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GI > Adjustment to exercise and regulation of food uptake > Flashcards

Adjustment to exercise and regulation of food uptake Flashcards

1
Q

How does pulmonary ventilation change with strenuous exercise relative to light?

A

no true plateau phase in heavy exercise

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2
Q

What is VO2 max used for?

A

estimation of cardiac output due to the close association

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3
Q

how does execise affect this?

A

oxygen extraction by muscle improves with exercise training due to increase capillarization of muscle fibers, increased mitochondria and increased aerobic enzymes

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4
Q

What is the ventilatory breakpoint? What causes it?

A

point during progressively increasing exercise intensity at which VE increases disproportionately to VO2; buffering of lactic acid increases CO2 levels which triggers the increase in VE

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5
Q

How is the lactate threshold found?

A

VE/VO2 and VE/VCO2 can be used to estimate it

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6
Q

What affect does training have on lactate levels during exercise?

A

decreases the rate of accumulation of lactate

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7
Q

What affect can respiratory muscles have during acute exercise?

A

15% of O2 consumed during heavy exercise; typically does not limit performance but can in highly trained individuals

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8
Q

What are respiratory adaptations to training?

A

tidal volume increases only during exercise, rate stays steady at rest, decreases with submaximal exercise and can increase dramatically with maximal exercise; VE increases during maximal effort after training; pulm diffusion increases at maximal work rates, a-VO2 difference increases with training due to increased extraction

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9
Q

what are the metabolic adptations to exercise?

A

improved submaximal aerobic endurance and max O2 consumption, improved blood and oxygen supply to working muscles, improved efficiency of energy production

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10
Q

What factors affect VO2 max?

A

level of conditioning (max within 8-18mo of heavy endurance training), heredity, age (decrease with age), gender- lower in women 20-25% in untrained and 10% in trained, and specificity of training

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11
Q

what happens to blood lactate levels due to training? why?

A

decrease in concentration, change of fast twitch glycolytic fibers to fast-twitch oxidative, increase in capillaries to muscles, increased myoglobin content, increase number and size of mitochondria, store more glycogen and triglyceride, increased triglyceride store increases use as a fuel and decreases lactate prod

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12
Q

What is hitting the wall?

A

run out of glycogen in the muscles; body typically tries to spare glycogen stores; why athletes supplement with glucose goo and sugary sports drinks

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13
Q

what is QO2?

A

maximal respiratory or oxidative capacity of muscle

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14
Q

What affect does training have on enzymes in the muscles? QO2?

A

increase in enzymes, increase in their activity, increase in QO2

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15
Q

What adaptations to training affect energy sources?

A

store more glycogen and triglycerides, FFAs better mobilized and more accessible, ability to oxidize fat increases

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16
Q

What happens to blood volume due to training?

A

increased blood volume due to increased plasma volume (increases ADH, aldosterone, and plasma proteins cause more fluid to be retained in the blood) RBC volume increases but hematocrit decreases (plasma increase greater), viscosity decreases, improving circulation and enhancing O2 delivery

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17
Q

What factors contribute to body heat lost?

A

radiation, conduction convection, evaporation (can be a method of gaining heat in certain circumstances)

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18
Q

What factors contribute to the gain of body heat?

A

metabolic heat and environmental heat

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19
Q

What is the main method of heat loss at rest? exercise?

A

radiation; evaporation

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20
Q

How do muscles adapt to increase in heat in the muscle?

A

increase heat shock proteins

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21
Q

What happens if body heat increases above 40? 41-42?

A

affect NS and reduce ability to thermoregulate; sensitive organs can be damaged-> GI and kidneys most sensitive; with heat stroke can develop sepsis 24-48 hours later due to GI break down and leak

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22
Q

What is the metabolic response to exercise?

A

body temp increases, O2 uptake increases, glycogen depletion is hastened, muscle lactate levels increase

23
Q

What is the difference between exercise in the cold and heat?

A

lactate builds up more rapidly in heat and glycogen is depleted at a slower rate

24
Q

How does the body acclimatize to heat exercise training?

A

sweat increases and is more dilute, blood flow to skin is reduced, blood volume increases, HR increase is less, SV increases, glycogen usage decreases

25
Q

How is fluid balance during exercise effected by dehydration (loss of H2O and electrolytes through sweat)?

A

reduced plasma volumes (increased hematocrit), decreased SV, higher HR, reduced sweat rate, increased core body temp, hypotension, increased risk for heat-related injury, reduced performance, increased renin-aldosterone and ADH, increased plasma osmolality and ANGII (promotes thirst)

26
Q

How does rehydration work during exercise?

