Chapter 6 Shit Flashcards

1
Q

What is cardiac output (Q)?

A

-amount of blood pumped by the heart in liters per minute.
-stroke volume x heart rate
-Increases rapidly during initial aerobic activity
-Followed by a gradual increase and plateau
-Resting level = 5L/min
-Can increase to a maximum of 20-22L/minute

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2
Q

How does stroke volume change during aerobic exercise or exercise in general?

A

-Rises during the onset of exercise
-Plateaus once oxygen uptake reaches 40-50% maximum
-Untrained stroke volume of college men - 100-120ml blood/beat
-Trained men = up to 150-160ml per beat
-Women = 25% less than men
-End=diastolic volume and catecholamine action determine stroke volume

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3
Q

How is venous return increased during exercise?

A

-Vasoconstriction (from sympathetic activation)
-Increased skeletal muscle pump
-Increased respiratory frequency and tidal volume
-Increased venous return results in more forceful heart contractions via the Frank-starling mechanism

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4
Q

What is Frank-starling mechanism?

A

-Increased end-diastolic volume stretches myocardial fibers resulting in more forceful contraction and increased systolic ejection
-Increased cardiac ejection characterized by increased ejection fraction - the fraction of the end-diastolic volume that is ejected during heart contraction

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5
Q

How is heart rate effected by aerobic exercise?

A

-Increased immediately before and at the beginning of exercise
-HR increases linearly with exercise intensity
-Increases during acute bout of aerobic exercise
-Proportional to the mass of muscle used

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6
Q

What is maximal oxygen uptake?

A
  • greatest amount of O2 usable at the cellular level
    -Correlates with degree of physical conditioning
    -Related to heart and circulatory system’s ability to transport O2 and body tissue’s ability to use it
    -Resting O2 uptake estimated - 3.5mL O2/kg bodyweight per minute - defined as one metabolic equivalent (MET)
    -Normal VO2 max = 25-80ml/kg/minute
    -Fick equation is used to determine oxygen uptake/beat
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7
Q

What is the fick equation?

A
  • VO2=Qxa-VO2 difference
  • a-VO2 = Arteriovenous difference - the difference in O2 content of arterial and venous blood
    EXAMPLE- I.E. HR=72bpm, stroke volume = 65ml blood, a-VO2=6, weight = 80kg
    VO2= 281mlO2/min/80KG
    VO2=3.5 ml
    kg
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8
Q

What happens to blood pressure with aerobic exercise?

A

-Systolic blood pressure = pressure during contraction
-Combined with HR to estimate oxygen consumption of the heart
-Rate-pressure product = heart rate x systolic blood pressure
-Diastolic blood pressure = BP exerted on arterial walls when no blood being ejected
-Typical resting BP = 120 mmHg/80mmHg
-Maximal exercise can raise BP to 220-260mmHg/90mmHgdiastolic
-Mean arterial pressure - average pressure throughout cardiac cycle
-Typically, lower than average of systolic and diastolic
-MAP = ((systolic - diastolic)/3) + diastolic

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9
Q

What happens to the control of local circulation for aerobic exercise?

A

-Vasoconstriction and vasodilation are the primary mechanisms regulating blood flow
-Blood flow to active muscles increased via local dilation of arteries
-Restricted in other areas by constriction of arterioles
-At rest 15-20% of cardiac output to muscles
-During work up to 90% of cardiac output to muscles

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10
Q

What happens to the ventilation of your body during aerobic exercise?

A

-During exercise breathing increases from 12-15 breaths to 35-45 breaths per minute
-Tidal volume (volume of air inhaled and exhaled with each breath) increases from between .4 and 1.0 L to upwards of 3L or greater
-Low-moderate exercise increases O2 uptake and CO2 removal in proportion to increased ventilation

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11
Q

What is the ventilatory equivalent?

A

-ration of minute ventilation to oxygen uptake
-Ranges from 20-25 L of air/liter of O2 consumed
-Intense exercise increases the role of breathing frequency
-Minute ventilation rises disproportionately to oxygen uptake
-Parallels the rise in blood lactate
-Upwards of 35-40 L of air per liter of O2 during intense exercise

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12
Q

What is the alveoli?

A
  • functional unit of pulmonary system where gas exchange occurs
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13
Q

What is anatomical dead space in the lungs?

A
  • the area not functional for gas exchange (trachea, nose, mouth)
    -150 mL in young adults
    -Increases with age
    -Area increases during deep breathing due to stretching of passages
    -Increases similar to tidal volume during deep breathing
    -Tidal volume increases more than anatomical dead space
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14
Q

What is physiological dead space in the lungs?

A

-Alveoli with poor blood flow, ventilation, or other problems
-Lung diseases can increase physiological dead space

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15
Q

What are the overall effects of aerobic exercise on the lungs?

A

-Larger amounts of O2 diffusion from capillaries to tissues
-Increased CO2 from blood to alveoli
-Increased minute ventilation to maintain gas concentrations

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16
Q

What are the gas responses to aerobic exercise?

