Why does systolic blood pressure increases and diastolic bp decrease during exercise? Watch

1drowssap
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I know that there is vasoconstriction by sympathetic NS and high cardiac output due to high stroke volume and heart rate.
I know that there is vasodilation in active muscle
In the scenario, the systolic BP increases and diastolic BP decreases.
The mean arterial pressure increases.
Pulse pressure also increases.
My question is how systolic BP can increase and diastolic BP can decrease at the same time?
Surely if the mean arterial pressure rises then vasoconstriction>vasodilation, which would at best support a case for increase systolic BP. But how does the diastolic BP decrease?
Am I not getting something here?
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The Only Rivo
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(Original post by 1drowssap)
My question is how systolic BP can increase and diastolic BP can decrease at the same time?
Surely if the mean arterial pressure rises then vasoconstriction>vasodilation, which would at best support a case for increase systolic BP. But how does the diastolic BP decrease?
Am I not getting something here?
This is from my 2nd year PBL notes so don't take it as dogma, but it is what I gathered at the time using two physiology textbooks (Martini's and Tortora) as well as leaked official PBL facilitators' notes (lol this took me back to the good ol' days!):

Short term CV changes in dynamic exercise (may be different in weightlifting and other static types of exercise)
-CO --> Increases (5 l/min up to 35 l/min) due to increased HR and SV
-SV --> Increases due to increased sympathetic activity to ventricular myocardium as well as increased EDV (preload) due to increased venous return --> both lead to increased force of contraction (Starling’s law)
-HR --> Increases due to increased sympathetic activity to SA node (N.B. this I think is not strictly true even though it was taken from a textbook. I believe the SA node doesn't get a lot of sympathetic innervation so a more accurate way to put it would be "decreased parasympathetic activity" - this is why atropine (anti-muscarinic) is the first drug of choice in supra-nodal bradycardia rather than an adrenergic agonist. Again this is just personal opinion)
-TPR --> Decreases due to vasodilation in muscle arterioles (with concomittant vasoconstriction in visceral organs)
-MABP --> Increases because the increase in CO > the reduction in TPR
-Pulse Pressure --> Increases due to increased SV and velocity of ejection


So basically to directly answer your question, there is an increased in MABP despite peripheral vasodilation because the increases in HR and SV and consequently CO are bigger than the decrease in TPR.
Systolic BP increases due to increased contractility which leads to increased stroke volume and increased ejection velocity.
Diastolic BP decreases due to peripheral vasodilation.
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1drowssap
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(Original post by The Only Rivo)
This is from my 2nd year PBL notes so don't take it as dogma, but it is what I gathered at the time using two physiology textbooks (Martini's and Tortora) as well as leaked official PBL facilitators' notes (lol this took me back to the good ol' days!):

Short term CV changes in dynamic exercise (may be different in weightlifting and other static types of exercise)
-CO --> Increases (5 l/min up to 35 l/min) due to increased HR and SV
-SV --> Increases due to increased sympathetic activity to ventricular myocardium as well as increased EDV (preload) due to increased venous return --> both lead to increased force of contraction (Starling’s law)
-HR --> Increases due to increased sympathetic activity to SA node (N.B. this I think is not strictly true even though it was taken from a textbook. I believe the SA node doesn't get a lot of sympathetic innervation so a more accurate way to put it would be "decreased parasympathetic activity" - this is why atropine (anti-muscarinic) is the first drug of choice in supra-nodal bradycardia rather than an adrenergic agonist. Again this is just personal opinion)
-TPR --> Decreases due to vasodilation in muscle arterioles (with concomittant vasoconstriction in visceral organs)
-MABP --> Increases because the increase in CO > the reduction in TPR
-Pulse Pressure --> Increases due to increased SV and velocity of ejection


So basically to directly answer your question, there is an increased in MABP despite peripheral vasodilation because the increases in HR and SV and consequently CO are bigger than the decrease in TPR.
Systolic BP increases due to increased contractility which leads to increased stroke volume and increased ejection velocity.
Diastolic BP decreases due to peripheral vasodilation.
Thanks for giving such a detailed reply. It makes a lot of sense.

