Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
117 Cards in this Set
- Front
- Back
conversions
|
3.5 ml/kg/min = 1 MET
26.8 m/min = 1 mph 1 watt = 6 kgm/min 2.2 lbs = 1 kg |
|
Endcrine System
|
- tissues & glands located throughout the body that secrete hormones
|
|
hormones
|
- hormones transproted in the blood to target tissues/cells that opssess specific hormone receptors
- upon binding to receptor sites, hormones can control activity of target tissue (lock & key) [p 93, Fig 6-1 p 96, Fig 6-3] |
|
steroid hormones
|
- chemical structure resembling cholesterol
- lipid soluble - pass easily through cell membranes (bi-lipid layer) |
|
nonsteroid hormones
|
- not lipid soluble
- cannot pass easily through cell membrane - examples in body: anterior pituitary (growth hormone) pancreas (insulin) |
|
steroid hormones in the body
|
- Adrnela cortex: cortisol & aldosterone
- Ovaries: estrogen & progesterone - Testes: testosterone - Placenta: estrogen & progesterone |
|
steroid hormones - mech. of action
|
- hormone enters cell and binds with a receptor
- hormone-receptor complex binds with cells DNA (direct gene activation) - mRNA activated and promotes protein sysnthesis - can have a direct effect ont he nucleus |
|
nonsteroid hormones - mech. of action
|
- polypeptide hormones
- made up of amino acids and bind to receptors on cell membrane of target tissue - triggers formation of intracellular second messenger (ie. cAMP - cyclic AMP) |
|
cAMP
|
activates protein kinases that lead to cellular changes & hormonal effects
|
|
negative feedback
|
- secretion of hormone will cause some change in body
- this change will inhibit further secretion |
|
Pituitary Gland
|
- master gland, although largely under control of hypothalamus
- hormones are secreted by anterior & posterior lobe |
|
Pit. Anterior Lobe secretions
|
-- GH: growth hormone
-stimulates tissue growth -inc. protein synthesis -mobilization of fats for energy use -dec. rate of carb use (glucose sparing) -important for child's normal growth -role in adapting to stress of resistance training -- TSH: thyroid stimulatin hormone -controls production & release of thyroxine & triiodothyronine by thyroid gland -- ACTH: adrenal corticotropic hormone -controls secretion of hormones from adrenal cortex |
|
Pit. Posterior Lobe secretions
|
-- ADH: antidiuretic horomone
-assists in controlling water secretions by kidneys -elevates BP w/ bv constriction -usually produced in hypothalamus & stored in pituitary -release triggered by neural impulses from hypothalamus -- Oxytocin -stimulates contraction of uterine muscles -milk secretion |
|
Thyroid Gland
|
- secretes thyronxin & triidothyronine
-stimulate oxidative metabolism in mitochondria & cell growth; inc. rate a& contractility of heart - release of homrones controlled by TSH |
|
Parathyroid Gland
|
- PTH
- increases calcium levels & decreases phosphate levels in blood - stimulates bone formation |
|
Adrenal Glands - adrenal medulla
|
- secretes catacholamines
- eleveate w/ exercise and decline ~30 min. post exercise - explaining EPOC |
|
Adrenal Glands - adrenal medulla: epinephrine
|
-mobilizes glycogen
-increases skeletal blood flow -increases HR, contractility & oxygen consumption (all important w/inc. activity levels; ;also stimulated w/ inc. stress levels -> fight or flight response) |
|
Adrenal Glands - adrenal medulla: norephinephrine
|
-constricts arterioles & venules causing inc. in BP
-if in time of non physical stress -> easily angered, hostile -- detrimental over time) |
|
Adrenal Glands - adrenal cortex: aldosterone
|
-- "mineralocorticoid"
-inc. sodium retention & potassium excretion in kidneys -help body hod onto water -positively influence BP -dec. plasma volume = inc. aldosterone -> w/ exercise |
|
Adrenal Glands - adrenal cortex: cortisol
|
-- "glucocorticoid"
-controls metabolism of carbs, fats & proteins -anti-inflammatory action -resistance exercise of high volume, large muscle groups & short rest periods = inc. serum cortisol values -chronic high levels = adverse catabolic effects -acute increases contribute to modeling of muscle tissue |
|
Pancreas secretions
|
-- Insulin
-stored glygocen in the liver, muscles, kidneys -promotes glucose entry into cell ultimately decreasing blood glucose levels -involed in protein -- Glucagon -inc. blood glucose levels |
|
Gonads - Testes
|
-- Testosterone
-stimulates growth, protein anabolism, develoment & maintenance of male sex characteristics -large muscle group exercises result in acute inc. serum total testosterone concentration in men |
|
Gonads - Ovaries
|
-- Estogen
-stimulated development of female sexual characteristics -- Progesterone -stimulates development of female sexual characteristics & mammary glands - maintains pregnancy |
|
Kidneys
|
- not really considered as one of endocrine organs
