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144 Cards in this Set
- Front
- Back
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Homeostasis
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Maintenance of a constant and
“normal” internal environment |
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Homeokinesis
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Achievement of equilibrium in
body functions by dynamic processes (fluctuations over time, but basically constant, blood pressure for instance) |
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Steady state
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– Physiological variable is unchanging, but not necessarily “normal”
– Balance between demands placed on body and the body’s response to those demands (change during exercise, for instance) – Examples: Body temperature Arterial blood pressure |
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Biological Control System
Components: |
Series of interconnected components that maintain a
physical or chemical parameter at a near constant Sensor or receptor: Detects changes in variable (notices stimulus and sends data to...) Control center: Assesses input and initiates response (response to stimulus caused by...) Effector: changes internal environment back to normal (negative feedback) |
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Examples of Intracellular control systems
Organ systems • Pulmonary and circulatory systems Replenish oxygen and remove carbon dioxide |
• Protein breakdown and synthesis
• Energy production • Maintenance of stored nutrients Organ systems • Pulmonary and circulatory systems Replenish oxygen and remove carbon dioxide |
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Give an example of negative feedback with blood pressure....
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1. Heart activity causes elevated blood pressure
2. Baroreceptors in carotid artery relay info to brain 3. Brain signals heart to contract more slowly and with less force 4. Blood pressure decreases |
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Positive Feedback
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Response increases the original stimulus
Example: • Initiation of childbirth stimulates receptors in cervix • Sends message to brain • Release of oxytocin from pituitary gland • Oxytocin promotes increased uterine contractions |
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Gain of a control system
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• Degree to which a control system maintains
homeostasis (is capable or) • System with large gain is more capable of maintaining homeostasis (correcting a disturbance) than system with low gain – Pulmonary and cardiovascular systems have large gains |
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Regulation of body temperature
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• Thermal receptors send
message to brain • Response by skin blood vessels and sweat glands regulates |
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Regulation of Blood Glucose Concentration
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The pancreas acts as
both the sensor and effector organ Negative feedback • Function of the endocrine system Requires the hormone insulin • Elevated blood glucose signals the pancreas to release insulin • Insulin causes cellular uptake of glucose |
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Homeokinesis: Physiological Control Mechanisms examples
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Water Balance
• Water Balance Inside/Outside Cells • I/O (Intake/ Output) Ionic (Electrolyte) Balance • Na + , K + , Ca ++ , Mg ++ , Cl - , O2 -2 , HCO3 - Gas Tension: O2 – CO2 Balance • Retain adequate O2 • Remove waste, CO2 Acid Base Balance • Concentration of H + • Buffer Systems Temperature Regulation • Central-Peripheral Modifiers • Factors Affecting Body Heat Metabolism • Fuels Utilized • Energy Types Produced Translocation • Diffusion (free and facilitated/mediated) • Osmosis • Filtration • Active Transport • Membrane gates/channels/etc.: Phagocytosis Pinocytosis Exocytosi |
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Failure of a Biological Control System Results in
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Disease
Failure of any component of a control system results in a disturbance of homeostasis Example: • Type 1 diabetes Damage to beta cells in pancreas Insulin is no longer released into blood Hyperglycemia results • This represents failure of “effector |
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Exercise disrupts homeostasis by changes in:
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pH
O2 CO2 Temperature |
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• Control systems are capable of maintaining steady
state during |
submaximal exercise in a cool
environment • Intense exercise or prolonged exercise in a hot/humid environment may exceed the ability to maintain steady state May result in fatigue and cessation of exercise |
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Exercise Improves Homeostatic Control Via:
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(it's a stress, with positive results)
Adaptation – Change in structure or function of cell or organ system – Results in improved ability to maintain homeostasis Acclimatization – Adaptation to environmental stresses Heat stress in a hot environment Cell signaling – Communication between cells using chemical messengers – Important for maintaining homeostasis |
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Stress Proteins Help Maintain Cellular
Homeostasis The cellular stress response |
Cells synthesize “stress proteins” when
homeostasis is disrupted, damaged proteins act as signals for the cell to produce stress proteins • Heat shock proteins repair damaged proteins in cell (after high temp due to exercise usually) Stresses include: • High temperature • Low cellular energy levels • Abnormal pH • Alterations in cell calcium • Protein damage by free radicals *Reduced cellular oxygen Exercise induces these stresses |
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Metabolism =
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Sum of chemical reactions in body
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Catabolic reactions
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• Breakdown of molecules to form energy
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Anabolic reactions
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• Synthesis of molecules or other work
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Bioenergetics
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Converting foodstuffs(fats, proteins,
carbohydrates) into energy (ATP) Conversion of chemical energy into mechanical energy |
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Energy =
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capacity to do work. Forms - electrical, chemical, mechanical
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Work
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Force x distance (kg*m or kpm, kcal, J (SI))
Types: chemical (synthesis), mechanical, transport |
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Power =
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Work/Time (rate, watts & kgm*m/min)
In body, Force = body weight, distance = distance segment moved, time = time elapsed moving from point a to b |
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Structure of ATP
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Adenosine - Ribose - Phosphate ~ Phosphate ~ Phosphate
~ = anhydride bonds, which release a lot of energy when hydrolized |
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ATP Hydrolysis
DOES NOT require |
Oxygen
Therefore its use is immediate ATPase breaks it down into ADP + P + energy + heat |
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Since ATP is the only energy “currency”,
how much ATP is stored? a. Enough to run a marathon b. Enough for only 2-3 seconds c. Enough for 30 min of exercise |
b. Enough for only 2-3 seconds, about 2 kcal
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What's the difference between cytoplasm and cytosol?
