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Metabolic Response to Exercise

Metabolic Response to Exercise. Foss ch. 3 Brooks - Exercise Phys. Ch. 10 selected sections - Brooks Ch. 5-7 Outline Fuel utilization - crossover concept Recovery Glycogen re-synthesis lactate performance Lactate shuttles Endurance Training effects lactate, Glycolysis, mitochondria

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Metabolic Response to Exercise

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  1. Metabolic Response to Exercise • Foss ch. 3 • Brooks - Exercise Phys. Ch. 10 • selected sections - Brooks Ch. 5-7 • Outline • Fuel utilization - crossover concept • Recovery • Glycogen re-synthesis • lactate • performance • Lactate shuttles • Endurance Training effects • lactate, Glycolysis, mitochondria • Anaerobic Threshold??

  2. Measurement of Metabolic Response • Evaluation provides info about absolute and relative intensity of exercise bout (fig 10.1a) • absolute VO2 (L/min or ml/Kg/min) • % of VO2 max • % of HR max • multiples of Metabolic Rate (MET’s) • 1kcal/Kg/hour at rest • determination of metabolic response allows estimation of • Total energy cost • Nutritional requirements • Efficiency calculations • Estimation of workload indicates metabolic system utilization, and the potential for fatigue

  3. Substrate Utilization • Brooks p 133 • Power output is the most important factor determining fuel utilization • Crossover concept • post absorptive and resting • lipid used predominantly • with increasing intensity • fuel mix switches from lipid to CHO • Fig 7-12 • training - displaces absolute intensity at which crossover occurs • epinephrine suppression • inc lactate clearance • inc mitochondria • prolong onset of glycogen breakdown, depletion and fatigue

  4. Fuel Utilization • Fig 7-11 • Glucose - fatty acid cycle • FFA breakdown inhibits glycolysis • PDH is inhibited by Acetyl-CoA from Beta oxidation • PFK is inhibited by inc citrate from Beta oxidation and ATP • in highly trained and glycogen depleted this is accentuated • Fig 7-10 - higher FFA utilization with higher mitochondrial enzyme activity following training • Hexokinase is inhibited by its product G6P, which builds up if glycolysis is not active.

  5. Recovery from Exercise • Ch. 3 - Foss • process of recovery from exercise involves transition from catabolic to anabolic state • breakdown of glycogen and fats to replenishment of stores • breakdown of protein to protein synthesis for muscle growth and repair • Our discussion of recovery will include; • oxygen consumption post exercise • Replenishment of energy stores • Lactate metabolism(energy or glycogen) • Replenishment of oxygen stores • intensity and activity specific recovery • guidelines for recovery

  6. Recovery Oxygen • Recovery O2 - Net amount of oxygen consumed during recovery from exercise • excess above rest in Litres of O2 • Fast and Slow components • Based on slope of O2 curve • first 2-3 min of recovery - O2 consumption declines fast • then declines slowly to resting • Fig 3.1 • Fast Component - first 2-3 minutes • restore myoglobin and blood oxygen • energy cost of elevated ventilation • energy cost of elevate heart activity • replenishment of phosphagen • volume of O2 for fast component = area under curve • related to intensity not duration

  7. Recovery Oxygen • Slow Component • elevated body temperature • Q10 effect - inc metabolic activity • cost of ventilation and heart activity • ion redistribution Na+/K+ pump • glycogen re-synthesis • effect of catecholamines and thyroid hormone • oxidation of lactate serves as fuel for many of these processes • duration and intensity do not modify slow component until threshold of combined duration and intensity • After 20 min and 80% • We observe a 5 fold increase in the volume of the slow component

  8. Energy Stores • Both phosphagens (ATP, CP) and glycogen are depleted with exercise • ATP/CP - recover in fast component • measured by sterile biopsy, MRS • rate of PC recovery indicative of net oxidative ATP synthesis (VO2) • study of ATP production • 20-25 mmol/L/min glycogen and all fuels • during exercise • CP can drop to 20%, ATP to 70 % • CP lowest at fatigue, rises immediately with recovery • Fig 3.2 - very rapid recovery of CP • 30 sec 70%, 3-5 min 100% recovery

  9. Phosphagen Recovery(cont.) • Fig 3.3 • occlusion of blood flow - no phosphogen recovery • ** requires aerobic metabolism • estimate 1.5 L of oxygen for ATP-PC recovery • Energetics of Recovery • Fig 3.4 • breakdown carbs, fats some lactate • produce ATP which reforms CP • high degree of correlation between phosphagen depletion and volume of fast component oxygen • Fig. 3.5 • Strong correlation between phosphagen depletion and volume of the fast component of recovery oxygen - sea level and altitude • anaerobic power in an athlete related to phosphagen potential - Wingate test

  10. Glycogen Re-synthesis • Requires 1-2 days and depends on • type of exercise and amount of dietary carbohydrates consumed • Two types of exercise investigated • continuous endurance (low intensity) • intermittent exhaustive (high intensity) • Continuous - (low- moderate intensity) • Fig 3.6 - diet effect • minor recovery in 1-2 hours, does not continue with fasting • complete re-synthesis requires high carbohydrate diet ~ 2 days • Recovery does not occur without high carbohydrate diet • depletion of glycogen related to fatigue • Fig 3.7 - heavy training