- do release hormaone erythropoietin: -regulates RBC production by stimulateing bone marrow cells - high altitude training results in inc. erythropoietin relase -> inc. in RBC production |
|
Glucose Metabolism (response to exercise)
|
--> stimulate glycogenolysis:
-glucagon -epinephrine -norepinephrine -cortisol - GH: inc. FFA mobilization, dec. cellular uptake of glucose (glucose sparing) - beneficial for endurance athletes - Thyroid hormones: enhanced glucose & fat metabolism (thyroxine more important) |
|
glucose uptake by muscles
|
- facilitated in presence of insulin
- studies indicate that blood insulin levels decline w/ exercise despite inc. concentrations of blood glucose - suggests inc. in insulin sensitivity -> dec. in amt. of insulin needed to facilitate glucose uptake - activity has insulin like affect -- sucking up glucose into cells (why good for diabetes to exercise) |
|
fat metabolism during exercise
|
- tryglycerides broken down to FFA's & glycerol by enzyme lipase
- lipase activty stimulated by: cortisol epinephrine norepinephrine growth hormone |
|
fluid & electrolyte balance
|
- muscles gain water at expense of you plasma volume during exercise
- endocrine sys. plays important role in monitoring & correcting imbalances in fluid & electrolytes |
|
endcrine system control of fluid & electrolyte balance during exercise
|
- angiotensin II triggers Aldosteron release from adrenal cortex = retention of sodium & water -> minimizing plasma volume loss
- ADH released in response to hemoconcentration that occurs as plasma volume is reduced w/ exercise - ADH promotes water reabsorption in kidneys in effort to restore normal plasma volume & BP |
|
post-exercise hormone activty & fluid balance
|
- Aldosterone & ADH leveles remain elevated for 12-48 hours post-exercise -> reducing urine output a& protecting from further dehydration
|
|
hemodilution
|
- expanded blood volume brought on by regular exercise
- solutes in blood (RBC, WBC & plateletes) become diluted despite no change in their absolute number - makes blood less thick/viscus by adding plasma to blood |
|
renin-angiotensin mechanism
|
- muscular activity promotes sweating & inc. BP
- sweating reduce plasma volume & blood flow to kidneys - red. renal blood flow stimulates renein release from kidneys -- renin lead to formation of angiotensin I that converts to angiotensin II (potent vasoconstrictor) - angiotensin II stim. release of aldosterone from adrenal cortex -> retain sodium; retention of fluid) - aldosterone inc. sodium & water reabsorption from renal tubules - plasma volume inc. & urine production dec. after several days |
|
ADH concerves body water
|
1. muscluar activty promotes sweating
2. sweating causes loss of blood plasma -> hemoconcentration & inc. blood osmolarity 3. inc. blood osmolarity stimulates hypothalamus 4. hypothalamus stimulates posterior pituitay gland 5. post. pit. glang secretes ADH 6. ADH acts on kidneys, increasing water permeability of renal tubules & collecting ducts -> inc. reabsorption of water 7. plasma volume inc -> blood osmolarity dec. after exercise & water ingestion |
|
renin-angiotensin mech. & ADH water conservation
|
occur at the same time -> during prolonged aerobic activity (especially in warm environments)
|
|
plasma volume drop
|
following inital drop, plasma volume remains relatively constant throughout exercise due to:
- action of adlosterone & ADH - water returning from exercising muscle to blood, & - inc. in amt. of water prouction by metabolic oxidation w/in plasma |
|
training adaptations
|
- specific to type fo training & muscles used in training program
- may differentiate responses associated w/ low-to-moderate intensity aerobic exercie to those associtaed with hight intensity |
|
anaerobic training energy system
|
-- Phosphagen system
-increase in stored ATP and PC -- Lactic acid system -anaerobic glycolysis -inc. muscle glycogen storage -inc. glycolytic enzymes (act as catalyst enhancing mvmt through cycle) -inc. lactate generating capacity & tolerance -- Oxidative system -no significant impact on oxidative enzyme content |
|
lactate tolerance
|
- several weeks of intense, but progressive, anaerobic workout will result in improved tolerance to reduce blood & msuce pH levels
- impmroved ability to buffer acids leading to inc. performance - most significant w/ intese training in 1-2 minute range |
|
"puke factor"
|
- intense anaerobic exercise, if progressed too quickly can cause nausea & vomiting
- indicator of excessive training stimulus -- not an indicator of a good workout |
|
methods of anearobic training (examples)
|
- PRE
- Sprints - Plyometrics - Interval training (repeat work bouts w/rest periods b/t) |
|
myocaridal adaptations
|
- inc. septal and left ventricular free wall thickness (tissue hypertrophy_
- a "physiological hypertorphy" that occurs in response to resistance training and not a "pathological" change |
|
muscle fiber adaptations
|
- hypertrophy or hyperplasia?
