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Chapter 14 - Energy Use
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- 1What is the slow component of O2 uptake?Increase in VO2 over expected steady state when exercising over anaerobic threshold
Usually starts after 3 min - 2Processes requiring ATPPrimary: 1) Myosin ATPase (50-70%), 2) Ca-ATPase (20-40%), 3) Na-K ATPase (6-10%)
Secondary: 1) Glycogen synthesis (in recovery), 2) Adenylate cyclase (glycogenolysis), 3) Phosphorylation reactions (MLC kinase, phosphorylase kinase) - 3How to quantify energy needs1) Measure O2 uptake (1 L ~ 5 kcal)
2) Measure heat generated (max optimal efficiency = 30% - 0% when isometric)
3) Measure ATP & CP use (must prevent resynthesis - inhibit mitochondria & glycolytic enzymes) - 4What is meant by efficiency in terms of muscle?Conservation of energy in a useful form
Mechanical efficiency = conservation of energy as work - calculated by measuring work done & energy cost (can often be 0, ex. walking)
Energy cost = steady state O2 uptake (L/min) * t (min) * 5 kcal/L * 4187 J/kcal - 5Influences on rate of ATP turnover by myosin ATPase1) CB turnover - depends on: myosin isoform dependent (IIX = fastest) + rate of length change (high velocity = less probability of CB attachment)
2) Number of CBs - depends on: activation (#/size of MUs, freq) + actomyosin overlap (20-40% is optimal) + lattice spacing (closer = more interaction) - 6What energy is required for activation processes?None - passive process
Ions move down electrochemical gradients - 7What energy is needed for restoration?Needed for Na-K ATPase & Ca ATPase
Found by: measure heat/O2 uptake at progressively longer lengths (decreases CB interaction without changing activation) -> determine total nrg use -> extrapolate to 0 force
Less ion exchange in fatigued m. - 8What energy is needed for activation?None - passive process
Ions move down electrochemical gradients - 9What energy is needed for restoration processes?Need for: Na-K ATPase & Ca ATPase
Found by: measure heat/O2 uptake at progressively longer lengths (decr CB interaction without activation change) -> determine total energy use -> extrapolate to 0 force
Less ion pumping in fatigued m. - 10O2 & work graphsO2:
incr = incr rate of CB turnover
decr = lower probability of attachment - 11Oxygen use, work, efficiency & power graph
- 12F-velocity relation & energy useFor submax, load & desired velocity dictate MU activation - 1 of main modulators of nrg cost (more MUs = more nrg)
Recruitment changes to maintain given PO at diff velocities
Lower F-v curve for ST vs. FT - 13Frequency & efficiencyEach m. has optimal freq for efficiency
FT: more efficient & optimal freq is lower, more efficient at high velocities - 14Effect of muscle length on energyLonger m. = greater energy cost (but faster movement)
- 15Effects of fatigueAffects max velocity (lower)
Economy of force development not affected - 16Age & training as factors in energy useAge = lower m. mass : total mass relation
Training = higher m. mass : total mass - 17What is McArdle's syndrome?Glycogen breakdown disorder
Lots of glycogen but no myophosphorylase (a) - can't mobilize it
-> pain, weakness & m. stiffness, no lactate production, rapid force decline (fatigue)
Get '2nd wind' if keep exercising in pain = switch from glycogen to fatty acid - 18Energy needed depends on:M. length
Level of activation (incl MU recruitment)
Velocity of shortening - 19How is [ATP] measured?Biopsy & freeze - not very precise for in vivo (can cause extra ATP loss)
MRS - non-invasive, phophate gives diff signal when bound to C vs. in ADP vs. ATP - 20Froce, ATP & PCr over time graph
- 21Immediate energy systemFastest rate of ATP production
1) ADP + PCr <-> ATP + Cr
Catalyzed by CK
PCR store 3-8x bigger vs. ATP
CR also shuttles nrg between mitochondria & myofibrils
2) 2 ADP <-> ATP + AMP
Catalyzed by MK (myokinase)
AMP is then deaminated
Keeps [ADP] low = stimulate metabolism - 22Short term energy systemGlycolysis
Rapid, local ATP formation
Regulated by Ca, energy charge, hormones & end products (also stimulate oxidative metabolism)
Start with glucose/glycogen -> pyruvic acid/lactic acid - 23Long term energy systemOxidative metabolism - in mitochondria
Beta oxidation -> citric acid/Krebs cycle -> ETC -> oxidative phosphorylation - 24MitochondriaVolume depends on fiber type & function (2-40%)
Connected in mitochondrial reticulum
Double membrane - inner separates matrix from intermembrane space
Crista - projections of intermembrane into middle
Inner membrane has F complexes - 25Krebs cycleStarts & ends with oxaloacetate - added to acetyl CoA -> decarboxylations release CO2 to recreate oxaloacetate
Requires: FAD, NAD+, Pi & H2O - NAD+ activates cycle
Produces: 3 NADH, 1 FADH2, 1 ATP - 26ETC & oxidative phosphorylationIn mitochondria
Energy from: 1) high-energy phosphate bond formed in GTP & broken to make ADP -> ATP, 2) Electron transfer
Electrons -> NAD+ & FAD -> passed along cytochromes of ETC -> nrg transports protons into intermembrane space -> diffuse down gradient back to matrix via F-complex & ATP synthase
O2 accepts electrons at end
24 ATP/glucose - 27Integration of systems
- 28Creatine phosphate shuttleCr -> mitochondria -> gets re-phosphorylated (CK catalyzes) -> PCr diffuses back to myofibril & ADP is formed in mitochondria -> stimulates oxidative metabolism
- 29Sequence of interaction between systemsGlycolysis -> NADH -> transfers to mitochondria -> drive oxidative metabolism
Glycolysis -> pyruvate -> used in Krebs - 30How energy sources enter systems- Glycerol/glucose/glycogen -> glycolysis
- Fatty acids -> beta oxidation (glycerol + 3 fatty acid chains) -> Krebs (fatty acids - longer ones require special transport)
- Proteins -> converted to pyruvate for oxidative metabolism - 31GlycogenolysisGlycogen = 10,000-30,000 glucose
Activated by: EPI, incr [Ca], incr ADP, decr ATP
Events: EPI binds β-receptor – coupled with adenylate cyclase → binds ATP to make cyclic AMP → activates protein kinase (can also be activated by Ca) → activates phosphorylase kinase → phosphates phosphorylase b to a & ADP to ATP → phosphorylase a is converted to glucose-phosphate - 32Glycogenolysis picture
- 33How is [ATP] regulated?Demand reduced by down-regulating E-C coupling - aka fatigue -> maybe fatigue is regulatory process to maintain [ATP]?
- 34Transfer of NADH to mitochondria1) Glycerol phosphate shuttle* - electrons transferred to FAD -> FADH2 -> ETC
2) Malate-aspartate shuttle - electrons transferred to mitochondrial NADH
3) Lactate shuttle - lactate dehydrogenase catalyzes -> lactic acid & oxidation of NADH -> NAD+ - 35Forms of metabolic regulationFEEDBACK = a reactant/product activates control system (wants to return to equilibrium)
Decr by ATP & H+, Incr by C, Pi & ADP
FEEDFORWARD = uses parallel activation system to turn on metabolism
ex. PFK -> incr enzyme activity -> faster ATP synthesis
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- (K485) Final stuff Fichas sobre Chapter 14 - Energy Use, creado por Megan Willerth el 08/12/2014.
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