BIOLOGY, TOPIC SEVEN,7. Flashcards
1
Q
HOW MANY DIFFERENT TYPES OF MUSCLE FIBRES ARE IN FACT FOUND IN MUSCLES?
A
THERE ARE IN FACT TWO,2, DIFFERENT TYPES OF MUSCLE FIBRES FOUND IN MUSCLES. THEESE INCLUDE BOTH FAST TWITH FIBRES, AND SLOW TWITCH FIBRES.
2
Q
WHAT ARE HUMAN MUSCLES MADE UP OF?
A
HUMAN MUSCLES ARE IN FACT MADE UP OF BOTH TYPES OF MUSCLE FIBRES. SOME MUSCLES DO IN FACT HAVE HIGHER PROPORTIONS OF A PARTICULAR FIBRE TYPE DUE TO THEIR DIFFERENT PROPERTIES.
3
Q
FAST TWITCH MUSCLE FIBRES, CONTRACTION.
A
FAST TWITCH MUSCLE FIBRES DO IN FACT CONTRACT RAPIDLY.
THE MYOSIN HEADS BIND AND UNBIND FROM THE ACTIN-BINDING SITES, FIVE,5, TIMES FASTER THAN SLOW TWITCH MUSCLE FIBRES.
THEIR RAPID CONTRACTION-RELAXATION CYCLE MEANS THAT THEY DO IN FACT NEED LARGE AMOUNTS OF CALCIUM IONS PRESENT TO STIMULATE CONTRACTION.
4
Q
FAST TWITCH MUSCLE FIBRES, ENERGY.
A
FAST TWITCH MUSCLE FIBRES DO IN FACT RELY ON ANAEROBIC RESPIRATION FOR ATP SUPPLY.
THEY ARE SUITED TO SHORT-BURSTS OF HIGH-INTESITY ACTIVITY AS THEY FATIGUE QUICKLY DUE TO THE LACTATE THEY PRODUCED FROM THE ANEAROBIC RESPIRATION.
5
Q
FAST TWITCH MUSCLE FIBRES, LOCATION.
A
FAST TWITCH MUSCLE FIBRES ARE IN FACT OFTEN FOUND IN HIGH PROPORTIONS IN THE LIMBS OF ANIMALS THAT FLEE A PREDATOR OR HUNT PREY AT HIGH SPEEDS.
FOR EXAMPLE, THE WINGS OF A ROBIN AND THE LEGS OF A CHEETAH.
6
Q
FAST TWITCH MUSCLES, THE EYE LIDS.
A
THERE ARE IN FACT A HIGH PROPORTION OF FAST TWITCH MUSCLES IN THE HUMAN EYE-LIDS.
THEY CONTRACT IN SHORT BURSTS AND DO IN FACT NOT NEED TO SUSTAIN THE RAPID MOVEMENT.
7
Q
FAST TWITCH MUSCLE FIBRES, BLOOD.
A
FAST TWITH MUSCLES DO IN FACT HAVE FEW CAPILLARIES.
BLOOD CONTAINING BOTH GLUCOSE, C6H12O6, AND OXYGEN, O2, DOES IN FACT FLOW THROUGH THE CAPILLARIES.
THIS MEANS THAT THEY DO IN FACT HAVE QUITE A SLOW SUPPLY OF OXYGEN, O2, AND GLUCOSE, C6H12O6, FOR AEROBIC RESPIRATION.
8
Q
MYOGLOBIN, FAST TWITCH MUSCLE FIBRE.
A
LOW AMOUNTS OF MYOGLOBIN ARE IN FACT PRESENT IN FAST TWITCH MUSCLE FIBRES.
MYOGLOBIN IS A RED PIGMENT MOLECULE THAT IS IN FACT SIMILAR TO HAEMOGLOBIN.
MYOGLOBIN DOES IN FACT FUNCTION AS A STORE OF OXYGEN, O2, IN MUSCLES AND DOES IN FACT INCREASE THE RATE OF OXYGEN, O2, ABSORPTION FROM THE CAPILLARIES.
DUE TO THIS FAST TWITCH MUSCLE FIBRES DO IN FACT APPEAR PALER IN COLOUR THAN SLOW MUSCLE FIBRES.
9
Q
SLOW TWITCH MUSCLE FIBRES, CONTRACTION.
A
SLOW TWITCH MUSCLE FIBRES DO IN FACT CONTRACT MORE SLOWLY, THAN FAST TWITCH MUSCLE FIBRES, AND ARE IN FACT SUITED TO SUSTAINED ACTIVITIES, LIKE WALKING AND PERCHING.
10
Q
SLOW TWITCH MUSCLE FIBRES, ENERGY.
A
SLOW TWITCH MUSCLE FIBRES DO IN FACT RELY ON AEROBIC RESPIRATION, FOR ATP.
THEY DO IN FACT FATIGUE LESS QUICKLY, DUE TO LESS LACTATE PRODUCTION, THUS IN TURN MAKING THEM IDEAL FOR ENDURANCE.
11
Q
SLOW TWITCH MUSCLE FIBRES, LOCATION.
A
SLOW TWITCH MUSCLE FIBRES, ARE IN FACT OFTEN FOUND IN HIGH PROPORTIONS IN THE LIMBS OF ANIMALS THAT MIGRATE OR STALK PREY OVER LONG DISTANCES.
FOR EXAMPLE, THE WINGS OF GEESE AND THE LEGS OF WOLVES.
12
Q
HUMAN BACK MUSCLES.
A
HUMAN BACK MUSCLES DO IN FACT HAVE A HIGH PROPORTION OF SLOW TWITCH MUSCLE FIBRES.
THESE MUSCLES DO IN FACT HAVE TO CONTRACT FOR LONG PERIODS OF TIME IN ORDER TO KEEP THE SKELETON ERECT WHEN STANDING OR SITTING.
13
Q
SLOW TWITCH MUSCLE FIBRES, BLOOD.
A
SLOW TWITCH MUSCLE FIBRES, DO IN FACT HAVE A DENSER NETWORK OF CAPILLARIES.
BLOOD CONTAINING BOTH GLUCOSE, C6H12O6, AND OXYGEN, O2, DO IN FACT FLOW THROUGH THE CAPILLARIES.
THIS MEANS THAT THEY DO IN FACT HAVE A SHORT DIFFUSION DISTANCE AND A GOOD SUPLY OF GLUCOSE, C6H12O6, AND OXYGEN, O2, FOR AEROBIC RESPIRATION.
14
Q
MYOGLOBIN, SLOW TWITCH MUSCLE FIBRES.
A
HIGH AMOUNTS OF MYOGLOBIN, HAEMOGLOBIN AND MITOCHONDRIA ARE IN FACT PRESENT IN SLOW TWITCH MUSCLE FIBRES.
THIS DOES IN FACT INCREASE THE RATE OF OXYGEN, O2, SUPPLY, OXYGEN, O2, ABSORPTION, AND AEROBIC RESPIRATION.
DUE TO THE HIGH AMOUNTS OF RED PIGMENT, SLOW TWITCH MUSCLE FIBRES DO IN FACT APPEAR A DARK RED.
15
Q
THICK FILAMENTS, COMPOSITION.
A
THE THICK FILAMENTS WITHIN A MYOFIBRIL ARE IN FACT MADE UP OF MYOSIN MOLECULES.
16
Q
MYOSIN MOLECULES
A
THEESE ARE IN FACT FIBROUS PROTIEN MOLECULES, WITH A GLOBULAR HEAD.
THE FIBROUS PART OF THE MYOSIN MOLECULE ANCHORS THE MOLECULE INTO THE THICK FILAMENT.
IN THE THICK FILAMENT, MANY MYOSIN MOLECULES LIE NEXT TO EACH OTHER WITH THEIR GLOBULAR HEADS ALL POINTING AWAY FROM THE M-LINE.
17
Q
THIN FILAMENT, COMPOSITION.
A
THE THIN FILAMENTS WITHIN A MYOFIBRIL ARE IN FACT MADE UP OF ACTIN MOLECULES.