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Cytosol is just the fluid part between the nucleus and cell membrane, while cytoplasm includes organelles.
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Endergonic reactions are...
vs... |
• Require energy to be
added • Endothermic Exergonic reactions • Release energy • Exothermic e.g. breakdown of glucose |
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Coupled reactions
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– Liberation of energy
in an exergonic reaction drives an endergonic reaction Oxidation and reduction are always coupled reactions |
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Reduction
Oxidation |
Addition/gain of
an electron (GER) Removing/loss of an electron (LEO) Oxidation and reduction are always coupled reactions Often involves the transfer of hydrogen atoms rather than free electrons • Hydrogen atom contains one electron • A molecule that loses a hydrogen also loses an electron and therefore is oxidized |
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___ and ____ are electron carriers and play an
important role in transfer of electrons |
NAD and FAD
Molecules can be both oxidizing agents and reducing agents, in turn: • NAD –Nicotinamideadenine dinucleotide • FAD -Flavinadenine dinucleotide NAD + 2H+NADH + H+ FAD + 2H+FADH2 |
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How do enzymes act as catalysts that regulate the speed of reactions
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• Lower the energy of activation, which increases the rate the reactions take place
Interact with specific substrates (reactant molecules) • Lock and key model • Rate-limiting enzymes |
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Factors That Alter Enzyme Activity/ turnover rate
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1. Temperature and pH
2. Concentration & activity of enzymes and substrates 3. Stimulatory or inhibitory effect of product on enzyme activity 4. Concentration and availability of cofactors and co-enzymes • Co-factors –derivatives of minerals –Mg, Ca, Zn • Co-enzymes –derivatives of vitamins – Niacin / Vitamin B3-NAD Riboflavin / Vitamin B2-FAD Pantothenic acid –Co-enzyme A Ubiquinone –derivative of Vitamin E -CoQ10 |
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• Co-factors =
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–derivatives of minerals –Mg, Ca, Zn
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• Co-enzymes –
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derivatives of vitamins –
Niacin / Vitamin B3-NAD Riboflavin / Vitamin B2-FAD Pantothenic acid –Co-enzyme A Ubiquinone –derivative of Vitamin E -CoQ10 |
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Niacin =
Riboflavin = |
Vitamin B3-NAD
Vitamin B2-FAD |
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Pantothenic acid –
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Co-enzyme A
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Ubiquinone –
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derivative of Vitamin E -CoQ10
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Enzyme activity is optimal at what temperature and pH?
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Higher than normal body temp, during exercise, around 104 F
pH between 7.35 and 7.45 |
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What does it mean for an enzyme to be "denatured"?
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Its shape is altered, making it not fit with the substrate
Happens with high temperature |
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Carbohydrates exist in three forms:
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1. Monosaccharides - simple sugars like glucose, fructose, galactose
2. Disaccharides - combos of 2 - sucrose, lactose, maltose 3. Polysaccharides - 3 or more mono. plant - cellulose and starch. Glycogen stored in animal tissue - hundreds to thousands of glucose molecules |
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Glycogen
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Glycogen
Storage form of glucose in liver and muscle Synthesized by enzyme glycogen synthase |
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Glycogenolysis-
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Breakdown of glycogen to glucose
(phosphorylase) can occur in liver or muscle cells |
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Glycogenesis
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Making of glycogen
glucose and enzyme glycogen synthase |
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Glycolysis - basic definition
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Oxidation of glucose
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Gluconeogenesis
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Production of "new" glucose from non-carbohydrate sources
glycerol, lactate, amino acids |
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What is the primary type of fat used by the muscle for energy?
