Energetics Flashcards
Homeotherm
Regulation of their own temperature
WHY do we maintain body temperature?
Keep kinetic energy high and optimum temperature of enzymes
Heat gain mechanisms
Conduction
Convection
Metabolism
Radiation
Types Of Heat Loss
Conduction
Convection
Evaporation
Radiation
What happens when heat gain exceeds heat loss?
Body temperature rises
Rate of heat production is…
Proportional to metabolic rate
Heat energy definition
Heat is a spontaneous flow of energy from one object to another caused by a difference in temperature between the two objects.
Heat balance equation
(metabolism - work) - (heat loss) = storage of heat (Hs)
Storage heat equation
Calculating the amount of heat energy which is transferred
H = mc delta T
Specific heat capacity
The amount of heat required to raise the temperature of 1kg mass by 1 Kelvin - depends on the composition of the object.
Conduction
Heat energy is transferred through a solid, liquid or gas by direct contact
Heat gain or loss is usually by conduction is minimal
Heat transfer is dependent on…
Thermal conductivity and the temp difference between the two objects
Convection
Transfers heat by fluid movement driven by a temperature gradient
Transfer of heat from skin to fluid warms the fluid, thereby reducing its density, it rises and is replacement by cooler fluid
Evaporation
Heat loss through the change of state of a liquid into gas.
Hevap = Kevap A.(P2-P1)
Evaporative heat transfer is dependent on the water vapor pressure gradient between the solution and the environment.
Radiation
Transfer of thermal energy by means of electromagnetic waves. It does not require a material medium
Modes of thermoregulation
Metabolism
Vasomotor regulation (blood flow)
Sweating
Shivering
Thermal regions (core + shell)
Core temp - tightly maintained
Shell or skin -highly variable
Mean body temperature = 0.64Tcore + 0.36shell
Core expands in a hot environment and contracts in a cold environment
Tcore females
Fluctuates with the menstrual cycle
Hormone levels, endometrial thickness and ovulation
Where is heat produced (organs)
At rest: Primarily at brain, heart, liver and kidneys
During exercise: primarily skeletal muscles
How is heat lost?
Overwhelmingly through the skin, via radiation, conduction, convection & evaporation
At normal temp 50-65% of heat is lost by radiation with most of it lost by evaporation
Insulation of the shell methods
Qualitative variation (vary the medium)
Fat
Feathers
Fur/Hair
Quantitative variation
(Vary the thickness)
Winter fat
Piloerection (air-trapping)
Variable blood-flow to the skin (vasodilation & vasoconstriction)
Thermoregulatory control feedback system
Receptors from the skin and the hypothalamus effects metabolism, vasomotor, sweating and shivering that increases body temperature
Temperature sensors - receptors
Warm receptors and cold receptors from these receptors project to the pre-optic hypothalamus
Regulation of heat transfers
Peripheral thermoreceptors and core thermoreceptors input signal compared with set point.
Effectors: shivering, vasomotor, sweat which activate/deactivate heat transfer
Effector locations for heat gain/loss
Metabolism - brown adipose tissue - mainly in newborns
Vasomotor - blood vessels - vasoconstriction at skin, vasodilation at core = heat retention
Sweat - sweat glands - increased sweat leads to evaporative heat loss in dry environments
Shivering - muscles - increases metabolic heat production
Piloerection - hair follicles - traps a layer of air between skin and hair = insulation
Brown adipose tissue
High density of mitochondria for high level of metabolic activity. Situated close to blood vessels so that heat produced by metabolism of fatty acids can be quickly distributed to the rest of the body.
Heat transfer within the body
Conduction: Slow
Advection/convection: fast -> blood flow
Heat transfer through vasodilation
To remove heat produced by metabolism, convection is the primary node of heat loss
Hyperthermia of exercise
Heat gain > heat loss so Tcore increases
The hypothalamic integrator outputs neural output to activate heat loss via skin blood flow and sweating. When heat loss = heat gain storage of heat decreases to zero. But the elevated T core persists as long as exercise is maintained.
Heat stroke
Occurs when the thermoregulatory system fails and core temperature increases to 41C or above.
Excessive vasodilation at skin causes drop in blood pressure & decreased brain perfusion - confusion, loss of consciousness
Treatment is to sponge with tepid water.
Only place ice packs over skin where large vessels are near surface
Fever hyperthermia
Set point is raised
Caused by cytokines from the immune system crossing the blood-brain barrier which increases Tset
Brain sends neural output to increase heat gain/retention to increase Tcore to new higher Tset.
Mechanical work
Muscle contraction
Movement of cells, organelles, appendages
Therapeutic hypothermia
Lowering core temp. can protect the brain from reperfusion. Damage post-stroke or cardiac arrest.
Decreased metabolism, ROS, cell death and glutamate
List of energy output processes
Mechanical work
Synthetic reactions
Membrane transport
Signal generation and conduction
Heat product
Detoxification and degradation
What are synthetic reactions?
