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Physio > Physiological Responses To Exercise > Flashcards

Physiological Responses To Exercise Flashcards

1
Q

Energy sources during exercise

A

. Onset of exercise: transfer of high energy P from creatine phosphate to ADP via creatine kinase
. First 10-20s of exercise: glycolysis most important source
. After 120s through hours depending on intensity, energy production dominated by mitochondrial oxidative phosphorylation using electrons derived from FFA and carbs

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2
Q

Relationship between metabolic rate during exercise and whole-body O2 consumption (VO2)

A

Linear

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3
Q

VO2 max

A

. Point where exercise intensity inc. but VO2 plateaus
. Reflects the apacity for anabolic energy transfer
. Used as standard index of cardiorespiratory fitness
. Reflects level of function and integration of physio systems involving uptake, delivery, and utilization of O2
. Inc. w/ exercise training, dec. w/ age, being sedentary, and O2 uptake issues
. Low levels are assoc. w/ higher risks of premature mortality

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4
Q

Metabolic equivalent (MET)

A

. Expression of energy expenditure as a multiple of resting metabolic rate (RMR)
. 1 MET = 3.5 ml O2/kg body weight/min
. Conversion: 5 kcal produced per liter of O2 consumed: (MET x 3.5 ml/kg/min x kg body weight)/200

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5
Q

Exercise intensities in METS for healthy adults)

A

. Light exercise: less than 3 METS or under 4 kcal/min
. Moderate exercise: 3-5.9 METS or 4-7kcal/min
. Heavy exercise: over 6 METS or 7 kcal/min

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6
Q

Clinical significant MET levels for max exercise capacity

A

. Under 5: poor prognosis, usual limit of functional capacity immediately after MI, peak cost of basic activities of daily living
. 10: healthy 50-60 y/o male
. 13 METS: excellent prognosis regardless of other exercise responses
. 18 METS: elite endurance athletes
. 20 METS: world-class athletes

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7
Q

ventilation in response to dynamic exercise

A

. Inc. immediately at onset
. Further inc. depend on intensity of exercise
. Reaches steady state after 3 min when performing submaximal exercise
. Inc. in tidal volume (VT) and frequency contribute to hypercapnia
. VT inc. up to 2L and frequency can inc. from 15 to 45/min
. Exercise VT doesn’t exceed 60% of forced vital capacity
. Combo of VT and frequency for given VE is set by brainstem

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8
Q

Arterial blood gas response to exercise

A

. PaO2 well maintained during submaximal and maximal exercise
. Slight arterial desaturation is typical at near maximal exertion ((7%-95%)
. PaCO2 dec. as exercise intensity exceeds moderate levels indicating relative hyperventilation
.pH dec. as exercise intensity exceeds moderate levels

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9
Q

Ventilatory threshold

A

. Point at which ventilation begins to inc. out of proportion to VO2
. Identified as a breakpoint in the linear relationship btw VE and VO2 that exists during mild to moderate exercise
. Causes: multiple inputs likely, inc, neural feedback from fatiguing exercising muscles, and inc. effort-related input from higher centers (central command), inc. in arterial acidosis, plasma cattecholamines, and K acting on carotid chemoreceptors, and inc. body temp.
. Excess ventilation results in 8-15 mmHg dec. in PaCO2 at max levels of exercise

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10
Q

Lactate threshold

A

. Exercise VO2 (or intensity) above which there is. Sustained inc. in blood lactate
. Accumulated attributed to inc. production of lactate (esp fast-twitch fibers) and dec. removal of lactate from blood

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11
Q

Anaerobic threshold

A

. Level of exercise VO2 above which aerobic energy production is supplemented by anaerobic mechanisms and is reflected by an inc. in lactate in muscle or blood

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12
Q

Significance of lactate threshold

A

. Exercise above this is assoc. w/ accelerated acidosis that interferes w/ contractile and enzymatic processes in muscle
. Changes in cellular function can contribute to fatigue development
. If exercise intensity at which the lactate threshold occurs is low then cellular acidosis will occur in simple activities
. Patients will report fatigue, dyspnea, and difficulty completing essential tasks

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13
Q

How to calculate VO2 and its interaction w/ cardiovascular system

A

. VO2 = CO x extraction of O2 (CaO2-CvO2)
. CaO2 highly dependent on ability to move O2 from air into blood and the adequate Hb levels to bind the O2
. CaO2 relatively constant during exercise in normal people
. CvO2 dec. during exercise so a-vO2 difference inc. from 4 to 15 at max exercise (inc. 3 fold)
. CO inc. linearly from 3-5l/min up to 20 L/min in untrained individual are up to 35 l/min in highly trained individual

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14
Q

Cardiovascular responses to inc. a-vO2 difference

A

. Inc. blood flow
. Capillary recruitment
. Low PO2 in tissue
. Dec. Hb affinity for O2

