Download Exercise Physiology Study Guide-Test 1 History of Exercise

Exercise Physiology Study Guide-Test 1
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History of Exercise Physiology
o First research paper in 1973, Seguin and Lavoisier-oxygen consumption
o First textbook, “The Physiology of Bodily Exercise”, Lagrange 1898
o Modern Day Olympics, 1896, Athens, Greece
Exercise Physiology Pioneers
o AO Atwater-developed first cycle ergometer, 1903
o John Haldane-Haldane apparatus, 1917
o August Krogh-Father of Exercise Physiology, Nobel Prize 1920 (blood flow, O2)
o AV Hill-muscle physiologist, Nobel Prize 1922 (heat production in muscle), force-velocity
relationship
o David Bruce Dill-born in Kansas, 40-40-40 club, Director of Harvard Fatigue Lab,
Environmental research, Army
American College of Sports Medicine
o Founded in 1954
Metabolism
o Sum of all chemical reactions in the body that take place in a living organism
 Catabolism-break down
 Anabolism-build up
Bioenergetics-Chemical conversion of foodstuffs into biological energy
Thermodynamics
o Energy can be neither created nor destroyed
 Energy in (food)=energy out (work) + energy out (heat) ± energy stored (fat)
o Processes move from a higher to a less order
 Conversion processes is inefficient; 60-70% of the energy used by the body is
released as heat; remaining energy is used for muscle activity and cellular
processes
 ΔEntropy=solid<liquid<gas=↑Entropy
Concept of Free Energy (ΔG)
o Helps determine if a chemical reaction will occur
Energy for Cellular Activity
o Carbohydrate (glucose and glycogen)
o Fat (triglycerides)
o Protein (amino acids)
 At rest, body uses CHO and fats for energy
 With mild to severe effort=CHO
 Protein provides little energy
 Enzymes provide a catalyst for metabolism
Carbohydrate
o Readily available and easily metabolized by muscles
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Fat
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Ingested, converted to glucose, taken up by the liver and muscles, then converted to
glycogen
Glycogen is stored in the liver and is converted back to glucose as needed
 Advantages:
 High energy yield per liter of O2 uptake (5.2kcal/LO2)
 Metabolized both aerobically and anerobically
 Rapid activation
 Glycogen concentration can be greatly increased by training and diet
 Can be the sole source of energy during heavy exercise
 Disadvantages:
 Stored with a lot of water (reduces caloric value of storage form)
 Small amount of glycogen stored
 Accumulation of lactate with anaerobic use of glycogen
 Muscle cells are dependent upon internal glycogen stores
Provides substantial energy during prolonged, low intensity activity
Larger reserves than carbohydrates
Less accessible for metabolism
 Advantages:
 Highest energy value of any fuel (9.3kcal/g)
 Fat can be stored in large amounts
 Disadvantages
 Total caloric value of intramuscular fiber lipid is small compared to
glycogen
 Energy release from fat only occurs with O2 uptake
 Oxidation of fat yields less energy per liter of O2 consumption than CHO
 Majority of fat is stored outside muscle
 Fats cannot serve as the sole energy source
CHO vs Fat
o Each gram of CHO yields 17 KJ (4 kcal)
o Each gram of Fat yields 37 KJ (9 kcal)
o For every 1 g of glycogen 2.7 g of H2O are stored
Protein
o Can be used as energy source if converted to glucose via glucogenesis
o Can generate FFAs in times of starvation through lipogenesis
o Only basic units of protein used for energy (Amino Acids)
o Approximately 20% of human body is protein
Time to Exhaustion (at 70% VO2max)
o CHO:2-2.5 hours
o Fat:3-5 days
o Protein:2.5 days
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Basic Energy Systems for APT production
