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UM / Kinesiology / KIN 321 / What is the study of energy exchange in physical science?

What is the study of energy exchange in physical science?

What is the study of energy exchange in physical science?

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School: University of Miami
Department: Kinesiology
Course: Introduction to Systemic Exercise Physiology
Professor: Kevin jacobs
Term: Fall 2016
Tags: KIN321 and SystemicPhysiology
Cost: 50
Name: KIN321 Exam 2 Study Guide
Description: Lecture 7-12
Uploaded: 10/15/2016
41 Pages 136 Views 8 Unlocks
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KIN321 Class Notes Week 1 (8/22­8/26)


What is the study of energy exchange in physical science?



________________________________________________________________________________ From previous sections

­ N/A

________________________________________________________________________________ Lecture 1 Bioenergetics and Calorimetry

● Thermodynamics = study of energy exchange in physical science. ○ 1800s ➙ ability to predict work output of steam engines. ● Bioenergetics = study of the exchange of energy in the biological world. ● 1st Law of Thermodynamics ➙ Energy can be neither created nor destroyed, but only converted from one form to another.

● 2nd Law of Thermodynamics ➙ The exchange of energy is imperfect and some energy will escape.


What is the study of the exchange of energy in the biological world?



○ Loss of heat

● ATP is used for many functions including:

○ Chemical work ➙ driving reactions that are not spontaneous ○ Transport ➙ movement of substances against concentration gradients (Na+ - K+ pump)

○ Mechanical work ➙ “crossbridge cycling”

● [ATP] changes very little even during intense exercise.

● Metabolism is sum of all energy transformations within an organism. ○ Impossible to measure ➙ ∴ metabolism is the rate of heat production.

● Calorimetry is measurement of heat to determine metabolic rate. ○ Direct calorimetry involves the measurement of heat production.


What is the content of the 1st law of thermodynamics?



■ Bomb Calorimeter determines caloric content of food Don't forget about the age old question of Is human conflict unavoidable?

■ Room Calorimeter determines heat production (closed room measuring temp change)

○ Indirect calorimetry involves the measurement of oxygen consumption

● Caloric Equivalents of Food

If you want to learn more check out How can you tell if someone is malingering?

○ Protein’s energy density is lower inside the body than outside the body because human can’t use nitrogen (in proteins) as energy ○ Protein is a building block for muscle, hence if using protein as fuel it breaks them down

○ Carb is prefered energy source during exercise as it gives more kcal/L of O2 consumption

● Vco2/VO2 ratio (R ratio)

○ Range 0.7~1.0

○ This number is determined because of the structures of protein and fat

____________________________________________________________ Lecture 2 Digestion & Absorption

● Functions of food

1. Energy

2. Growth & Development

3. Regulation of metabolism (how the body uses fuels) We also discuss several other topics like How does the vascular cambium give rise to xylem?

● Carbohydrates

○ Not good optimal energy to be stored because of low caloric density

○ Monosaccharides, Disaccharides,

Oligosaccharides/Polysaccharides

■ Only fructose, glucose, and galactose can be absorbed

■ Mono and Disaccharides are “simple sugar”

● Lipids

○ Simple: Triglycerides,

○ Compound: Phospholipids, Lipoproteins, Chylomicrons (how triglycerides appear in blood)

○ Derived (body can produce): Cholesterol

○ No double bond = saturated (tend to be solid in room temperature e.g. butter)

○ One double bond = monounsaturated

○ More double bond = polyunsaturated

○ Trans fat→ “partially hydrogenated” as code name

■ ^ shelf life

■ Bad, increases LDL-C and lowers HDL-C

● Protein

○ Combination of up to 20 dierent amino acids via peptide bonds. ■ C, H, amino group (Nitrogen), carboxylic acid group, and side chain.

● Why GI function is important to exercise?

○ Dehydration, Hyperthermia, and CHO depletions are common causes of fatigue during prolonged exercise If you want to learn more check out What sort of information do we rely on to form first impressions?

● Small intestine: absorbs macro nutrients, water, and electrolytes ○ Glucose and Amino Acids absorbed go into the Liver before they enter the circulation

● Large intestine: absorbs water and electrolytes ONLY

● Gastric Emptying:

○ Stomach is a holding tank-> only a small amounts of alcohol and vitamin B12 is absorbed here

○ Stomach’s elasticity (rebound eect) pushes food into small intestine, therefore, gastric emptying poses limiting factor for absorption

○ how to measure gastric emptying?

■ ingest uid with dye, put tube into the stomach through GI to extract samples to see how much does the dye go away ● Gastric emptying is controlled to ensure delivery of water and solute at rate slightly less than intestine’s absorptive capacity ● Factors inuencing gastric emptying:

○ Volume ➙ ↑ V = ↑ emptying rate. If you want to learn more check out Are polyunsaturated fatty acids good for you?

○ Energy content ➙ ↑ energy = ↓ emptying rate.

■ < 6-8% CHO, 6-8 g CH2O/L recommended.

○ Osmolality ➙ ↑ osmolality = ↓ emptying rate.

■ Glucose polymers

○ Exercise ➙ > 70-75% VO2max ↓ emptying rate.

○ Dehydration ➙ ↓ emptying rate.

○ Optimal uid/CHO replacement ➙ 30-60 g CHO/hour in a 6-8% solution ingested at a rate of 600-1200 ml/hour. We also discuss several other topics like What is the meaning of progressives?