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15
Q

Cardiovascular responses to inc. CO

A

. Inc. HR and inc. SV
. Dec. vagal and inc. SNS responses causing splanchnic venoconstriction and visceral vasoconstriction and inc. contractility
. Inc. SV causes inc. LVEDV and inc. venous return

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16
Q

Heart rate during exercise

A

. Inc. linearly w/ graded exercise
. Major determinant of CO during moderate to maximal exercise
. Onset of exercise: vagal withdrawal inc. HR followed by SNS activation to inc. it over 100 b/min (some contribution from circulation catecholamines too)
. Max HR = 220-age, when over 60 use 208-0.7(age), standard dev. =/- 10 to 12 beats
. At high HR (heavy exercise) the shortened time for ventricular filling would limit SV but the enhanced ventricular contractile performance, elevated filling pressures and EDV to maintain SV

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17
Q

SV during exercise

A

. Inc. from rest to light, then plateaus when moderate exercise reached in untrained individuals
. SV may inc. 10-35% over resting levels in untrained people
. May not show clear plateau in well-trained individual
. Inc. bc of inc. contractility from inc. SNS leading to dec. LVESV and higher ejection fraction), inc. preload (due to inc. venous return), and inc. HR

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18
Q

Venous return during exercise

A

. Venoconstriction: shifts blood into central circulation
. Muscle pump: moves venous blood centrally, believed to be major contributor to ability to maintain EDV during exercise
. Respiratory pump: enhanced respiratory effort (deeper inhalation) enhanced movement of venous blood into heart

19
Q

Arterial resistanceduring exercise in non-exercising tissue

A

. Inc. SNS to viscera causes vasoconstriction
. Initially skin circulation also received inc. in SNS
. Perfusion of these vascular beds dec. as function of exercise intensity
. Overall dec. % of the now higher CO is sent here
. Inc. SNS limits inc. perfusion of nonactive muscle and contributes to CO redistribution to non-exercising muscles

20
Q

Arterial resistance in active skeletal muscle during exercise

A

. SNS inc. but overall metabolic vasodilation (from hyperemia) results in huge inc. in muscle blood flow and O2 delivery
. Can reverse 75% of CO depending on exercise intensity and heat load

21
Q

Overall TPR during exercise

A

. Dec. during dynamic exercise

22
Q

Venous resistance during exercise

A

. Inc. SNS shifts BV into central circulation

. AIDS in maintaining cardiac filling pressure (LVEDV and SV) during exercise

23
Q

T/F rise in mean BP during exercise is minor compared to rise in CO

A

T

. Due to reduction in TPR

24
Q

Arterial blood pressure during exercise

A

. Sympathetic vasoconstriction in viscera and inactive muscle is important in maintaining adequate BP during heavy exercise
. SNS vasoconstriction in active muscle circulation prevents excessive falls in TPR due to metabolic vasodilation
. Systolic pressure rises more than diastolic (which may dec. a little) thus pulse pressure inc.

25
Q

How skin circulation effects BP during exercise

A

. Dilation of skin circulation diverts blood into skin for thermoregulation
. Compensation for slow dec. in BP involves further vasoconstriction in visceral beds
. Prolonged heat stress and exercise can result in dec. in central BV which can reduce CO and BP

26
Q

A-VO2 difference during exercise

A

. Extraction of O2 inc. during exercise
. Inc. blood flow during vasodilation
. Inc. SA for diffusion due to capillary recruitment
. Inc. conc. Frailest for O2 diffusion due to lower PO2 in interstitial fluid and in the muscle cell
. Reduction in Hb affinity for O2 bc of inc. temp., CO2, and H released from active muscle

27
Q

Central command during exercise

A

. Descending cortical commands drive both locomotion and influence the medullary (brainstem) control of SNS and vagal output
. Responsible for vagal withdrawal and to lesser extent the rise in SNS activity to viscera at the start of exercise

28
Q

Exercise pressor reflex

A

. Ascending sensory info from peripheral mm. Informs brainstem of skeletal mm. Activity and results in inc. in BP, HR, and DND
. Afferents: Group III/IV sensory endings at the muscle and muscle-blood vessel interface
. Mechanical sensitive endings (III): fire during contraction, engaged at tart of exercise and continues as mm. Contract
. Chemically sensitive endings (IV): fire when metabolites accumulate in interstitium, not strong until heavy exercise, attempts to inc. perfusion of active mm. When metabolites start to build up

29
Q

Arterial baroreflex control of HR and SNA

A

. Setpoint for baroreceptors moves up and towards the right at the start of exercise and facilitates the rise in the other variables
. Baroreflex continues to defend the new BP setpoint during exercise
. Shift in setpoint is a function of the CNS

30
Q

Acute CV response to static exercise

A

. Static contractions compress the vasculature in active mm. Inc. resistance to flow and possibly reducing perfusion to active mm.
. Higher levels of relative tension, the exercise pressor reflex will produce large inc. in HR and vasoconstriction in the nonactive mm. And viscera
. Inc. in CO is moderate as SV doesn’t inc.
. Net result is excessive inc. in SBP, DBP, and MAP relative to dynamic exercise
. Plates pressure load on heart and can disproportionally inc. myocardial work and O2 demand for level of exertion
. Not good to do w/ CAD

31
Q

CV response to dynamic exercise

A

Inc. in CO, HR, SV, and SBP
. TPR dec.
. DBP no change or dec.
. MAP no change or slightly inc.