o ATP-PCr system-quick explosive energy source
o Glycolytic system-short, high intensity energy source
 Anaerobic breakdown of CHO (glucose/glycogen)
o Oxidative System-long term aerobic energy production (CHO and fat metabolism)
 Glycolysis, Krebs Cycle, ETC, Beta-Oxidation
ATP-PCr System
o Can prevent energy depletion by forming more ATP
 Rapid, no O2 required
o Occurs in cytosol of the cell
o Provides energy (ATP) for only a few seconds (3-15 seconds) during intense muscular
effort
o 1 mole of ATP is produced per 1 mole of phosphocreatine
Immediate Energy Sources
o ATP
Ca2+
2+
 ATP+Actin+MyosinActomyosin+Pi+ADP+Energy
ATPase
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 ATP+H2OADP + Pi
Creatine Phosphate (CP) or Phosphocreatine (PCr)
Creatine kinase
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 PCr+ADPATP+Cr
Adenylate kinase/myokinase reaction
Adenylate kinase
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ADP+ADPATP+AMP
Glycolysis
o Breakdown of glucose, may be anaerobic or aerobic
o Requires 12 enzymatic reaction to breakdown glucose and glycogen into ATP
o When it occurs in glycolytic system is anaerobic
o Glycolysis occurs in the cytosol of the muscle cell
o Glycogenesis-process by which glycogen is synthesized from glucose to be stored in the
liver
o Glycogenolysis-process by which glycogen is broken into glucose-1-phosphate
o Glucose is broken down into two 3 carbon structures called pyruvic acid
 Crossroad for aerobic metabolism (with O2) or lactic acid (without O2)
o Pyruvic acid is then converted to lactic acid
o Breakdown of glucose yields 2 ATP, 3 ATP if glycogen
Lactic Acid Formation
o Pyruvic AcidLactic AcidLactate
↘H+
LDH
Oxidative System
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Relies on O2 to breakdown fuels for energy
Produces ATP in mitochondria of cells
Can yield much more energy (ATP) than anaerobic systems
Primary method of energy production during endurance events
 Oxidation of Carbohydrate
 Glycolysis, Kreb’s cycle, ETC
 Oxidation of Fat
 Beta Oxidation, Kreb’s cycle, ETC
Glycolysis-Kreb’s Cycle Link
o Glycolysis occurs in the cytosol of the cell
o Kreb’s cycle occurs in the mitochondria of the cell
o With O2 pyruvic acid is converted to acetyl coenzyme A (Acetyl CoA)
o Acetyl CoA enters Kreb’s cycle
Krebs Cycle Energy Production
o For each molecule of glucose:
 2 ATP
 6 NADHETC
 1 NADH=3 ATP
 2 FADHETC
 1 FADH=2 ATP
Electron Transport Chain
o ETC is coupled to the Krebs cycle
o Hydrogen ions produced from glycolysis and krebs cycle combine with NAD and FAD and
form NADH and FADH2
 Accomplishes:
 Prevention of H+ ions
 Carries H+ ions to ETC
 H+ combines with O2 to form water
End products of oxidative carbohydrate metabolism are carbon dioxide and water
Glycolysis
2 ATP
2 ATP
2 NADH
6 ATP
Acetyl CoA
2 NADH
6 ATP
Krebs Cycle
2 ATP
2 ATP
6 NADH
18 ATP
2 FADH
4 ATP
2
Total
38 ATP (glucose) 39 ATP (glycogen)
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Oxidation of Fat (Beta-Oxidation)
o Lypolysis-breakdown of triglyericde into glycerol and free fatty acids (FFA’s)
o Acetyle CoA enters Krebs cycle and ETC
o Fat oxidation requires more oxygen and generates more energy than CHO oxidation
o Once acetyl CoA enters Krebs cycle, it follows the same fate as CHO 2-carbon
compounds
o FFA’s can produce more ATP than CHO
o Example: Pamatate is a 16 carbon compound
8 Acetyl CoA molecules
96 ATP
7 NADH
21 ATP
7 FADH
14 ATP
2
Subtotal
131 ATP
- 2 for activation
TOTAL
129 ATP
3 FFA per triglyceride, therefore total ATP produced is 387 ATP
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Lipids
o Predominate fuel for heart and muscle at rest.
