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HES 403- Exam 2
| Question | Answer |
|---|---|
| 3 functions of hormones during exercise | fuel mobilization, cardiovascular actions, pulmonary actions |
| Which glut transporter is stimulated by insulin? | glut-4 |
| Which glut transporter is found in the liver? | glut-2 |
| What over-rides limited muscle glucose uptake in post-absorptive phase? | contracting skeletal muscle |
| High insulin during exercise | stimulates Rd and inhibits Ra (very bad) |
| Norepinephrine and epinephrine are derivatives of | tyrosine |
| Where is norepinephrine released? | leaking out of sympathetic neurons |
| Where is epinephrine released? | adrenal medulla |
| Synthesis pathway of tyrosine derivatives | tyrosine-> DOPA -> dopamine -> norepinephrine -> epinephrine |
| Physiologic effects of adrenergic receptors | can cause constriction or dilation of blood vessels; inhibit lipolysis or stimulate it; etc |
| Calorigenesis | heat production |
| Why is it ok to eat during exercise (with respect to insulin)? | epi/NE inhibit insulin secretion |
| Steroid hormone biosynthesis | testosterone to estradiol is only one step |
| Steroid hormones are synthesized from | acetate |
| Amine receptors | intracellular or extracellular |
| Neurotransmitters are | amines |
| Steroid hormones major effect | transcription |
| Amine/peptide hormones major effects | transcription/modification of existing proteins |
| Orthostatic intolerance | changing posture rapidly causes one to pass out (older) |
| 4 types of 2nd messengers | cAMP, Ca2+, IP3, phosphorylation/dephosphorylation cascades |
| epinephrine cascade | adenylyl cyclase, cAMP, activate PKA, phosphorylase kinase, activates phosphorylase |
| insulin action at muscle | GLUT1 always there, insulin tyrosine kinase makes GLUT4 translocate to the membrane |
| where does caffeine work (one) | blocks adenosine from binding to its receptor (which usually inhibits adenylyl cyclase) |
| A1 receptor | adenosine binds to it, and this inhibits adenylyl cyclase |
| PDE | phosphodiesterase; breaks down cAMP into AMP |
| 3 types of hormone action | endocrine, paracrine, autocrine |
| where hormones come from (classic) | hypothalamus, pituitary, thyroid, adrenal, pancreas, testes, ovaries |
| where hormones come from (novel) | adipose, endothelium, skeletal muscle, heart, stomach, small intestine |
| brain produces some of its own | insulin |
| does epi or NE have a higher concentration? | norepinephrine |
| what happens to insulin training vs. untrained? | goes down |
| what happens to plasma insulin during exercise? | decreases |
| what happens to NE/epi as O2 consumption increases? | up exponentially |
| lactate ___ and ____ improve with training | turnover and clearance |
| effect of varying O2 supply on performance | increased up to 100% (due to chemoreceptors? Or up from 97% saturation) |
| ADP/AMP intralipid vs. control | higher for all during exercising, but higher for control condition |
| Metabolic response to exercise for FFA/glycerol/glucose/H+ | both Ra and Rd increase (Ra may be more) |
| Metabolic response to exercise amino acids | flux reduced (leucine oxidation increases) |
| Turnover cannot be | assessed by blood concentration |
| Alveolar surface area | 90 square meters (about 1000 square feet) |
| Two pulmonary zones | conducting zone and respiratory zone |
| Muscle mechanics of breathing | diaphragm descends, ribs rise |
| Why does EPOC occur? | HR/ventilation do not immediately drop; lactate oxidation |
| Sea level pressure | 760 mm Hg |
| Peak O2 location | outside lungs |
| Peak CO2 location | in mitochondria |
| N2 % | 79.04% |
| O2 % | 20.93% |
| CO2 % | 0.03% |
| Why is alveolar O2 less than 21%? | gradient moves it inside, moistening air lowers O2 partial pressure |
| Bohr effect | higher acidity, CO2, higher temp allows more oxygen to be unloaded |
| Oxyhemoglobin dissociation is a | sigmoid curve |
| Haldane effect | opposite of Bohr effect; hemoglobin holds onto oxygen tighter at lungs |
| What affects oxygen carrying capacity other than hemoglobin saturation? | number of red blood cells |
| Tidal volume vs. pulmonary minute ventilation | directly proportional |
| Breathing frequency vs. pulmonary minute ventilation | directly proportional |
| Inspiratory time/expiratory time vs. pulmonary minute ventilation | inversely proportional |
| The ventilatory breakpoint | the point at which ventilation increases disproportionately to oxygen consumption (before VO2 max) |
| Anaerobic threshold | the point at which metabolism becomes more dependent on anaerobic pathways; reflects lactate under most conditions; increase in VE/VO2 without an increase in VE/VCO2 |
| Where are chemoreceptors found? | aortic bodies, carotid bodies; many others |
| Silent ischemia | mutation in H+ channel of sensory receptors on heart |
| Proof can dissociate ventilation threshold from lactate threshold | McArdle’s disease patients; ventilation threshold will still increase b/c of H+ from ATP hydrolysis |
| Dyspnea | inappropriate shortness of breath |
| Lungs are the right size for | CO2 release |
| Valsalva maneuver | involuntary breathing technique that traps and pressurizes air in the lungs and can raise blood pressure |
| Hematocrit | ratio of packed cells to total blood volume |
| Buffy coat | white blood cells in blood (<1%) |
| Hematocrit responses to endurance training | increase in plasma volume, increase in # RBCs (more of an increase in volume than blood cells so ratio goes down) |
| Arterial-venous oxygen difference | amount of oxygen extracted from the blood as it travels through the body (increases w/ exercise) |
| 4 factors that affect maximum race velocity | running economy, velocity at LT, VO2 max, % VO2 max at LT |
| pulmonary anatomy & training | does not change |
| what allows heart cells to contract together? | intercalated disks |
| arteries aka | conducting vessels |
| arterioles aka | resistance vessels |
| capillaries aka | exchange vessels |
| venules/veins aka | capacitance vessels (large fraction of total blood volume) |
| average blood volume | 5 L |
| venous return aided by (3) | one-way valves, smooth muscle bands, muscular contractions |
| parasympathetic stimulated by | vagus nerve; lower HR, force of contraction |
| why do endurance athletes have lower resting BP? | stronger signal from vagus nerve |
| the heart is dependent on | extracellular calcium ions (calcium induced calcium release) |
| preload | factors that contribute to filling (stretching) |
| 3 factors that affect preload | cardiac output, posture, intrathoracic pressure |
| afterload | tension during ejection; affected by anatomic impedance |
| 3 factors that affect contractility | loss of myocardium, ionotropic drugs, pharmacologic depressants |
| bradycardia | <60 bpm |
| tachycardia | >100 bpm |
| steady state HR | optimal heartrate for demands at that specific work; lower= more efficient |
| stroke volume | major determinant of endurance capacity at maximal rates of work |
| cardiac output average | 5 L/min |
| if 40-60% VO2 max, increase in cardic output is due to | heart rate, not stroke volume |
| functional sympatholysis | over-riding signal to constrict |
| cardiac output is determined by | the balance between mean arterial pressure and total peripheral resistance |
| distribution of cardic output in muscle at rest vs. exercise | 20%/1000mL; 84%; 21,000 mL |
| poiseuille’s law | radius^4 so that will affect flow more than pressure, length, or viscosity |
| cardiac output units | L/min |
| stoke volume units | mL/beat |
| counterregulatory hormones | raise the level of glucose in the blood by promoting glycogenolysis, gluconeogenesis, ketosis, and other catabolic processes |
Created by:
melaniebeale
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