18
Q
ACTIN MOLECULES.
A
THEESE ARE IN FACT GLOBULAR PROTIEN MOLECULES.
MANY ACTIN MOLECULES DO IN FACT LINK TOGETHER TO FORM A CHAIN.
TWO,2, ACTIN CHAINS TWIST TOGETHER TO FORM ONE THIN FILAMENT.
A FIBROUS PROTIEN, KNOWN AS TROPOMYOSIN IS TWSITED AROUND THE TWO,2, ACTIN CHAINS.
ANOTHER PROTIEN KNOWN AS TROPONIN IS ATTACHED TO THE ACTIN CHAINS AT REQULAR INTERVALS.
19
Q
HOW MUSCLES CONTRACT, THE SLIDING FILAMENT THEORY, INTRODUCTION.
A
MUSCLES DO IN FACT CAUSE MOVEMENT BY CONTRACTING.
DURING MUSCLE CONTRACTION, SARCOMERS WITHIN MYOFIBRILS SHORTEN AS THE Z-DISCS ARE PULLED CLOSER TOGETHER.
IT IS NOT THE MYOFILAMENTS THAT CONTRACT AS THE MYOSIN AS THE MYOSIN AND THE ACTIN MOLECULES REMAIN THE SAME LENGTH.
MYOSIN AND ACTIN FILAMENTS SLIDE OVER ONE ANOTHER.
THIS IS KNOWN AS THE SLIDING FILAMENT THEORY OF MUSCLE.
20
Q
EXPLINATION.
A
CONTRACTION OCCURS DUE THE FOLLOWING PROCESS.
AN ACTION POTENTIAL ARRIVES AT THE NEUROMUSCULAR JUNCTION.
CALCIUM IONS ARE RELEASED FROM THE SARCOPLASMIC RETICULUM, SR.
CALCIUM IONS BIND TO TROPONIN AND TROPOMYOSIN PROTIENS, TO CHNAGE POSITION ON THE ACTIN, THIN, FILAMENTS.
MYOSIN BINDING SITES ARE EXPOSED ON THE ACTIN MOLECULES.
THE GLOBULAR HEADS OF THE MYOSIN MOLECULES BIND WITH THESE SITES, FORMING CROSS-BRIDGES, BETWEEN THE TWO,2, TYPES OF FILAMENTS.
THE FOMRATION OF THE CROSS-BRODGES CAUSES THE MYOSIN HEADS TO SPONTANEOUSLY BEND, RELEASING ADP AND INORGANI PHOSPHATE.
THIS ALSO PULLS THE ACTIN MOLECULES TOWARDS THE CENTRE OF THE SARCOMERE ABD CAUSING THE MUSCLE TO CONTRACT A VERY SMALL DISTANCE.
ATP binds to the myosin heads producing a change in shape that causes the myosin heads to release from the actin filaments.
The enzyme ATPase hydrolyses ATP into ADP and inorganic phosphate which causes the myosin heads to move back to their original positions, this is known as the recovery stroke.
The myosin heads are then able to bind to new binding sites on the actin filaments, closer to the Z disc.
The myosin heads move again, pulling the actin filaments even closer the centre of the sarcomere, causing the sarcomere to shorten once more and pulling the Z discs closer together.
ATP binds to the myosin heads once more in order for them to detach again.
As long as troponin and tropomyosin are not blocking the myosin-binding sites and the muscle has a supply of ATP, this process repeats until the muscle is fully contracted.
21
Q
NEUROMUSCULAR JUNCTION.
A
THE NEUROMUSCULAR JUNCTION, IS IN FACT A SPECIALISED SYNAPSE BETWEEN A MOTOR NEURON NERVE TERMINAL AND ITS MUSCULAR FIBRE.
22
Q
HOMEOSTATSIS.
A
IN ORDER TO FUNTION PROPERLY AND EFFICENTLY ORGANSISMS HAVE DIFFERENT CONTROL SYSTEMS THAT ENSURE THEIR INTERNAL CONDITIONS ARE KEPT RELATIVELY CONSTANT.
23
Q
PHYSIOLOGICAL CONTROL SYSTEMS.
A
PHYSIOLOGICAL CONTROL SYSTEMS DO IN FACT MAINTAIN THE INTERNAL ENVIRONMENT WITHIN RESTRICTED LIMITS THROUGH A PROCESS CALLED HOMEOSTASIS.
24
Q
THE STATE OF DYNAMIC EQUILIBRIUM.
A
THE PROCESS OF HOMEOSTASIS DOES IN FACT KEEP THE INTERNAL ENVIRONMENT FLUCTUATING AROUND A SPECIFIC NORMAL LEVEL.
THIS IS IN FACT KNOWN AS A STATE OF DYNAMIC EQUILIBRIUM.
25
SENSORY CELLS.
SENSORY CELLS, KNOWN AS RECEPTORS, CAN IN FACT DETECT INFORMATION ABOUT THE CONDITIONS INSIDE AND OUTSIDE OF THE BODY.
26
HOMEOSTATSIS, TEMPERATURE.
HOMEOSTATSIS, IS IN FACT CRITICALLY IMPORTANT FOR ORGANISMS AS IT ENSURES THE MAINTENANCE OF OPTIMAL CONDITIONS FOR ENZYME ACTION AND CELL FUNCTION.
27
TEMPERATURE, ENZYMES.
AN INCREASE IN BODY TEMPERATURE ABOVE 40 DEGREES CELCIUS, WOULD IN FACT CAUSE ENZYMES TO DENATURE.
THIS IS IN FACT DUE TO AN INCEASE IN KINETIC ENERGY, WHICH WOULD RESULT IN THE BREAKAGE OF HYDROGE, H, BONDS, HOLDING THE ENZYME IN A SPECIFIC 3D SHAPE.
THE ACTIVE SITE WILL IN FACT CHANGE SHAPE AND WILL NO LONGER BE COMPLIMENTARY TO THE SUBSTRATE MOLECULE.
AN EZYME-SUBSTRATE COMPLEX CAN IN FACT NOT FORM AND THE ENZYME CANNOT CATALYSE THAT REACTION ANYMORE, LEADING TO LESS EFFICENT METABOLIC REACTIONS.
28
BLOOD GLUCOSE.
CELLS DO IN FACT NEED A CONSTANT SUPPLY OF ENERGY IN THE FORM OF ATP, TO WORK EFFICENTLY.
GLUCOSE IS RESPIRED TO IN FACT SUPPLY THIS ATP, MEANING THAT THE BODY NEEDS TO CARFEULY MONITOR BLOOD GLUCOSE CONCENTRATIONS.
CELLS IN THE PANCREASE, MONITOR BLOOD GLUCOSE CONCENTRATIONS.
29
WATER.
WATER, H2O, IS IN FACT ANOTHER ESSENTIAL REQUIREMENT FOR CELLS TO FUNCTION OPTIMALLY, ITS MAKE UP THE CELL CYTOPLASM AND IT DOES IN FACT TAKE PART IN METABOLIC REACTIONS.
IT IS THEREFORE CRUCIAL FOR THE AMOUTN OF WATER, H2O, IN THE BLOOD TO REMAIN CONSTANT.
WATER, H2O, IS LOST DURING EXCRETION OF WASTE PRODUCTS, SUCH AS URINE, AND IN SWEAT.
THE KIDNEYS ARE IN FACT RESPONSIBLE FOR REGULATING THE AMOUNT OF WATER, H2O, IN THE BLOOD.
30
CONTROL MECHANISMS FOR MAINTANINING THE BODY TEMPERATURE.
THE MAINTENANCE OF A CONSTANT INTERNAL BODY TEMPERATURE, IS IN FACT KNOWN AS THERMOREGULATION.
THIS PROCESS INVOLVES BOTH COOLING AND WARMING MECHANISMS DEPENDING ON WHETHER THERE IS IN FACT AN INCREASE OR DECREASE IN BODY TEMPERATURE.
31
COOLING MECHANISMS, VASODILATION.
VASODILATION OF THE BLOOD VESSELS THAT SUPPLY SKIN CAPILLARIES.