● 1.4g of CHO/min is the max avg rate for CHO to be absorbed ○ So don’t take more than ~70g of CHO per hour

● Intestinal Digestion:

○ The majority of CHO digestion happens in the small intestine ○ The majority of FAT digestion happens in the small intestine ■ Bile breaks down large fat droplets into smaller pieces for pancreatic lipase to further break down (breaks fat into FA, diacytlglycerols, and monoacytlglycerols)

○ The majority of PROTEIN digestion happens in the stomach ■ and it also extend into the intestinal epithelial cells

● Intestinal Absorption:

○ Small intestine divided into:

■ Duodenum

■ Jejunum

■ Ileum

● Surface area of small intestine is increased up to 600 fold by: ○ Circular folds (x3)

○ Villi (x10)

○ Brush border (x3)

● The time from ingestion to blood appearance for:

○ glucose ~15min

○ fat ~2-4hrs

CHO:

● Glucose and galactose are actively transported by sodium- and glucose-linked transporter molecule (SGLT-1)

○ SGLT-1: glucose, galactose, sodium, and water (like GLUT-4) ● Fructose moves by facilitated GLUT-5 transporter

● goes into the liver

LIPIDS:

● ingested long chained fat turns into chylomicrons in the epithelial cells, then into the lymph system, then into bloods

PROTEINS:

● active transport, go into the liver

H2O:

● Water always moves to where it has more particles, to dilute the uid ● Majority are absorbed in the small intestine (85%)

● Water absorption can occur passively via osmosis or actively via SGLT-1. ○ SGLT-1 mediated water absorption may account for up to 70% of total water absorption.

KIN321 Class Notes Week 2 (8/29­9/2)

________________________________________________________________________________ From previous sections

­ Bioenergetics and Calorimetry

­ Digestion & Absorption

________________________________________________________________________________ Lecture 3 ATP, CP, and Glycolysis

● 3 major ATP generating methods:

○ Creatine Phosphate (v. rapid)

○ Glycolysis (rapid)

○ Oxidative Phosphorylation (slow)

● Benet of low resting ATP: to maintain metabolic sensitivity ● Slow Glycolysis

○ All the pyruvate can be oxidized in the mitochondria

■ Doesn’t need to produce lactate

○ Rate of NAD+ regeneration is enough from shuttle

● Rapid Glycolysis

○ Rate of pyruvate production > pyruvate oxidation

○ Rate of NAD+ regeneration via mitochondrial shuttle is insucient ○ Therefore, lactate is produced to recycle o the rate-limiting factors

■ RBC all the time, take in glucose spit out lactate

■ Type IIB bers across a wide range of exercise intensities ● ∵ low mitochondrial density ∴rate of pyruvate

production > oxidation early

■ Type I bers only at max intensity because of high

mitochondrial density

■ Lactate can be oxidized at the production site, or be sent through blood to another site (heart mainly) to be oxidized. Or → liver (gluconeogenesis) → glucose

■ Lactate can be seen as a glucose (CHO)/Energy group to be donated from one muscle to another

■ The CORI cycle: Muscle produce pyruvate/lactate → liver take them to make glucose → muscle for fuel

● Lactate threshold test → the lactate threshold indicates the intensity at which one can withhold for a prolonged period of time

● Lactate is more metabolically ecient* ∵only 1 step Lactate → Pyruvate ∴Body oxidizes it more than glucose when it becomes more prevalent ● Intracellular lactate shuttle: NADH shuttle to produce NAD+ ○ Pyruvate/Lactate Carrier (MCT) is found on the mitochondrial membrane

○ LDH found inside the mitochondria turns lactate and NAD+ into pyruvate and NADH

○ This shuttle substrates into mitochondria for ATP production (while the other two shuttle NADH in)

○ This shuttle adds on to the other two shuttles when lactate level is really high

■ E.g. during rapid glycolysis and recover period

● Lactate causes fatigue by leading to lactate acidosis?

○ Lactate actually consumes H+ to buer muscle acidosis

____________________________________________________________________________ Lecture 4 Lipid Metabolism

● Lipid mobilization is dependent on:

1. Rate of lipolysis

2. Rate of re-esterication

3. Rate of fatty acid export via circulation

○ Fatty acid is either re-esteried or enter the circulation

○ Glycerol always goes to the blood → liver

■ Therefore glycerol level in blood is a good lipolysis rate indicator ● At times of stress, you always mobilize energy

○ Epi → Lipolysis

○ Insulin (storage) → Lipolysis inhibitor

● Proportion of fatty acid re-esteried is high during

○ rest (body doesn’t need much fuel)

○ high intensity exercise (reduced blood ow to adipose tissue & increased need for glucose)

○ FA → circulation is 30-50% during rest, but 65-80% during

low/moderate exercise, 10-30% during high intensity exercise

■ Railroad switch, provide immediate supply of FA for energy

● FA are transported in the plasma in association with protein albumin → thre high anity FA binding sites

● Lipid uptake is likely facilitated transport instead of passive diusion because of Saturated Kinetic, which the plasma FFA Uptake level plateaus with increasing FFA concentration in blood

○ Only that many transporters can work simultaneously at a time ● Three key fatty acid transporters identied:

1. Sarcolemmal FABP → membrane bound (low rate, working 24/7) (at sarcolemma)

2. FAT/CD36 → translocated from sarcoplasm (move when needed, recruited after meal, during or after exercise) (at sarcolemma) 3. Cytosolic FABP (moves fat within the cytosol)

● Abundance of fatty acid transporters increase with:

1. Endurance training (pushing ability to oxidize fat)

2. High fat/low CHO diets

● FA in the sarcoplasm have two potential fates:

○ Prior to either fates, FAs are activated using ATP and forms fatty-acyl CoA

1. Esterication into intramuscular triglyceride (IMTG)

a. IMTG is important for exercise recovery

2. Transport into mitochondria for oxidation

● Fatty acids must enter mitochondrial matrix to undergo oxidation ○ Short- and medium-chain fatty-acyl CoA enter via specic carrier protein → little or no regulation

○ Long-chain fatty-acyl CoA enter via carnitine and carnitine acyl transferase enzymes (CAT1 and CAT2)