32
Q

Factors that contribute to enhances max SV with training

A

. Inc. ventricular size and compliance cause inc. BV which inc. preload/EDV that inc.SV
. Contractility remains the same

33
Q

How does training result in inc. maximal a-vO2 difference?

A

. Inc. aerobic capacity of muscle (inc. mitochondrial enzymes)
. Inc. blood flow at maximum exercise (inc. capillary density, inc. CP, inc. redistribution of CO)
. Overall inc. VO2max

34
Q

Adaptations at muscle to improve the ability to utilize O2 during submaximal exercise

A

. After training skeletal mm. Produce higher ATP levels aerobically at a given level submaximal exercise
. Adaptation reduces reliance on anaerobic pathways (leads to disturbance of intracellular pH) and delays perception of fatigue during prolonged submaximal exercise

35
Q

Central cardiovascular adaptations to exercise training at rest

A

. Sam CO but generated using lower HR and higher SV
. Some individuals (esp hypertensive persons) experience a dec. in resting SBP (-8mmHg), DBP (-6 mmHg) and mean BP
. Thus exercise training lowers myocardial rate-pressure product (HRxSBP) and reduces myocardial O2 demand

36
Q

Central cardiovascular adaptations to exercise trainings during submaximal exercise at same absolute workload

A

. Same CO but lower HR and higher SV
. Myocardial O2 demand at this absolute workload is less bc of lower HR
. SBP response to exercise may be lower in hypertensive individuals, which is also beneficial to the heart

37
Q

Guidelines for physical activity in adults

A

. Do 150 min (2 hrs and 30 min) to 300 min (5 hrs) a week of moderate-intensity or 75 min (1 hr and 15 min) to 150 min (2 hrs and 30 min) a week of vigorous intensity aerobic physical activity, or equivalent combo of moderate and vigorous intensity aerobic activity
. Additional health effects are gained by engaging beyond 5 hrs of physical activity
. Adults should also do muscle strengthening activities of moderate or greater intensity w/ all muscle groups on 2 or more days per week

38
Q

How much exercise for optimal weight loss

A

. Over 200 min/wk or burn over 2000 kcal/week

. 60 min/day 5 days per week is what is suggested

39
Q

What is moderate physical activity

A

. 3-5.9 METS or 4-7 kcal/min
. Brisk walking: 3.5 METs
. Should break light sweat and have inc. ventilation and HR but should still be able to speak short sentences (ventilatory threshold)

40
Q

Benefits assoc. w/ regular physical activity

A

. Dec. Risk of CAD
. Dec. resting systolic/diastolic BP
. Inc. HDL, dec. serum triglycerides
. Dec. body fat or prevention of weight gain
. Antithrombotic effect: dec. platelets adhesiveness and aggregation last bout of exercise effect)
. Improved glucose tolerance, enhanced insulin sensitivity

41
Q

Major effects that muscular contraction has on muscle glucose uptake in active skeletal muscle

A

. During exercise and continuing for several hours postexercise there is an insulin-independent, contraction-initiated inc. in glucose uptake
. During the next 18 hrs postexercise, there is an inc. in insulin sensitivity of skeletal m.
. Single bout of exercise also initiates protein synthesis and results in inc. number of GLUT4 transporters in the muscle cell

42
Q

Mechanism of insulin-independent, contraction-initiated glucose uptake

A

. Occurs by enhancing movement of pre-formed GLUT4 transporters to cell membrane
. An inc. in cell cytosolic Ca and inc. in cell AMP: ATP ratio and/or creatine:phosphocreatine ratios initiate cell signaling pathways
. Changes reflect metabolic stress
.

43
Q

Mechanism of skeletal muscle inc. in insulin sensitivity 18 hrs after exercise

A

. Means glucose uptake in response to submaximal insulin stimulus is enhanced
. Due to inc. movement of previously recruited GLUT4 transporters back to the membrane
. transporters that were recruited during exercise are temporarily sitting in highly recruitable cell compartment
. Weak insulin signal can shift them into cell membrane

44
Q

How a single bout of exercise initiates protein synthesis and inc. GLUT4 transporters in muscle cells

A

. Responsible for inc. in max insulin responsiveness evident 16 hrs after exercise
. Not responsible for immediate inc. in sensitivity
. Elevated levels of GLUT4 in trained muscle enhance glucose disposal, insulin action, and glycogen storage

Physio (62 decks)

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