HEAT EXCHANGE DURING BOTH WARMING AND COOLING OCCURS AT THE BODY'S SURFACE AS THIS IS WHERE THE BLOOD COMES INTO CLOSE PROXIMITY WITH THE ENVIRONMENT.
THE WARMER THE ENVIRONMENT, THE LESS HEAT IS IN FACT LOST FROM THE BODY'S SURFACE.
ONE WAY TO INCREASE THE HEAT LOSS, IS IN FACT TO SUPLY THE CAPILLARIES IN THE SKIN WITH A GREATER VOLUME OF BLOOD, WHICH THEN LOSES HEAT TO THE ENVIRONMENT VIA RADIATION.
ARTERIOLES DO IN FACT HAVE MUSCLES IN THEIR WALLS, THAT CAN RELAX OR CONTRACT, TO ALLOW MORE OR LESS BLOOD TO FLOW THROUGH THEM.
DURING VASODILATION, THESE MUSCLES DO IN FACT RELAX, CAUSING THE ARTERIOLES NEAR THE SKIN TO DILATE AND ALLOWING MORE BLOOD TO FLOW THROUGH SKIN CAPILLARIES.
THIS IS IN FACT WHY PALE-SKINNED PEOPLE GO RED WHEN THEY ARE HOT.
32
SWEATING.
SWEAT IS IN FACT SECRETED BY SWEAT GLANDS.
THIS DOES IN FACT SERVE TO COOL THE SKIN BY EVAPORATION, HEAT ENERGY FROM THE BODY CONVERTS LIQUID WATER, INTO VAPOUR.
SWEATING IS IN FACT LESS EFFECTIVE AS A COOLING MECHANISM IN HUMID ENVIRONMENTS; SWEAT DOES IN FACT EVAPORATE MORE SLOWLY DUE TO THE REDUCED CONCENTRATION GRADIENT BETWEEN THE SWEAT, AND THE SURROUNDING AIR.
33
FLATTENING OF HAIRS.
THE HAIR ERECTOR PILI MUSCLES IN THE SKIN DO IN FACT RELAX, CAUSING HAIRS TO LIE FLAT.
THESE MUSCLES CAN IN FACT BE DESCRIBED AS EFFECTORS, AS THEY RESPOND TO A CHANGE IN BODY TEMPERATURE.
THIS DOES IN FACT STOP THEM FROM FORMING AN INSULATING LAYER OF TRAPPED AIR AND ALLOW AIR TO CIRCULATE OVER SKIN; HEAT CAN THEREFORE LEAVE BY RADIATION.
34
VASOCONSTRICTION.
VASOCONSTRICTION OF BLOOD VESSELS THAT SUPPLY SKIN CAPILLARIES.
ONE WAY TO DECREASE HEAT LOSS, IS IN FACT TO SUPPLY THE CAPILLARIES IN THE SKIN WITH A SMALLER VOLUME OF BLOOD, MINIMISING THE LOSS OF HEAT TO THE ENVIRONMENT BY RADIATION.
DURING VASOCONSTRICTION, THE MUSCELS IN THE ARTERIOLE WALL DO IN FACT CONTRACT, CAUSING THE MUSCLES IN THE ARTERIOLE WALLS TO CONTEACT, CAUSING ARTERIOLES NEAR THE SKIN TO CONSTRICT, AND ALLOING LESS BLOOD TO FLOW THROUGH SKIN CAPILLARIES.
INSTEAD, THE BLOOD IS IN FACT DIRECTED THROUGH SHUNT VESSELS, WHICH ARE DEEPER IN THE SKIN, AND THEREFORE DO NOT LOSE HEAT TO THE ENVIRONMENT.
DOES NOT WARM THE BODY, BUT IT DOES IN FACT REDUCE HEAT LOSS FROM THE BLOOD, AS IT FLOW THROUGH THE SKIN.
35
BOOSTING METABOLIC RATE.
MOST OF THE METABOLIC REACTIONS IN THE BODY ARE IN FACT EXOTHERMIC, AND THIS PROVIDES WARMTH TO THE BODY.
IN COLD ENVIRONMENTS, THE HORMONE THYROXINE, RELEASED FROM THE THYROID GLAND, DO IN FACT INCREASE THE BASAL METABOLIC RATE, BMR, INCREASING HEAT PRODUCTION, IN THE BODY.
ADRENALINE, MAY IN FACT ALSO BE RELEASED, TO SPEED UP THE METABOLIC RATE AND RELEASE MORE HEAT.
36
SHIVERING.
SHIVERING IS IN FACT A REFLEX ACTION, IN RESPONSE TO THE CORE BODY TEMPERATURE.=
THIS DOES IN FACT MEAN THAT IT IS A NERVOUS MECHANISM, NOT A HORMONAL ONE.
IN THIS CASE THE MUSCLES ARE IN FACT EFFECTORS, AND THEY CONTRACT IN A RAPID AND REGULAR MANNER.
THE METABOLIC REACTIONS REQUIRED TO POWER THIS SHIVERING, DO IN FACT GENERATE SUFFICENT HEAT TO WARM THE BLOOD, AND RAISE THE CORE BODY TEMPERATURE.
37
ERECTION OF HAIRS.
THE ERECTOR PILI MUSCLES, IN THE SKIN, DO IN FACT CONTRACT, CAUSING THE HAIR TO STAND ON END.
THIS DOES IN FACT FORM AN INSULATING LAYER OVER THE SKINS SURFACE, BY TRAPPING AIR BETWEEN THE HAIRS, AND STOPS HEAT FROM BEING LOST BY RADIATION.
A HEAT RETENTION MECHANISM, RATHER THAN A HEAT WARMING MECHANISM.
38
LESS SWEATING.
THE SWEAT GLANDS, WILL IN FACT SECREATE LESS SWEAT WHEN IT IS COLD.
THIS WILL IN FACT REDUCE, THE AMOUNT OF HEAT LOST THROUGH THE EVAPORATION OF SWEAT.
A HEAT RETENTION MECHANISM, RATHER THAN A HEAT WARMING MECHANISM.
39
THE HYPOTHALAMUS.
THE HYPOTHALAMUS, IS IN FACT AN AREA OF THE BRAIN THAT IS RESPONSIBLE FOR CONTROLLING MANY FUNCTIONS IN THE BODY, INCLUDING:
HORMONES,
SLEEP,
GROWTH,
BODY TEMPERATURE,
AND
BLOOD PRESSURE.
40
THERMORECEPTORS.
MAMMALS CAN IN FACT DETECT EXTERNAL TEMPERATURES VIA THERMORECEPTORS, WHICH ARE IN FACT FOUND IN THE SKIN AND MUCOUS MEMEBRANES.
41
TEMPERATURE RECEPTORS.
THERE ARE IN FACT RECEPTORS FOR BOTH HEAT AND COLD.
THESE COMMUNICATE WITH THE HYPOTHALAMUS ALONG SENSORY NEURONS.
THE HYPOTHALAMUS WILL IN FACT SEND IMPULSES ALONG MOTOR NEURONS TO EFFECTORS, TO BRING ABOUT A PHYSIOLOGICAL RESPONSE, TO CHANGING EXTERNAL TEMPERATURES.
42
HYPOTHALAMUS, THE BLOOD.
THE HYPOTHALAMUS, DOES IN FACT ALSO HELP TO REGULATE BODY TEMPERATURE, BY MONITORING THE TEMPERATURE OF THE BLOOD, FLOWING THROUGH IT, AND INITIATING HOMEOSTATIC RESPONSES, WHEN IT GOES TOO HIGH OR TOO LOW.
43
CONTRACT V.S CONSTRICT.
MUSCLES CONTRACT.
ARTERIOLES CONSTRICT.
44
MAINTAINING HOMEOSTATIC BALANCE.
ACHIEVING THIS.
THE MAJORITY OF HOMEOSTATIC CONTROL MECHANISMS IN ORGANISMS, DO IN FACT USE NEGATIVE FEEDBACK, TO MAINTAIN HOMEOSTATIC BALANCE.