■ CAT1 takes CoA o, puts on carnitine

■ CAT2 reverses the process, takes carnitine o, put on CoA from the matrix

■ ∴ CAT is the rate-limiting enzyme of long chain fat oxidation ● High intensity exercise inhibits CAT1

● Carnitine-decient patients have reduced capacity to oxidize lipids

● Beta oxidation

○ Creates Acetyl-CoA → TCA cycle; FADH2, NADH → Electron Transport Chain

○ Promoters = low Acetyl-CoA, low NADH/NAD+ 

■ Low intensity exercise

■ CHO depletion

○ Inhibitors = high Acetyl-CoA, high NADH/NAD+ 

■ High exercise intensity

■ CHO supplementation

● Metabolism during recovery

○ Need to rebuild glycogen storage

○ Thus increased fat oxidation as fuel

○ Low RER values during recovery from exercise = heavy reliance on fat as a fuel source

○ Although CHO is primary energy source during moderate to high intensity exercise, lipid oxidation is substantial during recovery ○ Lipid oxidation is the same during recovery from 45 and 65% VO2peak as long as exercise energy expenditure is the same

■ “Fat burning zone” is not necessary/valid

■ ^ energy expenditure (cal burned) = ^ fat burned afterwards

KIN321 Class Notes Week 3&4 (9/5­9/13)

________________________________________________________________________________ From previous sections

­ ATP, CP, and Glycolysis

­ Lipid Metabolism

________________________________________________________________________________ Lecture 5 Amino Acid Metabolism & Exercise Metabolism

● Nitrogen is metabolically useless; we can’t use it as fuel

● Use of amino acids as fuel sources limited to fasting and prolonged exercise (depletion of CHO)

● Nitrogen can be removed from amino acids by one of two ways: ○ Oxidative deamination

■ Occurs ONLY in the mitochondria of the LIVER and involves NAD+ as an oxidizing agent

○ Transamination

■ Occurs in many tissues (including muscles) and involves the transfer of nitrogen

○ They all compounds the nitrogens to get rid of it through the Urea Cycle ■ When ppl consume excess protein, Nitrogen content goes up in the urea

■ High protein diet → increased urea amount & frequency → loss of water weight

● Most amino acids carbon skeletons are converted to either:

1. Pyruvate

2. Acetyl-CoA

3. TCA cycle intermediates

○ BCAAs are preferentially oxidized

■ Use of BCAA as a fuel source begins with transamination to glutamate ● Gluconeogenesis

○ ONLY IN LIVER (& small portion in kidney)

○ Pyruvate → Alanine → Gluconeogenesis

○ Enzymes for conversion: Alanine/Lactate → Pyruvate → Pyruvate Carboxylase → PEPCK → F1, 6BP (reverse PFK) → G6P → Glucose ● Regulation of CHO metabolism

● Regulation of Lipid metabolism

● Endogenous fuel stores

○ Fat is a very ecient form of energy storage

■ 9 kcal/g for fat vs. 4 kcal/g for CHO

■ Each gram of CHO stored with 3g H2O → compounds storage ineciently

○ CHO is a more ecient source of energy during exercise

○ AA contributes 15% of energy fasting/prolonged exercise, 5% when fed ● Substrate partitioning during exercise

○ Exercise intensity is primary factor, all others are secondary

○ Duration

○ Fuel availability → Diet and exercise duration

○ Gender (During prolonged moderate exercise, female tend to use more fat than male)

○ Ambient temperature

● Why does relative contribution of lipids decrease with increasing intensity? ○ Higher necessary ATP re-synthesis rates

○ CHO metabolism regulates lipid metabolism → inc. glycolytic ux likely decreases long-chain FA transport into mitochondria (inhibits CAT enzymes) ○ Inc. recruitment of fast twitch bers

○ Decreased FFA availability → reduced adipose blood ow and lactate

● Exercise duration

○ Inc. exercise duration results in:

■ Inc. reliance on plasma sources of fuel (glucose and FA) and dec. reliance on intramuscular fuel sources (glycogen, IMTG)

■ Inc. reliance on lipids and dec. reliance on CHO

○ Approx. depletion times of CHO during moderate exercise

■ Muscle glycogen: 60-90 min

■ Liver glycogen: 80-120 min

● Ingestion of CHO during exercise spares liver glycogen (glucose absorbed goes right into circulation and to muscles) → protect blood glucose level → support longer exercise, and higher race pace/intensity

● Training adaptations

○ Endurance training → adaptations that favor greater reliance on lipids at the same absolute intensity

■ Inc. capillary density

■ Inc. expression of sarcolemmal FA transporters

■ Inc. mitochondrial density

● Higher activities of beta-oxidative enzymes

● Higher activities of TCA cycle enzymes

○ However, pattern of use at the same relative intensity is unaltered by endurance training

■ CHO needs are not reduced by such training and instead are likely increased due to:

● Improved ability to sustain higher exercise intensities

● Improved ability to sustain longer exercise durations

∴ People think CHO doesn’t matter that much in a trained state is wrong

________________________________________________________________________________ Lecture 6 Neural-Endocrine Control of Metabolism

● Hormones - chemical messengers that act either locally (acetylcholine, Nepi) or generally (Epi, Nepi, insulin, glucagon, etc.)

