Direct calorimetry uses the measurement of heat production as an indication of metabolic rate. * Indirect calorimetry estimates metabolic rate via the measurement of oxygen consumption. * Energy expenditure can be expressed in L•min-1, kcal•min-1, ml•kg-1•min-1, METs, and kcal•kg-1•hr-1.
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* To convert L•min-1 to kcal•min-1, multiply by 5. 0 kcal•L-1. * To convert L•min-1 to ml•kg-1•min-1, multiply by 1000 and divide by body weight in kilograms. * To convert ml•kg-1•min-1 to METs or kcal•kg-1•hr-1, divide by 3. 5 ml•kg-1•min-1. Efficiency: * Exercise work rate Efficiency decreases as work rate increases * Speed of movement
* There is an optimum speed of movement and any deviation reduces efficiency * Muscle fiber type * Higher efficiency in muscles with greater percentage of slow fibers SUMMARY: Net efficiency is defined as the mathematical ratio of work performed divided by the energy expenditure above rest, and is expressed as a percentage. * The efficiency of exercise decreases as the exercise work rate increases. This occurs because the relationship between work rate and energy expenditure is curvilinear. To achieve maximal efficiency at any work rate, there is an optimal speed of movement. * Exercise efficiency is greater in subjects who possess a high percentage of slow muscle fibers compared to subjects with a high percentage of fast fibers.
This is occurs because slow muscle fibers are more efficient than fast fibers. * Not possible to calculate net efficiency of horizontal running * Running Economy * Oxygen cost of running at given speed * Lower VO2 (ml•kg–1•min–1) at same speed indicates better running economy * Gender difference * No difference at slow speeds At “race pace” speeds, males may be more economical that females 170-188 CIRCULATORY RESPONSE TO EXERCISE Organization: arteries branch to form vessels, vessels become microscopic and form arterioles, which develop into “beds” called capillaries. Capillaries are the smallest and most numerous of blood vessels—exchange of oxygen, CO2, and nutrients. Blood passes from capillary beds to venules that move back to heart and increase in size becoming veins. Mixed venous blood= mixture of venous blood from both upper and lower body in the right side of the heart. *it represents an average of venous blood from entire body.
HEART: Right/left side separated by muscular wall called interventricular septum (prevents mixing blood from sides). Valves: Bicuspid/mitral = left atrioventricular valve **atrioventriculars close when heart contracts to prevent backflow. Tricuspid= right atrioventricular valve Semilunar valve (pulmonary semilunar)- b/w right ventricle and pulmonary artery. Prevents backflow from arteries into ventricles. Aortic valve (aortic semilunar)= b/w left ventricle and aorta. Also prevents backflow… Right side pumps deoxygenated blood to pulmonary circuit so oxygen can be loaded and CO2 released.
Left side pumps oxygenated blood to body via systemic circuit. RIGHT: to lungs LEFT: to body Heart sounds are due to closing of atrioventricular valves (first sound-systole) and the closing of aortic and pulmonary valves (second sound-diastole) Wall of heart is 3 layered: 1) outer layer is epicardium, 2) muscular middle layer called myocardium, 3) inner layer endocardium. Myocardium contracts to force blood out. Right and left coronary arteries supply myocardium Cardiac muscle fibers are shorter than skeletal and are branched and involuntary. Heart muscle fibers are all connected via intercalated discs- transmit electrical impulses.
They are leaky membranes that allow ions to cross b/w fibers (contract together= functional syncytium). *atria contract separate from ventricles because there is a separating layer of CT *heart is only type 1, slow fiber- highly aerobic, many mitochondria (more than skeletal). Cardiac cycle: Systole- contraction phase (blood ejected) Diastole- relaxation period (arterial BP decreases– filling) There is also an atrial systole and diastole. Atrial contraction during ventricular diastole, atrial relaxation when ventricular systole. *SO there are TWO steps of heart pumping. *atria contract together, which empties arterial blood into ventricles. . 1 second and then ventricles contract to deliver blood to systemic and pulmonary circuits.