FOR EXAMPLE, TO KEEP CERTAIN PHYSIOLOGICAL FACTORS, SUCH AS INTERNAL TEMPERATURES OR BLOOD GLUCOSE CONCENTRATION, WITHIN CERTAIN LIMITS.
45
NEGTIVE FEEDBACK LOOPS, ACTION.
NEGATIVE FEEDBACK LOOPS, DO IN FACT INVOLE:
A RECEPTOR DETECTS A STIMULUS, THAT IS INVOLVED IN A PHYSIOLOGICAL FACTOR.
SUCH AS A CHANGE IN TEMPERATURE, OR BLOOD GLUCOSE LEVEL.
A COORDINATION SYSTEM TRANSFERS INFORMATION BETWEEN DIFFERENT PARTS OF THE BODY,
THIS COULD BE THE NERVOUS SYSTEM OR THE HORMONAL SYSTEM.
AN EFFECTOR CARRIES OUT A RESPONSE.
EFFECTORS ARE MUSCLES OR GLANDS.
46
EFFECTORS.
EFFECTORS, ARE IN FACT MUSCLES OR GLANDS.
47
NEGATIVE FEEDBACK LOOP, OUTCOME.
THE OUTCOME OF A NEGATIVE FEEDBACK LOOOP IS:
IF THERE IS IN FACT AN INCREASE IN THE FACTOR, THE BODY RESPONDS TO MAKE THE FACTOR DECREASE.
IF THERE IS IN FACT A DECREASE IN THE FACTOR, THE BODY RESPONDS TO MAKE THE FACTOR INCREASE.
48
NEGATIVE FEEDBACK SYSTEMS, HOW DO THEY IN FACT WORK?
NEGATIVE FEEDBACK SYSTEMS DO IN FACT WORK BY, REVERSING A CHANGE IN THE BODY, TO BRING IT BACK WITHIN ITS NORMAL LIMITS.
IF THE BODY TEMPERATURE RISES, A NEGATIVE FEEDBACK SYSTEM WILL IN FACT ACT TO LOWER BODY TEMPERATURE, BRINGING IT BACK TO NORMAL.
IF BLOOD GLUCOSE LEVEL DROP, A NEGATIVE FEEDBACK SYSTEM WILL IN FACT ACT TO RAISE BLOOD GLUCOSE, BRINGING IT BACK TO NORMAL.
49
THE CONTROL OF NEGATIVE FEEDBACK, RECEPTORS.
RECEPTORS DO IN FACT DETECT ANY DEVIATIONS IN A FACTOR FROM THE NORMAL RANGE, THIS RESULTS IN A CORRECTIVE MECHANISM TO RETURN THE FACTOR BACK TO ITS NORMAL RANGE.
50
NEGATIVE FEEDBACK LOOP, THE CORRECTIVE MECHANISMS?
IN NEGATIVE FEEDBACK LOOPS, THERE ARE IN FACT USUALLY TWO,2, CORRECTIVE MECHANISMS:
ONE FOR THE FACTOR BECOMES TOO LOW,
AND ONE FOR WHEN THE FACTOR BECOMES TOO HIGH.
51
CORRECTIVE MECHANISMS, THE SYSTEMS INVOLVED.
THE CORRECTIVE MECHANISMS MAY IN FACT INVOLVE THE NERVOUS SYSTEM OR THE ENDOCRINE SYSTEM.
52
POSITIVE FEEDBACK.
IN POSITIVE FEEDBACK LOOPS THE ORIGINAL STIMULUS PRODUCES A RESPONSE THAT CAUSES THE FACTOR TO DEVUATE EVEN MORE FROM THE NORMAL RANGE.
THEY DO IN FACT ENHANCE THE EFFECT OF THE ORIGINAL STIMULUS.
53
POSITIVE FEEDBACK LOOPS, USEFUL FOR.
POSITIVE FEEDBACK LOOPS ARE IN FACT USEFUL TO QUICKLY ACTIVATE A PROCESS.
POSITIVE FEEDBACK LOOPS, MAY IN FACT ALSO KICK IN WHEN HOMEOSTATIC MECHANISMS BREAK DOWN.
54
HORMONES, AFFECT.
HORMONES, CAN IN FACT ALTER THE EVENTS INSIDE A CELL, BY INFLUENCING GENE EXPRESSION.
55
EUKARYOTES, TRANSCRIPTION FACTORS.
EUKARYOTES DO IN FACT USE TRANSCRIPTION FACTORS TO CONTROL GENE EXPRESSION.
56
HORMONES, ENTERING A CELL.
HORMONES THAT CAN IN FACT CROSS THE CELL SURFACE MEMBRANE, SUCH AS STERIOD HORMONES AND THYROID HORMONES, ARE ABLE TO ENTER THE NUCLEUS AND BIND TO TRANSCRIPTION FACTORS, THAT ARE PRESENT THERE.
57
STERIOD HORMONES.
STERIOD HORMONES, ARE IN FACT LIPID SOLUBLE, ALLOWING THEM TO PASS BETWEEN THE PHOSPHOLIPIDS OF THE CELL SURFACE MEMBRANE.
58
AFFECT OF HORMONES, FROM OUTSIDE CELLS.
HORMONES THAT CAN IN FACT NOT CROSS THE CELL MEMBRANE, SUCH AS PROTIEN AND PEPTIDE HORMONES, BIND TO RECEPTORS IN THE CELL SURFACE MEMBRANE.
SCUH AS:
ADRENALINE,
INSULIN,
GLUCAGON,
AND
ADH.
59
WHAT HAPPENS WHEN HORMONES, DO IN FACT BIND TO CELL SURFACE MEMBRANE RECEPTORS?
THE BINDING OF THEESE HORMONES TO CELL SURFACE MEMBRANE RECEPTORS, DOES IN FACT INITIATE A PROCESS THAT ACTIVATES MESSENGER MOLECULES IN THE CYTOPLASM OF THE CELL, KNOWN AS SECOND MESSENGERS.
THE ACTIVATED SECOND MESSENGERS MOLECULES ACTIVATE ENZYMES CALLED PROTIEN KINASES.
ACTIVE PROTIEN KINASE ENZYMES, DO IN FACT TRIGGER A CHAIN OF REACTIONS, KNOWN AS A CASCADE, INSIDE THE CELL.
THE CASCADE, MAY IN FACT RESULT IN CHANGES TO THE ACTIVITY OF TRANSCRIPTION FACTORS, WHICH MAY THEN EFFECT GENE EXPRESSION IN THE CELL.
60
CONTROL OF THE BASIC HEARTBEAT.
CONTROL OF THE BASIC HEARTBEAT, IS IN FACT MYOGENIC, WHICH MEASN THE HEART WILL IN FACT BEAT WITHOUT ANY EXTERNAL STIMULUS.
61
THE INTRINSIC RHYTHM.
THE INTRINSIC RHYTHM, DOES IN FACT MEAN THAT THE HEART BEATS AROUND SIXTY, 60, TIMES PER MINUTE.
62
THE SINOATRIAL NODE, SAN.
THE SINOATRIAL NODE, SAN, IS IN FACT A GROUP OF CELLS IN THE WALL OF THE RIGHT ATRIUM.
THE SAN, INITIATES A WAVE OF DEPOLARISATION, THAT CAUSES THE ATRIA TO CONTRACT.
63
DEPOLARISATION.
DEPOLARISATION, IS IN FACT WHEN THE CHARGE ACROSS THE MEMBRANE IS REVERSED.
64
THE SPREAD OF DEPOLARISATION.
THERE IS IN FACT A REGION OF NON-CONDUCTING TISSUE, WHICH PREVENTS THE DEPOLARISATION, SPREADING STRAIGHT TO THE VENTRICLES.
INSTEAD, THE DEPOLARISATIOSN IS CARRIES TO THE ATRIOVENTRICULAR NODE, AVN.
THIS IS IN FACT A REGION, OF CONDUCTING TISSUE BETWEEN ATRIA AND VENTRICLES.