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Fatty Acids Are!
– Stored as Triglycerides Storage form of fat in muscle and adipose tissue Breaks down into glycerol and fatty acids (each with one glycerol and 3 fatty acids) Process called lypolysis, enzymes lipases |
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Fats can be classified into which four general groups?
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1. Fatty Acids - long chains of carbon attoms linked to a carboxyl group at one end.
2. Triglycerides - storage form 3. Phospholipids - not used as an energy source during exercise. Provide structural integrity and sheath around nerves 4. steroids - not used as energy source for exercise, cholesterol |
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How can proteins be used as an energy source?
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Must be broken down into amino acids.
Alanine can be converted in the liver to glucose. Many amino acids ( alanine, Branched chain amino acids - isoleucine, leucine, valine...) can be converted into metabolic intermediates in muscle cells and directly contribute as fuel in the bioenergetic pathways Overall, not a primary energy source for exercise |
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Nutrients are broken down with exergonic catabolism to produce, CO2, H20, heat, and ATP, which is used to fuel energy-requiring processes such as...
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Muscular contraction (mechanical work)
Biosynthesis anabolism (chemical work) Active transport (osmotic work) |
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Muscle cells can produce ATP by these three metabolic pathways
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1. Phosphocreatine (PC or CP) breakdown
2. Degradation of glucose or glycogen - Glycolysis 3. Oxidative/aerobic with Oxidative phosphorylation, which includes generation of Acetyl-CoA, Krebs cycle (citric acid cycle, Tri Carboxylic Acid Cycle) and electron transport chain |
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Three steps of Phosphagen system (ATP-PC system)
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Quick and powerful process, but low capacity
1. Breakdown of ATP for energy (myosin ATPase -> ADP + P + E) 2. Reformation of ATP with phosphocreatine and ADP (creatine kinase -> ATP + C 3. Formation of ATP with 2 ADP (adenylate kinase/myokinase -> ATP + AMP |
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How long does ATP-PC system last?
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20-30 seconds, usually
For high-intensity activities Important for onset of exercise, immediate But, only a small amount of PC stored in cells |
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Where in the cell do the metabolic processes take place?
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ATP-PC and Glycolysis in cytosol
Oxidative phosphorylation in mitochondria |
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What happens during the energy investment phase of glycolysis?
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Five reactions
Glucose is phosphorylated by ATP in 2 steps Split into two 3-carbon G3P molecules Uses 2 ATP |
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What happens during the energy generation phase of glycolysis?
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Each 3-carbon G3P is oxidized and phosphorylated, energized phosphate groups are removed, oxidation, and removal of energized phosphate groups...
Overall produces 4 ATP, 2NADH and 2 pyruvate OR 2 lactate |
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What happens if glycogen is the substrate for glycolysis?
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Net gain is 3 ATP instead of 2
(glycogen can be phosphorylated by inorganic phosphate) |
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What happens in the "committing" step of glycolysis?
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Hexokinase adds phosphate group to glucose, which makes transporters not recognize it so it can't be sent out of the cell
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What is the rate-limiting enzyme for glycolysis?
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Phosphofructokinase (PFK)
It uses another ATP molecule to transfer a phosphate group to fructose 6-phosphate to form fructose 1, 6-bisphosphate. That's then broken into two 3-carbon molecules |
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How is NADH produced in glycolysis converted back to NAD?
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• By converting pyruvic acid to lactic acid
The addition of two H+ (from NADH) to pyruvic acid forms NAD and lactic acid or • By “shuttling”H+into the mitochondria • Malate-aspartate shuttle |
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Does lactic acid/lactate cause acidosis?
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It is produced as a consequence of cellular acidosis, not the cause. Pyruvate absorbs protons and converts to lactate
Actually acts as a buffer to the accumulation of protons Each time ATP is broken down, H+ is released It's a good "indirect marker" for the metabolic condition of the cell |
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What are the potential fates of pyruvate?
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1. Converted to lactate
2. Converted to glucose in the liver 3. Converted to oxaloacetate (Krebs cycle) 4. Converted to acetyl Co-A (Krebs cycle) |
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What metabolic process is predominately used in the first few minutes of exercise? Why do you have to slow down?