*when atria relax, blood flows into them from venous circulation as they fill, pressure inside increases. Increase in HR less time spent in diastole (not as much impact on time in systole until at high HR) Arterial Blood Pressure: -greatest in arteries BP = the force exerted by blood against the arterial walls. Determined by how much blood is pumped and the resistance to blood flow. -male: 120/80, female: 110/70 systolic/diastolic dif between the two is calls “pulse pressure” “mean arterial pressure”= av pressure during cardiac cycle. determines rate of blood flow through systemic circuit Mean arterial pressure = DBP + . 33 (pulse pressure) (DBP: diastolic blood pressure) (pulse pressure: dif between systolic and diastolic pressure) SO, if someone has bp 120/80, Mean arterial pressure= 80mmHg + . 33(120 – 80) = 93 mmHg *but this calculation is only used for cardiac cycle at rest.
Hypertension- increases workload on left ventricle so cardiac mass increases, but this eventually results in diminished pumping capacity. Also increase risk for other disease/damage of body parts like brain and kidneys. 20% all US adults Factors influencing arterial BP: ) cardiac output—amount of blood pumped from heart 2) total vascular resistance – sum of resistance to blood flow by all systemic blood vessels. —blood volume, blood viscosity Mean arterial blood pressure = (cardiac output x total vascular resistance) *so increase in either will increase the mean art. BP Blood pressure increases when increase in: blood volume, HR, SV, blood viscosity, peripheral resistance. And it decreases when any of those decrease. BP regulated short term by the sympathetic NS, long term by the kidneys (bc they control blood volume). Baroreceptors- sense arterial blood pressure in carotid artery and aorta.
Increase in pressure send impulses to CV control center which will decrease the sympathetic activity (lowers cardiac output and/or reduces vascular resistance lowers BP). Decrease in BP reduction of baroreceptors activity to brain CV control center increases sympathetic activity raise BP to normal Electrical Activity of the Heart: Sionatrial node (SA node)- in the right atrium (by the vena cava). responsible for spontaneous electrical activity in normal heart, it’s the pacemaker. Occurs due to decay of resting membrane potential (bc of diffusion of NA during diastole).
When SA is depolarized and reaches threshold, a wave of depolarization is spread over the atria contraction! Wave of atrial depolarization needs special conductive tissue to transport it to the ventricles. This conductive tissue is called the atrioventricular node (AV node- in floor of right atrium). When blood from atria empties into ventricles, the conductive pathways branch into smaller fibers called purkinje fibers that spread the wave of depolarization through ventricle so it can contract. Electrocardiogram (ECG)- recording of electrical charges in myocardium during cardiac cycle. –ability of hear to conduct impulses.
P wave- depolarization of atria QRS complex- depolarization of ventricles and atrial repolarization(during beginning of systole, aprx . 10 seconds after Pwave) T wave- ventricular repolarization (same time as QRS, but at the beginning of diastole) CARDIAC OUTPUT (Q): Q = HR X SV Regulation of heart rate: -because SA node controls HR, changes in HR involve factors influencing SA node. Most influence over HR: parasympathetic and sympathetic NS Parasympathetic NS- acts as braking system to slow HR using vagus nerve which touches SA and AV node and releases acetylcholine decrease activity of SA and AV nodes due to hyperpolarization= reduce HR. —initial increase in HR during exrcise up to 100bpm is due to decrease in parasympathetic tone. Sympathetic fibers use cardiac accelerator nerves to innervate both SA node and ventricles.
Increase HR and myocardial contraction when they release norepinephrine. –beta receptors *all beta-blocking drugs will decrease resting HR and exercise HR. CV control center regulates- pressure receptors in right atrial respond when there is increased pressure by increasing Q to reduce the BP. Body Temp also influences HR. increase temp = increase HR Regulation of stroke volume: ) end-diastolic volume (EDV aka “preload”) (volume of blood at end of diastole) 2) average aortic BP 3) strength of ventricular contraction EDV- Frank and Starling, stronger contraction with higher EDV bc there is more stretch of ventricles. EDV influenced by rate of venous return to heart- more return= higher EDV. Venous return regulated by: 1) venoconstriction – reduced volume capacity of veins to store blood. *sympathetic control- activates organ increase HR (the parasympathetic inhibits activation decrease HR) 2) muscle pump—muscles contract and compress veins blood pushed to heart.