AFTER A SLIGHT DELAY, THE AVN IS STIMULATED AND PASSES THE STIMUALTION ALONG THE BUNDLE OF His.
THIS DELAY MEANS THAT THE VENTRICLES CONTRACT AFTER THE ATRIA.
THE BUNDLE OF His, IS IN FACT A COLLECTION OF CONDUCTING TISSUE ON THE SEPTUM, THE MIDDLE, OF THE HEART.
THE BUNDLE, OF His, DOES IN FACT DIVIDE INTO TWO,2, CONDUCTING FIBRES, CALLED THE PURKYNE TISSUE, AND CARRIES THE WAVE OF EXCITATION ALONG THEM.
PURKYNE FIBRES SPREAD ALONG THE VENTRICLES AND INITIATE THE DEPOLARISATION OF THE VENTRICLES FROM APEX, BOTTOM, OF THE HEART.
THIS DOES IN FACT MAKE THE VENTRCLES CONTRACT FROM THE BOTTOM UPWARD, AND BLOOD IS FORCED OUT OF THE VENTRICLES INTO THE PULMONARY ARTERY, AND THE AORTA.
65
ELECTROCARDIOGRAPHY, WHAT IS IT IN FACT USED FOR?
ELECRTROCARDIOGRAPHY, CAN IN FACT USED TO MONITOR AND INVESTIGATE THE ELECTRICAL ACTIVITY OF THE HEART.
66
ELECTRODES.
ELECTRODES, THAT ARE CAPABLE OF DETECTING SIGNALS, ARE IN FACT PLACED ON THE SKIN.
THESE ELECTRODES, DO IN FACT PRODUCE AN ELECTROCARDIOGRAM, AN ECG.
67
WHAT DOES AN ECG, IN FACT SHOW?
AN ECG, DOES IN FACT SHOW A NUMBER OF DISTINCTIVE ELECTRICAL WAVES, PRODUCED BY THE ACTIVITY OF THE HEART.
68
THE P-WAVE.
THE P-WAVE IS IN FACT CAUSED BY THE DEPOLARISATION OF THE ATRIA, WHICH RESULTS IN ATRIAL CONTRACTION, SYSTOLE.
69
THE QRS COMPLEX.
THE QRS COMPLEX IS IN FACT CAUSED BY THE DEPOLARISATION OF THE VENTRICLES, WHICH RESULTS IN VENTRICULAR CONTRACTION, SYSTOLE.
THIS IS IN FACT THE LARGEST WAVE, BECAUSE THE VENTRICLES, DO IN FACT HAVE THE LARGEST MUSCLE MASS.
70
THE T-WAVE,
THE T-WAVE IS IN FACT CAUSED BY THE REPOLARISATION OF THE VENTRICLES, WHCIH DOES IN FACT RESULT IN VENTRICULAR RELAXATION, DIASTOLE.
71
TACHYCARDIA.
WHEN THE HEART BEATS TOO FAST, IT IS IN FACT TACHYCARDIA.
AN INDIVIDUAL, WITH A RESTING HEART RATE ABOVE 100bpm, IS IN FACT SAID TO HAVE TACHYCARDIA.
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BRADYCARDIA.
WHEN THE HEART BEATS TOO SLOW, IT IS IN FACT BRADYCARDIC.
AN INDIVIDUAL, WOTH A RESTING HEARYT RATE BELOW 60bmp, IS IN FACT SAID TO HAVE BRADYCARDIA.
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ECTOPIC HEARTBEAT.
THIS CONDITION IS IN FACT CAUSED BY AN EARLY HEARTBEAT, FOLLOWED BY A PAUSE.
THIS COULD IN FACT BE DUE TO AN EARLIER CONTRACTION OF EITHER THE ATRIA, OR THE VENTRICLES.
IT IS IN FACT COMMON IN THE POPULATION, AND USUALLY REQUIRES NO TREATMENT UNLESS VERY SEVRE.
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FIBRILATION.
AN IRREGULAR HEARTBEAT, WILL IN FACT DISRUPT THE RHYTHM OF THE HEART.
THE ATRIA OR VENTRICLE, DO IN FACT STOP CONTRACTING PROPERLY.
SEVRE CASES OF FIBRILATION, CAN IN FACT BE VERY DANGEROUS, EVEN FATAL.
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CARDIC OUTPUT.
CARDIAC OUTPUT, CO, IS IN FACT THE TERM USED TO DESCRIBE THE VOLUME OF BLOOD THAT IS PUMPED BY THE HEART, THE LEFT AND THE RIGHT VENTRICLE, PER UNIT OF TIME.
AN AVERAGE ADULT, DOES IN FACT HAVE A CARDIAC OUTPUT OF ROUGHLY 4.7. LITRES OF BLOOD PER MINUTE WHEN AT REST.
INDIVIDUALS WHO ARE FITTER, DO IN FACT OFTEN HAVE HIGHER CARDIAC OUTPUTS, DUE TO HAVING BOTH THICKER AND STRONGER VENTRICULAR MUSCLES IN THEIR HEARTS.
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CARDIAC OUTPUT, WHEN EXERCISING.
CARDIAC OUTPUT DOES IN FACT INCREASE WHEN AN INDIVIDUAL IS EXERCISING.
THIS IS IN FACT SO THE BLOOD SUPPLY CAN MATCH THE INCREASED METABOLIC DEMANDS OF THE CELLS.
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HEART RATE.
HEART RATE IS IN FACT THE NUMBER OF TIMES A HEART BEATS PER MINITE.
THE NUMBER OF CARDIAC CYCLES PER MINUTE.
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STROKE VOLUME.
STROKE VOLUME, IS IN FACT THE VOLUME OF BLOOD PUMPED OUT OF THE LEFT VENTRICLE, DURING ONE CARDIAC CYLE.
79
CARDIAC OUTPUT, CALCULATION.
CARDIAC OUTPUT.= THE HEART RATE X THE STROKE VOLUME.
THE CARDIAC OUTPUT, cm^3min^-1.
HEART RATE, BEATS PER MINUTE, bpm.
STROKE VOLUME, cm^3.
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dm^3 to cm^3.
1dm^3.= 1000cm^3
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MUSCLE CONTRACTION, EXERCISE.
DURING EXERCISE, MUSCLE CONTRACTION DOES IN FACT OCCUR MORE FREQUENTLY, REQUIRING MORE ENERGY.
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AEROBIC RESPIRATION, EXERCISE.
THE RATE OF AEROBIC RESPIRATION, DOES IN FACT INCREASE, TO MEET THE INCREASE IN ENERGY DEMAND.
THIS DOES IN FACT MEAN, THAT CELLS REQUIRE MORE OXYGEN TO BE DELIVERED TO THEM, WHILE PRODUCING MORE CARBON DIOXIDE, CO2, AS A WASTE PRODUCT OF RESPIRATIOM.
THE BODY WILL IN FACT ACCOMODATE THIS, BY MAKING THE FOLLOWING CHANGES:
INCREASE THE RATE AND DEPTH OF BREATHING, WHICH WILL INCREASE THE AMOUNT OF OXYGEN ENTERING THE LUNGS AND THE BLOODSTREAM, WHILE GETTING RID OF MORE CARBON DIOXIDE, CO2.
INCREASE THE HEART RATE, WHICH WILL TRANSPORT THE OXYGEN, AND THE GLUCOSE, C6H12O6, TO THE MUSCLE MUCH FASTER, WHILE REMOVING THE ADDITIONAL CARBON DIOXIDE, CO2, PRODUCED DUE TO THE INCREASED RATE OF RESPIRATION.
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BREATHING RATE, CONTROLL.
BREATHING RATE, IS IN FACT CONTROLLED BY THE VENTILATION CENTRES, ALSO CALLED THE RESPITORY CENTRES, IN THE MEDULLA OBLONGATA.
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THE MEDULLA OBLONGATA.
THE MEDULLA OBLONGATA, IS IN FACT ONE,1, OF THE THREE,3, REGIONS THAT MAKE UP THE BRAINSTEM, IT TRANSFERS NERVE MESSAGES FROM THE BRAIN, TO THE SPINAL CORD.
