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Lecture 8

Lecture 8 (revised).docx

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Kinesiology&Physical Education
EDKP 395
Russell T Hepple

12/5/2012 8:54:00 PM Regulation of local blood slow  Skeletal muscle vasodilation (arterioles o Autoregulation via SNS  BF increased to meet metabolic demands of tissue  i.e. rvasodilation regulated by metabolic need of muscel  Due to changes in  O2 tension  CO2 tension product of metabolism  Metabolites  Adenosine  Nitric oxide o Produced in endothelium/arterioles  Nitric oxide synthase o Promotes smooth muscle relaxation  Overrides SNS stimulation  Causes vasodilation & inc. BF o Important in autoregulation  Potassium  pH  Vasoconstriction to visceral organs and inactive tissues o Via SNS regulated by cardiovascular control center Summary:  O2 delivery to exercising muscle increased due to o Increased CO  As a linear function of O2 uptake during exerise  SV reaches a pleateau at ~40-60% VO2max  After that increases in CO are due to HR alone o Redistribution of BF from inactive organs to contracting skeletal muscle Changes in HR and BP  Depend on o Type, intensity, duration of exercise  Arm vs leg exercise  HR/BP arm >> leg o Environmental condition  Hot/humid vs cool o Emotional influence  Can raise pre-exercise HR and BP  Onset of exercise o Rapid inc. in HR, SV, CO o Plateau of SV during sub-maximal (below lactate threshold) & steady state exercise @ 40% VO2max  CO continues to inc. due to HR  During recovery o Decrease HR, SV, CO towards resting levels  Slower/longer than rapid increase at onset of exercise o Depends on  Duration/intensity of exercise  Training state of subject  More trained, less time for recovery b/c don’t obtain as high a HR as untrained  Slower during hot humid invoontmentsdue to elevated body temp HR/CO  Increases linearly with increasing work rate o Highly regulated  Reaches plateau at 100% VO2max BP  MAP increases linearly o Systolic BP inc. o Diastolic BP remains fairly constant  Due to vasodilation  In active muscle causes a decrease in total peripheral resistance which is why BP doesn’t change Double product (rate-pressure product)  Increases linearly with exercise intensity  Indicates work of the heart (i.e. metabolic demand placed on heart- increased during exercise)  DP = HR x systolic BP  Used as a guideline to predscirbe exercise for patients w/ CHD 12/5/2012 8:54:00 PM Arm vs Leg  At same O2 uptake ARM work results in HIGHER o HR  Higher SNS stimulation o BP  Vasoconstriction of large inactive muscle mass Interval exercise  CO/HR inc in direct proportion to O2 uptake o BF increase too o CO Iinc. Achieved through  Dec. vascular resistance  Inc. MAP  CO/HR reach plateau @ 100% VO2max o Increases in exercise intensity result in elevation of body HR and SBP which increases workload placed on heart Intermittent exercise- discontinuous  recovery of HR and BP b/w bouts depends on o fitness level  shorter time to resting levels for trained indv. o temp/humidity  sweat helps maintain body temp  in high temp/humid environments you get the most amount of sweat produced o duration and intensity of exercise Prolonged exercise  CO maintained  Gradual decrease in SV o Due to dehydration and reduced plasma volume  Dehydration  dev. BV  major dec in venous return  dec. diastolic volume  dec. systolic volume  Gradual increase in HR o Called “Cardiovascular drift” - signal that shows the point of change b/w steady sate to prolonged exercise: where HR becomes the main contributor the CO while SV decreases note that HR increases in the same proportion as SV decreases in order to maintain a constant CO Summary  Changes in HR and BP during exercise area function of o Type & intensity of exercise o Duration o Environmental conditions 12/5/2012 8:54:00 PM Suddent cardiac death during exercise  Uncommon- 1/200,00 youth athletes  Caused by abnormal, lethal heart rhythms o Children/adolescents, due to:  Genetic abnormailities or coronary arteries  Cardiomyopathy  Conduction system is messed up  Myocarditis  Infection that attacks heart cells o Adults  Coronary artery disease  Cardiomyopathy  can be identified those at risk through medical exams o Cardiac ejection fraction <40% = cardiac issues CO  Increased in HR (cardiac rate), SV o Which is a function of SNS activation via adrenal glands o SV:  Skeletal muscle activity leads to improved venous return (muscle pumps) that increases SV  Deeper breathing increases venous return via increase in negativity of intrathoracic pressure sucks blood into thorax/vena cava BF to skeletal muscles  Skeletal muscle activity leads to accumulation of metabolites which causes vasodilation in active muscles increasing BF  Sympathetic vasoconstriction in viscera (i.e. in inactive tissue/organs) leads to increase in BF Central command theory  Initial signal to drive cardiovascular system comes from higher brain centers o Due to centrally generated motor signal o Primary drive is to inc HR, but cardiovascular response is fine tuned feed  Fine tuned fee
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