Venous return reduced when muscles are contracted. isometric exercise, mechanical. 3) respiratory pump- breathing decreases pressure in chest and increases abdominal pressure so venous blood flows from abdominal into thorax and increases return. *more respiration in exercise Aortic pressure (mean arterial pressure/afterload)- to eject blood, pressure in left ventricle must be more than in the aorta. Increase in aortic pressure= decrease SV. Less afterload during exercise bc arteriole dilation reduces afterload. Circulating epinephrine-norepinephrine (increase Ca+ entry) and direct sympathetic stimulation of heart by cardiac accelerator nerves.
Increase in sympathetic stimulation of heart increases SV at any level of EDV. HEMODYNAMICS: -blood flow is in a continuous loop. Physical characteristic of blood- composed of plasma (watery portion, contains ions/proteins/hormones) and cells (called the hematocrit: RBC/platelets/WBC). Hematocrit= 42% of blood (38% in college women), the rest is plasma. RBCs are largest part of a blood cell—influence viscosity. Anemia decreases RBC, so decreases viscosity Relationships among pressure, resistance, and flow: Rate of flow is proportional to pressure difference. Inversely proportioned to resistance.
Blood Flow= change in pressure/ resistance -Change in pressure is the dif between the two ends of the circulatory system -resistance due to length of vessel and viscosity, and radius of vessel **Blood flow increases with increase in BP or with decrease in resistance. -during exercise blood flow increases mainly due to decrease in resistance with small rise in pressure. Resistance = (length x viscosity)/ radius^4 (**so radius is VERY important-vasoconstriction/vasodilation) Sources of vascular resistance: -vasoconstriction/vasodilation the greatest vascular resistance in blood flow occurs in arterioles.
Pg 188 – 196 Changes in oxygen delivery to muscle during exercise: Metabolic need for O2 increases so there is an increase in blood flow to muscle- increase O2 delivery by 1) increased cardiac output and 2) redistribution of blood flow from inactive organs to working skeletal muscle. Changes in cardiac output during exercise: -cardiac output increases in proportion to metabolic rate for task -maximal cardiac output decreases after 30 yrs of age mostly bc of decreased maximal heart rate with age. Cardiac output = heart rate X stroke volume Max HR = 220 – age (years)
Changes in Arterial-Mixed Venous O2 content during exercise: -change in arterial-mixed venous oxygen difference (a – VO2 diff)during exercise. It represents the amount of O2 taken from 100 ml of blood by the tissue during 1 systemic circuit. The relationship between cardiac output (Q), a – VO2 diff, and oxygen uptake is given by the Fick equation: VO2 = Q X (a- VO2 diff). Fick equation: VO2 is equal to the product of cardiac output and the a-VO2 diff. *SO INCREASE IN CARDIAC OUTPUT OR (a – VO2 diff ) WOULD ELEVATE VO2. Redistribution of Blood Flow During Exercise:
Increase flow to skeletal muscles and decrease to less-active organs like liver, kidneys, GI tract. Increase in muscle blood flow and decrease in splanchnic blood flow change as a linear function of %VO2 max. -at rest aprx 15-20% total cardiac output is directed to skeletal muscles. -during maximal exercise 80-85% of total cardiac output goes to skeletal muscle (to help meet oxygen needs for contracting) -during heavy exercise % that goes to brain is reduced compared to rest. -total coronary blood flow increases due to increase in cardiac output -reduction of blood flow to skin and abdominal organs
Regulation of local blood flow during exercise: Regulated with arterioles in skeletal muscles that have a high vascular resistance at rest (due to adrenergic sympathetic stimulation which causes vasoconstriction). This results in low blood flow to muscle (4-5 ml/min per 100g muscle) but this is still 20-25% total flow from heart. **autoregulation (an intrinsic metabolic control) -vasodilation (opens vessels) results from local changes during exercise like decrease in O2 tension, increase in CO2 tension, nitric oxide, potassium and adenosine concentrations, increase in acidity.
Vasodilation reduces vascular resistance and therefore increases blood flow. Also aided by recruitment of cappilaries- at rest only 5-10% of capillaries are open, all are open during heavy exercise. **level of vasodilation regulated by metabolic need of the muscle (intensity and # of motor units recruited determines blood flow to active muscle fibers) during exercise, vascular resistance in skeletal muscle decreases and vascular resistance to flow in the visceral organs/other inactive tissue increases. *because on increased sympathetic output to these organs regulated by CV control center. increase in visceral vasoconstriction during exercise decreases blood flow to viscera by 20-30% resting value. During exercise in upright position, SV reaches plateau at 40% VO2 max, therefore, at work rate about 40% VO2 max, the rise in cardiac output (Q) is due to increased HR only.