○ Polypeptide hormones interact with receptors on cell surface

○ Steroid hormones move through cell membrane and interact with cell nucleus

○ Hormones generally have three eects:

■ Alter permeability of cell membrane to metabolites or ions

■ Activate an enzyme or second messenger (Epi → cAMP → HSL → Lipolysis)

■ Activate genetic apparatus to manufacture intracellular proteins (Steroid Hormones)

● Insulin

○ Translocates GLUT-4 to cell membrane to increase glucose storage into the cell

● Cyclic AMP

○ Increase 1) Glycogenolysis 2) Lipolysis 3) Hormone release

● Hormone regulation and action

○ Endocrine Glands:

■ Hypothalamus and pituitary glands (growth hormone)

● Hypothalamus controls activity of the anterior and posterior

pituitary glands; it also receives neural input and is sensitive to

blood metabolite concentrations (esp glucose, some lactate)

● Growth hormone is essential for normal growth (protein

synthesis and bone growth)

○ It increases during acute exercise

○ Mobilizes fatty acids from adipose tissue (secondary to Epi)

○ Aids in the maintenance of blood glucose by increasing

gluconeogenesis and reducing uptake by adipose tissue

■ THyroid and parathyroid glands

■ Adrenal glands (Cortisol/Catecholamines i.e. Epi, Nepi)

● Adrenal medulla secretes Epi and Nepi

○ Promotes lipolysis, liver and muscle glycogenolysis (glucose

breakdown)

○ ^VO2max intensity ^CATs (positive linear correlation due to

sympathetic signals)

● Adrenal cortex secretes

○ Aldosterone → maintain plasma Na+/K+ and regulates BP

○ Cortisol → promotes lipolysis, protein catabolism, and

gluconeogenesis

■ Pancreas

● Secretes digestive enzymes and bicarbonate into small intestine ● Insulin → promotes the storage of glucose, amino acids, and fats ● Glucagon → promotes the mobilization of glucose from the liver and FA from adipose tissue

■ Testes and ovaries (Testosterone/Estrogen)

● Estrogen may promote lipolysis BUT progesterone seems to have anti-estrogen eects on metabolism

● Estrogen spikes late follicular phase → higher rate of lipolysis,

countered by spike of progesterone during mid luteal phase of

the menstrual cycle

● Hormone potency is a function of:

○ Concentration (High [epi]=0.003mg/5L blood)

○ Receptor density (^receptor ^potency)

○ Durability and half-life

● Hormone eects:

○ Metabolism

■ Supply or mobilization

■ Use

○ Fluid Balance

○ Blood pressure

○ Muscle repair and hypertrophy

● Eect of acute and chronic exercise on Insulin, Glucagon, and Epi ○ Insulin

■ Acute: Reduction in [insulin] from rest to exercise

● Increasing time since last meal

● Epi-induced inhibition of insulin secretion

● Increased importance of contraction for glucose uptake (Insulin not needed for GLUT-4 anymore since muscle contraction can do the trick)

■ Chronic: Reduction in [insulin] at rest following training

● Training-induced increase in insulin sensitivity

○ Glucagon (not important for exercise, important during starvation) ○ Epinephrine

■ Acute: Increase in [epi] from rest to exercise

● Sympathetic stimulation of the adrenal medulla that is

proportional to the intensity of exercise

■ Chronic: Lower [epi] during at the same absolute intensity, but similar [epi] at the same relative intensity following training

● Catecholamine (CAT) release scales to relative exercise intensity whether the subject is untrained or trained

KIN321 Class Notes Week 5 (9/19­9/23)

________________________________________________________________________________ From previous sections

­ Amino acid metabolism

­ Neural­endocrine control of metabolism

________________________________________________________________________________ Lecture 7 The Heart and the Cardiac Cycle

● Cardiovascular Functions

○ Distribution

■ O2 to tissues and CO2 from tissues to lungs

■ Nutrients to tissues

■ Hormones

■ Waste products

○ Hemostatic regulation

■ Fluid balance and blood pressure (blood ow)

■ Maintain pH

■ Maintain thermal balance

● Vasodilation to get rid of heat

● Vasoconstriction to keep warm

○ Protection

■ Prevention of blood loss (vasoconstrict)

■ Prevention of infection

● Basics of Heart

○ Size of st → approx. ½ pound

○ Four chambers

■ Left & Right Atria (thin myocardium because of low resistance & short distance)

■ Left ventricle

● Thicker and usually larger ventricle, pump blood to the whole

body

● Left ventricle hypertrophy is due to:

○ Hypertension, increased resistance & pressure in the aorta

○ Endurance training, volume overload overtime

○ Resistance training, pressure overload

■ Right ventricle pump blood to the lungs

● Thinner due to low BP in the lungs (due to very high surface area)

● Right ventricle hypertrophy is due to COPD, increased pressure in lungs

○ Base at 2nd rib

○ Apex at 5th or 6th rib

■ Important for placing electrodes for ECG

○ Non-contractile layers:

■ Pericardium → double-walled, loose-tting sac

● Parietal → brous protection, anchor + smooth surface

● Pericardial cavity

● Visceral (epicardium) → smooth surface + coronary arteries

○ Contractile layers:

■ Myocardium → Cardiac muscle

○ Endocardium (innermost layer)

○ Valves of the heart assure unidirectional ow of blood

■ Atrioventricular

● Tricuspid on right

● Mitral on left

● Chordae tendonae and papillary muscles hold valves closed

during ventricular contraction

■ Semilunar

● Pulmonic on right

● Aortic on left

● The Cardiac Cycle

○ Systole - Contraction phase (ventricular contraction)

○ Diastole - Relaxation phase (lling of the ventricle)

■ Where the perfusion to myocardium occurs

○ When HR goes up, time for diastole decreases dramatically

1. Waste-carrying, oxygen-poor blood enters the right atrium from the superior and inferior venae cavae

2. Blood ows from the right atrium into the right ventricle; from there it is pumped through the pulmonary arteries into the lungs

3. In the lungs, blood picks up oxygen and discards carbon dioxide; it then ows through the pulmonary veins into the left atrium

4. Oxygen-rich blood ows from the left atrium into the left ventricle; from there it is pumped through the aorta into the rest of the body’s blood vessels ● The Myocardium

