Chapter 9 - Cardiorespiratory Responses to Acute Exercise

cardiovascular responses to acute exercise

• increases blood flow to the working muscle

• driven by metabolism

• involves altered heart function, peripheral circulatory adaptations

Altered heart function, peripheral circulatory adaptations include

• heart reare

• stroke volume

• cardiac output

• blood pressure

• blood flow

Normal heart rate

• a measure of stress in a multitude of ways

• affected by neural tone (resting heart rate, temperature, and altitude)

Untrained resting heart rate

60-80 beats per minutes due to the parasympathetic nervous system

Trained resting heart rate

30-40 beats/min

Anticipatory response

• heart rate above resting heart rate just before start of exercise

• vagal tone goes down

• norepinephrine and epinephrine go up

Heart rate during exercise

• directly proportional to exercise intensity

maximal heart rate

highest heart rate acheived in all-out efforts to volitional fatigue

• highly reproducible

• slight decline with age

estimated max heart rate

220 - age in years

steady-state heart rate

point of plateau , ptimal heart rate for meeting circulatory demands at a given submaximal intensity

• increases with intensity

• takes 2-3 minutes to adjust to new intensity

• hasis for simple exercise tests estimating aerobic fitness and heart rate max

heart rate variability

measure of heart rate rhythmic fluctuation

• due to continuous changes in sympathetic and parasympatheic balance

• at rest and during exercise

Factors that influence heart rate variability

• body core temperature

• sympathetic nerve activity

• respiratory rate

• analyzed with respect to requency (spectral analysis), not time

Stroke volume

• increases with intensity to 40%-60% of VO2max

  • beyond this, plateau to exhaustion

  • possible exception: elite endurance athletes

Maximal exercise stroke volume

• double standing stroke volume

• maximal exercise SV is only slightly higher than supine SV

Factors that increase stroke volume

• increase preload

• increase contractibility

• decrease after load

increased preload

end-diastolic volume ventricular stretch

• before the valve

• increased strecth means increased contraction strength

• Frank-Starling mechanism

Frank-Starling mechanism

if you get more blood = better squeeze and emptying

Increased contractibility

inherent ventricular property

• squeezing

• increased norepinephrine or epinephrine

• independent of EDV (increase ejection fraction instead)

decreased after load

aortic resistance (R)

• push against less resistance, get more blood out = higher stroke volume

Stroke volume changed during exercise

• increased preload at lower intensities

• increase in heart rate

• increased contractility at higher intensities

• decreased afterload via vasodilation

increased preload at lower intensities

• increase stroke volume

• increase venous return making EDV increase which means a higher preload

• muscle and respiratory pumps, venous reserves

increase in heart rate

• decreased filling time

• slight decrease in EDV

• decreased stroke volume

increased contractility at higer intensities

increased stroke volume

decreased afterload via vasodilation

increased stroke volume (after load)

Cardiac output

• Q= HR x SV

• increase with increase in intensity

• plateau near VO2 max

Normal resting cardiac output volume

about 5 L/min

Normal untrained cardiac output

about 20 L/min

Normal trained cardiac output

about 40 L/min

Q max

a function of body size and aerobic fitness

Fick principle

• calcuation of tissue of O2 consumption depending on blood flow, O2 extraction

blood pressure

• during endurance exercise, increase in mean arterial pressure (MAP)

• MAP = Q x total peripheral resistance (TPR)

• rate-pressure product = HR x SBP

• resistance exercise → periodic larger increases in MAP

During endurance exercise, increase in mean arterial pressure (MAP)

• systolic blood pressure increases proportional to exercise intensity

• diastolic blood pressure slight decreases or increases (at max exercise)

MAP = Q x total peripheral resistance

• Q increases, TPR slightly decreases

• muscle vasodilation vs. sympatholysis

reate-pressure product = HR x SBP

related to myocardical oxygen uptake and myocardial blood flow

resistance exercise → periodic large increases in MAP

• up to 480/350 mmHg

• more common when using the Valsalva meneuver

Blood floow redistribution

• increased cardiac output → increased available blood flow

• increased blood flow redirected to areas with the greatest metabolic need (exercising muscle)

• blood shunted away from less active regions by sympathetic vasoconstriction

• local vasodilation permit additional blood flow in exercising muscle

• as temperature rises, skin vasodilation also occurs

blood shunted away from less active regions by smpathetic vasoconstriction

• splachnic circulation (liver, pancreas, GI)

• kidneys

local vasodilation permits additional blood flow in exercising muscle

• local VD triggered by metabolic, endothelial products

• smypathetic vasoconstriction in muscle offset by smpatholysis

• local VD > neural VC

as temperature rises, skin VD also occurs

• decrease sympathetic VC, increase sympathetic VD

• heat loss permitted through skin

cardiovascular responses

• cardiovascular drift

• competition for blood supply

• blood oxygen content

• plasma volume

• hemoconcentration

• central regulation

• integration of the exercise response

cardiovascular drift

• associated with increase in core temperature and dehydration

• SV drift decreases

• HR drift increases to compensate (Q maintained)

SV drift decreases

• skin blood flow increases

• plasma volume decrease (sweating)

• venous return/preload decreases

competition for blood supply

• exercise and other demands for blood flow create competition for limited Q

• multiple demands may decrease muscle blood flow

Exercise and other demands for blood flow create competition for limited Q

• exercise (muscles) + eating (splanchnic blood flow)

• exercise (muscles) + heat (skin)

blood oxygtgen content

• (arterial - venous) O2 difference (mL O2/100 mL blood)

• mixed venous O2 less than or equal to 4 mL O2/100 mL blood

(arterial - venous) O2 difference (mL O2/100 mL blood)