CIRCULATORY RESPONSES TO EXERCISE: HR and blood pressure at any VO2 (oxygen uptake) are higher in arm than in leg -higher HR in hot/humid conditions emotional influence- HR increase with high emotion because increase in sympathetic NS activity. Does not generally alter peak HR or blood pressure during exercise itself but does elevate pre-exercise HR. ransition from rest to exercise- increase in HR and SV and cardiac output at beginning of exercise (after 1st second! ) then if work is constant it plateaus recovery from exercise- recovery from short-term/low intensity is rapid. Recovery after exercise better in trained individuals bc their HR doesn’t get as high. Recovery from long-term is slower because elevated body temp. incremental exercise- HR and cardiac output increase in direct proportion to O2 uptake. More O2 uptake = more blood flow to muscles. Plateau of cardiac output and HR at 100% VO2 max (no more hemoglobin to transport O2).
The increase in HR and systolic BP results in increased workload on the heart (increased metabolic demand on heart estimated by: double product = HR x systolic BP) maximal exercise increases workload on heart by 500% Useful equation to tell patients with coronary artery blockage how they can exercise. **cardiac output increases because decrease in vascular resistance to flow and increase in mean arterial blood pressure. Arm vs. Leg exercise- HR and BP higher in arm because greater sympathetic outflow to heart during arm work when compared to leg work.
Large increase in BP for arms because of vasoconstriction in inactive muscle groups. Large muscles (legs) have more resistance vessels dialated, so there is lower peripheral resistance and lower BP (cardiac output x resistance= pressure). Intermittent exercise- (interval training), recovery of HR and BP depends on level of fitness, environmental conditions, and duration and intensity. Recovery not complete if the temperature is high because that increases HR. with repeated bouts of light exercise, many repetitions can be preformed. Prolonged exercise- cardiac output at constant level.
SV declines while HR increases because the increase (cardiac output constant bc HR increases and balances SV decrease). Cardiovascular drift= increase in HR and decrease in SV during prolonged exercise. , it is due to rising body temp and reduction in plasma volume. Reduction in plasma volume reduces venous return to heart and thus decrease in SV REGULATION OF CARDIOVASCULAR ADJUSTMENTS TO EXERCISE –increase in sympathetic stimulation of heart and vasodilation of arterioles and increase resistance of vessels in less-active areas= increase cardiac output so that blood flow to muscle matches metabolic needs.
Central command- CV change due to centrally generated cv motor signals **also modified by heart mechanoreceptors, muscle chemoreceptors, muscle mechanoreceptors, and pressure-sensitive receptors (baroreceptors) “tuners” during exercise: muscle chemoreceptors- muscle metabolites (K, lactic acid, etc. ) muscle mechanoreceptors- force and speed of muscular movement baroreceptors- change in arterial BP- regulate arterial BP Page 267-269, 277-280 VO2 max = HR max X SV max X (a- vO2 dif)max STROKE VOLUME SV = End diastolic volume(EDV) – End systolic volume (ESV) *EDV increase ecause increase in ventricle size/increase in venous return (“preload”), increase in myocardial contractility, and decrease in resistance to blood flow out of heart (“afterload”) End diastolic volume (EDV) Left ventricle increase with endurance training bc of volume loading during exercise Plasma volume increases with endurance training (loss of plasma volume = decrease VO2 max in first weeks of detraining) **EDV increase with training. FRANK-STARLING MECHANISM: increase stretch of ventricle = increased SV Cardiac contractility- strength of contraction when fiber length, afterload, and HR are constant.
Afterload- peripheral resistance against which the ventricle contracts in order to push portion of EDV into aorta. Decrease in resistance = increase max cardiac output, SO arterial BP is unchanged (MAP = Q x TPR) **endurance training lower resistance in working muscle to facilitate higher blood flow blood pressure falls when muscles capacity for blood flow exceeds hearts ability to provide it.. —to maintain BP some of muscle mass is vasoconstricted (other is vasodialated) training decrease resistance of vascular bed to match increase in max cardiac output to maintain BP Arteriovenous O2 difference: increase in difference could be due to elevation of the arterial oxygen content, or decrease in the mixed venous oxygen content. -increase capacity of muscle to extract O2 after training probably because increase in capillary density (mitochondria too) accommodate more blood flow *training-induced increase in maximal SV due to increase in preload and a decrease in afterload.