o Storage form of fat: triglycerides, diglycerides, monoglycerides
o Primary storage: adipose tissue
o “trans fats”: make liquid fats solid, increase LDL, decrease HDL
o Esterification: formations of triglycerides from fatty acids; uses O2
o Hydrolysis: breakdown of fatty acids from triglycerides
Mobilization
o Lipolysis-breakdown of triglycerides to fatty acids
 Important enzymes in adipose tissue
o ATGL-adipose tissue lipase
o HSL-hormone sensitive lipase
 Stimulated by
o Fast-catecholamines
o Slow-growth hormone
 Epinephrine, SNS (norepinephrine), hGH, cortisol increases
 Insulin, ketones, lactate decreases
Circulation
o Fatty acids exit adipocytes
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o Fatty acids circulate bound to albumin
o Must increase blood flow through tissue
Uptake
o FFA released from albumin and binds to fatty acid binding protein
o Lipoprotein lipase (LPL)
o Increased by endurance training
Activation
o Occurs in cytosol
o Fatty acid is attached to coenzyme A (CoA)
o Requires ATP
Translocation
o Outer mitochondrial membrane – carnitine replaces CoA
o Inner membrane – CoA replaces carnitine
o Carnitine acyl transferase I
 Inhibited by malonyl CoA an intermediate of fatty acid synthesis
o Carnitine acyl transferase II
o Enzyme content increases with training due to increased mitochondrial density
Beta oxidation
o Cleaves 2 carbons at a time from fatty acyl CoA
o Rate limiting enzyme is B-ketoacyl-CoA thiolae
o Results in acetyl CoA and NADH and FADH2
Lipid Oxidation
o Activation costs 2 ATP
o 1 FADH2 x 2 ATP
o 1 NADH x 3 ATP
o N represents the # of carbons in a fatty acid chain
 ((n/2) - 1) FADH2 x 2 ATP
 ((n/2) - 1) NADH x 3 ATP
 (n/2) acetyl CoA x 12 ATP
 Activation = - 2 ATP
 129 net ATP
Intramuscular Fat
o Lipoprotein lipase (LPL)
 Hydrolyzes intramuscular triglycerides for β oxidation
 Endurance training increases LPL activity
 Regulated by:
o Glucagon (+)
o Growth hormone (+)
o Insulin (-)
o Uptake of FAs during exercise is low, but training increases FA uptake and oxidation –
glycogen sparing
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IMTG likely recruited following glycogen depletion
IMTG mobilized during recovery from prolonged exercise – leads to glycogen depletion
Primarily occurs in the heart and liver
Brain/red blood cells rely mostly on glycolysis
Skeletal muscle cells
 White fibers (Type IIb; “Fast glycolytic”) also rely on glycolysis
o Low blood supply
o Low mitochondrial density
o Low [FABPs]
 Red skeletal muscle (Type I) better equipped to use fat as fuel
o High blood supply
o Innervated with high number of capillaries
o High myoglobin/mitochondrial content
o Endurance training ↑ mitochondrial capacity to use fat
o Fuel Selection
 Exercise onset – increased uptake/oxidation LCFA
 Low intensity exercise – enhanced lipid utilization at expense of CHO as energy
fuel
 Increased intensity – increased CHO/decreased fat utilization
 Endurance training – shifts towards lipid utilization
o Crossover concept
 Rest – lipid oxidation dominates
 As exercise starts and intensity increases – crossover from lipid to CHO
utilization
 Endurance training=higher cross over
o Increases lactate clearance capability
o Reduced epinephrine secretion
o Increased mitochondrial mass
 Glycogen sparing-reduced glycogenolysis
Keotacidosis
o Ketogenolysis – usage of ketone bodies for energy
o Ketogenesis – creating of ketone bodies
o Occurs mostly in the liver
o Utilized by kidney, brain, and muscle
o Ketone Bodies:
 Acetone
 Acetoacetic acid
 3-hydroxybutyrate
o Generated during fasting, starvation, diabetes, endurance exercise or low carbohydrate
intake
o Acidic-decreases blood pH
o Made in liver
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Ketoacidosis:
 Fruity breath
 Acetone excreted in urine
Lipid oxidation summary
o Lipid oxidation predominates at rest and decreases with exercise
o Beta oxidation breaks down fatty acids 2 carbons at time
o Intramuscular fat used during exercise
o Ketone bodies-alternative fuel source
o Mitochondrial adaptations occur with endurance training
Protein metabolism