A

Increased diffusion of O2 and CO2 due to decrease in partial pressure of O2 (40mmHg - 3,,Jg) in interstitial fluid and increase in CO2 (46mmHg - 90mmHg) partial pressure

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17
Q

What are the mechanisms of blood transport of gasses and metabolic by-product?

A

Oxygen and Carbon dioxide

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18
Q

How is oxygen involved in blood transport of gasses and metabolic by-product?

A

-Either dissolved in plasma or carried by hemoglobin
-Low fluid solubility of oxygen - less than 3ml oxygen per liter of plasma
Most oxygen is carried in hemoglobin
-15-16g hemoglobin per 100mL blood in men
-14g hemoglobin/100mL blood in women
-One gram of hemoglobin can carry 1.34mL of oxygen
-Oxygen capacity of 100mL blood around 20mL in men and slightly less in women

19
Q

How is Carbon dioxide involved in blood transport of gasses and metabolic by-product?

A

-Removal more complex than oxygen delivery
-Diffuses across cell and then transported to lungs
-Around 5% of metabolic CO2 in plasma
-Some CO2 via hemoglobin (small amount)
-Some CO2 removed via bicarbonate (HCO3+)
-Reversible reaction
+Formation of carbonic acid with the water in red blood cells
+Sped up by carbonic anhydrase
+Acid broken into H+ and bicarbonate
+H+ combines with hemoglobin due to its buffering properties
+Maintains blood ph
+Bicarbonate diffuses to plasma while chloride diffuses into red blood cells
-Lactic acid begins to accumulate when O2 availability cannot meet exercise demands

20
Q

What are the chronic cardiovascular adaptations to aerobic exercise?

A

-Increased maximal cardiac output
-Increased stroke volume
-Reduced resting and submaximal exercise heart rate
-Increase capillary density in muscle fibers
+Function of volume and intensity of training
+Decreases diffusion distance for oxygen and metabolic substrates

21
Q

Why is increased maximal oxygen uptake crucial for aerobic performance?

A

-Enhanced cardiac output results in lowering discharge rate due to increased stroke volume
-Slow resting heart rate (bradycardia) seen in highly conditioned athletes (40-60bpm)
-Slow HR rise in response to standardized submaximal efforts a hallmark of aerobic endurance training
-Over 6-12 months of aerobic training results in large increase in cardiac output
-Increased left ventricle chamber volume and wall thickness increases stroke volume

22
Q

What are Respiratory adaptations to aerobic training?

A

-Increased tidal volume with maximal exercise
-Increased breathing frequency with maximal exercise
-Reduced tidal volume and breath frequency at submaximal exercise
-Adaptations largely occur in the specific muscles being trained

23
Q

What are neural adaptations to aerobic training?

A

-Increased efficiency
-Delayed fatigue in contractile mechanisms
-Rotations of neural activity between synergists and motor units within the muscle
-More efficient locomotion and lower energy expenditure

24
Q

What are muscular adaptations to aerobic training?

A

-Increase in glycogen-sparing (decreased glycogen use)
-Increased fat-utilization within the muscle
+Raises the intensity at which OBLA occurs - up to 80-90% aerobic capacity
-Increased oxidative capacity of type 2a fibers
+Reduced glycolytic enzymes and some size reduction will occur
+Conversion of type 2x to type 2a fibers
+No evidence of type 2 to type 1 transitions
-Some limited hypertrophy of type 1 muscle fibers
-Increased mitochondrial density
+Mitochondria produce ATP from oxidation of glycogen and free fatty acids
+In combination with increased O2 availability more mitochondria increase the oxidative capacity of muscle tissue
-Increased myoglobin content - a protein that transports oxygen within the muscle cell
-Increased activity of the enzymes involved in aerobic metabolism
-Increase in glycogen and triglyceride stores

25
Q

What are bone and connective tissue adaptations?

A

-Intense aerobic activities stimulate bone growth most successfully
-Must exceed the minimum threshold intensity and strain frequency for bone growth
-Must systematically increase to continually overload the bone
-Eventually bone growth may be limited due to the inability to continually overload via aerobic exercise
-High-intensity intervals provide greater osteogenic stimulus along with the benefits of aerobic exercise
-Ligaments, tendons, and cartilage grow stronger in proportion to the intensity
-Weight-bearing surfaces in joints show increased thickness in response
-Requires full range of motion for optimal results

26
Q

What are endocrine adaptations to aerobic exercise?

A

-Increases circulating hormones
-Increased number of receptors
-Increased hormone turnover rate
-Increased cortisol secretion - increases catabolic activity
-Offset by increased IGF and testosterone
-Net protein synthesis does occur in endurance-trained athletes
-Likely associated with increased mitochondrial proteins, not contractile proteins

27
Q

How does altitude influence adaptations to acute and chronic aerobic exercise?