Preload increased because end diastolic ventricular volume and associated increase in plasma volume. Afterload decreased because decrease in arteriolar constriction in trained muscles increases maximal muscle blood flow but no change in mean arterial BP. in young, sedentary ppl, 50% of increase in VO2 is bc of increase in systemic a-VO2 dif (due to increase in capillary density). Decrease in VO2 max when you stop training because decrease in max SV and decrease in oxygen extraction. 277-280 net cost of walking is ? of net cost running use pace maker test for kids field test for CRF use walking, running, stepping. Can test many ppl at low cost. Hard to measure response for some, and motivation can be a variable. VO2 max estimates from all-out run tests are based on the linear relationship b/w running speed and oxygen cost of running.
VO2 max estimated in endurance test is influences by CV function and % body fat. Canadian home fitness test: submaximal, uses lowest two 8-inch steps in a staircase. Evaluates cardiorespiratory fitness using post-exercise HR. 1 mile walk test: VO2 based on age, weight, sex, time, HR improved fitness: lower HR and/or time and higher VO2 max cardiorespiratory fitness measured using: treadmill, cycle ergometer, stepping bench measured by: palpation (carotid/radial artery), stethoscope (systolic- 1st korotkoff sound, diastolic- 4th sound), ECG ncreased metabolic demand on heart estimated by: double product= HR x systolic BP -double product is estimate of myocardia O2 demand arrhythmia- irregularity in normal electrical rhythm: atrial fibrillation, premature contractions conduction disturbances- depolarization is slowed/blocked (first-degree AV block or bundle branch block) myocardial ischemia- inadequate perfusion of the myocardiumflow limitation= O2 insufficiency (angina pectoris- symptom)(ST segment depression-sign upsloping, horizontal, downsloping—downsloping is worst) teady state:
HR measured over 15-30 seconds post exercise HR: measured for 10 seconds within first 15 seconds of stopping exercise, then multiple the # by 6 HR and systolic BP increase with exercise intensity * Typical measurements obtained during a graded exercise test include heart rate, blood pressure, ECG, and rating of perceived exertion. * Specific signs (e. g. , fall in systolic pressure with an increase in work rate) and symptoms (e. g. , dizziness) are used to stop GXT. VO2 max: “gold standard” to measure CRF VO2 increases with increasing loads on a GXT until max capacity reached- VO2 estimated based on final work rate achieved in graded exercise test- can also be estimated from HR responses to submaximal exercise using age, also consider environmental factors.
Estimation of VO2 max from last work rate: Poorly fit individuals take longer to achieve the steady state at moderate/heavy work rates may overestimate the VO2 max when using formula Estimation of VO2 max from submaximal HR response: HR plotted against work rate (or estimated VO2) until termination criterion of 70%- 85% of age-adjusted maximal HR reached (220-age). careful of environmental factors- dehydration, temp, emotions, medication * VO2 max Estimation of VO2 max from Last Work Rate Estimation of VO2 max from Submaximal HR Response CRITERIA FOR ACHIEVING VO2 MAX: * Leveling off of VO2 with higher work rate <150 ml•min–1 or <2. 1 ml•kg–1•min–1 * Post-exercise blood lactate >8 mmoles•L–1 * R >1. 15 * HR within 10 beats•min–1 of age-predicted maximal HR * Usefulness has been questioned * Should not expect subjects to meet all criteria * Graded Exercise Test: Protocols Treadmill Cycle Ergometer Step Test * Graded Exercise Tests: Measurements
Heart Rate Blood Pressure ECG Rating of Perceived Exertion Termination Criteria Treadmill- don’t have to adjust for body weight in calculation because subject is carrying their own weight ( so VO2 is proportional to weight). Health or cardiac risk inventory—PAR-Q (physical activity readiness questionnaire) – heart condition, pain in chest when doing physical activity, lose balance/dizziness/lose consciousness, bone/joint probs, drugs/meds for BP or heart condition * Estimating VO2 max * Based on extrapolating submaximal HR during incremental test * YMCA protocol