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explain sea level
less than 500 m, no effects
explain low altitude
500-2000 m, performance may decrease then acclimize
explain moderate altitude
2000-3000 m, affects well being in unacclimized people, performance and aerobic capacity decrease
explain high altitude
3000-5500, mountain sickness, not restored by acclimation
extreme high altitude
above 5500 m, severe hypoxic effects
explain what happens to VO2 max when you have acute altitude
decrease as altitude increases past 1500m, due to decreased arterial PO2 and Q max, 8-11% drop per 1000 m of ascent
explain what happens to anaerobic performance at altitude change
unaffected, may increase performance because thinner air and less air resistance, sprints and jumps inreace in performance
explain pulmonary ventilation from acute altitude exposure
increases immediatly, decreased PO2 stimulates aortic arch and carotids, hyperventilation, TV increases for several hours
explain what happens when you start hyperventilating
alveolar PCO2 decreases, blowing off CO2 so alkalosis happens (high pH), oxyhemoglobin curve shifts left and the body has higher affinity for O2
what do the kidneys do when expose to acute altitude
excrete more bicarbonate, minimizes blood buffering capacity, reverses alkalosis so lowers blood pH
what happens to plasma volume when exposed to acute altitude
decreases within a few hours, respiratory water loss and increased urine production, short term increase in hematocrit
what happens to CO when acute altitude exposure
increases at rest and submaximal exercise, more O2 delivered to tissues per minute, increased sympathetic activity and HR, short term adaption
what happens to gas exhanged when acute altitude exposure
decreases at muscles due to lower PO2 gradient so O2 diffusion into muscles is reduced
pulmonary adaptions to acclimation
increased ventialtion at rest and submaximal exercise, 40% higher resting and 50% higher submaximal than at sea level
Explain what happens to the blood when body is acclimated
EPO release increases for 2-3 days, stimulates polycythemia, elevated RBC, more hemoglobin, the plasma volume is first lowered to stimulate high hematocrit and then it is lowered and polycythemia takes over to elevate hematorcrit
what happens to the muscle when acclimated
cross sectional area decreases and muscle mass decreases, capillary density increases
what happens to muscle metabolic potential when acclimated
decreases, mitochondrial function and glycolytic enzymes decrease, oxidative capacity decreases
Explain the proposed benefits, demonstrated effects, and risks of bicarbonate loading
proposed benefits: increased blood pH and buffering capactiy, delayed onset of anaerobic fatigute
Demonstrated effects: increase performance in 1-7 min, enhance H removal from muscles
Risks: GI issues
explain the proposed benefits, demonstrated effects, and risks of caffiene
Caffeine: central nervous system stimulant, adenosine receptor antagonist
Prop benefits: increased alertness/concentration/energy, faster response, delayed fatigue
Dem Effects: elevated mood, decreased fatigue, increase fat metabolism, decrease perception of effort
risks: nervousness, tremors, addiction, insomnia
Explain proposed benefits, demonstrated effects, and risks of creatine
Prop benefits: enhance peak power, improved recovery from high intensity exercise, enhanced muscle mass
dem effects: increased muscle PCr content, enhanced performance in high power exercise, strength gains
risks: short term weight gain
explain proposed benefits, demonstrated effects, and risks of nitrate
proposed benefits: increased delivery of O2 and nutrients to active muscle
dem effects: improved time to exhaustion, reduced O2 consumption, reduced systolic blood pressure
risks: opposite effects when taking meds that affect NO metabolism
what are the 3 criteria of anti doping code
has potential to enhance performance, has potential to harm athlete, violates spirit of sport
explain what anabolic steroids are, prop benefits, dem effects, dose threshold, and risks
anabolic androgenic
prop benefits: increase muscle mass/strength, reduced fat mass, facilitation of recovery after exhaustive exercise
dem effects: increase body mass/ffm, increase FFM markers, increase muscle strength, decrease muscle fiber damage
large chronic doses = effective
risks: smaller statue, men = more estrogen, large breasts, testicular atrophy, reduced sperm, impotence, women = male characteristics, affected menustration/ovulation, cancer prostate/liver, cardiac conditions, hypertentions, lower HDL and higher LDL, aggression/violence