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Glycolysis
Slowing down is not because of a lack of glucose * Accumulation of metabolites (levels of pH, K+) * Interfere with enzymes *Can't regenerate NAD as well *Slower intensity allows time for pyruvate to get into mitochondria |
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The 3 Stages of Oxidative
Phosphorylation |
1.Pyruvicacid (3 C) is
converted to acetyl-CoA(2 C) (Generation of Acetyl-CoA) 2.Krebs cycle -production of : 3 NADH 1 FADH 1 molecule of GTP (Oxidation of Acetyl-CoA) 3.Electron Transport Chain Oxidative Phosphorylation The ETC uses the potential E. available in NADH and FADH to rephosphorylate ADP to ATP |
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The Tri Carboxylic Acid Cycle is also known as
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the Krebs Cycle, Citric Acid Cycle
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Important steps of the Tri Carboxylic Acid Cycle (Krebs)
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Krebs Cycle / Citric Acid Cycle
1. Pyruvic acid (3 C) is converted to acetyl-CoA (2 C) CO 2is given off 2. Acetyl-CoA combines with oxaloacetate(4 C) to form citrate (6 C) 2. Citrate is metabolized to oxaloacetate Two CO2 molecules given off 2. Produces 3 NADH and 1 FADH 2. Also forms 1 molecule of GTP Produces one ATP Substrate-level phosphorylation GTP: Guanosine Triphosphate • donates a Pi to make ATP |
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What is the purpose of the Krebs Cycle / Citric Acid Cycle?
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To regenerate oxaloacetate while producing C02 and NADH & FADH
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The Chemiosmotic Hypothesis of ATP formation:
Process of oxidative phosphorylation (of ADP to form ATP) List the steps involved in the Electron Transport Chain |
1. H+are removed from NADH and FADH
2. The e- are passed along cytochrome molecules 3. This movement of the e- releases energy, which is used to pump the p+ (H+) into the intermembrane space 4. The accumulation of p+results in a concentration gradient across the inner mitochondrial membrane 5. The p+ diffuse back across the membrane, releasing energy to form ATP 6. The H+ p+and e- from NADH and FADH are ultimately accepted by O2 to form water |
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What can cause a lack of O2, and what effect does that have on the electron transport chain?
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Unclear notes...
Pollution or high demand can deplete availability of O2. If you can't pump in ETC, you can't generate ATP. (no O2 available to accept H+ and e- from NADH and FADH to produce energy for pump) |
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How much ATP can be formed from the energy given off by every NADH molecule going through the electron transport chain?
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2.5 molecules of ATP
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How much ATP can be formed from the energy given off by every FADH molecule going through the electron transport chain?
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1.5 molecules of ATP
Less than NADH because it enters the cytochrome pathway afterward, bypassing one of the sites of ATP formation |
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What are the products of one turn of the Kreb's cycle?
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3 NADH
1 FADH 2 or 3 (counting pyruvate step) CO2 1 GTP which makes 1 ATP |
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How much ATP is produced from the aerobic breakdown of one molecule of glucose? Glycogen?
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32 ATP, 33
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What is the efficiency of aerobic respiration?
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34%, 66% of the free energy of glucose oxidation released as heat
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Allosteric enzymes are
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enzymes that are regulated by modulators
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CoQ10 is essential for what process?
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All three hydrogen pumps of the electron transport chain
What does it actually DO? "CoQ10 functions as an electron carrier from enzyme complex I and enzyme complex II to complex III in this process" |
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What is the rate-limiting enzyme of the ATP-PC system?
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Creatine kinase, activated by increasing sarcoplasmic concentration of ADP
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What is the rate-limiting enzyme of the Krebs cycle?
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Isocitrate dehydrogenase, stimulated by ADP and inhibited by ATP, also stimulated by Ca++ levels in the mitochondria.
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What is the rate-limiting enzyme in the electron transport chain?
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Cytochrome Oxidase
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How are fats used in aerobic metabolism?
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Fats
– Triglycerides -> glycerol and fatty acids – Fatty acids ->acetyl-CoA *Beta-oxidation - activated fatty acid chopped into 2C fragments forming acetyl=CoA – Glycerol can be converted to glucose during exercise (gluconeogenesis) |
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How are proteins used in aerobic metabolism?
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Protein
– Broken down into amino acids – Converted to glucose (gluconeogenesis), pyruvic acid, acetyl-CoA, and Krebs cycle intermediates Only makes up about 2-15% of fuel during exercise |
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Aerobic ATP Tally
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32 ATP if starting from glucose. (glycolysis - 2 and 5 from the 2 NADH, Pyruvic acid to acetyl-coA gives 5 from 2 NADH, Krebs cycle gives 2 from 2 GTP, 15 from 6 NADH, and 3 from 2FADH.)