Creation of essential functional molecules
Membrane transport
Minerals
Organic anions/cations
Amino acids
How is heat produced?
Temperature regulation
Inefficient chemical reactions
Detoxification and degradation
Urea formation
Conjugation
Oxidation
Reduction
Energy released equation
energy released = mc(delta)T
Bomb calorimeters and energy
Overestimate energy available for cellulose
Oxidation of glucose
Produces 32ATP
Oxidation of Fat (palmitate)
Produces 129 ATP
Oxidising fuel
Oxidising different fuels yields similar amounts of energy per unit O2 consumed
Glucose metabolism
Glucose is split during glycolysis into 2 pyruvate. This enters TCA cycle, NADH produced, ETC produces ATP
Fast-twitch muscle ATP production
30ATP per glucose
Exact number of ATP produced by glucose
Initial estimates of 36 or 38 ATP were done at room temperature
Metabolic wastes
Main waste products are CO2 and NH3. Both are water soluble & carried in the blood. CO2 excreted by diffusion and HCO3- by kidney. NH3 carried to liver as glutamine, converted to urea and excreted.
Ammonia toxicity and glutamate dehydrogenase
NH3 + a ketoglutarate -> glutamate + H2O by glutamate dehydrogenase.
a-ketoglutarate
Important for oxidative phosphorylation. Reaction with NH3 means that it is not available for oxidative phosphorylation and can be harmful for the brain.
Fick principle
Used to measure VO2. Subject breathes using a respiratory valve, inspired gas content known. Expired air analysed for O2 & CO2 content and volume expired is measured.
Energy efficiency
Efficiency = output / input
Output = demand for energy
Input = source/supply of energy
= power/ VO2
Energy consumption in muscle involves: signalling and mechanical. How much ATP is used?
30-40% of ATP consumed during isometric contraction fuels Na+ and Ca2+ pumping
Different types of work
Chemical work: moving a molecule against its concentration
Electrical work: moving a molecule against its electrical gradient
Mechanical work e.g muscle contraction
Chemical work
Molecules can passively transport across a membrane down their concentration gradient (from high to low)
Chemical work equation
work = RT lnC1/C2
R is the universal gas constant
T is absolute temperature
C is concentration
Electrical work
Positively charged particles that are free to move will always tend to shift towards the direction of lower voltages
Electrical work equatiion
Work elec = zFEm
Sarcolemmal ATPase
A membrane bound electrogenic enzyme that moves Na+ out of the cell (efflux) and K+ into the cell (influx) against their concentration gradients and electrical gradient (Na+)
W total equation
RT ln(ci/co) + zFEm
Cost of a contraction trigger
Ca2+ ions are release from the sarcoplasmic reticulum and bind to the myofilaments to trigger contraction. Ca2+ is then taken back up into the SR by the SRCa2+- ATPase pump.
Work total for SERCA
Wtotal = RT ln (Csr/ccytoplasm) + zFEsr
ATP and cross-bridge relation
1 ATP is needed to detach a cross-bridge.
First law of thermodynamics
Energy can be transferred and transformed, but it cannot be created or destroyed (energy of the universe is constant)
Second law of thermodynamics
Every every transfer or transformation makes the universe more disordered (every process increases the entropy of the universe)
Gibbs free energy equation
∆G = ∆H - T∆S
Favourable
∆H < 0
∆S > 0
Entropy
Quantitative measure of disorder that is proportional to randomness
Energy is stored in molecules which are ordered such as glucose
Energy transfer from glucose breaks down the molecule into smaller parts and creates a more disordered state (increases entropy)
Open systems
The entropy of a system may decrease, but the entropy of the system plus its surroundings must always increase
Anaerobic reactions
Alactic (doesn’t produce lactate):
Creatine phosphokinase reaction
Adenylate kinase reaction
Lactic:
Glycolysis and glycogenolysis
Aerobic pathway
Oxidative phosphorylation
Sprinter uses…
Alactic anaerobic
Crp, AMP
400m uses
Lactic anaerobic dominates (glycolysis)
Marathon runner
Aerobic (oxidation)
Creatine phosphokinase reaction
CrP + ADP -> Cr + ATP
Catalysed by creatine phosphokinase
CrP acts as a buffer to maintain ATP high
Creatine phosphokinase reaction kinetics
Extremely rapid
Of small extent
Creatine phosphate shuttle
Creatine phosphate shuttles chemical energy from mitochondria to various cellular locations of the ATPases to phosphorylate ADP
Adenylate Kinase reaction
2ADP -> AMP + ATP
catalysed by adenylate kinase
last ditch process used only when ATP is v.low
Adenylate kinase reaction degradation products
IN the absence of ATP, AMP is deaminated to inosine monophosphate:
AMP -> IMP + NH4+
catalysed by AMP deaminase and the products inhibit muscle contraction
Glycolysis/Glycogenolysis yields from splitting
Glucose yields 2 ATP and glycogen yields 3 ATP
Glycogen
Consists of long chains of glucose molecules joined end-to-end with many branches. Up to 6000 glucose residues
Converting G6P to glycogen is that it compacts all the molecules into single large polymers for storage by the cell as large granules of sugar.