• arterial O2 content - mexied venous O2 content

• resting: about 6 mL O2/100 mL blood

• max exercise: about 16-17 mL O2/100 mL blood

mixed venous O2 less than or equal to 4 mL O2/100 mL blood

• venous O2 from active muscle about 0 mL

• venous O2 from inactive tissue > from active muscle

• increase in mixed venous O2 content

plasma volume

• capillary fluid movement into and out of tissue

• upright exercise → decreased plasma volume

capillary fluid movement into and out of tissue

• hydrostatic pressure

• oncotic, osmotic pressures

upright exercise → decreased plasma volume

• compromise of exercise performance

• increased MAP → increased capillary hydrrostatic pressure

• metabolic build up → increased tissue osmotic pressure

• sweating further decreases plasma volume

hemoconcentration

• decreased plasma volume → hemoconcentration

• net effects

decreased plasma volume → hemoconcentration

• fluid percentage of blood decreases, cell percentage of blood increases

• hematocrit increase up to 50% (or even beyond)

net effects of hemoconcentration

• red blood cell concentration increases

• hemoglobin concentration increases

• O2 carrying capacity increases

central regulation

• what stimulates rapid changes in heart rate, cardiac output, and blood pressure during exercise?

• central command

What stimulates rapid changes in heart rate, cardiac output, and blood pressure during exercise?

• precede metabolite buildup in muscle

• heart rate increases with 1 second of onset exercise

central command

• higher brain centers

• coactivation of motor and cardiovascular centers

integration of the exercise response

• cadiovascular responses to exercise: complex, fast, and finely tuned

• priority: maintenance of blood pressure

priority: maintenance of blood pressure

• blood flow can be maintained only if BP remains stable

• BP is prioritized before other needs (e.g. exercise thermoregulation)

respiratory responses

• ventilation during exercise

• breathing irregularities

• ventilation and energy metabolism

• estimating lactate threshold

• limitations on performance

• acid-base balance

ventilation during exercise

• immediate increase in ventilation

• gradual second phase of increase in ventilation

• ventilation increases proportional to metabolic needs of muscle

• ventilation recovery after exercise delayed

immediate increase in ventilation

• before muscle contractions

• anticipatory response from central command

gradual second phase of increase in ventilation

• driven by chemical changes in arterial blood

• increase in CO2, H+ sensed by chemoreceptors

• right atrial stretch receptors

ventilation increase proportional to metabolic needs of muscle

• at low exercise intensity, only tidal volume increases

• at high exercise intensity, rate also increases

ventilation recovery after exercise delayed

• recovery takes several minutes

• may be regulated by blood pH, PCO2, temperature

respiratory irregularities

• exercise-induced asthma

• dyspnea (shortness of breath)

• hyperventilation (excessive ventilation

• valsalva maneuver

exercise-induced asthma

• lower airway obstruction: coughing, wheezing, or dyspnea

• more water evaporated from airway surface

• disruption of airway epithelium and injury of microvasculature

dyspnea

• shortness of breath

• common with poor aerobic fitness

• caused by inability to adjust to high bloodd PCO2, H+

• fatigue in respiratory muscles despite drive to increase ventilation

hyperventilation

• excessive ventilation

• anticipation or anxiety about exercise

• increased PCO2 gradient between blood, alveoli

• decreased PCO2 → increased blood pH → decreased drive to breathe

valsalva maneuver

• potentially dangerous, but accompanies certain types of exercise

  • close glottis

  • increased intra-abdominal P (bearing down)

  • increased intrthoracic P (contracting breathing muscle)

great veins collapsed by high pressure →

decreased venous return → decreased cardiac output → decreased arterial blood pressure

estimating lactate threshold

• Ventilatory threshold as a surrogate measure?

  • excess lactic acid + sodium bicarbonate

  • result: excess sodium lactate, H2O, CO2

  • lactic acid, and CO2 accumulated simultaneously

• refined to better estimate lactate threshold

Ventilatory threshold as a surrogate measure?

• excess lactic acid + sodium bicarbonate

• result: excess sodium lactate, H2O, CO2

• lactic acid and CO2 accumulated simultaneously

refined to better estimate lactate threshold

• anaerobic threshold

limitations on performance

• ventilation normally not limiting factor

• airways resistance and gas diffusion normally not limiting factors at sea level

• restrictive or obstructive respiratory disorders possibly limiting

• exception: elite endurance-trained athletes exercising at high intensities

ventilation normally not limiting factor

• The respiratory muscles account for 10% of VO2, 15% of Q during heavy exercise

• respiratory muscles are very fatigue resistant

exception: elite endurance-trained athletes exercising at high intensities

• ventilation possibly limitied

• ventilation-perfusion mismatch

• exercise-induced arterial hypoxemia (EIAH)

acid-base balance

• metabolic processes produce H+ → decrease pH

• H+ + buffer = H-buffe3r

• at rest, body is slightly alkaline

• during exercise, body is slightly acidic

• Physiological mechanisms control pH

• active recovery facilitates pH recovery

at rest, body is slightly alkaline

• 7.1 - 7.4

• higher pH = alkalosis

during exercise, body is slighly acidic

• 6.6 - 6.9

• lower pH = acidosis

physiological mechanisms control pH

• chemical buffers include bicarbonate, phosphates, proteins, hemoglobin

• increased ventilation helps H+ bind to bicardonate

• kidneys remove H+ from buffers, excretes H+

active recovery facilites pH recovery

• passive recovery: 60 - 120 minutes

• active recovery: 30 - 60 minutes

recovery from acute exercise: cardiovascular variables

• postexercise hypotension (aerobic)

• postexercise hypotention (resistance)

postexercise hypotension (aerobic)

• driven by peripheral vasodilation

• can last several hours

• histmine is an important mediator of this response

postexercise hypotension (resistance)

• driven by decreased cardiac output