33 from glycogen (one more in glycolysis) (2.5 ATP per NADH in ETC, 1.5 per FADH b/c it enters ETC later in process. 1 ATP per 4 H+) |
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How does endurance training affect mitochondrial content in skeletal muscle fibers?
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Mitochondria number are increased in the muscle, some right below the membrane (subsarcolemmal) and some within (intermyofibrillar - around contractile proteins)
Increases quickly! Can by 50-100% in first 6 weeks, depending on intensity and duration of training. Having a greater number leads to more enzymes and greater efficiency although each mitochondria doesn't get more efficient. |
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What stimulates mitochondrial ATP production?
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ADP concentration. All mitochondria respond to the same concentration, so if there are more mitochondria, there's more of a response (ATP production and V02).
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How does increased mitochondrial number increase endurance performance? Effect on blood pH?
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Increased FFA oxidation and decreased PFK activity -> decreased pyruvate formation -> decreased lactate and H ion formation (also from increased mitochondrial uptake of pyruvate and NADH) so blood pH is maintained
other notes: more mito means more fats are able to be oxidized. Rely less on glycolysis, so less pyruvate and lactic acid. LDH converts pyruvate to lactate. Pyruvate sent to mitochondria (go to Krebs cycle) more than making lactate. H+ also generated by ATP. |
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Process of beta oxidation
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fatty acids from triglyceride (glycerol w/ 3 fatty acids and ester bonds). Free fatty acids activated by attaching acetyl-coA. Enter mitochondria, where fatty acetyl-CoA is "chopped" into 2C fragments forming acetyl-CoA, then enters the Krebs cycle and ETC to make ATP.
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Do all intermediates stay in the Krebs cycle?
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No, a lot are pulled away for other processes.
Amino acids can enter at different places as intermediates (need to regenerate oxaloacetate) |
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What are the non-carb sources of glucose for gluconeogenesis?
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Glycerol, Lactate, and Amino Acids come in to form glucose
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What's the problem with incomplete combustion during metabolism of fats?
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Accumulation of Ketone bodies changes the pH of the system. Need a certain amount of carb, need glycolysis, for fat metabolism to run smoothly.
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Work Capacity:
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the total amount of E that can be produced by that system with no regard to time. Aerobic processes have the highest capacity.
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How does the energy supply from different systems differ for an endurance trained vs. sprint trained athlete?
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Sprint trained has greater initial energy supply from ATP-PC and Glycolysis, but beyond around 30sec the endurance trained athlete has a greater energy supply from aerobic metabolism
(graph with solid and dotted curves) |
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Direct calorimetry
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measurement of heat production as an indication of metabolic rate
food + 02 -> ATP + Heat Commonly measured in calories (1 kcal = 1,000 calories = 4.186 kJ) |
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Indirect Calorimetry
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Measurement of oxygen consumption as an estimate of metabolic rate
Foodstuffs + 02 -> Heat + C02 + H20 V02 of 2.0 L/min = ~10 kcal or 42 kJ per minute Depends on the type of nutrient (carb or fat) metabolized |
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Open-circuit spirometry
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Type of indirect calorimetry
Determines V02 by measuring amount of 02 consumed V02 = volume of 02 inspired - volume of 02 expired Subject -> breathing valve -> mixing chamber -> analyzer (C02 & 02) -> and Flowmeter -> computer -> programmed to make calculations v02 = vo2inspired - V02 expired |
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Absolute V02 (L/min) Example:
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60kg subject,
ventilation (STPD) = 60 L/min (measured) inspired 02 = 20.93% (does not change) Expired 02 = 16.93% (measured) 60 L/min x (20.93% - 16.93%) = 2.4 L/min |
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Relative V02 (ml*kg/min)
Example: |
Allows you to compare different people
V02 = 2.4 L/min Body weight = 60kg 2.4 L/min x 1000 ml/L divided by 60 kg = 40 ml/kg*min |
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V02 =
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the capacity to transport and utilize 02
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What happens as you transition from rest to exercise?