- hypertrophy -> result of inc. in size & # of myofibrils - Type I vs. type II: both tend to undergo hypertrophy w/ biggest inc. in type II - stimulus for muscle hypertrophy is intramuscular tension |
|
capillary density
|
- PRE w/ significant muscle hypertrophy -> dec. in capillary density (capillary volume per area of muscle fiber)
- may have negative impact on aerobic performance |
|
mitochondrial adaptations
|
- no change in size or # with anaerobic training
- possible dec. in motochondiral density due to dilution effect caused by muscle hypertrophy (dec. 25%) - no change in quantity or activity of oxidative enzymes |
|
aerobic training
|
- results in specific skeletal muscle adaptations that allow for improved delivery of oxygen & nutrients to working muscles (at cellular level)
- improved utilization of O2 & nutrients for generation of ATP - improved VO2 max, lactate threshold, & endurance time |
|
myocardial adaptations
|
- inc. diameter of left ventricle (volume hypertrophy)
-> inc. stroke volume - inc. left ventricular wall thickness (tissue hypertrophy) |
|
mitochondrial adaptaitons
|
- inc. size & #
- inc. Krebs cycle enzymes - inc. dependence on fat oxidation -> glucose sparing - dec. lactate accumulation ofr given submax workload |
|
triglyceride metabolism
|
- inc. intramuscular storage of triglycerides
- inc. ability to breakdown triglycerides into FFA's - inc. enzymes for mobilization & metabolism of fat - de. serum triglyceride levels (better cholesterol & lipid profiles) |
|
energy systems
|
-- Phospagen system
-inc. sotred ATP & PC (not to extend of anaerobic) -- Lactic Acid system -little change in both type I & type II muscle fiber concentration of glycolytic enzymes -- Oxidative system -significant inc. inoxidate enzyme content |
|
glycogen storage
|
- inc. glycogen synthase activty
= greater glycogen storage |
|
muscle fiber adaptations
|
- type I: inc. oxidative capacity
- type II: some type II may take on characteristics of type I fibers (= better suited for aerobic activty) - muscle size: no significant change in size (possible hypertrophy of type I fibers) |
|
glycogen depletion patterns
|
- glycogen depletion patterns: preferential glycogen depletion in type I fibers
- most depend on glygocgen -> easliy depleted |
|
capillary density
|
- inc. in size & # of capillaries per muscle fiber in endurance training
- improved ability to deliver oxygen & nutrients to muscle |
|
heart rate
|
- resting = 60-80 bpm
- >100 = tachycardia - <60 = bradycardia (can be exercise induced) - deconditioned: > 100 bpm - endurance trained: <40 bpm - anticipatory rise in HR -inc. symp. NS activty -dec. vagal tone (associated w/ parasymp. NS = dominant system at rest) |
|
HR during exercise
|
- inc. in direct proportion to exercise intensity
- mas HR dec. w/ age - estimateing HR max: 220 - age |
|
steady-state HR
|
- HR inc. at beginning of exercise & plateau w/ submax workload
- w/ inc. in intensty: HR will again rise & plateau (1-2 min) - w/ intese exercise: take longer to reach steady-state |
|
stroke volume
|
- inc. in direct proportion to exercise intensity up to 40-60% VO2 max
- may cont. to rise in highly endurance trained - untrained: rest=50-60; exer=100-120ml - highly training: rest=80-110; exer=160-200ml - stroke volume is greatest in supine b/c of inc. venous return |
|
Frank-Starling mechanism
|
- inc. venous return results in greater EDV & inc. SV due to greater stretch of ventricle
|
|
increased contractility and/or decreased peripheral vascular resistance
|
- PVR declines due to vascular dilation
- could lead to increase SV |
|
cardia output (Q)
|
- Q = HR x SV
- rises in direct proportion to exercise intensity - resting Q ~5 L/min - max exercise Q ~20-40 L/min (depending on size & level of fitness) - inc. Q w/ activity is a result of inc. in HR & SV up to ~40-60% VO2 max - further inc. dependent on inc. HR |
|
Fick Equation
|
Q = VO2 / a-vO2 diff
VO2 = Q x a-vO2 diff |
|
blood flow to muscles
|
