ENERGETICS AND METABOLIC RATE
Importance of ATP in metabolism
-large quantity of free energy in its high energy phosphate
bonds (7000cal /mol)
Transfer of energy from diff foodstuff to functional system of the cell
Phosphate bonds – release stored energy
PHOSPHOCREATINE
Storage depot for energy
Buffering the concentration of ATP
Most abundant substance that stores energy
Can’t act as ATP but can transfer energy with ATP
-extra amount of ATP synthesis of phosphocreatine
when ATP is used up energy from phosphocreatine
is transferred back to ATP
- concentration of ATP is maintained at high level-
ATP buffer system
ANEROBIC/AEROBIC ENERGY
Anaerobic – energy derived from foods without the
use of O2
Aerobic –energy derived from foods by oxidative
metabolism
Glycogen storage is the only food for anaerobic
metabolism - glycolysis
What happens to Pyruvate
If oxygen is present it is converted to Acetyl-CoA and enters citric acid cycle
If oxygen is not present is will become lactic acid and /or ethanol
Oxidative Respiration
aerobic metabolism
occurs in mitochondria
conversion of pyruvate to Acetyl-CoA
citric acid cycle
electron transport
Anaerobic Metabolism (fermentation) occurs when oxygen is not available.
ethanol fermentation (Yeast)
Pyruvate is converted to acetaldehyde, by removal of CO2. Which then accepts H from NADH to produce ethyl alcohol.
Lactic Acid Fermentation
takes H from NADH and attaches it to pyruvate to produce lactic acid (Muscles)
Oxidative Respiration
aerobic metabolism
occurs in mitochondria
conversion of pyruvate to Acetyl-CoA
citric acid cycle
electron transport
How Cells Make atp
by
PHOSPHORYLATION... adding a phosphate to ADP
ADP + P ------> ATP
) substrate level phosphorylation...
where a substrate molecule ( X-p ) donates its P to ADP making ATP
b) chemiosmosis - [Oxidative Phosphorylation of Krebs cycle & ETC]...
food substrates donate e- & protons to acceptor molecules [NADH], i.e., oxidation.
NADH gives up electrons & protons are pumped out of mitochondria
protons diffuse back into mito thru an enzyme - ATPase,
the ATPase enzyme makes ADP + P --> ATP
Complex I
NADH dehydrogenase (or)
NADH-coenzyme Q reductase
Complex II
Succinate dehydrogenase (or)
Succinate-coenzyme Q reductase
Complex III
Cytochrome C - coenzyme Q oxidoreductase-
Complex IV
Cytochrome oxidase
Complex VATP synthase
ANAEROBIC ENERGY DURING HYPOXIA
Acute hypoxia – O2 in the lungs/hemoglobin is good only
for 2 mins – glycolysis
Anaerobic energy usage during strenuous bursts of activity
-energy is derived from
1. ATP already present in the muscle cells
2. phosphocreatine in the cells
3. anaerobic energy from glycolysis
4. oxidative energy from oxidative process
Max. amount of ATP in a liter of intracellualr fluid – 5 millimoles - can maintain contraction for a second
Phosphocreatine is 3 to 8 times this amount – can
maintain contraction for few more seconds
Energy from glycolysis can occur rapidly than from oxidative
process
Glycogen content of the muscle during exercise is reduced
while lactic acid increases
After exercise – reconversion of lactic acid to glucose
Oxygen debt – rapid breathing after exercise
Excess O2 is used to
1. reconvert lactic acid to glucose
2. reconvert ATP/ phosphocreatine to normal
3. restablished normal conc of O2 in Hg/ myoglobin
4. O2 in the lungs
SUMMARY OF ENERGY UTILIZATION
glycogen energy for
synthesis and growth
Glucose ATP muscular contraction
glandular secretion
Lactic acid pyruvic acid nerve conduction
active absorption
Acetyl-coA
Deaminated a.a. phosphocreatine
Other substrate AMP
CO2 +H2O creatine+phosphate
CONTROL OF ENERGY RELEASE IN THE CELL
1. rate control of enzyme-catalyzed reaction
2. role of enzyme conc. in the regulation of
metabolic reaction
3.role of substrate concentration
4. rate limitation in a series of reaction
5. ADP conc. as rate controlling factor
THE METABOLIC RATE
Metabolism – all chemical reaction in the body
Heat – end product of energy released in the body
35% of energy in the foods becomes heat during ATP
formation
Only 27% of energy from food is utilized by the cell’s
functional system
But all eventually becomes heat
Calorie – unit for expressing the quantity of energy released
from foods or expended by diff. functional process
in the body
MEASUREMENT OF METABOLIC RATE
1. direct calorimetry
-quantity of heat liberated from the body at any
given time(not doing external work)
- uses calorimeter- insulated air chamber
- heat gain by cool water bath
2. indirect calorimetry- oxygen utilization
3. metabolator –floating drum with O2 chamber to a