85
THE INSPIRATORY CENTRE.
THE INSPIRATORY CENTRE, DOES IN FACT CONTROL THE MOVEMENT OF AIR, INTO THE LUNGS.
INHILATION.
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THE EXPIRATORY CENTRE.
THE EXPIRATORY CENTRE, DOES IN FACT CONTROL THE MOVEMENT OF AIR, OUT OF THE LUNGS.
EXHALATION.
87
THE INSPIRATORY CENTRE, EFFECT ON BREATHING.
THE INSPIRATORY CENTRE IN THE MEDULLA OBLONGATA HAS THE FOLLOWING AFFECT ON BREATHING:
IT DOES IN FACT SEND NERVE IMPULSES ALONG MOTOR NEURONS TO THE INTERCOSTAL MUSCLES OF THE RIBS AND DIAGHRAGM MUSCLES.
THESE MUSCLES WILL IN FACT CONTRACT, AND CAUSE THE VOLUME OF THE CHEST TO INCREASE.
THIS DOES IN FACT LOWER THE AIR PRESSURE IN THE LUNGS, TO SLIGHTLY BELOW ATMOSPHERIC PRESSURE.
AN IMPULSE IS IN FACT ALSO SENT TO EXPIRATORY CENTRE, TO INHIBIT ITS ACTION.
DUE TO THE DIFFERENCE IN PRESSURE BETWEEN THE LUNGS, AND THE OUTSIDE AIR, AIR WILL IN FACT FLOW INTO THE LUNGS.
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STRETCH RECEPTORS.
STRETCH RECEPTORS IN THE LUNGS, ARE IN FACT STIMULATED, AS THEY FILL WITH AIR.
89
THE EXPIRATORY SYSTEM, EFFECT ON BREATHING.
NERVE IMPULSES ARE IN FACT SENT BACK TO THE MEDULLA OBLONGATA, WHICH WILL INHIBIT THE INSPIRATORY CENTRE.
THE EXPIRATORY CENTRE, IS NO LONGER INHIBITED AND WILL BRING ABOUT THE FOLLOWING CHANGES:
IT DOES IN FACT SEND NERVE IMPULSES TO THE INTERCOSTAL AND DIAPHRAGM MUSCLES.
THE MUSCLES WILL IN FACT RELAX, AND CAUSE THE VOLUME OF THE CHEST CAVITY TO DECREASE.
THIS DOES IN FACT INCREASES THE AIR PRESSURE IN THE LUNGS, TO SLIGHTLY ABOVE ATMOSPHERIC PRESSURE.
DUE TO THE HIGHER PRESSURE IN THE LUNGS, AIR WILL IN FACT FLOW OUT OF THE LUNGS.
AS THE LUNGS DEFLATE, THE STRETCH RECEPTORS DO IN FACT BECOME INACTIVE, WHCIH MEANS THAT THE INSPIRATORY CENTRE IS NO LONGER INHIBITED, AND THE NEXT BREATHING CYCLE CAN BEGIN.
90
EFFECTS OF EXERCISE, CARBON DIOXIDE, CO2.
THE EXTRA CARBON DIOXIDE, CO2, THAT IS IN FACT PRODUCED DUE TO THE INCREASED RATE OF RESPIRATION DURING EXERCISE, DISSOLVES IN THE BLOOD TO FORM CARBONIC ACID.
THIS DOES IN FACT QUICKLY DISSOCIATE INTO HYDROGEN, H+, IONS, AND HYDROCARBONATE IONS, HCO3^-.
THE INCREASE IN THE CONCENTRATION OF H+, IONS, WILL IN FACT DECREASE THE pH, IT BECOMES MORE ACIDIC.
THE DECREASE IN pH, IS DETECTED BY RECEPTORS SENSITIVE TO CHANGES IN THE CHEMICAL COMPOSITION OF THE BLOOD.
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CHEMORECEPTORS.
CHEMORECEPTORS, ARE IN FACT SENSITIVE TO CHANGES IN THE CHEMICAL COMPOSITION OF THE BLOOD.
THEY ARE IN FACT LOCATED IN SEVERAL PLACES:
IN THE VENTILATION CENTRE OF THE MEDULLA OBLONGATA.
THEY ARE IN FACT ALSO PRESENT, AS CLUSTERS OF CELLS IN THE AORTA, AORTIC BODIES, AND THE CAROTID ARTERIES, CAROTID BODIES.
ONCE THEY ARE STIMULATED, A NERVE IMPULSE IS SENT TO THE MEDULLA OBLONGATA.
THE MEDULLA OBLONGATA, WILL THEN SEND MORE FREQUENT NERVE IMPULSES TO THE INTERCOSTAL AND DIAPHRAGM MUSCLE, TO INCREASE THE RATE AND THE STRENGTH OF CONTRACTIONS.
THIS RESULTS IN MORE OXYGEN, ENTERING THE LUNGS AND THE BLOODSTREAM, WHILE MORE CARBO DIOXIDE, CO2, CAN BE EXHALED AND THUS BE REMOVED FROM THE BLOOD STREAM.
THE DECREASE IN CARBON DIOXIDE, CO2, LEVEL WILL RESULT IN THE BLOOD pH RETURNING BACK TO NORMAL,WHICH LEADS TO THE BREATHING RATE RETURNING TO NORMAL.
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VENTILATION RATES.
THE VOLUME OF AIR, THAT DOES IN FACT MOVE IN AND OUT OF THE LUNGS DURING A SET TIME PERIOD, SUCH AS A MINUTE, IS KNOWN AS THE VENTILATION RATE.
THE VENTILATION RATE, DOES IN FACT INCREASE DURING EXERCISE, DUE TO THE INCREASE IN BREATHING RATE AND DEPTH.
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CONTROL OF THE HEART RATE, INTRODUCTION.
THE CARDIOVASCULAR CONTROL CENTRE, IN THE MEDULA OBLONGATA, DOES IN FACT UNCONSCIOUSLY CONTROL THE HEAR RATE, BY CONTROLLING THE RATE AT WHICH THE SINOATRIAL NOD, SAN, GENERATES ELECTRICAL IMPULSES.
THESE ELECTRICAL IMPULSES DO IN FACT CAUSE THE ATRIA TO CONTRACT, AND THEREFORE DETERMINES THE RHTHYM OF A HEARTBEAT.
94
CHANGES IN THE HEART RATE, CAUSES.
CHANGES IN THE INTERNAL ENVIRONMENT OF THE BODY, SUCH AS BLOOD PRESSURE, AND OXYGEN LEVELS, CAN IN FACT RESULT IN A CHANGE IN THE HEART RATE.
95
CHANGES OF THE HEART RATE, DETECTORS.
THE CHANGES IN THE INTERNAL ENVIRONMENT, ARE IN FACT DETECTED BY BARORECEPTORS AND CHEMORECEPTORS.
96
BARORECEPTORS.
BARORECEPTORS, ARE IN FACT FOUND IN THE AORTIC AND CAROTID BODIES, AND THEY ARE STIMULATED BY HIGH AND LOW BLOOD PRESSURE.
97
CHEMORECEPTORS, LOCATION.
CHEMORECEPTORS, ARE IN FACT FOUND IN THE MEDULLA OBLONGATA, AS WELL AS THE AORTIC AND CAROTID BODIES.
THEY ARE IN FACT STIMULATED, BY CHANGES IN THE LEVELS OF CARBON DIOXIDE, CO2, AND OXYGEN, O2, IN THE BLOOD, AS WELL AS BLOOD pH.
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WHAT HAPPENS AFTER, THE BARORECEPTORS AND CHEMORECEPTORS HAVE IN FACT BEEN STIMULATED?
ONCE STIMULATED, THESE RECEPTORS WILL IN FACT SEND ELECTRICAL IMPULSES TO THE MEDULLA OBLONGATA.
THE CARDIOVASCULAR CONTROL CENTRE, IN THE MEDULLA OBLONGATA, WILL RESPOND BY SENDING IMPULSES TO THE SINOATRIAL NODE, SAN, ALONG SYMPATHETIC AND PARASYMPATHETIC NEURONES.