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ATP production increases IMMEDIATELY
Oxygen uptake increases rapidly (brief delay) *Reaches steady state within 1-4 minutes *After steady state is reached, ATP requirement is met through aerobic ATP production Initially through anaerobic pathways (immediate sources) *ATP-PC system *Glycolysis |
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Oxygen deficit is
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the lag in oxygen uptake at the beginning of exercise, while not using 02 to make ATP. Difference between oxygen uptake in the first few minutes of exercise and an equal time period after steady state (shaded area on graph)
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When do PC stores recover?
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After aerobic processes start. A graph of PC shows a steady amount for the first few minutes, a rapid decrease around min 4-7, and an increase (is that timing right?)
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Why do trained subjects have a lower oxygen deficit?
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Though the need for ATP is the same,
Better developed aerobic bioenergetic capacity Cardiovascular or muscular adaptations (capillary density increases, more mitochondria/enzymes) Results in less production of lactic acid and H+ |
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What was originally thought about "oxygen debt"?
Now? |
Elevated oxygen uptake following exercise (while resting)
A.V. Hill reasoned that it was ~80% repayment of O2 deficit through oxidative conversion of lactic acid to glucose in the liver Now, it's called EPOC, excess post-exercise oxygen consumption, and only ~20% of elevated O2 consumption is used to "repay" O2 deficit |
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What does a graph of VO2 over time look like during heavy, exhausting exercise? Mention O2 deficit and EOC
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VO2 increases at the same rate as during moderate exercise for the initial phase, however, O2 requirement is above the highest level of VO2 obtainable, so O2 deficit is larger. VO2 plateaus at the highest possible level, but cannot be maintained (for more than 2 minutes?), so exercise is stopped more quickly. Slow (and rapid?) components of EPOC take longer to decline
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What factors contribute to EPOC? 6
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Resynthesis of PC in muscle
Lactate conversion to glucose Restoration of muscle and blood oxygen stores Elevated body temperature Post-Exercise elevation of HR and breathing Elevated hormones |
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What occurs during the "rapid" portion of EPOC?
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Some O2 is consumed immediately following exercise (within the rapid portion of 3 minutes) to...
restore PC in muscle and replenish O2 stores in blood and tissues. Heart rate and breathing are elevated, requiring more O2 for the muscles. |
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How many O2 molecules are consumed as a RBC circulates through a body at rest? At maximal exercise?
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About 1 out of the 4 (25%)
At max, 3 out of 4 (75%) |
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Where is phosphocreatine re-synthesized?
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At the mitochondrial membrane. Breakdown is anaerobic , but synthesis is aerobic.
ATP in mitochondria becomes ADP as C becomes CP |
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What accounts for the "slow" portion of EPOC?
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Heart rate and breathing are elevated, requiring more O2 for the muscles.
Elevated body temperature = increased metabolic rate (Q10 effect, factor by which processes increase with 10 C rises in temp) Elevated epinephrine and norepinephrine = increased metabolic rate (helps break down glycogen and raises heart rate) Conversion of lactic acid to glucose (gluconeogenesis) ~20% of EPOC used to "repay" O2 deficit |
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Why is the epoc larger after heavy exercise?
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higher body temp
greater depletion of PC (more O2 for resynthesis) Greater blood concentrations of lactic acid (greater gluconeogenesis) Higher levels of blood epinephrine and norepinephrine |
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Removal of lactic acid following exercise:
classical theory Recent evidence shows... |
Classical - majority of lactic acid converted to glucose in liver (gluconeogenesis)
Evidence that... 70% of lactic acid is oxidized (used as a substrate by heart and skeletal muscle) 20% converted to glucose 10% converted to amino acids |
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What affects blood lactate removal following strenuous exercise?
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It's removed more rapidly with light exercise in recovery, optimal intensity of 30-40% VO2 max, otherwise you'd start accumulating again.
Graph of concentration during recovery time with no ex and 35% VO2 |
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Metabolic responses to short-term, intense exercise
First 1-5 seconds longer than 5 seconds longer than 45 seconds |
1-5: ATP-PC system
>5: shift to predominately glycolysis >45: ATP-PC, glycolysis, and aerobic systems 70% anaerobic/30% aerobic at 60 seconds 50% anaerobic/50% aerobic at 2 minutes |
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What happens to VO2 during prolonged exercise?
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Steady-state can usually be maintained during submaximal exercise in a cool enough environment
ATP production primarily from aerobic metabolism. A slow rise in O2 uptake (upward drift) occurs in 2 cases: high work rate - >75% VO2 max or Hot and humid environment |
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Why does a slow rise in O2 uptake (upward drift) occur in a hot and humid environment?
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Increasing body temperature
and rising blood levels of the hormones epinephrine and norepinephrine increase the metaboilic rate. |
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How does VO2 change during incremental exercise tests?