A

drive to drink lags behind losses in body water (dehydrated already); adequate fluid replacement should offset due to losses to sweating so no more than 2% of body mass is lost, sweat rates more than 1 liter per hour is common

27
Q

What is the risk for hyponatremia with exercise?

A

exercise during ultraendurance events, plasma Na 115-125, usually from over replacement of sweat losses with dilute fluids containing low sodium; symptoms- weakness, disorientation, seizures, and coma if not reversed

28
Q

What is clinical obesity? complications?

A

BMI greater than 30; 25-30 is overweight; hypertension, CAD, diabetes, cancers

29
Q

What is anorexia nervosa?

A

relentless pursuit of thinness that results in serious weight loss

30
Q

What is bulimia nervosa?

A

excessive food consumption followed by inappropriate behavior to avoid weight gain

31
Q

What are the components of the food intake control system?

A

environmental (avail, palatability, social, habits), brain physiological events (NT-metabolic ineractions), physiological events (hunger, craving, hedonic sensations, cognition), behavior operations (meals, snacksm energy/macronutr selection), and systemic physiological events (GI processing and metabolism)

32
Q

What is the difference between isolated eating patterns and typical environment eating patterns?

A

dinner larger in environ as opposed to breakfast; meals eaten with people are 45% larger, 20% increase on weekends, 15% increase in the fall

33
Q

How does the body change due to caloric concentration?

A

hyperphagia due to decrease in diet caloric concentration and hypophagia with increase in caloric concentration (weak compensation in humans)

34
Q

What affect does palatability play in eating?

A

highly hereditary component; 44% larger meal if food is palatable

35
Q

How does portion size affect intake?

A

30% larger meals when portion size was doubled

36
Q

What response does the body have to fasting and overeating?

A

hyperphagia to fasts, hypophagia to overeating (generally weaker in humans)

37
Q

What affect does ambient temperature have on intake of food?

A

hyperphagia to cold, hypophagia to hot

38
Q

What affect does physical activity have on food intake

A

hyperphagia to increased activity, hypophagia to decrease in activity (weaker response in humans)

39
Q

What is the homeostatic regulation of food intake?

A

high reserves slowly decreases intake; low reserves greatly increases intake

40
Q

What is the non-homeostatic portion of the regulation of reserves?

A

in the modern environment there is little physical activtity and in increase intake due to environmental factors

41
Q

How long does it take for regulation to occur?

A

daily no but within a week

42
Q

What are the types of mechanisms that control food intake?

A

short-term that control initiatation and termination of individual meals, and long term that modulate size and frequency of individual meals to regulate energy reserves

43
Q

What is the glucostatic hypothesis?

A

blood glucose depletion and repletion model, decreased blood glucose causes a central excitatory response through ghrelin which increases food intake which negatively feeds back on blood glucose, food intake causes metabolic/gut factors which feedback negatively on CNS

44
Q

What is the satiety cascade model?

A

satiety signals via gastric mechanism, SI mechanism, pancreatic mech, and hepatic mechanism

45
Q

What is the gastric mechanism of satiety?

A

stimulus distention, mediators- vagal sensory nerves

46
Q

What is the SI mechanism of satiety?

A

simtuli vol, distention, osmolarity and calories; mediators, vagal and splanchnic nerves, hormonal-CCK, PYY, GLP

47
Q

What is the pancreatic mechanism of satiety?

A

stimuli- interaction of plasma nutrients and gut hormones (GIP, GLP, CCK), mediators- amylin, insulin

48
Q

What is the hepatic mechanism of satiety?

A

stimuli- portal vein nutrients, insulin; mediators- vagal sensory neurons

49
Q

What are the humoral signals associated with adiposity?

A

leptin (synthesized by adipocytes, plasma levels correlate with adiposity) and insulin (basal plasma levels correlate with adiposity

50
Q

Where are leptin receptors found? What does each affect?

A

in choroid plexus (mediates saturability transport of leptin into brain), hypothalamus (thought to mediate food intake and weight regulatory function), lung, kidney, liver and skeletal muscle

51
Q

What increases plasma leptin levels

A

increase in adipose mass increases leptin production

52
Q

What does systemic injection of leptin cause?

A

decreased food intake, activates hypothalamic neural networks linked to control of food intake in rodents

53
Q

Leptin and insulin effect what in the hypothalamus?

A

increasing POMC which decreases food intake and decreasing NPY which increases food intake; they are peptide intermediary’s

54
Q

What affect does leptin have on CCK?

A

increase leptin increases CCK activity so smaller meals

GI (9 decks)

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