- rest: ~15% of blood flow
- max exercise: ~85% of blood flow -- mediated by inc. sympathetic activity & autoregulation - w/ inc. temp., more blood will be directed toward skin to help w/ heat dissipation at expense of muscles needs |
|
cardiovascular drift
|
- prolonged exercise in hot environment = upward "drift" in HR & downward "drift" in SV
-> results from: -inc. % Q directed to skin -loss of blood plasma in sweat |
|
blood pressure
|
- SBP: inc. linearly w/ exercise intensity -- due to inc. Q
- DBP: normally shows little change w/ acute aerobic exercise - w/ max PRE: BP may rise dramatically in response to inc. intrathoracic pressure |
|
UE exercise and BP
|
- tend to result in greater BP resaonse when compared to LE exercise using same absolute load
- due to smaller muscle mass & vasculature of upper body |
|
myocardial O2 demand
|
- MVO2
- directly related to RPP (rate pressure product/"double product") RPP = HR x SBP - great RPP = greater demand of O2 to keep up work level |
|
blood
|
- can carry 20 ml O2/100 ml blood
- resting a-v O2 = 5-6 ml O2/100 ml blood - a-v O2 diff widens w/ inc. intensity of exercise due to inc. O2 demands - w/ max exercise: a-v O2 may reach 15-16 ml O2/100 ml blood |
|
plasma volume
|
- dec. w/ acute exercise while interstitial fluid inc.
- inc. faster than RBC w/ training |
|
causes of dec. plasma volume
|
- inc. BP forces fluid out of blood
- build-up metabolic waste products will create an intramuscular osmotic pressure that will draw fluid (water) from the blood - excessive sweating can lead to impaired performance due to loss of plasma volume - dec. plasma volume will result in inc. hematocrit & blood viscosity -> impaired blood flow |
|
hemoconcentration
|
- 45% of blood volume
- results from loss of plasma volume (elderly/young; dehydration) - formed elements will represent a greater % of blood volume - inc. RBC concentration -> improved O2 carrying capacity of blood (training at high altitudes) - advantage of inc. O2 carrying capacity may be negated if inc. viscosity impair flow |
|
hemodilution
|
- w/ recurrent (chronic) aerobic exercise -> inc. plasma volume
- b/c inc. in plasma volume is not matche by inc. in volume of RBC -> dec. in hematocrit - expanded plasma volume results in hemodilution effect - in reality, have greater absolute # of RBC, but they represent less % of blood volume |
|
blood pH
|
- normal: 7.4
- intensities >50% of max lead to dec. in pH - due to build up of acidic waste products (lactic acid and/or hydrogen) - blood pH may drop to 7.0, muscles to 6.5 -> muscles tighten & get heavy; fatigued; slowed down; will correct itself - muslce to |
|
control of HR
|
-- autonomic nervous system
-Parsympathetic: dominatnt in reasting -Sympathetic: takes over w/ inc. activty & exercise; withdrawl of vagal tone |
|
carida cycle
|
-> all events (electrical & mechanical) that occur b/t two consecutive heartbeats
--Electical events: -depolarization (QRS wave) -repolarization (T wave) --Mechanical events: -systole (contraction) -diastole |
|
PNS
|
- predominates at rest
- vagal control - vagal stimulation: acetylcholine release -dec. HR -dec. force of contraction -coronary arteries dilate |
|
SNS
|
- adrenergic
- stimulation leads to relase of: norepinephrine epinephrine - receptors: alpha receptors beta receptors - predominates during times of stress |
|
adrenergic stimulation
|
-- Beta 1
-inc. HR -inc. force of contraction --Beta 2 -coronary arteriolar vasodilation -bronchiolar smooth muscle dilation -- Alpha 1 -coronary arteriolar vasoconstriction |
|
other factors influencing HR
|
- baroreceptors: aorta, carotid arteries
- pressoreceptors: vena cave near R atrium - chemoreceptors: aortic & carotid bodies - hormonal: adrenal glands - body temp - ion concentration |
|
stroke volume depends on
|
-- preload: volume of blood in ventricle at end of diastole; depends on:
venous return ventricular distensibility -- ventricular contractility -- afterload: aortic or pullmonary pressure against which ventricle must contract |