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Oxygen uptake increases linearly until maximal (VO2 max) is reached. No more increase even though work rate is still increasing.
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What is VO2 max and what affects it?
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"Physiological ceiling" for delivery of O2 to muscle
Affected by genetics and training (only about 10-20%) Physiological factors are maximum ability of cardiorespiratory system to deliver oxygen to the contracting muscle, and the muscle's ability to take up the oxygen and produce ATP aerobically |
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What's the lactate threshold and how does it differ in trained and untrained subjects?
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It is the point at which blood lactic acid rises systematically during incremental exercise
~ 50-60% of VO2 max in untrained ~ 65-80% in trained Not called anaerobic threshold anymore because it's not necessarily related to lack of oxygen. |
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What factors affect the lactate threshold?
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1. Low tissue/muscle oxygen (not so accepted as true anymore)
2. Reliance on glycolysis (accelerated by increasing epinephrine and norepinephrine, NADH production may exceed transport capacity of hydrogen shuttles, making pyruvate accept more and form lactate) 3. Activation of fast-twitch fibers (LDH isozyme in fast fibers promotes lactic acid formation, use glycolysis) 4. Reduced rate of lactate removal |
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Practical Uses of the Lactate Threshold
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For planning training programs - marker of intensity, choose a training HR based on LT
For prediction of performance - combined with other physiological measurements such as VO2 max |
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What are the two types of lactate shuttles?
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Intracellular - lactate formed by glycolysis in the cytoplasm is transported by MCT (monocarboxylate transporters) into mitochondrion
Extracellular lactate shuttle - something about moving lactate into slow twitch fibers and out of fast twitch. Skin excretion, heart oxidation, and liver gluconeogenesis are involved... enters bloodstream and goes to heart, liver, and muscle |
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Maximum velocity in distance races is determined by velocity at lactate threshold, which is influenced by what three factors
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VO2 max
% VO2 max at LT (depends on capillary density and oxidative enzymes) Running economy |
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Example of how to predict performance based on VO2 and LT
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If lactate threshold is at 40 ml/kg/min O2, find running speed at which VO2 is 40ml/kg/min.
Graph shows 200 meters/min, so 10k running time = 10,000 m/200 m/min = 50 min |
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Do you run out of O2 when you hold your breath?
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No! it's the buildup of CO2 that sucks
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How is the lactate threshold (aka metabolic or gas exchange threshold) different from the "ventilatory threshold" (or "respiratory compensation point")?
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LT is where lactate begins to accumulate, but it is buffered effectively during moderate exercise by bi-carbonate
2nd point is VT, where a steeper inflection point occurs as buffers aren't effective enough (going into severe range, breath more w/ more CO2) |
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Measures obtained (info gained) from open circuit spirometry:
Used for determining: |
• VO2
• VCO2 • % O2 • % CO2 • MET’s • VE • RR (respiratory rate) • Tidal volume (air inhaled or exhaled in a single breath) • RQ (respiratory quotient) Used For: • O2 deficit • EPOC • REE (resting energy expenditure) • Energy expenditure • Pulmonary functions • Gas Exchange threshold • Ventilatory threshold • Substrate use |
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Respiratory Exchange Ratio (RER or R, also called Respiratory Quotient, but that's a little different) is determined how?
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R = VCO2/VO2
VCO2 is always on top |
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What is the RER for fat?
For carbohydrate (glucose)? |
Respiratory exchange ratio is
VCO2/VO2 = 16 CO2/23 O2 = 0.70 Glucose - 6 CO2/6 O2 = 1.00 (non-protein R, assume it doesn't contribute significantly) |
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Caloric Expenditure rate is calculated by...
Range between fats and carbs |
multiplying VO2 by kcal/L O2 by minutes of exercise
1 L O2 = 5 kcal/L on average, 4.7 kcal/L for fats to 5.05 kcal/L for carbohydrates For example, VO2 of 2.4 L/min x 5 kcal/L O2 = 12 kcal/min x 30 min = 360 kcal total caloric expenditure |
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What qualifies as "low-intensity" exercise and what is the primary fuel source?
High intensity? |
< 30% VO2 max
Fats are primary fuel >70% VO2 max, carbs are primary |
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Describe the "crossover" concept
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The shift from fat to carbohydrate (CHO) metabolism as exercise intensity increases
At 10% VO2, about 70% from fat and 30% from carbs, about 50/50 at 35% VO2, 70% from carb and 30% from fat at 70% VO2. Due to: recruitment of fast muscle fibers (more glycolysis) and increasing blood levels of epinephrine |
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Regulation of glycogen breakdown during exercise is dependent on what enzyme?