mouthpiece thru 2 tubes
\
The Formula
B x 10 x A x C = Your Basic Metabolic Rate
FACTORS AFFECTING METABOLIC RATE
1. exercise – most dramatic effect
- may increased to 2000%
2. energy requirements for daily activity
- avg. 70 kg. man lying in bed -1650cal/day
- process of eating and digesting of food- 200cal
- daily requirement for existing – 2000cal/day
3. effects of diff. types of work
4. specific dynamic action of protein
5. age – rate of cellular reaction
6. sympathetic stimulation- increase cellular activity
increase liver muscle glycogenolysis
-non shivering thermogenesis
7. male sex hormones
8. Growth hormones
9. fever
10. climate
11. sleep – decrease muscle tone – sympathetic stimulation
12. malnutrition
BASAL METABOLIC RATE
Rate of energy utilization in the body during absolute rest
but while a person is awake
Conditions for measuring BMR
1. NPO at least 12 hours
2. after a night of restful sleep
3. no strenuous activity preceding 1 hour
4. psychic and physical factors causing excitement be
eliminated
5. temperature of air must be comfortable
METHODS FOR MEASURING BMR
Expressing BMR in terms of surface area
- percentage above or below normal
Constancy of BMR in same person
- person to person
BODY TEMPERATURE: REGULATION AND FEVER
Normal body temperature
-core temperature – deep tissue of the body
-constant
Skin temperature – rises and falls
Body temperature – balance of heat production
and heat loss
Heat production from :
1. BMR of all cells
2. metabolism cause by muscle activity
3. effect of thyroxin
4. sympathetic stimulation
5. increase in temperature
Heat production – generated in deep organs
liver, brain, heart, skeletal muscle
Heat transferred to the skin
Rate of heat loss
1. rate of conduction from core to skin
2. rate of transfer from skin to surrounding tissue
THE INSULATOR SYSTEM OF THE BODY
Skin, subcutaneous tissue and fat - insulator
Fat conducts heat only one third as readily
Effect of blood flow
-venous plexuses below the skin
-arteriovenous anastomosis
-increase rate of blood flow heat loss
Control of heat conduction to the skin is regulated
by sympathetic nervous system
PHYSICS OF HEAT LOSS FROM SKIN
1. radiation – in the form of infrared heat rays
- 60% of heat loss
2. conduction - to objects to air air convection
3 convection – heat loss thru air currents
- cooling effect of wind
-water adjacent to the skin
4. evaporation – when water evaporates from the
body heat is also loss
- insensible heat loss
SWEATING
Its regulation – anterior hypothalamus pre
optic area
Sweat glands – sympathetic cholinergic fibers –
responsive to epinephrine
MECHANISM OF SWEAT SECRETION
Sweat gland – tubular – 2 parts
1. deep subdermal – coiled portion
2. duct portion
Epithelial lining in coiled portion forms the primary or
precursor secretion ( similar to plasma secretion)
Composition is modified by reabsorption of sodium and
potassium
Depends on sympathetic stimulation
Acclimatization of sweat mechanism
Rarely 700cc/hr if not acclimatized
Progressive sweating occurs when exposure to hot temperature is increased
-Maximum of 2 liters/ hr
Decrease sodium chloride loss - 3 – 5 gms/day – due aldosterone
REGULATION OF BODY TEMPERATURE
Anterior hypothalamus preoptic area
– heat /cold sensitive neurons
When stimulated
– profuse sweating and vasodilation
DETECTION OF TEMPERATURE
Receptors from skin and deep tissues
More cold receptors than warm receptors
When skin is chilled – reflex reaction
1. shivering
2. inhibit sweating
3. vasoconstriction
Both receptors are important in prevention of
hypothermia
ROLE OF HYPOTHALAMUS
Integration of peripheral and central
temperature signals
Responsible for providing either heat producing
or heat conserving reaction
TEMPERATURE DECREASING MECHANISM WHEN BODY IS TOO HOT
1. vasodilatation
2. sweating
3. decrease heat production
1. vasodilatation
2. sweating
3. decrease heat production
1. skin vasoconstriction
2. piloerection
3. increase in heat production
-shivering- primary motor center in hypothalamus
- sympathetic excitation of heat production
chemical thermogenesis – uncoupled oxidation
-thyroxine secretion- release of thyrotropin-
releasing hormone—throid stimulating hormone
thyroxin chemical thermogenesis
SET POINT FOR TEMPERATURE CONTROL
Critical core body temperature --- 37.1 degree centigrade
Above or below this temperature –
- change in the rate of heat loss or heat production
by temperature regulating mechanism of the body
Heat temperature receptors in the ant hypothalamic-preop-
-tic area
Can be altered by temperature signals from the peripheral
