Energetics Flashcards

(109 cards)

1
Q

Homeotherm

A

Regulation of their own temperature

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2
Q

WHY do we maintain body temperature?

A

Keep kinetic energy high and optimum temperature of enzymes

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3
Q

Heat gain mechanisms

A

Conduction
Convection
Metabolism
Radiation

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4
Q

Types Of Heat Loss

A

Conduction
Convection
Evaporation
Radiation

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5
Q

What happens when heat gain exceeds heat loss?

A

Body temperature rises

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6
Q

Rate of heat production is…

A

Proportional to metabolic rate

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7
Q

Heat energy definition

A

Heat is a spontaneous flow of energy from one object to another caused by a difference in temperature between the two objects.

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8
Q

Heat balance equation

A

(metabolism - work) - (heat loss) = storage of heat (Hs)

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9
Q

Storage heat equation

A

Calculating the amount of heat energy which is transferred
H = mc delta T

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10
Q

Specific heat capacity

A

The amount of heat required to raise the temperature of 1kg mass by 1 Kelvin - depends on the composition of the object.

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11
Q

Conduction

A

Heat energy is transferred through a solid, liquid or gas by direct contact

Heat gain or loss is usually by conduction is minimal

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12
Q

Heat transfer is dependent on…

A

Thermal conductivity and the temp difference between the two objects

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13
Q

Convection

A

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

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14
Q

Evaporation

A

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.

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15
Q

Radiation

A

Transfer of thermal energy by means of electromagnetic waves. It does not require a material medium

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16
Q

Modes of thermoregulation

A

Metabolism
Vasomotor regulation (blood flow)
Sweating
Shivering

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17
Q

Thermal regions (core + shell)

A

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

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18
Q

Tcore females

A

Fluctuates with the menstrual cycle
Hormone levels, endometrial thickness and ovulation

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19
Q

Where is heat produced (organs)

A

At rest: Primarily at brain, heart, liver and kidneys

During exercise: primarily skeletal muscles

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20
Q

How is heat lost?

A

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

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21
Q

Insulation of the shell methods

A

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)

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22
Q

Thermoregulatory control feedback system

A

Receptors from the skin and the hypothalamus effects metabolism, vasomotor, sweating and shivering that increases body temperature

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23
Q

Temperature sensors - receptors

A

Warm receptors and cold receptors from these receptors project to the pre-optic hypothalamus

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24
Q

Regulation of heat transfers

A

Peripheral thermoreceptors and core thermoreceptors input signal compared with set point.
Effectors: shivering, vasomotor, sweat which activate/deactivate heat transfer