EACH OF THESE NEURONES, WILL IN FACT RELEASE DIFFERENT NEUROTRANSMITTERS, WHICH WILL AFFECT THE SAN DIFFERENTLY.
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SYMPATHETIC NEURONES.
SYMPATHETIC NEURONES, WILL IN FACT INCREASE THE RATE AT WHICH THE SAN GENERATES ELECTRICAL IMPULSES, THUS SPEEDING UP THE HEART RATE.
THESE NEURONES, DO IN FACT FORM PART OF THE SYMPATHETIC NERVOUS SYSTEM, WHICH PREPARES THE BODY ACTION, FIGHT OR FLIGHT RESPONSE, AND INCREASES THE HEART RATE DURING EXERCISE.
100
PARASYMPATHETIC NEURONES.
PARASYMPATHETIC NEURONES, WILL IN FACT DECREASE THE RATE AT WHICH THE SAN FIRES, THUS SLOWING DOWN THE HEART RATE.
THESE NEURONES, DO IN FACT FORM PART OF THE PARASYMPATHETIC NERVOUS SYSTEM, WHICH CALMS THE BODY DOWN AFTER ACTION, REST AND DIGEST RESPONSE, AND DECREASE THE HEART RATE AFTER EXERCISE.
101
THE HEARTS RESPONSE, TO DIFFERENT STIMULUS.
THE HEART, WILL IN FACT RESPOND IN DIFFERENT WAYS DEPENDING ON THE STIMULUS THAT IT RECIEVES.
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THE HEARTS RESPONSE, HIGH BLOOD PRESSURE.
HIGH BLOOD PRESSURE, IS IN FACT DETECTED BY BARORECEPTORS, WHICH SEND IMPULSES TO THE CARDUOVASCULAR CONTROL CENTRE.
IT SENDS IMPULSES, ALONG PARASYMPATHETIC NEURONES, WHICH SECRETE THE NEUROSTRNASMITTER, ACETYLCHOLINE.
ACETYLCHOLINE, BINDS TO RECEPTORS ON SAN, CAUSING IT TO FIRE LESS FREQUENTLY.
HEART RATE SLOWS DOWN, AND BLOOD PRESSURE DECREASES BACK TO NORMAL.
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THE HEARTS REPSONSE, LOW BLOOD PRESSURE.
LOW BLOOD PRESSURE, IS IN FACT DETECTED BY BARORECEPTORS, WHICH SEND IMPULSES TO THE CARDIOVASCULAR CONTROL CENTRE.
IT SENDS IMPULSES ALONG SYMPATHETIC NEURONES, WHICH SECRETE THE NEUROTRANSMITTER NORADRENALINE.
NORADRENALINE, BINDS TO RECEPTORS ON SAN CAUSING IT TO FIRE MORE FREQUENTLY.
HEART RATE SPEEDS UP, AND BLOOD PRESSURE INCREASES BACK TO NORMAL.
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HIGH BLOOD O2, LOW CO2, HIGH pH LEVELS.
DETECTED BY CHEMORECEPTOTS, WHICH DO IN FACT SEND IMPULSES TO THE CARDIOVASCULAR CONTROL CENTRE.
IT SENDS IMPULSES ALONG PARASYMPATHETIC NEURONES, WHICH SECRETE THE NEUROSTRANSMITTER ACETYLCHOLINE.
ACETYLCHOLINE, DOES IN FACT BIND TO RECEPTORS ON SAN, CAUSING IT TO FIRE LESS FREQUENTLY.
HEART RATE SLOWS DOWN, AND O2 AND CO2, AND pH LEVELES RETURN TO NORMAL.
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LOW BLOOD O2, HIGH CO2, AND LOW pH LEVELS, DURING EXERCISE.
DETECTED BY CHEMORECEPTORS, WHICH DO IN FACT SEND IMPULSES TO THE CARDIVASCULAR CONTROL CENTRE.
IT SEND IMPULSES, ALONG SYMPATHETIC NEURONES, WHICH SECRETE THE NEUROTRANSMITTER NORADRENALINE.
NORADRENALINE, BINDS TO RECEPTORS ON SAN, CAUSING IT TO FIRE MORE FREQUENTLY.
HEART RATE SPEEDS UP AND O2, CO2, AND pH LEVELS, DO IN FACT RETURN TO NORMAL.
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MEASURING BREATHING.
THERE ARE IN FACT FOUR,4, MAIN WAYS THAT BREATHING CAN BE SCIENTIFICALLY MEASURED.
107
TIDAL VOLUME.
TIDAL VOLUME, THIS IS IN FACT THE VOLUME OF AIR THAT IS BREATHED IN OR OUT, DURING NORMAL BREATHING, AT REST.
TO CALCULATE,
CALCULATE THE AVERAGE DIFFERENCE IN THE VOLUME OF GAS, BETWEEN EACH PEAK AND TROUGH.
UNIT.= dm^3.
108
BREATHING RATE.
THIS IS IN FACT THE NUMBER OF BREATHS TAKEN IN ONE,1, MINUTE.
ONE BREATH.= TAKING AIR IN AND BREATHING IT BACK OUT AGAIN.
TO CALCULATE, COUNT THE NUMBER OF PEAKS ON A TRACE IN ONE,1, MINUTE.
UNIT.= breaths min^-1.
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OXYGEN, O2, CONSUMPTION.
THIS IS IN FACT THE VOLUME OF OXYGEN, O2, USED UP BY SOMEONE IN A GIVEN TIME.
110
REPSITORY MINUTE VENTILATION.
THIS IS IN FACT THE VOLUME OF AIR, THAT CAN BE BREATHED IN OR OUT IN A MINUTE, AND CAN BE CALCULATED BY MEANS OF THE FOLLOWING FORMULAE:
RESPITORY MINUTE VENTILATION.=
TIDAL VOLUME X THE BREATHING RATE, BREATHS PER MINUTE.
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SPIROMETERS.
THE BREATHING MEASUREMENTS, CAN IN FACT ALL BE MADE USING A PIECE OF APPARATUS, KNOWN AS A SPIROMETER.
THE PERSON, SUBJECT, BEING EXAMINED BREATHES IN AND OUT, THROUGH THE SPIROMETER.
CARBON DIOXIDE, CO2,
IS ABSORBED FROM THE EXHALED AIR, BY SODA LIME, IN ORDER TO STOP THE CONCENTRATION OF CARBON DIOXIDE, CO2, IN THE RE-BREATHED AIR FROM GETTING TOO HIGH, AS THIS CAN CAUSE BREATHING DISTRESS.
AS THE SUBJECT BREATHES THROUGH THE SPIROMETER, A TRACE IS DRAWN ON A ROTATING DRUM OF PAPER, OR A GRAPH IS FORMED DIGITALLY, WHICH CAN BE VIEWED ON A COMPUTER.
FROM THIS TRACE, THE SUBJECT'S RESPITORY MINUTE VENTILATION, TIDAL VOLUME AND BREATHING RATE CAN ALL BE CALCULATED.
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INVESTIGATING THE EFFECTS OF EXERCISE.
EXERCISE CAN IN FACT CAUSE AN INCREASE IN BREATHING RATE AND TIDAL VOLUME, INCLUDING AN INCREASE IN OXYGEN, O2, CONSUMPTION AND VENTILATION RATES.
113
INVESTIGATING THE EFFECTS OF EXERCISE, APPARATUS.
SPIROMETER,
TREADMILL,
AND A STOPWATCH.
114
INVESTIGATING THE EFFECTS OF EXERCISE, METHOD.
A PERSON AT REST, WILL IN FACT BREATHE INTO THE SPIROMETER FOR ONE,1, MINUTE.
RECORD THE RESULTS.
THE PERSON WILL THEN EXERCISE FOR TWO,2, MINUTES WHILE THE SPIROMETER CHAMER IS REFILLED WITH OXYGEN, O2.