Enzyme is activated by... |
Phosphorylase
1. Calmodulin activated by calcium released from sarcoplasmic reticulum - active calmodulin activates phosphorylase 2. Epinephrine binding to receptor results in formation of cyclic AMP - cyclic AMP activates phosphorylase Exercise leads to both processes and phosphorlyase leads to glycogen degradation and glycolysis |
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Is low-intensity exercise best for burning fat?
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It's not the fastest. A higher percentage of energy expenditure is derived from fat (~60% at 20% VO2 max) but total energy expended and fat oxidized is low.
At higher intensity, a smaller percentage is from fat but the total expenditure is higher making fat oxidization higher |
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What energy source is used during prolonged low-intensity exercise?
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Shift from carbohydrate metabolism to fat metabolism due to an increased rate of lipolysis
- breakdown of triglycerides -> glycerol + FFA by enzymes called lipases - stimulated by rising blood levels of epinephrine |
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What happens as glycogen is depleted during prolonged high-intensity exercise?
What's an example of this? |
Reduced rate of glycolysis and production of pyruvate
Reduced Krebs cycle intermediates Reduced fat oxidation - fats are metabolized by Krebs cycle Marathon is a good example. People have enough glycogen for about 2 hours without supplementation, then you "hit the wall". Rely on blood glucose levels and the rate of glycolysis, have to slow intensity if glycolysis can't keep up blood glucose, which is vital for your brain "Fats burn in the flame of carbohydrates" |
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What is the ratio of fat to carb metabolism at 10 minutes of exercise? At 100 minutes?
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A little more than 50% carb at 10 minutes to only 40% at 100 minutes (60% fat)
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What are the body's sources of carbohydrate during exercise?
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Muscle glycogen - primary source during high-intensity, supplies much of the carbohydrate in the first hour of exercise
blood glucose - from liver glycogenolysis, primary source of carbohydrate during low-intensity exercise, important during long-duration exercise as muscle glycogen levels decline |
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What are the body's sources of fat during exercise?
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Intramuscular triglycerides - primary source of fat during higher intensity exercise
Plasma Free Fatty Acids - From adipose tissue lipolysis - Triglycerides -> glycerol + FFA - FFA converted to acetyl-CoA and enters Krebs cycle - Primary source of fat during low-intensity exercise - Becomes more important as muscle triglyceride levels decline in long-duration exercise |
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Influence of Exercise Intensity on muscle fuel source
Which sources decrease and which increase as exercise intensity increases? |
FFAs are the main source at 25% VO2 max, but decrease
Muscle glycogen hardly contributes at 25%, a little less than half at 65%, and more than half at 85% VO2 max Blood glucose is maintained in a certain range and doesn't change much as a fuel source Muscle triglycerides are used most at 65% |
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Effect of exercise duration on muscle fuel sources
Which sources decrease and which increase as exercise duration increases |
Assume low intensity level
Muscle glycogen starts close to 50% and steadily reduces to about 20% in two hours, 10% in three hours, and almost none in four hours Muscle triglycerides begin around 25% and decrease Plasma FFA begin around 25% of energy expenditure and increase to around 45% within 4 hours Blood glucose barely contributes initially but grows to around 20% in two hours and 45% in four Think about how these changes occur along with changes in the percentage of carb and fat metabolism |
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Muscle can directly metabolize which amino acids?
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Branched chain amino acids and alanine
Liver can convert alanine to glucose |
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How much does muscle contribute to total energy production during normal exercise?
Prolonged-duration? |
about 2%
up to 5-10% late in prolonged exercise Enzymes that degrade proteins (proteases) are activated in long-term exercise Intermediates for Krebs cycle may be lacking, spots filled by proteins |
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Lactate can be used as a fuel source by which parts of the body?
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Skeletal muscle and the heart
converted to aceyl-CoA and enters Krebs |
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Lactate can be converted to what in the where?
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to glucose in the liver
Cori cycle - lactic acid produced by skeletal muscle is transported to the liver Liver converts lactate to glucose (gluconeogenesis) Glucose is transported back to muscle and used as a fuel |
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Lactate shuttles (again?)
a and b |
a. cell to cell shuttle - lactate produced in one tissue and transported to another
b. intracellular shuttle - lactate produced in a cell is transported and oxidized in the mitochondria |