o Skeletal muscle proteins
 Major storehouse for AA’s
 Liver, intestinal wall, blood
o Skeletal muscle can catabolize its own protein content into AAs
 Transaminase enzymes
o Exchange amine groups to amino and keto acids
 Net degradation of AAs limited in skeletal muscle
 Liver major site for AA degradation
o Carbon skeletons of AAs are degraded:
 Converting the carbon atoms to glucose
o Glucogenic
 Converting the carbon to the ketone acetoacetate or acetyl-CoA
o Ketogenic
 After removal of N+ groups, most AA residues appear as:
o Pyruvate
o Krebs cycle intermediates
o Nitrogen Removal
 Cleave nitrogen from protein
 Nitrogen removal has 2 major mechanisms
o Oxidative deamination
 Occurs in mitochondrial matrix of liver
o Involves NAD+ (oxidizing agent)
o Glutamate dehydrogenase
o Sufficient substrates:
 NAD+  NADH = glutamate
o Insufficient substrates:
 Glutamate  -ketoglutarate and NADH
 NADH yields several ATP
o Transamination
 Most common route for exchange of AA’s
 Transfer amine group
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Key transaminases
o Glutamate-pyruvate transaminase (GPT) (uses alanine)
or alanine aminotransferase
 Pyruvate + glutamate alanine +  Ketoglutarate
o Glutamate-oxaloacetate transaminase (GOT) (or
aspartate aminotransferase
 OAA + glutamate aspartate +  Ketoglutarate
Gluconeogenic AAs
 AAs can supply carbon for gluconeogenesis
o Catabolized AAs from proteins are important
 Glucose levels (kidney and brain)
o Starving
o Fasting
o Prolonged exercise can simulate fasting
o Caloric demands in excess of supply (glucose)
 Body must find ways to make glucose in these situations
o Phosphoenolpyruvate (PEP)
o PEP (phosphoenolpyruvate)
 AAs can supply carbon for gluconeogenesis
o AAs that give rise to:
 Pyruvate
 Oxaloacetate
 Malate
o Can become precursors for PEP
o PEP  Glucose
 Expensive (significant energy input)
o PEP Pathways
 Mitochondria in liver and kidneys
 Mitochondrial and cytoplasmic processes
 Pyruvate  Oxaloacetate PEP
 Malate  PEP
o Glucose-Alanine Cycle
 Can provide 130g of glucose per day during fasting or starvation
o Review of Protein metabolism
 Protein contributes very little as source of fuel
 Except for BCAAs, skeletal muscle is NOT a site for degradation
 Can be site of transaminase reactions only – not net change in concentrations
 Oxidative deamination occurs in the liver
Risk Stratification for exercise testing
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High risk: known cardiovascular, pulmonary, or metabolic disease or symptoms—need
physician present to supervise sub or max testing
 cardiovascular- cardiac, peripheral vascular (DVT or claudication),
cerebrovascular (stroke)
 pulmonary- COPD, asthma, lung disease, cystic fibrosis
 metabolic- diabetes (type 1 or 2), thyroid, renal or liver disease
 symptoms:
o Pain or discomfort in chest,
neck, jaw, arms from ischemia
o Shortness of breath at rest or
mild activity, fatigue
o Dizziness or syncope
o Ankle edema
o Palpitation or tachycardia
o Intermittent claudication
o Heart murmur
Moderate risk: Asymptomatic with 2 or more risk factors- Physician recommended for
max testing, recommend to see physician before vigorous training
Low risk: Asymptomatic with 1 or less risk factors
Risk Factors
 Age
o men 45 and older, women 55 and older
 Family History
o first degree relative (immediate family or grandparents) with MI,
coronary revascularization, or sudden death before the age of 55 for
men or 65 for women
 Smoking
o Current smoker or stopped within 6 months
 Sedentary lifestyle
o Less than 30 minutes of moderate intensity activity, 3 days a week for 3
months
 Obesity
o BMI over 30
o Waist girth >102 cm (40 inches) for men, >88 cm (35 inches) for women
 Hypertension
o > or= to 140/90 on a least 2 separate occasions
o On hypertensive medicine
 Dyslipedimia
o > or= to 130 LDL
o <40 HDL, *if > or = 60, then Negative risk factor*
o >or= to 200 total CHO
o On lipid-lowering medication
 Prediabetes
o Fasting glucose >or = to 100 but less than 126
o Oral glucose tolerance test > or= to 140 but less than 200 on two
separate occasions