Exercise Physiology > Test One > Flashcards
Test One Flashcards
oxidation
removal/ loss of H+ in bioenergetics (electrons)
reduction
addition of e- or H+
Reducing agent
oxidation
Oxidizing agent
reducer
metabolism-
Net result of conversion processes including synthesis (anabolic) and breakdown of molecules (catabolic)
Catabolic
break down of molecules
anabolic
synthesis of molecules
Who accepts electrons?
oxidizing agent/ reduction
Who donates electrons?
reducing agent/ oxidation
Example of Reducing agent in Bioengertics
NADH
NAD+ is what ?
oxidizing agent
How do enzymes work?
Enzyme role is increasing rate of chemical reactions in bioenergetics. Reactions have energy of activation, which is energy needed to start the reaction, and reactions needs to overcome EOA to access free energy of the rxn. Enzymes catalyze reactions by reducing the EOA.
Importance of ATP; the chemical rxn of its hydrolysis
ATP is the primary source of energy to do metabolic work. ATP is molecule that has energy in the three phosphate bonds, and ATP used to harness the energy in the bond. It is a hydrolysis reaction because it requires water to break it down along with ATPase (enzyme catalyzing rxn). It creates H+, which is an acidic condition.
ATP hydrolysis exothermic exogonic reaction
Hydrolysis rxn: ATP + H20 —ATPase-→ ADP + Pi+ H+ + energy
Immediate energy system rxn
PC+ADP—-Creatine Kinase-→ ATP + Creatine
(Kinase-
enzyme that phosphorylates/adds a phosphate molecules)
Glycolysis- know the products
Start: glucose molecule, 2 ADP, and 2 oxidizing agents (NAD+)
END: 2 pyruvates, 2 ATP, 2 reducing agents (NADH)
Glucose gets oxidized to pyruvate; NAD+ reduced to NADH; 1 glucose yields 2 ATP.
PDH rxn – know details
Pyruvate dehydrogenase (PDH) enzyme allows formation of acetyl CoA
1) Removes CO2 (decarboxylates)
2) Adds CoA (cofactor)
3) NAD oxidizes pyruvate (NAD is reduced to NADH and pyruvate is oxidized to acetyl CoA.
Products of Krebs cycle:
6 NADH per glucose and 3 per acetyl CoA
2 FADH2 per glucose and 1 per acetyl CoA
2 GTP per glucose and 1 per acetyl CoA
Importance behind Krebs products
These products are important because it creates lots of energy potential in matrix of mitochondria. Used to harness energy from original glucose molecule to undergo oxidative phosphorylation.
ETC – how does it work? How is ATP produced?
ETC occurs in inner membrane of mitochondria. It works by utilizing reducing potential of NADH and FADH2 to phosphorylate ADP to ATP. It consists of 4 protein complexes (embedded in inner membrane) that can undergo redox reactions. The first step is NADH and FADH2 (e- carriers) transfer their electrons to the electron-transport chain. (However, in the ETC, O2 must be present in the mitochondrial matrix to accept electrons from the protein complex and H+ coming from the outer mitochondrial space.) As the electrons move through the electron-transport chain, some of the energy is used to pump H+ into the outer compartment, resulting in a higher concentration of H+ in the outer than in the inner compartment. Then, H+ diffuses back into inner compartment through special channels, ATP synthase, that couple the H+ movement with the production of ATP. The electrons, H+, and oxygen combine to form H2O (metabolic water; think about hydrolysis reaction). ATP is transported out of the inner compartment by a carrier protein that exchanges ATP for ADP. A different carrier protein moves phosphate into the inner compartment.
The three components of oxidative phosphorylation include
PDH rxn, to Krebs, to ETC
Know the beneficial effects of aerobic training on factors of VO2max (relate to Fick equation)
Aerobic training increased maximal cardiac output, by increased max SV and increased plasma volume. Increased maximal a-v o2 diff is increased due to increased capillary density and diameter, and increased mitochondria density and size. This results in decreased submaximal heart rate and increases VO2max. Thus, the more aerobically trained one is the training duration will increase along with VO2max since heart becomes more efficient at pumping blood to muscles and muscles are more efficient at extracting oxygen from blood.
Fick EQN: VO2= Q x a-v o2 diff or hr x sv x a-v o2 diff. Q= sv x hr
How does detraining impact VO2max? how quickly does it occur?
VO2max will decrease with detraining, and about 50% of the increase in mitochondrial content will be lost after one week of detraining, and 100% after 5 weeks. It will take 4 weeks of retraining to regain adaptations lost in first week of detraining. Initially, this is due to decrease in SV (rapid loss of plasma volume) (about 12 days after) and later decrease of maximal a-v o2 difference since mitochondria decrease and oxidative capacity of muscle decrease along with type IIa fibers and increase in type IIx fibers
Know the utility of measuring citrate synthase activity; what is the difference in CS activity in type IIa vs. IIx fibers? Effect of exercise intensity?