Glycogen energy
Provides fuel for muscle contraction and liver glycogen is converted to glucose that exits liver cells and enters the bloodstream by Cori cycle
Consequences of anaerobic energy production (knock on effects)
Extensive glycolytic activity leads to decreased cellular pH.
Protons: inhibit Ca2+ release from the sarcoplasmic reticulum and compete with Ca2+ for binding sites on Troponin-C, thereby potentially diminishing contractile force.
Lactate production as a function of exercise intensity
Lactate begins to accumulate and rise exponentially at 55% VO2 max for an untrained subject
Process of oxidative phosphorylation
Glycogen, fats & proteins can be broken down & enter the CAC or Kreb’s cycle
slow kinetics
enormous extent
Citric acid cycle process
Pyruvate enters the mitochondria and is a substrate for the CAC. CAC produces ATP and NADH & FADH2 for the ETC
ETC - complexes
NADH & FADH2 produced by the CAC is used in the ETC chain at complex 1&2
Transmembrane charge is set up generated ATP at complex V
Muscle fatigue definition
Defined as a reversible failure to maintain the required or expected power output, leading to reduced muscle performance
Protective strategy to prevent cellular damage
Central fatigue
CNS command
- reduced excitatory input
- Motor neuron signal decreased by altered input from sensory fibres
Peripheral fatigue is caused by
Neuro-muscular transmission
Muscle fibre action potential
Excitation-contraction coupling
Depletion of substrates for metabolism
Accumulation of waste-products
How is fatigue studied?
- Trained athlete
- Exercising volunteer subject (sedentary vs active)
- Experimental animals
- Isolated whole muscle
- Isolated single fibre (myocyte)
- Contractile proteins in a test-tube
Tetanus
Prolonged contraction of a muscle caused by rapidly repeated stimuli
Force time fatigue graph
Fatigue occurs at the intersection of maximum force and required output
Time taken to fatigue factors
Required force
Maximum force
Intrinsic fatigability
Fast-twitch fiber
Easily fatigued
Decreased Ca2+ and force over time
Soleus fibre
Fatigue resistant
Ca2+ and force relatively stable, even after 1000 pulses
Fatigue in fast twitch fiber
Type II easily fatigued
Predominantly anaerobic metabolism
Short bursts of fast contractions (e.g sprinters)
Slow-twitch fibre
Type I, fatigue-resistant e.g Soleus
Predominantly aerobic metabolism
Rich in capillaries and mitochondria (dark)
Continuous extended contractions over time (e.g marathon runners)
Fatigue at cellular level
Changes in pH (due to accumulation of waste products)
Accumulation of phosphate
Decrease Gibbs free energy of ATP
Excitation-contraction coupling impairment
Effects of decreased pH
Decrease in relative force
Competition of H+ with Ca2+ for binding sites on Troponin-C right-shift of the Force-Ca2+ relation = Ca2+ sensitivity of myofilaments
Inhibition of Na-K-ATPase, myosin ATPase, cross-bridge interaction
How do you measure the amount of inorganic phosphate?
Nuclear magnetic resonance (NMR) imaging used to quantify Pi and PCr. Decreased PCr with and increased Pi with exercise. Coincident with decreased force production
Possible actions Pi
Direction inhibition of rotation of the actomyosin cross-bridge
Reduce Ca2+ release and increase Ca2+ force activation threshold from SR.
Reduction of Free energy of ATP hydrolysis
Gibbs Free energy of ATP
∆G = Go + RTln [ADP][Pi]/[ATP]
Energy released by ATP hydrolysis
Depends on concentrations
Usually negative because release of energy
∆G required by ATPases
∆G required by ATPases is positive b/c they gain energy from ATP
Changes in ∆GATP for [CrP]
As [CrP] falls, [Pi] rises but [ATP] and [ADP] stay constant
What happens at exhaustive exercise?
ATP preserved at expense of CrP& Pi
Increased Pi will cause a decrease in ∆GATP
If ∆GATP falls sufficiently then work of ATPases will be compromised
Metabolic end-products may inhibit muscle activation & force development
Fatigue effect on excitation-contraction coupling
Na+ and K+ ionic gradients not fully restored = impaired membrane excitability
Signal to open Ca2+ channels is impaired
Inhibition of SERCA pump = decreased SR Ca stores
Decreased transient Ca and decrease force
Effects of aerobic training: Heart
Increased cardiac output, increases O2 delivery to the muscles
Effects of aerobic training: Circulation
Increased plasma volume, increases stroke volume and thus cardiac output. Increases skin blood flow to optimise thermoregulation
Effects of aerobic training: Blood vessels
Increased capillary proliferation, increases O2 delivery and diffusion into muscles
Effects of aerobic training: Myocytes
Increased mitochondria, increases O2 extraction. Enzyme adaptation, optimizes metabolism, increases reliance on fat thus reduced lactate production
