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Physiology > Unit 7 - Exercise Physiology > Flashcards

Unit 7 - Exercise Physiology Flashcards

1
Q

what is resting O2 ventilation as an index of EE?

A

O2 consumption

  • 250 ml/min
  • 3.5 ml/min/kg = 1 MET
  • to translate to calories, need to know caloric equivalent of consuming 1 L of O2, which needs you to know the type of fuel metabolized (known if RQ is known)
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2
Q

respiratory quotient and kcal/L O2 for CHO, fat, and PRO

A

CHO: 1.0 RQ, 5.05 kcal/L O2
fat: 0.7 RQ, 4.7 kcal/L O2
PRO: 0.8 RQ, 4.5 kcal/L O2

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3
Q

what is respiratory exchange ratio?

A

RER = RQ whenever body’s total o2 content stays constant (usual) AND when total CO2 content stays constant (variable depending on breathing strategies)

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4
Q

what is a rough approximation of caloric expenditure?

A

O2 consumption x 5.0 kcal/L (noting that 1 MET = 1 kcal/kg/hr)

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5
Q

how is O2 consumption determined?

A

via measuring inspired and expired air passing through flow meter and O2 and CO2 gas analyzers
-O2 inspired - O2 expired = volume inspired * flow of inspiration - volume expired * flow of expiration

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6
Q

how does O2 consumption change with increasing work rate?

A

initially increases, but doesn’t continue indefinitely, and at some point increases in work rate won’t elicit further increase

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7
Q

what pulmonary, cardiovascular, and muscle factors that limit max VO2?

A
  1. ventilatory capacity and diffusion
  2. cardiac output, distribution of CO, and capillarity of skeletal muscle
  3. mitochondrial content
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8
Q

how does cardiac output change with increasing O2 consumption? max amount? distribution?

A

increases linearly; at max is 4-5x resting (5.5 L/min)

  • arterioles controlling blood flow to active skeletal muscle will dilate to get up to 80-85% of total CO
  • blood flow to inactive muscles and splanchnic area decrease due to vasoconstriction
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9
Q

how does heart rate change with increasing O2 consumption? how do nervous systems play into this?

A

HR increases fairly linearly with O2 consumption

-sympathetic input to SA node increases, and parasympathetic input decreases

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10
Q

how does stroke volume change with exercise? with venous return? contractility?

A

exercise: increases initially at mild to moderate exercise, but may level off or decline at higher work rates (due to shorter filling time and lower EDV)

venous return or contractility: SV increases

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11
Q

why does the arterial-venous O2 difference widen with increasing exercise?

A
  1. better capillary perfusion
  2. decreased myocyte PO2
  3. right shift in O2-Hb dissociation curve
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12
Q

what is max O2 ventilation limited by?

A

left ventricular output, but if heart could deliver more O2 to exercising muscle, the muscle would use it

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13
Q

what is the exception where the ability of skeletal muscle to consume O2 limits VO2 max?

A

highly deconditioned individuals (bed rested, COPD, dialysis patients)
-not usually in normal, healthy individuals

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14
Q

what are 4 things that affect the blood pressure response?

A
  1. type of muscle mass being use din exercise
  2. whether exercise is static or dynamic
  3. body position
  4. temperature
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15
Q

why does CO increase more than TPR decreases, causing MAP to increase?

A

due to an increase in SBP rather than DBP, which is expected to remain near resting levels during exercise in a healthy person

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16
Q

what happens to SBP and DBP during large muscle work (leg) VS small muscle work (arm)?

A

leg: vasodilation to large active group, and vasoconstriction to small inactive group
- SBP increases much more than DBP increases, so MAP only increases a bit

arm: MAP is higher due to increasing TPR

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17
Q

dynamic VS static contractions

A

static/isometric contractions occlude flow when contraction exceeds more than 30% of max tension

  • total occlusion of blood flow at 70% of max voluntary contraction, so MAP increase as TPR increases
  • extremely large increases in MAP are seen when setatic muscle contractions are performed with large muscle groups (competitive weight lifting)
  • -exacerbated with Valsalva maneuver
  • dynamic exercise in a large muscle group will have minimal BP response
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18
Q

what are the components of the metabolic response to exercise?

A
  1. anaerobic ATP production - fast to turn on in response to need, powerful in terms of max rate of ATP turnover, but limited in capacity to sustain repeated contractions
    - “stored” ATP in muscle cells can support only 2-3 contractions (4-6 mM)
    - levels of CrP are 3-4x greater than ATP
    - glycolysis has greatest capacity of anaerobic mechanisms
  2. aerobic ATP production - slower to turn on and less powerful, but greater in capacity to sustain prolonged bouts of muscle contraction
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19
Q

what is the myokinase reaction? what is it important for?

A

creatinine phosphate + ADP –> ATP + creatine

-important to maintain ATP/ADP ratio to determine muscle contractile ability in anaerobic ATP production

20
Q

when is anaerobically provided ATP important?

A
  1. during transition period from one level of activity to a higher level of activity
  2. whenever exercise demands exceed anaerobic threshold of the individual
21
Q

what is the O2 deficit?

A

when ATP need&raquo_space; ATP being made aerobically

-anaerobic ATP sources are mobilized to create “deficit” that is repaid post-exercise

22
Q

what is the anaerobic threshold? what is it if trained VS untrained?

A

when anaerobic processes supplement ATP production (also “lactate threshold”)

  • untrained: at 50% VO2 max
  • trained: 85 or 90% VO2 max
23
Q

what does the RER value during exercise depend on?

A
  1. exercise intensity
  2. prior dietary history
  3. exercise duration
  4. fitness level
24
Q

how does RER change as VO2 changes? what if if exercise intensity is prolonged?