|
regulation of Q
|
-- intrinsic
-Frank-Starling mechanism -- extrinsic -neural -hormonal |
|
blood vessels
|
-- arteries
-carry blood away from heart -distributing vessels*; resistance vessels; high resistance & low volume -- veins -carry blood toward the heart -collecting vessels; capacitance vessels*; low resistance & high volume -one way valves -muscular pump from gross mvmt -respiratory pump (breathing facilitated) -- capillaries -exchange vessels |
|
structure of blood vessels
|
- adventitia: CT w/ elastic & collagenous fibers (outer layer)
- media: fibromuscular layer (middle, muscula layer) - intima: endothelium & a CT membrane |
|
determinant of BP
|
- Q
- peripheral resistance (PR) - resistance in vascularture system |
|
PR
|
-> resistance to blood flow t hrough the blood vessels
- influenced by blood viscosity & arteriolar tone |
|
hematocrit
|
% of fomred elements in the blood
|
|
oxygen transport
|
- ~97% O2 bound to hemoglobin (Hb)
- oxygen carrying capacity of Hb = 20 ml O2/ 100ml blood |
|
CO2 transport
|
transported as bicarbonate (65%)
|
|
CDC/ACSM recommendations
|
all people over age of 2 should accumulate at least 30 minutes of endurance type physical activity of at least moderate intensity on most - preferably all - days of the week
|
|
purpose of a graded exercise test (GXT)
|
- functional capacity (FC)
- diagnostic/prognositc values - follow-up |
|
ACSM guidelines for stress testing
|
??
|
|
components of physical fitness
|
- cardiorespiratory endurance
- muscluar strength - muscular endurance - flexibility - body composition - balance & cooridnationj |
|
prescribing an exercise program
|
-- Program components:
- warm-up - aerobic conditioning - muscular strength/endur. - cool-down |
|
benefits of warm-up
|
- allows for circulatoy and respiratory adjustments
- inc. blood flow to working muscles - red. risk of injury & muscle soreness - inc. rate of O2 release - inc. muscle temp/dec. muscle viscosity - inc. speed of contraction - dec. incidence of ischemia in CAD patients |
|
passive vs. active warm-up
|
-- passive:
-hot shower, sauna, hot packs -- active: -general -specific -felxibility exercises can be included in both warm-up & cool-down, but NEVER vigorously stretch a cold muscle |
|
conditioning phase - aerobic
|
- frequency: 3-5 days/wk
- duration: 20-60 min - intensity: -60-90% HRmax -50-85% VO2 reserve or HRRmax -RPE (rate of perceived exertion) of 12-16 -- 11-14 for cardiac patients - must keep THR at least 10 beats below ischemic threshold in those with CAD |
|
increasing of frequency, duration & intensity
|
- with these inc., so does the risk of injry
- intensity is most critical variable in improving/maintaining aerobic fitness - once can derive similar benefits at lower intensit if frequency & duration are increased -> if main objective is to improve health & dec. risk of chronic disease vs. optimizing aerobic fitness -- exercise intensity need not be high |
|
PRE
|
- progressive resistance exercise
- as part of comprehensive exercise program, ACSM recommends: ->8-10 exercises covering all major muscle groups ->8-12 reps to volitional fatigue ->at least 2 days/wk (no more than 3 days/wk) ->strict attention to good technique ->perform thru full ROM |
|
flexibility
|
- perform at least 3 days/wk
- take stretch to a position of mild discomfort - hold for 10-30 seconds (static vs. ballistic) - repeat each stretch 3-5 times - emphasize low back and thigh area (tight hamstrings are likely to cause low back pain) |
|
cool-down
|
-- purpose:
-facilitate venous return -prevent pooling of blood in extremities that may lead to syncope -allows for respiratory adjustment (return to pre-exercise levels) ->arrhythmias occur more frequently in ind. that do not cool-down properly |
|
initial level of fitness
|
- the lower the initial level of fitness -> greater improvement
- improvements in aerobic capacity & muscluar strength w/ comprehensive exercise program tend to average about 20% |