areas of the body
ABNORMALITIES OF BODY TEMPERATURE REGULATION
Fever – body temperature above normal
- causes: 1. bacterial diseases
2. brain tumors
3. environmental conditions
Resetting of the hypothalamic temperature regulating center
in febrile conditions
Illness- effects of pyrogens(Proteins, breakdown products of
proteins,lipopolysacharride,toxins)
- cause set point to increase
- activates mechanism for increasing body temperature
MECHANISM OF ACTION OF PYROGENS IN CAUSING FEVER
Directly acting on hypothalamic regulating center
Indirect action – bacterial pyrogens(endotoxin)
bacterial phagocytosis by blood cells digestion
release of interleukin1 hypothalamus
One 10,000,000th of a gram
Formation of prostaglandin acts on hypothalamus
fever
Aspirin – blocks formation of prostaglandin
CHARACTERISTICS OF FEVER
Change of set point to higher level
-since blood temperature is lower
- body respond to increase temperature
- chills, cold vasoconstriction
- equalized hypothalamic setting
Crisis or flush
--removal of factor causing fever
--set point returns to normal
--body temperature still high
--heating of hypothalamus from peripheral recptors
--activates temperature regulating mechanism
--sweating
--vasodilatation
The danger of dehydration and heat stroke
can be life-threatening if left untreated.
What is heat stroke?
What is heat stroke?
It is the result of long, extreme exposure to the sun, in which a person does not sweat enough to lower body temperature.
The elderly, infants, persons who work outdoors and those on certain types of medications are most susceptible to heat stroke.
It is a condition that develops rapidly and requires immediate medical treatment.
Limits of heat one can withstand – dry/wet
Limitation of losing heat by heat regulating capacity
Thalamus is also depressed
Body temperature of 106-108OF heat stroke
symptoms -dizziness, abdominal distress, delirium
-loss of consciousness, circulatory shock
Hyperpyrexia – brain damaging
Could be fatal
prevention – ice-water bath – uncontrollable
shivering
- sponge or spray cooling
Harmful effects of high temperature
-local hemorrhages
-parenchymatous degeneration of cells
ACCLIMATIZATION TO HEAT
Increase maximum rate of sweating
Increase plasma volume
Decrease salt loss in sweat and urine
-due to aldosterone
EXPOSURE OF BODY TO EXTREME COLD
30 mins. exposure to ice water
-heart stand-still or fibrillation
Loss of temperature regulation at low temperature
Loss of chemical heat production in the cell
Sleepiness/coma
-depress cns heat control mechanism
-prevents shivering
Hypothermia is defined as a core temperature of less than 35 degrees Celcius.
the clinical state of sub-normal temperature when the body is unable to generate sufficient heat to efficiently maintain functions.
The healthy individual's compensatory responses to heat loss via conduction, convection, radiation, evaporation and respiration may be overwhelmed by exposure.
Once hypothermia develops, the heat deficit is shared by two body compartments, the shell and the core.
Medications may interfere with thermoregulation. Acute or chronic central nervous system processes may decrease the efficiency of thermoregulation
Hypothermia
Warnings signs of Hypothermia are uncontrollable shivering
memory loss
disorientation
incoherence
slurred speech
drowsiness
and apparent exhaustion.
Patients cold, stiff and cyanotic, with fixed pupils and no audible heart tones or visible thoracic excursions have been successfully resuscitated.
The only certain criterion for death in hypothermia is irreversibility of cardiac arrest when the patient is warm.
Conclusions regarding the potential reversibility of coexisting conditions should be withheld until the patient is rewarmed.
Resuscitation, including CPR if necessary, should be continued until either failure after hospital rewarming to 35 degrees Celcius or danger through exposure to rescuers exists.
If medical care is unavailable
start warming the body slowly
warm the body core first
use your own body heat to help
get the victim into dry clothing
and wrap them in a warm blanket covering the head and neck.
Frost bite
-freezing of surface area of the body
-ears, digits of hand/feet
-gangrene
Protection against frost bite – vasodilatation
Artificial hypothermia
-sedation
-depress cns temperature regulating mech.
- ice, cooling blankets
- alcohol
ARTIFICIAL HYPOTHERMIA
Strong sedative-depressing the reactivity of hypothalamic temperature controller
Cooling with ice
Used in heart surgery
Organ transport
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