  11. Glycogen Re-synthesis • Intermittent (high intensity) exercise • Fig 3.8 • significant re-synthesis in 30 min-2 hrs • does not require food intake • complete re-synthesis does not require high carbohydrate intake • only ~ 24 hrs for 100 % recovery • rapid recovery in first few hours • Continuous vs. intermittent • amount of glycogen depleted • Much higher with long duration • precursor availability • lactate, pyruvate and glucose available after high intensity exercise • Muscle fiber type involved in activity • re-synthesis is faster in type II fibers which are utilized with higher intensity activity

  12. Lactate Recovery • Blood lactate levels are fairly constant with rising intensity until a threshold of intensity is reached(10.1b) • After threshold, you observe a sharp rise in [lactate] along with intensity • [Lactate] is influenced by the duration of exercise and rest interval between repeated bouts • Fig 10-2 - lactate turnover • fig 3.10 - exhaustive exercise • ~25 min for 1/2 recovery (passive) • passive recovery - minimal activity • Fig 3-11 active vs passive recovery • Fig 3-12 intensity of active recovery • untrained 30- 45% VO2 Max • trained up to 50-60% - in some studies • glycogen re-synthesis is slowed with higher intensity active recovery

  13. Recovery • fig. 3.13(fate of lactate) • Fig 3.14 (lactate vs slow component) • close association between the slow component of O2 recovery and the removal of lactate - but not exact • restoration of O2 stores • fast component - 10-80 seconds • Ion concentrations • pH - rapid return after light exercise • heavy exercise dec. From 7-6.4 • ~20 min for recovery • close correlation to lactate and fatigue • Recovery of Maximum Voluntary Contraction correlates with Pi (both factors are restored in ~5 min)

  14. Performance Recovery • How quickly do we regain performance? - force, power, MVC • Guidelines Table 3.2 • Dependant on • energy system utilized • Intensity of exercise and type of recovery • Aerobic fitness (VO2 max) is an important influence as well • good correlation between fast recovery of muscle function and VO2 max • why? • Fast component requires O2

  15. Lactate Shuttles • Intracellular lactate shuttle (Brooks p 69) • Within one cell • evidence of LDH in mitochondria of muscle, liver and other cells • evidence that mito in liver and heart oxidize lactate more than pyruvate • lactate- more than pyruvate - is link between glycolytic and oxidative met • Fig 5-13, 14 (Brooks) • rapid glycolysis -creates a rise in cytosolic lactate • lactate enters mitochondria via MCT pyruvate/lactate carrier (Brooks p79) • oxidized to pyruvate in mito • continues through TCA (Krebs) • NADH formed inside mitochondria, as well as recycled in cytosol

  16. Intercellular Lactate Shuttle • Between different cells (Brooks p 78) • Lactate actively oxidized - preferred fuel in heart and slow twitch muscle • produced in Type IIb fibers • transported directly between cells in same muscle • or through blood circulation to type I fibers or heart muscle cells • Fig 5-20 (Brooks)

  17. Muscle as Consumer of Lactate • P 202 - 209 (Brooks) • Similar to discussions in Foss • EPOC - Excess post-exercise oxygen consumption- instead of Recovery Oxygen • Causes for excess oxygen used in recovery • 13 % increase in BMR / degree Celsius • similar to Q10 effect • Fig 10-11 - uncoupling of mitochondria - inc ATP needs • Calcium- accumulates with contraction - mitochondria may sequester Ca++- ATP required to remove it, which may alter net oxidative phosphorylation

  18. Endurance Training • Table 6-1, 6-2 • With endurance training, we observe • a doubling of enzyme activity • TCA and ETC - in all muscle fiber types • a doubling of mitochondrial content • Table 6-3 • improvements in oxidative capacity correlate well with running endurance • ~ 90 percent correlation • Correlation between oxidative capacity and VO2 max is not as strong • ~ 70 percent correlation • ~ 10- 15 % increase in VO2 max with training vs. ~100% for oxidative capacity • With an increased mitochondrial content • The given rate of O2 consumption can occur at a much higher ATP/ADP ratio • Fig 6-13 • This reduces carbohydrate breakdown in favor of lipid metabolism

  19. Anaerobic Threshold?? • Brooks p 215 • Historically, the non linear rise in blood lactate at ~60% VO2 Max was termed the anaerobic threshold • does not however provide info about anaerobic metabolism • reflects balance between lactate entry and removal from blood (turnover) • Lactate inflection point is now the preferred term • Inflection often corresponds to ventilatory threshold • (non linear rise in ventilation) (talk test) • However; Fig 10-17 • Patients with McArdles syndrome • lack of phospohorylase - unable to breakdown glycogen • Have normal ventilatory threshold • Association, therefore, is not causal

  20. Lactate Inflection Point • Many factors may influence either the production or removal of lactate • Type II b fiber recruitment - increases with intensity - results in higher lactate production • Sympathetic NS activity increases with intensity of exercise • vasoconstriction (many tissues) • Leads to reduced oxidation of circulating lactate - ie. less removal • *local factors (paracrines) in muscle • Stimulate vasodilation • raising % of Cardiac Output to muscle • Epinephrine and glucagon • stimulate glycogenolysis and glycolysis • higher lactate production • increased Calcium with contraction - activates glycogenolysis - (Fig 10-18)

  21. Learning Objectives • Understanding of metabolic influences in glucose fatty acid cycle • Distinction between fast and slow components of recovery oxygen • What contributes to the volume of each component • Pathways for recovery of energy stores - • Phosphagens, glycogen • Recovery of resting lactate concentrations • Active vs passive recovery • Performance recovery • Force, power, MVC • Lactate shuttles • Oxidative use of lactate - intra vs inter cellular • Training impacts on fuel use and recovery • Influences on lactate inflection point

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