|
specificity of exercise
|
- training should be specific to finess component that you are trying to improve
- testing should be specific to type of training involved in |
|
age & gender considerations
|
- rate of improvement may be slightly slower in elderly due to low intensity levels
- men & women respond similarly to exercise programs -- can expect same relative improvements |
|
metabolic equations
|
- useful in determining appropriate workloads when developing aerobic conditioning program
- walking: R+H+V - cycling: R+V |
|
inspiration
|
- active process involving diaphragm & external intercostals
- diaphragm descends w/ inspiration - chest & lungs expansion create negative intrapulonary pressure, allowing atmospheric air flow into the lungs - scaleni, SCM & pectorals assist with labored breathing |
|
expiration
|
- usually a passive process
- diaphragm relaxes & ascends to its upward arched position - lung recoil results in inc. intrapulonary pressure & exhalation of air into the atmosphere - internal intercostals, quadratus lumborum & abdominals activated with forced expiration |
|
O2 delivery & CO2 removal
|
- pulmonary ventilation (inhale & exhale)
- pulmonary diffusion (external respiration):vgas exchange at level of the lung - trasport of O2/CO2 in the blood - capillary gas exchange (internal respiration): gas exchange at level of the tissue/cell |
|
pulmonary diffusion
|
- replenishes O2 content of the blood
- blood releases CO2 that is the exhaled - gas exchange occurs across the respiratory membrane (alveolar-capillary membrane) -alveolar wall -capillary wall -basement membrane |
|
partial pressure of gases
|
- standard atmospheric pressure = 760 mmHg
Partial pressures of atmosphere: - O2=159.1 mmHg -> 20.93% - CO2=0.2 mmHg -> 0.03% - N2=600.7 mmHg -> 79.04 --> PP drop from atmosphere air to into system/lungs |
|
hemoglobin saturation
|
- binding of O2 to hemoglobin is dependent on PO2 & affinity/bonding strength b/t hemoglobin and O2
- inc. PO2 = hemoglobin saturation - inc. tissue temp = enhanced O2 unloading |
|
Bohr Effect
|
- hemoglobin saturation dec. w/ inc. acidity of the blood (dec. pH)
- enhance O2 uploading at the tissues - w/ strenuous exercise -- become more acidit & receive more oxygen |
|
CO2 exchange
|
- although the difference in CO2 PP b/t alveoli & pulmonary capillary blood is only 6 mmHg, CO2 membrane solubility is 20 times greater than of O2
|
|
ventilatory equivalent for O2
|
- VE/VO2 = ratio of ventilation & oxygen consuption per unit time
- measured in L/min - indicated breathing economy - resting VE/VO2 ~23-28 - max exer VE/VO2 >30 (doesn't change much due to ventilation of O2 consumption inc. at ~same rate) |
|
limitations
|
-> pulmonary ventilation is not a limiting factor in exercise
-> central limitation: inability/limit to send O2 to muscles ->periphperal limitation: inability to use O2 sent to them |
|
ventilaroty breakpoint
|
- point during exercise when ventilation rises disproportionately as compared to VO2
- occurs b/t 55-70% VO2max in response to anaerobic glycolysis & subsequent inc. in lactic acid accumulation - HLa is buffered in blood & blown off as CO2 in lungs |
|
post-exercise pumonary ventilation
|
- pulmonary ventilation remains elevated post-exercise secondary to:
dec. pH elevated PCO2 elevated blood temp. -> consistent with elevated O2 post-exercise |
|
factors influencing O2 delivery & uptake
|
-- O2 content of the blood
-hemoglobin normally 98% saturated w/ O2 -- blood flow -flow to muscles inc. with exercise -- local changes (unloading of O2) -inc. acidity (lactate) -muscle temp -CO2 concentration at tissue level |
|
respiratory limitations to performance
|
- rest: ventilation requires ~2% of total energy requirements (VO2)
- heavy exercise: >15% of VO2 used to support needs of respiratory muscles - recovery: ~9-12% of VO2 - ventilation is NOT normally throught to be a limiting factor in exercising except perhhpas in highly trained individuals |