A

RER increases as VO2 increases, reflecting increased CHO use (and less fat use) at steady state conditions, or hyperventilation at non-steady state

if exercise is prolonged, RER decreases if normal of high CHO diet, but if higher fat diet, the RER is already low and while they can’t work as long, RER doesn’t change

25
Q

how much does blood glucose supply for total energy costs?

A

10-40%

26
Q

when is liver glycogenolysis and liver gluconeogenesis more important?

A

glycogenolysis: major source of E especially during intense exercise
gluconeogenesis: provides up to 40% of liver glucose output with mild, very prolonged exercise

27
Q

why does glucose uptake by muscle increase despite decreased insulin?

A

enhanced insulin sensitivity

28
Q

how does glycogenolysis rate change as work rate changes? what happens if muscles are depleted of glycogen?

A

glycogenolysis rate increases exponentially as work rate increases
-severe local muscle fatigue apparent when muscles depleted

29
Q

blood free fatty acid utilization

A

mobilization stimulated by increased circulating levels of E, NE, GH, glucagon, and cortisol (inhibited by insulin and lactate)

  • major E substrate at low exercise intensities
  • contribution to total E supply decreases as exercise intensity increases
30
Q

blood triglyceride utilization

A

5-15% of energy provision

-especially important in high oxidative red muscle fibers

31
Q

muscle triglyceride utilization

A

significant depletion in high oxidative, red muscle fibers with prolonged exercise

32
Q

what do higher lactate levels in untrained people do?

A

inhibit FFA release from adipose tissue

-so a fit person will use more fat than CHO, and thus less likely to use up all CHO in muscles

33
Q

what happens if people undergo bedrest for extended periods of time?

A

VO2 max decreases rapidly

  • much more pronounced than simple cessation of training, or decrease in habitual activity level
  • restored with aerobic training
34
Q

what is VO2 max the product of? why does it increase with exercise?

A

max CO x max (a-v)O2 difference

  • increase with exercise due to increased SA and mitochondria, and decreased distance for diffusion of O2
  • CO increases due to increase in SV (trained athlete has lower HR and higher SV)
35
Q

what is the rate pressure product? how does it compare between fit and unfit people?

A

RPP = HR x SBP

  • non-invasive index of myocardial blood flow, thus O2 needs
  • lower at any given work rate in fit VS unfit
  • -consequences: heart needs less O2, thus needs less blood flow, and operates more efficiently
36
Q

how does a trained VS untrained person manage stress?

A

trained body perceives any given work rate as less stressful due to lower rates of circulating NE and E

37
Q

what is the rating of perceived exertion scale?

A

scale of 6 to 20 (*10 to get HR) for patients to sense how hard they are working

38
Q

what are muscle adaptations to aerobic exercise?

A
  • aerobically trained muscle has increased mitochondrial content, thus increased capacity to synthesize ATP aerobically from FFA
  • all muscle fiber types can increase mitochondrial content if used and stressed appropriately during training program (production doesn’t cease)
  • increase in mitochondrial content is associated with marked improvement in endurance capacity (ability to work at higher percent of VO2 max for a prolonged period of time) and greater reliance on fat as a metabolic fuel at any given work rate
  • with long-term training, VO2 max may not further increase, but ability to sustain progressively higher % of VO2 max does, causing improved endurance performance
39
Q

what is a good frequency of aerobic exercise to train?

A

3x per week (minimum) to 5x per week, for 20-60 continuous minutes (excluding warm up and cool down)
-any more is detrimental and doesn’t provide further benefit

40
Q

what is the overload principle?

A

in order to improve, body systems must be expoesd to sufficient stress
-as training adaptations occur, the exercise stress must increase in order to continue to provide adequate stimulus for adaptation

41
Q

what can stronger muscles do? what do these factors favorably impact?

A

stronger muscles can:

  • maximally generate more force and power
  • do more work
  • above can be achieved at a lower recruitment level, thus reducing fatigue with repeated contractions

these favorably impact:

  • balance and fall prevention
  • ability to perform ADLs
  • performance in most athletic endeavors
  • bone mineral density
42
Q

what 2 properties does muscle strength depend on?

A
  1. muscle properties (size, length, and velocity of contraction)
  2. neural properties (recruitment level, frequency of firing of motor units)
43
Q

resistance training to increase muscle strength

A
  • initial strength gains primarily due to neural mechanisms
  • later gains due to hypertrophy (increased actin and myosin content), not usually not hyperplasia
  • genetic limitations can be stretched with steroids
44
Q

if you are training for strength, what are steps you should take?

A
  1. use a variety of exercises for any muscle group (due to the large neural component); UE, LE, and trunk for 8-10 exercises
  2. exercise to fatigue so that motor units that are most difficult to recruit, but most potential to hypertrophy, are used (lift 8-12 times, at 60-80% of 1 RM or repetition max)
    - start with less than max effort to avoid severe delayed onset muscle soreness (DOMS)
  3. 1-3 sets per session
  4. 2-3 times a week (24-48 hours should elapse for recovery and synthesis of actin and myosin)
    - 1 time/week for maintenance
  5. employ overload principles
45
Q

what are the 4 main risk factors for CVD?

A
  1. smoking
  2. hyperlipidemia
  3. hypertension
  4. sedentary behavior (even independent of HLD and HTN)
46
Q

what does regular exercise do for hyperlipidemia?

A
  • decreases total serum TG
  • increases HDL to increase HDL:LDL ratio
  • -total cholesterol usually stays the same
47
Q

effect of exercise on HTN

A

small, but important effect of lowering SBP and DBP in normotensive people

  • severe HTN patients need pharmacologic intervention and cautious exercise
  • most benefit for borderline HTN (don’t need drug therapy)

Physiology (60 decks)

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