○ Similarities to skeletal muscle:

■ Striated with myobrils containing actin (thin) and myosin (thick) laments

■ Surrounded by sarcolemma

■ Depolarize before contracting

○ Dierences from skeletal muscle:

■ Tightly connected by intercalated disks and gap junctions → complete synchronous contraction (contract at the same time; no lag/delays) ● Minimal electrical resistance → all or none contraction of entire heart compared to entire motor unit of skeletal muscle

■ More developed capillary network

■ Greater mitochondrial volume (~40%) than skeletal muscle (~2-6%) ■ Inherent rhythm (involuntary) → no need for neural innervation ■ 10-15min lack of Q to myocardium can cause death of tissue

● Action Potentials in Cardiac Tissue

○ Atrial and ventricular syncytium separated by atrioventricular brous tissue ■ This allow time for blood to ll the ventricle before the action potential arrives and forces the contraction to pump blood out

1. Sinus node (SA node)

a. SA node is leaky to Na2+ → less negative resting membrane potential i. Thus it has an inherent rhythm of 100-120bpm

b. Parasympathetic nervous system (Vagal tone) slows it down to 60-80bpm

2. Atrioventricular node (AV node)

a. Impulse delayed at AV node to allow ventricular lling

3. Right & Left bundle branch

4. Purkinje bers

a. Nearly instantaneous transmission → 0.03s from top bundle of branches to furthest ends

b. Ventricular muscle bers wrap around heart in double spiral → ventricles are emptied in a wringing motion ( )

● Normal ECG

○ Atrial repolarization is hidden behind QRS

○ Shape of QRS curve is due to the spread of action potential is AV node → 2 branches → tons of purkinje bers

● Blood Vessels

●SystemicandPulmonaryBloodPressure

● Physical Characteristics of Blood

○ Plasma

■ Liquid portion of blood

■ Contains ions, proteins, hormones

○ Cells

■ Red Blood Cells

● Contain hemoglobin to carry oxygen

■ White Blood Cells

■ Platelets

● Important in blood clotting

________________________________________________________________________________ Lecture 8 Control of Circulation; Cardiovascular dynamics during exercise

● Vascular Smooth Muscle

● Vascular smooth muscle designed to:

○ Regulate blood ow to active tissue

○ Maintain systemic BP

● Dierences from skeletal muscle bers include:

○ Smaller and not striated

○ Contract more slowly

○ Capable of maintaining vascular tone with little energy

● Controlled by factors including:

○ Local → (exclusively vasodilator)

○ Humoral → substances owing in the blood

○ Neural → (exclusively vasoconstrictor)

● Determinants of Blood Flow

○ Rate of Q is determined by blood pressure

○ BP = CO x TPR

○ At constant cardiac output (rest, steady state exercise), Q is regulated by changing TPR via vasoconstriction or dilation

○ Increased TPR is common cause of hypertension

○ Q is aected by:

■ Pressure dierence between inow and outow → ^P1-P2 = ^ow ● CO primarily inuences P1

■ Radius → ^R = ^ow (small changes in radius, big changes in ow) ■ Viscosity → ^V = dec. ow (higher viscosity more sticky)

○ How do you accomplish 25 fold increase in Q to active skeletal muscle during exercise?

■ ^CO (^P1)

■ Vasodilate at areas of need (decrease P2)

■ Vasoconstric at areas of unnecessity

■ Maintain viscosity

○ Perfusion to brain unchanged during exercise

● Local control of Q

○ Q increases exponentially with increased metabolism

○ Increased rate of local metabolism signaled by:

■ Metabolites → ^adenosine, ^lactate

■ Gas partial pressures → dec. PO2 and ^PCO2 

■ Ions → ^H+ and ^K+ 

■ NO, potent vasodilator at endothelium

● Damage to the arterial wall is the rst step for coronary diseases ■ Flow mediated dilation: decrease when people have disease, ^ with endurance training

● Renin-Angiotensin System

1. Reduced blood ow through kidneys

2. Kidneys secrete hormone renin

3. Renin splits angiotensinogen from liver to produce angiotensin I 4. Angiotensin converting enzyme (ACE) from the lungs converts angiotensin I to angiotensin II

a. Vasoconstriction

b. Aldosterone release by adrenal cortex → water retention by kidneys 5. Increased BP

- Caused by:

- Dehydration (^viscosity, decreased ow, decreased BP)

- Acute blood loss from injury

● Neural Control of Blood Flow

○ Sympathetic nerve bers innervate all blood vessels except capillaries → almost exclusively vasoconstrictor 

○ Kidneys, gut, and skin most heavily innervated → skeletal muscle and brain under less inuence

○ Neural control does not distinguish between active & inactive muscles ■ It needs to be layered with local factors, so Q goes to desired places ■ Therefore neural and local controls need to work together for it to work

● Myocardial Blood Supply

○ Danger of high DBP: Even during diastole that BP is high → low perfusion to myocardium (low pressure dierence to pump blood into myocardium) ○ DBP don’t usually drift that much during exercise; so if DBP goes up, exercise needs to stop

● Cardiovascular Regulation and Control

○ Ultimate goal of neural regulation of cardiovascular function is to maintain arterial BP

○ Heart is directly innervated by both the parasympathetic and sympathetic division of the ANS

■ Parasympathetic nervous system

● Vagus nerve innervates SA and AV nodes, atrial myocardium

● Slows HR by inhibiting SA node

● Decreases atrial contractility

■ Sympathetic nervous system

● Innervates SA and AV nodes and ventricular myocardium (wide spread eects)

● Increases HR by stimulating SA node

● Increases ventricular contractility (^SV)

■ (Parasympathetic inuence predominates at rest)

○ HR has a linear increase with exercise intensity and VO2 

○ HR is the most important factor increasing CO during exercise. (SV can only goes up so much)