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25
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
26
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.
27
Heat transfer within the body
Conduction: Slow Advection/convection: fast -> blood flow
28
Heat transfer through vasodilation
To remove heat produced by metabolism, convection is the primary node of heat loss
29
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.
30
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
31
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.
32
Mechanical work
Muscle contraction Movement of cells, organelles, appendages
32
Therapeutic hypothermia
Lowering core temp. can protect the brain from reperfusion. Damage post-stroke or cardiac arrest. Decreased metabolism, ROS, cell death and glutamate
32
List of energy output processes
Mechanical work Synthetic reactions Membrane transport Signal generation and conduction Heat product Detoxification and degradation
33
What are synthetic reactions?
Creation of essential functional molecules
34
Membrane transport
Minerals Organic anions/cations Amino acids
35
How is heat produced?
Temperature regulation Inefficient chemical reactions
36
Detoxification and degradation
Urea formation Conjugation Oxidation Reduction
37
Energy released equation
energy released = mc(delta)T
38
Bomb calorimeters and energy
Overestimate energy available for cellulose
39
Oxidation of glucose
Produces 32ATP
40
Oxidation of Fat (palmitate)
Produces 129 ATP
41
Oxidising fuel
Oxidising different fuels yields similar amounts of energy per unit O2 consumed
42
Glucose metabolism
Glucose is split during glycolysis into 2 pyruvate. This enters TCA cycle, NADH produced, ETC produces ATP
43
Fast-twitch muscle ATP production
30ATP per glucose
44
Exact number of ATP produced by glucose
Initial estimates of 36 or 38 ATP were done at room temperature
45
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.
46
Ammonia toxicity and glutamate dehydrogenase
NH3 + a ketoglutarate -> glutamate + H2O by glutamate dehydrogenase.
47
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.
48
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.
49
Energy efficiency
Efficiency = output / input Output = demand for energy Input = source/supply of energy = power/ VO2
50
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
51
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
52
Chemical work
Molecules can passively transport across a membrane down their concentration gradient (from high to low)
53
Chemical work equation
work = RT lnC1/C2 R is the universal gas constant T is absolute temperature C is concentration
54
Electrical work
Positively charged particles that are free to move will always tend to shift towards the direction of lower voltages
55
Electrical work equatiion
Work elec = zFEm
56
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+)
57
W total equation
RT ln(ci/co) + zFEm
58
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.
59
Work total for SERCA
Wtotal = RT ln (Csr/ccytoplasm) + zFEsr
60
ATP and cross-bridge relation
1 ATP is needed to detach a cross-bridge.
61
First law of thermodynamics
Energy can be transferred and transformed, but it cannot be created or destroyed (energy of the universe is constant)
62
Second law of thermodynamics
Every every transfer or transformation makes the universe more disordered (every process increases the entropy of the universe)
63
Gibbs free energy equation
∆G = ∆H - T∆S Favourable ∆H < 0 ∆S > 0
64
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)
65
Open systems
The entropy of a system may decrease, but the entropy of the system plus its surroundings must always increase
66
Anaerobic reactions
Alactic (doesn't produce lactate): Creatine phosphokinase reaction Adenylate kinase reaction Lactic: Glycolysis and glycogenolysis
67
Aerobic pathway
Oxidative phosphorylation
68
Sprinter uses...
Alactic anaerobic Crp, AMP
69
400m uses
Lactic anaerobic dominates (glycolysis)
70
Marathon runner
Aerobic (oxidation)
71
Creatine phosphokinase reaction
CrP + ADP -> Cr + ATP Catalysed by creatine phosphokinase CrP acts as a buffer to maintain ATP high
72
Creatine phosphokinase reaction kinetics
Extremely rapid Of small extent
73
Creatine phosphate shuttle
Creatine phosphate shuttles chemical energy from mitochondria to various cellular locations of the ATPases to phosphorylate ADP
74
Adenylate Kinase reaction
2ADP -> AMP + ATP catalysed by adenylate kinase last ditch process used only when ATP is v.low
75
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
76
Glycolysis/Glycogenolysis yields from splitting
Glucose yields 2 ATP and glycogen yields 3 ATP
77
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.
78
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
79
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.
80
Lactate production as a function of exercise intensity
Lactate begins to accumulate and rise exponentially at 55% VO2 max for an untrained subject
81
Process of oxidative phosphorylation
Glycogen, fats & proteins can be broken down & enter the CAC or Kreb's cycle slow kinetics enormous extent
82
Citric acid cycle process
Pyruvate enters the mitochondria and is a substrate for the CAC. CAC produces ATP and NADH & FADH2 for the ETC
83
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
84
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
85
Central fatigue
CNS command - reduced excitatory input - Motor neuron signal decreased by altered input from sensory fibres
86
Peripheral fatigue is caused by
Neuro-muscular transmission Muscle fibre action potential Excitation-contraction coupling Depletion of substrates for metabolism Accumulation of waste-products
87
How is fatigue studied?
1. Trained athlete 2. Exercising volunteer subject (sedentary vs active) 3. Experimental animals 4. Isolated whole muscle 5. Isolated single fibre (myocyte) 6. Contractile proteins in a test-tube
88
Tetanus
Prolonged contraction of a muscle caused by rapidly repeated stimuli
89
Force time fatigue graph
Fatigue occurs at the intersection of maximum force and required output
90
Time taken to fatigue factors
Required force Maximum force Intrinsic fatigability
91
Fast-twitch fiber
Easily fatigued Decreased Ca2+ and force over time
92
Soleus fibre
Fatigue resistant Ca2+ and force relatively stable, even after 1000 pulses
93
Fatigue in fast twitch fiber
Type II easily fatigued Predominantly anaerobic metabolism Short bursts of fast contractions (e.g sprinters)
94
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)
95
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
96
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
97
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
98
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
99
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
100
∆G required by ATPases
∆G required by ATPases is positive b/c they gain energy from ATP
101
Changes in ∆GATP for [CrP]
As [CrP] falls, [Pi] rises but [ATP] and [ADP] stay constant
102
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
103
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
104
Effects of aerobic training: Heart
Increased cardiac output, increases O2 delivery to the muscles
105
Effects of aerobic training: Circulation
Increased plasma volume, increases stroke volume and thus cardiac output. Increases skin blood flow to optimise thermoregulation
106
Effects of aerobic training: Blood vessels
Increased capillary proliferation, increases O2 delivery and diffusion into muscles
107
Effects of aerobic training: Myocytes
Increased mitochondria, increases O2 extraction. Enzyme adaptation, optimizes metabolism, increases reliance on fat thus reduced lactate production