CS is a marker of mitochondrial oxidative capacity and a rate-limiting enzyme in Krebs cycle that catalyzes synthesis of citrate, and is found in mitochondria. It will increase speed of Krebs, so increase ATP production. CS increases in type IIa fiber with all training intensities, but duration has no impact in type IIa fibers with CS levels. However, with type IIx longer duration and higher intensity is required to increase CS levels.
How does aerobic training affect oxygen deficit? Why?
Aerobic training will lower oxygen deficit because there is more mitochondria. This makes the body more sensitivity to the energy level making it faster to make ATP at a lower concentration of ADP. [ADP] stimulates mitochondrial ATP production. Increased mitochondrial numbers following training, thus, lowering [ADP] needed to increase ATP production and VO2. VO2 is at same but at lower concentraton of ADP. More energy requirement can be met by aerobic ATP production at the onset of exercise so there is a faster rise in VO2 curve and steady state is reached earlier. Results in less lactate and H+ formation and less PC depletion.
Why is aerobic training considered “carbohydrate-sparing”?
Aerobic training is considered “carb-sparing” because there is increased use of fat and less plasma glucose and glycogen. Carbohydrates are made up of glucose molecules. This is because this kind of training uses more oxygen, and fatty acids do not go through glycolysis, but they go through the aerobic process beta-oxidation. It will use more transport of FFA into the muscles through increased capillary density and increased FABP and FAT. Transport of FFA from cytoplasm to the mitochondria increases mitochondrial number so there is more mitochondrial oxidation of FFA since increased enzymes of beta-oxidation. Also, increased capillary density results in slower blood flow in muscle and increased FFA transporters that cause increased uptake of FFA, which will cause the body to increase FFA use and spare plasma glucose. Mitochondrial number increase causes increase in fatty acid cycle enzymes and carnitine transferase that will increase FFA use and spare plasma glucose.
Hypoxemia – why do well-trained endurance athletes experience it?
Well-trained endurance mofo’s experience hypoxemia because at near-max work they have decreased PO2 of 30-40 mm Hg. This is due to ventilation/perfusion mismatch and short RBC transit time in pulmonary capillary due to high Cardiac Output. So the blood is being ejected very quickly causing less ability to extract oxygen.
Know ventilatory response to exercise (trained vs. untrained; steady state vs. incremental) and in the heat
From rest to exercise, at the onset of constant load submax exercise: Initially, ventilation increases rapidly and then a slower rise toward steady state happens. PO2 and PCO2 are relatively unchanged and going to be maintained by increasing ventilation, and slight decrease in PO2 and increase PCO2 then normalize occurs while ventilation gradually increase until steady state since ventilation is catching up metabolism.
In hot environment, during prolonged submax exercise (long duration, steady state), ventilation tends to drift upward (slight increase) because of increase in blood temperature affects respiratory control center (trying to get heat out of body). Also, there is little change in PCO2 and higher ventilation is not due to increased PCO2, but due to higher body temp, way of body cooling down. Untrained person incremental ventilation is linear increase up to approx. 50-75% vo2max (linear increase ventilation), and afterwards there is an exponential increase beyond this point, and this is point is called Ventilatory Threshold (Tvent), or the inflection point where VE/V increases exponentially. Unlike, trained people, untrained people has maintained within 10-12 mm Hg of resting values (they don’t get hypoxemia). Trained person incremental: Ventilation = Tvent happens at higher % VO2max since they are better trained. The big difference between trained and untrained is P02. Decrease of 30 to 40 mm Hg at near-maximal work so there is a higher decrease in PO2, resulting in hypoxemia.
Know chemistry behind CO2 transport in blood – how does ventilation maintain acid-base balance?
CO2+H20 ←Carbonic Anhydrase→ H2CO3 (carbonic acid) ← → H+ + HCO3-
To the lungs (left) To the muscles right
At the tissue, CO2 leaves into RBC (passes through membranes) and becomes Carbonic Acid, which dissociates rapidly in an aqueous solution to form bicarbonate (HCO3-). Then, H+ binds to Hb in red blood cell and then HCO3- diffuses out of RBC in plasma, and Cl- diffuses into RBC to take bicarbonates spot at the negative stabilizing the cell (Cl shift/ hamburger).
@ lung, oxygen binds to Hb and drives off H+ causing bicarbonate to come back into cell. Thus, rxn reverses to release CO2. (cell is impermeable to H+) Gettting rid of H+ makes acidic condition thus go away.
Know oxyHb dissociation rxn; know Bohr Effect (temp & pH causing rightward shift of curve)
(Tissues/left) Deoxyhemoglobin + O2 ←-→ Oxyhemoglobin (at lungs/ right)
Bohr Effect: anything that impacts affinity of Hb- o2; favors offloading of O2 to the tissues. This is good in tissues since it will increase O2 to tissues, but bad in lungs because it can pick it up.
- Increased Temp= lowers Hb-o2 affinity, resulting in a rightward shift of the curve
- Decreased pH/ Increased Acidity: lowers Hb-o2 affinity, resulting in a rightward shift of the curve
- This increases PO2 of blood and more available for tissues.
Difference between Hb and myoglobin
Mb: shuttles O2 from the cell membrane into the mitochondria, and has higher affinity for O2 than Hb even at low PO2, which allows Mb to store o2 and continue delievery to mitochondria, so O2 reserve for muscle
Ventilation/perfusion ratio – why is it different at different parts of the lung?