○ SV plateaus ~40-50% VO2max 

■ SV = EDV - ESV

● ^EDV when:

○ ^HR

○ ^Venous Return

○ ^Ventricular compliance

● ^ESV when: ^Afterload (pressure the heart must pump against to eject blood)

● Decreased ESV when: ^Contractility

■ Frank-Starling mechanism:

● Greater preload results in stretch of ventricles and in a more

forceful contraction

● ^venous return = ^contractility

● Intrinsic to the heart (can beat on its own)

● Length-tension relationship of muscle cross bridges

■ ^Venous return → ^EDV (stretch of cardiac muscle bers + sympathetic stimulation) → ^contractility → deceased ESV → ^SV

● Oxygen Delivery During Exercise

○ ^O2 delivery accomplished by:

■ ^CO

■ Redistribution of Q to skeletal muscle

● (a-v)O2 Dierence

○ VO2max = COmax x (a-v)O2 dierence 

○ Range of ~ 5 to 16 ml O2/100ml

○ VO2max is limited by max CO

KIN321 Class Notes Week 6 (9/26­9/30)

________________________________________________________________________________ From previous sections

­ The Heart and the Cardiac Cycle

­ Control of Circulation; Cardiovascular dynamics during exercise

________________________________________________________________________________ Lecture 9 Pulmonary Anatomy and Physiology

● Pulmonary Anatomy

○ Conducting zone: Trachea, bronchial tree, bronchioles (Anatomical dead space)

■ Conduct air to respiratory zone

■ Humidify and warm air

○ Respiratory zone: Respiratory bronchioles, alveolar sacs

■ Exchange of gases between air and blood

○ Alveoli structure optimizes gas exchange:

■ Extremely large alveolar surface area → 50m2 for an avg. person with body surface area of 1.5m2 

■ Minimal distance from pulmonary capillaries

● Exercise increases capillary count

■ High fat content (gas are more soluble in fat than liquid H2O) ○ Muscles of inspiration: (always active)

■ External intercostals

■ Diaphragm!

○ Muscles of expiration: (only active during exercise)

■ Internal intercostals

■ Abdominal muscles

● Mechanics of Ventilation

○ Rest:

■ Contract diaphragm and external intercostals

■ Lower oor of thorax, increase thoracic volume, and decrease intrapulmonary pressure

■ Atmospheric air rushes in to equilibrate pressure gradient ■ Passive expiration

○ Exercise: (needs more rapid gas exchange)

■ Contract diaphragm and external intercostals + supplementary inspiratory muscles

■ Lower oor of thorax, increase thoracic volume, and decrease intrapulmonary pressure

■ Atmospheric air rushes in to equilibrate pressure gradient ■ Active expiration by contracting internal intercostals and abdominal muscles

○ Minute ventilation (VE) is a function of both tidal volume (VT) and breathing frequency (fb)

○ VE (L/min) = VT (L/breath) x fb (breath/min)

○ Optimum minute ventilation during exercise is achieved by increasing the breathing frequency (similar to increasing heart rate to increase CO) due to the plateau of TV

○ Physiological dead space → some alveoli are ventilated, but not adequately perfused with blood

■ Usually at the top of the lungs when in an upright position ■ Larger V/Q ratio

■ People with emphysema have increased physiological dead space ● O2 Transport in the Blood

○ O2 has low solubility in water → ~99% of O2 is transported in the blood bounded to hemoglobin

○ Hb binds to O2 according to PO2 (partial pressure)

■ ^PO2 = ^Hb anity for oxygen (stick together)

○ Opposite to Hb, myoglobin has a higher anity to oxygen in a lower PO2 to facilitate O2 transport from blood to muscles

○ Drop in pH causes a right shift of the oxyhemoglobin dissociation curve ■ Decreased anity of O2 at tissues with lower PO2 

● Allows oxygen to be released easier in tissues in need

○ Increased body temperature causes a right shift of the oxyhemoglobin dissociation curve

■ Easier o load of O2 

● CO2 Transport in Blood

○ Hb plays critical role in CO2 transport as well

○ ~5% of CO2 dissolve in blood, freely oating

○ ~25% of CO2 bind to Hb

○ ~70% of CO2 go into RBC and form bicarbonate

● Gas diusion

○ Gases move down concentration gradients

○ Optimal gas exchange achieved via:

■ Structure of alveoli

■ High capacity to transport gases in blood

■ Maintenance of concentration gradient with PAO2 of 105mm Hg and PACO2 of 40mm Hg

● Primary goal of ventilation regulation

■ Adequate capillary transit time

● Capillary transit time becomes a limit when exercise

intensity is too high (CO too high), Q to lungs is too fast, no time for gas exchange to occur

○ Pulmonary ventilation increases exponentially as exercise intensity increases

■ Maintenance of PAO2 

■ Maintenance of PaO2 

○ Fick’s Law of Diusion

● Control of Ventilation

○ Large increase/inuence: Neural → Motor Cortex

○ Fine tune: Humoral → Peripheral chemoreceptors sensing changes of PO2, PCO2, pH

○ Central input to respiratory center from:

■ Motor cortex

■ Hypothalamus

■ Cerebellum

■ Reticular formation

■ Central chemoreceptors

○ Peripheral input to respiratory center from:

■ Peripheral chemoreceptors → aortic arch and carotid bodies; sensing changes of PO2, PCO2, pH

■ Muscle aerents → active limb movement (muscle contraction) ■ Mechanoreceptors in lungs → prevent over-ination -- inhibit inspiration

■ Mechanoreceptors in muscles → active and passive limb

movement -- stimulate inspiration

● During active movements, there is a additive eect of

muscle aerents + mechanoreceptors in muscles, thus a

much higher VE 

○ Inspiration is largely regulated by the body (both central and peripheral input) because it is always active (voluntary)