AFTER THEY STOP EXERCISING, THEY WILL BREATHE IMMEDIATELY INTO THE SPIROMETER FOR ONE,1, MINUTE.
RECORD THE RESULTS.
COMPARE THE RECORDINGS, TAKEN BEFORE AND AFTER EXERCISING.
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EFFECTS OF TOO LITTLE EXERCISE ON HEALTH.
EXERCISE IS IN FACT AN IMPORTANT PART OF A HEALTHY LIFESTYLE.
NOT DOING ENOUGH EXERCISE CAN IN FACT HAVE A DETRIMENTAL EFFECT ON THE HEALTH OF AN INDIVIDUAL.
INCREASED RISK OF OBESITY, CARDIOVASCULAR DISEASE, CVD, AND DIABETES.
116
EFFECTS OF TOO MUCH EXERCISE ON HEALTH.
EXERCISING TOO MUCH, CAN IN FACT ALSO HAVE A NEGATIVE IMPACT ON HEALTH.
JOINTS MAY BECOME DAMAGED, DUE TO INCREASE WEAR AND TEAR ON THEM.
EXCESSIVE EXERCISE MAY IN FACT ALSO SUPPRESS THE IMMUNE SYSTEM, MAKING THE INDIVIDUAL MORE SUSCEPTIBLE TO DISEASE.
117
SPORTS INJURIES.
SPORTS INJURIES, ARE IN FACT A COMMON OCCURENCE, SINCE THE BODY IS PLACED UNDER STRESS, WHEN PARTICIPATING IN SPORTING ACTIVITIES.
SOME OF THESE INJURIES, CAN IN FACT RESILT IN PERMANENT DAMAGE, BUT WITH CORRECT TRATMENT IT IS POSSIBLE TO MAKE A FULL RECOVERY FROM SPORTS INJURIES.
ADVANCES IN MEDICAL TECHNOLOGY HAS ENABLED PROFESSIONAL ATHLETES TO RECOVER FROM INJURIES, THAT PREVIOUSLY MAY HAVE ENDED THEIR CAREER.
118
KEYHOLE SURGERY.
KEYHOLE SURGERY, IS IN FACT ONE EXAMPLE OF THE MEDICAL ADVANCES THAT HAVE BEEN MADE,
IT IS A LESS INVASIVE PROCEDURE, AS ONLY SMALL INCISIONS ARE MADE IN THE SKIN.
A SMALL VIDEO CAMERA IS INSERTED INTO THE INCISION, ALONG WITH SPECIALISED MEDICAL INSTRUMENTS, WITH WHICH TO PERFORM THE SURGERY.
119
KEYHOLE SURGERY, ADVANTAGES.
THERE ARE MULTIPLE ADVANTAGES TO KEYHOLE SURGERY, COMPARED TO CONVENTIAL SURGERY:
LESS BLOOD LOSS, AND SCARRING OF THE SKIN.
LESS PAIN AFTER SURGERY, AND A QUICKER RECOVERY.
THIS LEADS TO A SHORTER HOSPITAL STAY, AND THE PATIENT CAN QUICKLY RETURN TO DOING NORMAL ACTIVITIES.
120
PROSTHESES.
INJURIES MAY IN FACT SOMETIMES RESULT IN PEOPLE LOSING OR DAMAGING A BODY PART, TO THE EXTENT THAT THEY CAN NO LONGER USE IT.
IN SOME CASES, A PERSON MAY BE BORN WITHOUT CERTAIN BODY PARTS.
IN BOTH THESE CASES, THE MISSING OR DAMAGED BODY PART, MAY BE REPLACED WITH AN ARTIFICIAL VERSION, CALLED A PROSTHESIS.
THEY MAY REPLACE ENTIRE LIMBS, SUCH AS LEGS OR HANDS, OR PARTS OF LIMBS, SUCH AS A HIP OR A KNEE JOINT.
SOME PROSTHESES, MAY IN FACT BE CONNECTED TO ELECTRONIC DEVICES THAT CAN 'READ" INFORMATION FROM THE NERVOUS SYSTEM, IN ORDER TO OPERATE PARTS OF THE BODY.
PROSTHESES ENABLES INDIVIDUALS TO PARTICIPATE IN SPORTS AGINS, EVEN AFTER MORE SERIOUS INNJURIES.
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PERFORMING ENHANCING DRUGS.
DRUGS THAT CAN IN FACT IMPROVE A PERSON'S PERFORMANCE, IN SPORT OR ATHLETIC ACTIVITIES, ARE KNOWN AS PERFORMANCE-ENHANCING DRUGS.
WHEN TAKEN BY PEOPLE PARTICIPATING IN COMPETITIVE SPORTING EVENTS, IT WILL GIVE THEM AN UNFAIR ADVANTAGE.
DUE TO ENHANCED PERFORMANCE AND HEALTH RISKS ASSOCIATED WITH TAKING THESE DRUGS, THEY ARE BANNED FROM MOST COMPETITIVE SPORTS.
RANDOM DRUG TESTS ARE IN FACT PERFORMED ON ATHLETHES, AND IF THEY ARE POSITIVE, THEY MAY BE BANNED FROM COMPETING AND MAY LOSE ANY MEDALS OR AWARDS THAT THEY WON IN THE PAST.
122
ANABOLIC STERIODS.
ANABOLIC STERIODS, WHICH INCREASE MUSCLE SIZE, TO GIVE THE USER INCREASED STRENGTH, SPEED, AND STAMINA, BUT MAY LEAD TO ORGAN DAMAGE AND INCREASED AGGRESSION.
123
STIMULANTS.
STIMULANTS, WHICH MAKE THE USED MORE ALERT, AND ABLE TO REACT FASTER, THEY WILL HAVE GREATER ENDURANCE, BUT IT MAY ALSO LEAD TO AGGRESSIVE BEHAVIOUR.
124
NARCOTIC ANALGESICS.
NARCOTIC ANALGESICS, WHICH ARE VERY STRONG PAINKILLERS, THAY ENABLES USERS TO MAINTAIN THEIR PERFORMANCE DESPITE SUFFERING FROM INJURIES.
125
RATIONALISTS.
RASIONALISTS, THINK THERE BE TIMES WHEN THEIR USE IS JUSTIFIED.
DRUGS SHOULD BE ALLOWED UNDER CERTAIN CIRCUMSTANCES.
ATHLETES, SHOULD HAVE THE FREEDOM TO CHOSE WHETHER THEY WANT TO DEAL WITH THE RISKS OF TAKING THESE DRUGS.
PERFORMANCE-ENHANCING DRUGS, MAY HELP OVERCOME INEQUALTIES IN COMPETITIVE SPORT, SINCE ATHLETES THAT DO NOT HAVE THE SAME OPPORTUNITIES TO IMPROVE THEMSELVES,
SUCH AS FACILITIES, TRAINING OR COACHES.
COMPETING AT A HIGHER LEVEL, MAY ONLY BE POSSIBLE FOR SOME ATHLETES IF THEY ARE USING PERFORMING-ENHANCING DRUGS.
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ABSOLUTISTS.
THINK THAT THEY ARE MORALLY WRONG, AND SHOULD BE BANNED FROM ALL SPORT.
BELIEVE THESE DRUGS SHOULD BE BANNED, FROM ALL SPORTS AND NOT TAKEN UNDER ANY CIRCUMSTANCE.
THESE DRUGS GIVE ATHELTES AN UNFAIR ADVANTAGE, OVER THOSE WHO DO NOT TAKE THEM.
PERFORNCE SHOULD BE THE RESULT OF TRAINING AND HARD WORK ONLY.
THE HEALTH RISKS ASSOCIATED WITH THESE DRUGS ARE SERIOUS, AND INCLUDE A VARIETY OF SIDE EFFECTS.
THERE IS A QUESTION, OF WHETHER ATHLETES ARE FULLY INFORMED, ABOUT THE HEALTH RISKS INVOLVED WITH TAKING THESE DRUGS.
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WHAT DO HORMONES BIND TO, IF THEY ENTER THE CELL?
TRANSCRIPTION FACTORS.