V/Q indicates matching of blood flow to ventilation where ideal is 1.0. The apex of lung (top of lung) is Underperfused because of GRAVITY, and the ration will be greater than 1.0 because perfusion (Q) is smaller value which will make a whole number greater than. At the base (bottom) of lung, it is overperfused (GRAVITY IS WHY) because perfusion Q is greater value and since it is denominator is make ratio less than 1. However, during light exercise, it improves V/Q ratio and can equalize, but hard exercise results in V/Q inequality because body is close to hyperventilation (ventilation more than perfusion).
Know pulmonary volumes VC, RV, TLC, FEV1, FEV1/VC ratio – what is the usefulness of these?
VC= Vital Capacity, which is the maximum amount of gas that can be expired after maximal inhalation/inspirations. Testing in spirometry.
FEV1: Forced Expiratory Volume-1 is the volume of air expired in one second during maximal expiration, and is part of VC. Tested in Spirometer test. Most air is exhaled in first second of VC. FEV1/VC ratio: determines if person has healthy pulmonary system.
RV= Residual Volume, which is the volume remaining in the lungs after maximum expiration/ exhalation. Prevents lung collapse.
TLC: Total Lung Capacity: Amount of gas in the lungs after a maximum inhalation/ inspiration
Know % of the air components; how Fick’s law of diffusion determines gas diffusion rate
V gas= A/T x D x (P1-P2)
Ventilation- know the difference between V, VT, VA, VD
V or Ve is pulmonary ventilation/ minute ventilation, which is the movement of air in or out of the lungs per minute. Can be calculated by:
V= VT X f or V=VA+ VD
VT: tidal volume: amount of air moved per breath (inspiration and expiration)
f = breathing frequency= # of breaths/ min
VA= Alveolar Ventilation; the volume of air that reaches the respiratory zone (where alveoli and alveolar sacs are located)
VD: Dead-space ventilation (VD) that is the volume of air remaining in the conducting zone (trachea, secondary and tertiary bronchioles)
Know the difference between asthma and COPD. What are the types of COPD?
Know the difference between asthma and COPD. What are the types of COPD?
Asthma: narrowing of the airways bronchospasm, which causes increased work of breathing and dyspnea (shortness of breath). There are many potential causes. Another form is exercise-induced asthma, which happens during or right after exercise (this may impair performance).
Chronic Obstructive Pulmonary Disorder/ Disease (COPD): increased airway resistance due to constant airway narrowing and decreased expiratory airflow.
2 Lung diseases that make up COPD:
1.) Chronic bronchitis- inflammation of bronchiole tube that causes excessive mucus that blocks the airway resulting little air in and out (increases R).
2.) Emphysema- airway collapse and increased resistance manifested in bronchi tubes and alveoli sacs, and requires supplemental oxygen just to get little o2 in. A person reaching their VO2max when just walking can exemplify this condition, and smoking is a direct cause.
Both conditions lead to dyspnea (shortness of breath) and may interfere with exercise and activities of daily living.
What determines airflow? Formula?
Pressure difference between 2 ends of the air way (alveoli sacs where gas exchange occurs) and resistance of the airways. The formula is: P1-P2/ R= Air flow
What explains the mechanics of inhalation/exhalation?
During inhalation, the diaphragm pushes downward and ribs lift outward. Volume of lungs increases and intrapulmonary pressure decreases. During expiration, diaphragm relaxes, ribs pulled downward, volume of lungs decrease and intrapulmonary pressure increases. (Boyle’s law)
Know pulmonary vs. cellular respiration
Pulmonary respiration is ventilation and exchange of oxygen and carbon dioxide in the lungs
Cellular respiration is oxygen and co2 production by the tissues
Know the 2 functions of lungs
Ventilation= mechanical process of moving air into and out of lungs Diffusion= molecules move via concentration gradient
Know muscular strength vs. muscular endurance
Muscular strength is maimal force a mucle or muscle group can generate such as 1RM. Involves high resistance about 2-10 RM. Muscluar endurance increases ability to make repeated contractions against a submax load. It is high rep, low weight/R, RM 20+
Effect of aerobic training on lactate production, clearance
Increased mitochondria causes less carb use, causing less pyruvate formed, thus, less lactate formed. More fatty acid acids are mobilized so more type one fibers are used, which causes less ATP hydrolyzed so less H+ made to make less acidic condition so blood pH is maintained better, body is working more efficiently with type one fibers. Also, it makes more lactate removable via nonworking muscle, liver, and kidneys. Lactate will be made energy via gluconeogenesis in liver called Cori Cycle to make glucose. Also, increased capillary density causes muscle to extract same o2 with lower blood flow. There is then redistribution of blood flow to liver and kidney, which increases lactate removal. Redistribution of blood flow: Increased Q causes increased blood flow in liver which causes increased lactate removal so lactate in blood decreases. Also, increased Q will cause decrease blood velocity resulting in more O2 extraction in the working muscle resulting in decreased lactate production so less lactate in the blood.