________________________________________________________________________________

Lecture 10 Acid-Base Balance

● As well as H+, CO2 also decreases pH

● Sources of H+:

○ ATP Hydrolysis (ATP → ADP + H+)

○ Oxidation-Reduction Reactions (NAD+ + P → NADH + H+)

○ Buering of CO2 (CO2 + H2O → H+ + HCO2-)

● Sources of CO2:

○ TCA cycle

● pH and Performance

○ A signicant drop in muscle pH inhibits glycolytic rate and pyruvate oxidation

■ Because key enzymes are inhibited by low pH

■ Reduced high intensity exercise performance

○ Hydrogen ions compete with calcium for binding sites on troponin ■ Signicant drop in muscle pH interferes with

excitation-contraction coupling, thereby decreasing power

production

● Muscle pH declines more dramatically than blood pH with increasing exercise intensity

○ Muscle is site of majority of H+ production and has lower buering capacity than blood

● Blood relies upon multiple systems to buer:

○ 1st line of defense: (only pick o small numbers of H+, sucient during rest/low intensity exercise)

■ Intramuscular proteins, phosphates, and bicarbonate

■ Blood proteins and hemoglobin

○ 2nd line of defence: (during rapid glycolysis)

■ Blood bicarbonate + ventilatory compensation → primary buering system

● Ventilatory Compensation

○ Peripheral chemoreceptors senses the increase in PCO2 in the blood produced by buering H+ 

■ ^ventilation

○ Metabolic production of CO2 (mitochondria) increases linearly with the increase in intensity

○ When the intensity gets high enough (achieve rapid glycolysis rate), the addition of non metabolic CO2 production causes the rate of ventilation to increase exponentially (from linearly)

○ Ventilation threshold is absolute because beyond that threshold body pH would drop dramastically, which causes all sorts of dysfunction ■ However, vent. threshold can change with intense exercise training (e.g. sprint, HIIT)

KIN321 Class Notes Week 7&8 (10/3­10/14)

________________________________________________________________________________ From previous sections

­ Pulmonary Anatomy and Physiology

­ Acid­Base Balance

________________________________________________________________________________ Lecture 11 Thermoregulation I

● Heat Production

○ We are capable of producing a lot of heat during exercise

■ During intense exercise (80-90%VO2max), 20min to life threatening, 40min to death if no heat lost to environment

○ We are better at producing heat than to get rid of them

○ A majority of produced heat is transferred to the core by convective ow of venous blood, while small portion is lost to environment

● Heat Exchange

○ Radiation, conduction, and convection are driven by temperature gradient (from hot → cold) → less eective means of heat loss with increasing ambient

temperature

○ Radiation → infrared exchange of heat with environment

■ 60% of heat loss at rest in neutral environment

○ Conduction → Exchange of heat with objects in contact with skin

○ Convection → Exchange of heat with surrounding air or water

■ Eectiveness improved by movement of air or water

○ Heat loss to environment via evaporation

■ 25% of heat loss at rest in neutral environment

■ Evaporation of sweat from skin surface

● Sweat needs to evaporate o the skin, cannot be wiped/dripped o

(no heat loss)

■ Vaporization from respiratory passages

■ Only mean of heat loss when ambient temperature greater than skin temperature

■ Major mechanism of heat loss

■ Evaporation inuenced by:

● Relative humidity and ambient temperature

● Surface area exposed

● Convective air currents

■ Counterproductive sweating → water loss without cooling in hot, humid environment

● Temperature Measurement During Exercise

○ Deep-body (core) temperature

■ Rectal, tympanic (ear), esophageal, and stomach (pill)

○ Skin temperature

● We over produce heat, and we are bad at losing heat

● Thermoregulation

○ Hypothalamus = thermostat → protect from heat loss and heat gain ■ Heat loss mechanisms → Vasodilation + increased HR + sweating

■ Heat conservation/production mechanisms → Vasoconstriction + shivering ■ Cold-induced phase vasodilation: keep core temp + maintain peripheral tissue temp

● Exercise in the Heat

○ Two competing cardiovascular demands:

■ Oxygen and nutrient delivery to skeletal muscle

■ Heat delivery to the periphery for cooling

○ Plasma volume decrease during exercise in the heat → increased blood pressure + sweat loss (sweat is derived from plasma)

■ Decreased venous return → increased HR to maintain cardiac output ● Dehydration → ^HR

○ Sweat rate highly related to exercise intensity → may be as high as 1.5-2.0 L/h in unacclimatized situations

● Acclimatization (repeatedly exposed to heat → make body more ecient to get rid of heat)

○ Eects:

■ Lower sweating threshold → pre-emptive (start sweating sooner, get a jump start on heat loss)

■ Increased sweat rate → approximately 4 L/h compared to 1.5-1.8 L/h ■ More dilute sweat → less electrolyte loss

■ Increased plasma volume → greater sweating capacity, maintenance of stroke volume and HR

■ Decreased skin blood ow

○ Acclimatization is fairly rapid

■ Majority of adaptations develop in rst week, then more slowly in week two ■ Plasma volume and HR changes most rapidly, while increased sweat rate may take 14 days

■ Two weeks of acclimatization is needed to optimize aerobic performance in hot ambient conditions

○ To induce adaptations you must create heat stress → increase core and skin temperatures until profuse sweating evident

■ Likely need to reach core temp of ~ 38.5oC

■ Heat stress from environment + heat stress from exercise = rapid

acclimatization

■ Gradual loss of adaptations if you remain active when heat exposure is reduced

○ Heat acclimatization in dry heat improves exercise performance in humid heat and vice versa

○ Training in articially hot indoor environment will induce some adaptations

■ Outdoor training always considered optimal for preparing for competition ○ Individual dierences in rate of heat acclimatization exist