explain blood doping, prop beneftis, dem effects, risks
any means by which RBC count is increased
benefits: enhance O2 carrying capacity, improved endurance performance
effects: increase VO2 max long term, increased endurance performance, benefits evident in 2nd half of race
risks: blood too viscous - heart failure, blood matching complications, blood borne diseases
explain how VO2 max is affect with age in sedentary and athletes
sedentary: 10% decline with every decade
active: steady decline from 25-75, 1% every year, men: 5-6% per decade
previously active: 15% decline per decade
explain how max HR changes with age
reduced, varies, same for active and sedentary
explain how SV changes with age
decreases due to decreased contractility (catecholamines) and decreased preload (LV stiffness) and increased afterload (arterial stiffening), attenuated by exercise
explain how VO2 max changes with age
decreased due to decreased Q max, more to HR than SV, attenuated by exercise
explain how peripheral blood flow changes with age
decreases due to increased vasoconstriction and decreased vasodilation, decreased function sympatholysis (weakening of sympathetic induced vasoconstriction), decreased flow compensated by increase aO2 difference during submaximal exercise
explain how body comp changes with age
increase fat, ffm decrease starting at at 40, decreased muscle and bone mass, sarcopenia (decreased protein synthesis), decrease growth hormone, resistance training highly treats these effects,
explain what happens to type 2 fiber loss with age
decrease in type 2 motor neurons, so type 1 neurons innervate old type 2 fibers and results in more type 1 fibers, training stops fiber type change
explain what happens to mitochondrial function with age
declines due to reduced mitochondrial protein synthesis, respiration, max rate of ATP production, all improved by exercise
what percentage of adults have at least 1 form of CVD
48%
how has CV disease changed since the 60s
decreased due to improved awareness and lifestyle changes, we have better/earlier diagnosis but still a major health concern
explain what coronary artery disease is
largest form of CV disease
progressive narrowing of coronary arteries due to fatty plaque formation, atherosclerosis, results in blood supply to myocardium being compromised and mycardial ischema (chest pain)
atherosclerosis can begin early in life by being what in childhood/teens and then what in 20s
fatty streaks then fibrous plaques
vessel walls are composed of what
tunica intima, tunica media, tunica adventitia
explain tunica intima
endothelium, inner layer in contact with blood and produces agents to vasodilate when blood makes frictional force against blood vessel wall
tunica media
middle layer, smooth muscle cells and elastin, contractile element
tunica adventitia
outer layer composed of collagen
what does endothelial injury result from
high LDL, free radicals, hypertension, diabetes, high plasma homocytesine, infectious microorganisms
what does plaque consist of
smooth muscle cells, inflammatory cells, lipids, fibrous cap (thick or thin)
what happens when a fibrous cap is thin
more unstable and more likely to rupture, when rupture - thombrous formation
unctonrollable and controllable risk factors for CAD
uncontrollable - heredity, race (black), male>females, age
controllable - smoke, hypertension, abnormal blood lipid profile, physical inactivity, obese/overweight, diabetes/insulin resistance
explain hypertension
high blood pressure when systolic is above 130, and diastolic is above 80, 46% of adult population has this, heart has to work harder to eject blood, greater strain on arteries, leads to atherosclerosis, more common in blacks
controllable risk factors of hypertension
insulin resistance, obese, diet, tobacco, oral contraceptives, stress, physcial inactvitiy
explain ischemic stroke
most common, o2 delivery to brain obstructed by cerebral artery, cerebral thrombrosis/embolism, FAST
hemorrhagic stroke
intracebral or subarachnoid hemorrhage, rupture of vessel in brain, result of anaurism
strokes in right brain
vision problems/memory loss, quick behavior
strokes in left brain
speech/language problems, memory loss, slow cautious behavior
explain heart failure
chronic progressive weakening of heart, edema/pulmonary edema, hypertension is a major contributor, heart transplant may be required
HFrEF
reduced ejection fraction, myocardium thin, myocardium fractions
HFpEF
preserved ejection fraction, myocardium thick, older obese/diabetic women