A

-Elevations above 3900 ft (1200m) cause acute physiological adjustments to compensate for reduced partial pressure of oxygen
-Immediate adjustments:
+Increased pulmonary ventilation at rest and during exercise (hyperventilation)
+Caused by increasing breathing frequency
+Over time, tidal volume will increase
-Increased resting and submaximal cardiac output
+Up to 30-50% increase over sea level value
+Reflects increased need for blood flow
-Longer term adjustments (3-6 weeks)
+HR and cardiac output return to normal values (10-14 days after altitude exposure)
+Increased red blood cell concentration - 30-50% increase
+Increased hemoglobin formation - 5-15% increase
+Increased diffusing capacity of O2 through pulmonary membranes
+Increased renal excretion of HCO3+ to maintain acid-base balance
+Improved performance relative to initial altitude
++Generally still less aerobic performance than at sea level

28
Q

How does hyperoxic breathing influence chronic and acute adaptations to aerobic exercise?

A

-Breathing oxygen-enriched gas mixtures
-Performed during rest periods or following exercise
-May positively affect some performance measures
-Effects not fully elucidated
-Sea level blood O2 saturation already near 98%

29
Q

How does Smoking influence chronic and acute adaptations to aerobic exercise?

A
30
Q

How does Blood doping influence chronic and acute adaptations to aerobic exercise?

A

-Process of artificially increasing the red blood cell mass
-Accomplished through
+Infusion of blood cells from the individual or another person
+Administration of erythropoietin (EPO) - stimulates red blood cell production
-Increases blood’s ability to carry oxygen
+More oxygen available for working muscles
-Up to 11% increased oxygen uptake from blood doping and/or EPO administration
-Decreases HR, blood lactate levels
-Increases pH levels
-Increases resistance to environmental impacts on performance
+Decreases acute effects of altitude
+Increases submaximal exercise tolerance in hot conditions
++Mostly applies to acclimatized athletes

31
Q

How does Genetic potential influence chronic and acute adaptations to aerobic exercise?

A

-Limit of physical adaptations to exercise largely determined by genetic potential
-Gains harder to achieve as athletes get closer to genetic potential
-Small performance differences in elite athletes determine huge variations in victory
+Careful program design crucial to elite athletes

32
Q

How does age and sex influence chronic and acute adaptations to aerobic exercise?

A

-Maximal aerobic power decreases with age
-Women typically have 73-85% of the values men
-Physical responses to endurance training similar in men and women
-Max aerobic power difference in men and women may be caused by
+Higher body fat
+Lower blood hemoglobin
+Larger heart size in men

33
Q

What are health risks to blood doping?

A

-Increased hematocrit increases the risk of:
+Stroke
+Myocardial infarction
+Deep vein thrombosis
+Pulmonary embolism
-EPO use may also result in
+Increased arterial pressure
+Flu-like symptoms
+Increased plasma potassium levels

34
Q

What is overtraining?

A

Continuum of responses to intensified training without proper recovery (3 stages)

35
Q

What are the three stages of overtraining?

A

Functional overreaching
Nonfunctional overreaching
Overtraining syndrome

36
Q

What is functional overreaching?

A

-Short period of intensified training
-Can be used strategically before competition for a performance boost
-Intense training followed by days or weeks of recovery and volume reduction is called tapering
-Leads to supercompensative improvement

37
Q

What is nonfunctional overreaching?

A

-An extended period of excessive training beyond FOR
-Leads to significant drop in performance
-Requires weeks to months to return to baseline
-Leads to OTS when not managed

38
Q

What is overtraining syndrome?

A

-Causes significant drop in performance
-Altered nervous system and immune function
-Requires months to return to baseline

39
Q

What is the cardiovascular response to overtraining?

A

-Decreased heart rate variability with onset of OTS
+Indicates reduced parasympathetic input or excessive sympathetic input
-Lowered maximum heartrate from exercise
-Resting blood pressure generally unaffected
+Potential for increased diastolic pressure, no change in systolic pressure

40
Q

What is the biochemical response to OTS?

A

-High level of creatine kinase
-Decreases or no change in lactate concentrations increase
-Blood lipids and lipoproteins unaffected
-Decreased muscle glycogen content
+Often diet-related
+May result in lowered lactate response

41
Q

What is the endocrine response to overtraining?

A

-Lowered total testosterone levels in men
-Decreased testosterone-cortisol levels
+Associated with catabolic state
+30% decrease in ratio from baseline may indicate OTS
-Decreased growth hormone secretion from the pituitary gland
-Decreased nocturnal epinephrine - represent basal levels
-Increased epinephrine and norepinephrine responses to a given workload
+Maximum levels do not change
-Decrease basal dopamine levels
-Decreased dopamine response to relative workloads

42
Q

What are some good general strategies to prevent overtraining?

A

-Follow proper nutritional guidelines
-Ensure sufficient sleep and recovery
-Provide variety in intensity and volume
-Keep accurate performance records to catch OTS early
-Ensure athlete has access to multidisciplinary health team
+Coach
+Physician
+Nutritionist
+Psychologist

43
Q

What is detraining?

A

-The partial or complete loss of training-induced adaptations in response to insufficient training stimulus
-Aerobic adaptations most susceptible due to their enzymatic basis
-Exact cellular mechanisms unknown
-In highly trained athletes
+Short term - decrease in VO2 max between 4 and 14%
+Long term - decrease in VO2 max between 6 and 20%
++Result of
+++Decreased blood volume
+++Decreased stroke volume
+++Decreased maximal cardiac output