■ Heat acclimatization should take place 1-2 months prior to event

■ Monitor signs of heat acclimatization including: (during standardized submaximal exercise bout)

● Decreased HR

● Increased sweat rate

● Decreased sweat Na+ content

● Reduced core temperature

● Dehydration

○ Dehydration is dened as %loss of body weight

■ 5% dehydration → discomfort, loss of appetite, fatigue

■ Greater than 7% dehydration extremely dangerous

● 10% → Discoordination, spasticity

● 15% → Extreme delirium, diculty swallowing

● 20% → Skin cracks and bleeds

○ Thirst is not a reliable sign of uid need → drinking to thirst results in body water decit of 2-3% body weight when exercise in warm-hot environments + high sweat rates

■ Need to drink ahead of thirst, BUT DON’T OVER DO IT

○ Moderate dehydration decreases aerobic capacity & performance

■ 2% body weight loss → 10-20% reduction in VO2max, 3-5% reduction in long running

■ 4-5% body weight loss → 30-50% reduction in VO2max

○ Fatigue during prolonged exercise may be as much from dehydration as substrate (CHO) depletion

○ Primary reasons for decreased performance with dehydration are: ○

________________________________________________________________________________ Lecture 12 Thermoregulation II

● Cardiovascular Stress in the Heat

○ More cardiac output to skin in a hot environment (to reduce core temperature) ● Heat Injuries

○ Heat exhaustion → rapid weak pulse, hypotension, faintness, profuse sweating ■ Acute plasma volume loss + concurrent vasodilation to skin and active muscle → low BP

■ Normal to slight elevation of core temperature (>39.5oC)

■ Alleviated by rest in cool environment and uid replacement for next 24h ○ Heat syncope → loss of consciousness with cessation (at the end) of exercise in the heat

■ Independent or secondary to heat exhaustion

■ Happens due to dropped perfusion to the brain (because lack of muscle pump, vasodilation in lower body, and lack of BP)

○ Heat stroke → failure of hypothalamic temperature regulation → decreased sweat rate → massive heat storage

■ Mortality rate greater than 20% → heart failure and cerebral edema

■ High core temperature (>41oC), hot dry skin, central nervous system

dysfunction

■ Either hyper- OR hypotension

■ Damage to sweat glands

■ At risk include obese, unt, dehydrated, unacclimatized

■ Immediately cool with water, fanning, and ice packs (on neck, groin, armpit - major arteries)

● Hyponatremia

○ Exercise-associated hyponatremia (EAH) = serum of plasma Na+ < 135 mmol/L ■ Results in symptoms of altered function of CNS → weakness, dizziness, lethargy (lack of energy of enthusiasm), vomiting, headache, seizure

■ Can result from:

● Signicant uid consumption and retention → dilution of plasma Na+ ● Signicant dehydration → large amount of unreplaced Na+ loss

○ Predisposing factors for EAH among marathon runners are:

■ Substantial weight gain

■ Race time over 4 hours

■ Female

■ Low body mass index (underweight)

○ EAH likely less common among competitive athletes

■ Recreational endurance athletes should be cautious of over-hydration ● Preventing Heat Injuries

○ Allow for acclimatization → 2-4 weeks

○ Do not rely on sensation of thirst → people normally only replace 33-66% of sweat loss

○ Rely on clinical symptoms of hyperthermia more than temperature measurements ■ Hypo- or hypertension

■ Profuse sweating or dry & hot skin

○ Recognize conditions that predispose one to hyperthermia, including ■ Fever

■ Lack of adequate sleep

■ Glycogen depletion

■ Hypoglycemia

■ Heavy alcohol consumption (diuretic → dehydrate)

○ Record body weight every day before practice

■ ↓ 2-3% → consume extra uid

■ ↓ 4-6% → consume extra uid + reduce intensity

■ ↓ >7% → consult physician

● Proper Hydration

○ Can gauge hydration status by several means:

■ Changes in body weight → in the morning after peeing

■ Color of urine → precaution when taking vitamin B supplements

■ Urine osmolality → 100-300 mOsmol/kg normal, >900 dehydrated

○ Goal to replace sweat loss with uid intake during exercise is dicult because: ■ It is uncomfortable to drink that much uid when sweat rate is high ■ High variability of sweat rates between individuals

■ Thirst no a good indicator of uid need

■ Rules of sports

○ Pre-exercise hydration

■ General recommendation → consume 6 ml H2O/kg BW every 2-3 hrs in the days prior to exercise in heat

● Weight uctuates only tiny bit (<1%) in a well-fed & hydrated state ■ Consume ~16-24 uid ounces 2 hrs before practice or event, and 12 uid ounces 15 min before

■ Hyperhydration → lower HR and core temperature during exercise in the heat

● Problem with uid retention → improvement with glycerol

co-ingestion

● Some evidence for improvement in performance

○ During exercise hydration

■ Consume ~8-12 uid ounces every 15 min during practice or event lasting longer than 1 hr

● 6-8% CHO solution

● Small amount of electrolytes (500-700mg/L of Na+)

■ Increase Na+ intake to 1.5g/L if you routinely experience cramping ■ Inclusion of electrolytes help to:

● Increase palatability and maintain thirst

● Prevent hyponatremia

● Increase water absorption (SGLT-1 works better when both CHO & Na+ & H2O present)

● Increase uid retention

○ Rehydration after exercise is optimized by the inclusion of sodium and CHO → promote active water absorption

■ Plain water consumption → reduction in plasma sodium and osmolarity → reduced thirst and increased urine output → delay in rehydration

■ ^Na+ + uid = ^Rehydration

○ Should try to ingest 150% of weight loss after exercise (1.5 L for every kg of weight loss)

■ Conventional 1 L/kg weight loss did not account for obligatory urine loss after drinking

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