  Feul utilization, Fatigue and Training                                           N L3 356 -80 

  2. Introduction · Interaction among motor proteins by: ionic, hydrogen and hydrophobic bonds and Vander Waals interaction (temp) · Chemical energy (ATP) converted into motion: muscle contraction, organelles migration, flagella rotation ·  Muscle proteins: myosin : actin (80%) undergo transietnt interaction and slide past each other (arranged filaments aggregation) for contaction fig5.29, fig5.30 ·  Skeletal muscle consist of fibres (multinucleated cells) each contain 1000 myofibrils, that each consists of vast numbers of thick & thin filaments & sacroplasmic reticulum surrounds each myofibres fig5.31, fig5.32 ·  Signal from nervous system lead to sacroplamic retic release Ca++, which bind to tropomysin-troponin complex at troponin part fig5.33 ·   Skeletal muscle uses free FA, KB, glc as fuel fig23.17 ·   Heavy breathing lead to high O2 intake lead to ATP production causing high Lact that promotes gluconeogenesis leading to glc production (cori cycle) fig23.18 ·   The heart (aerobic, mitochondria) use mainly glc, KB

  3. Sprinting Energy expenditure in 100m for 10 seconds (approx 200KJ.min–1) 1. Fibre types: Most abundant are white muscle fibre (type II) Innervated by large neurines trasnsmit rapid signals Simultaneous contraction of all or most fibres Act-myosin interaction cycle is short Poor blood supply, no mitoch

  4. Sprinting Energy expenditure in 100m for 10 seconds (approx 200KJ.min–1) 2. Fuel: Engery from breakdown of phosphocreatine in the first 4 seconds Muscle glycogen is used to produce ATP () through anaerobic glycolysis 3. Fuel Utilization: Hormonal function during resting For initiation of sprinting, high myofibrillar ATPase activity resulting in low ATP, then phosphocreatine + AMP, Pi F1,6P2  creatine kinase (CK)  ATP Also protein kinase High F6P phosphorylation  by protein kinase (PK)  lead to formation of F1,6P2 Glycogen  glycogen phosphorylase  glc When ATP utilization is greater than ATP recovery lead to oxygen debt

  5. Sprinting Energy expenditure in 100m for 10 seconds (approx 200KJ.min–1) 3. Fuel Utilization: Hormonal function during resting For initiation of sprinting, high myofibrillar ATPase activity resulting in low ATP, then phosphocreatine + AMP, Pi F1,6P2  creatine kinase (CK)  ATP Also protein kinase High F6P phosphorylation  by protein kinase (PK)  lead to formation of F1,6P2 Glycogen  glycogen phosphorylase  glc When ATP utilization is greater than ATP recovery lead to oxygen debt

  6. Sprinting Energy expenditure in 100m for 10 seconds (approx 200KJ.min–1) 4. Fatigue: Failure of neurons, nerve, neuromusclular jusnction, muscle fibre a) peripheral:  High protons, low pH during phosphocreatine degradation and glycogen conversion to lactate High Ca++ may play role Limiting quantity of muscle b) central: central inhibition produced by sensory signal (mood) from fatigue muscle

  7. Sprinting Energy expenditure in 100m for 10 seconds (approx 200KJ.min–1) 5. Training: a) weight training: increase fibre size lead to increase in creatine kinase and glycolysis b) slow running start: development of contraction-relaxtion cycle coordination c) start running: increase substrate cycle capacity in response to catecholamine

  8. Marathon Running Energy expenditure in 42Km for 2 hours (approx 12000KJ) 1. Fibre types: Most abundant are red muscle fibre (type I) Innervated by slow nerve conduction Contract time is slow good blood supply and mitoch

  9. Marathon Running Energy expenditure in 42Km for 2 hours (approx 12000KJ) 2. Fuel: At start blood glc and FA The muscle glycogen and adipose tissue FA rate of glc release by liver & uptake by muscle is similar 30% O2 uptake, 60% FA oxid in later stages Glycogen depletion is gradual FA (50% supply of fuel) in bld increase during time leading to high glycerol

  10. Marathon Running Energy expenditure in 42Km for 2 hours (approx 12000KJ) 3. Fuel Utilization: a) Glc from liver glycogen (glycogen phosphorlase) increase epinephrine, norepinephrine and glucagons and decrease in insulin b) Glc from muscle glycogen (G6P, ATP, AMP, Pi, high phosphorylase a) c) FA oxidation: TG from adipose tissue lease to high FA causing acetyl CoA synthase and carnitine palmitoyl transferase Bld glc 14min, hep glycogen 18min, muscle glycogen 71min, TG 4018min

  11. Marathon Running Energy expenditure in 42Km for 2 hours (approx 12000KJ) 4. Fatigue: When carbohydrate store is depleted (glc, glycogen) lead to high FA oxid to provide 50% of power causing fatigue Caffeine stimulates FA release from AT by inhibiting cAMP phopshodiestrase leading to increase in cAMP

  12. Marathon Running Energy expenditure in 42Km for 2 hours (approx 12000KJ) 5. Training: a) untrained: physiological change: respiration(^O2), central circulation(^heart rate & size), peripheral circulation(^bld to liver leading to gluconegenesis and vbld to muscle) metabolic change: ^ oxidative pathway and ^ myoglobin b) elite: high aerobic metabolism (enz)              utilize all glc that enters TCA cycle (no lactate)              increase responsiveness of substrate cycle to hormones Marathon runners at risk of death from FA, cardiac arrhythmia, fibrillation (hypoxia), stress (thromboses) Lack of fitness means poor aerobic capacity

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