Just a question though,so does the pressure in the arteries rise due to increase contractility of the heart and increased stroke volume?
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carcinoma
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(Original post by 1drowssap)
Thanks for giving such a detailed reply. It makes a lot of sense.

Just a question though,so does the pressure in the arteries rise due to increase contractility of the heart and increased stroke volume?
Yes, MABP=CO*TPR

CO=SV*HR


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1drowssap
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(Original post by carcinoma)
Yes, MABP=CO*TPR

CO=SV*HR


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Thanks. Do you happen to know how afterload has an effect on cardiac output during exercise?
I only know that a greater afterload can cause longer isovolumetric contraction and decreased cardiac output. In exercise, would afterload be reduced due to fall in TPR?
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Hype en Ecosse
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(Original post by The Only Rivo)
This is from my 2nd year PBL notes so don't take it as dogma, but it is what I gathered at the time using two physiology textbooks (Martini's and Tortora) as well as leaked official PBL facilitators' notes (lol this took me back to the good ol' days!):

Short term CV changes in dynamic exercise (may be different in weightlifting and other static types of exercise)
-CO --> Increases (5 l/min up to 35 l/min) due to increased HR and SV
-SV --> Increases due to increased sympathetic activity to ventricular myocardium as well as increased EDV (preload) due to increased venous return --> both lead to increased force of contraction (Starling’s law)
-HR --> Increases due to increased sympathetic activity to SA node (N.B. this I think is not strictly true even though it was taken from a textbook. I believe the SA node doesn't get a lot of sympathetic innervation so a more accurate way to put it would be "decreased parasympathetic activity" - this is why atropine (anti-muscarinic) is the first drug of choice in supra-nodal bradycardia rather than an adrenergic agonist. Again this is just personal opinion)
-TPR--> Decreases due to vasodilation in muscle arterioles (with concomittant vasoconstriction in visceral organs)
-MABP --> Increases because the increase in CO > the reduction in TPR
-Pulse Pressure --> Increases due to increased SV and velocity of ejection


So basically to directly answer your question, there is an increased in MABP despite peripheral vasodilation because the increases in HR and SV and consequently CO are bigger than the decrease in TPR.
Systolic BP increases due to increased contractility which leads to increased stroke volume and increased ejection velocity.
Diastolic BP decreases due to peripheral vasodilation.
Sports science intercalatee here! This is roughly my understanding as well: my only caveats would be that the response varies with exercise type and intensity (and also to say weightlifting, bodyweight movements, etc. are all still forms of dynamic exercise!).

For HR: Initially (before exercise starts): increased SNS activity with reciprocal decreased PSNS activity. As exercise starts, most change is due to further PSNS withdrawal (like you said): but the more intense you get, the more SNS contribution there is. Feedback from peripheries (how much blood; how much o2; what pH etc.) also ends up playing an indirect role.

Increased skeletal muscle pump action contributes to the increased MAP in exercise, also.

Systolic shoots up as soon as you start exercise, then slowly increases with exercise intensity (this is mostly the CO). Diastolic has no big drop, but again, only slowly decreases with increased intensity (would drop due to vasodilation, but is counterbalanced by the CO: hence why you can see no change to a small change, vs the big changes in systolic). For exercise intensities you could keep up for a long time (like in a 10K), there's not usually a change on DBP.

The weightlifting response is totally different: concentric contraction compresses arteries -> "I'm not getting blood!!!!" response -> huge spike in CO & MAP. Both SBP and DBP increase a large amount here. More intense the lift, the bigger the jump.

(Original post by 1drowssap)
Thanks. Do you happen to know how afterload has an effect on cardiac output during exercise?
I only know that a greater afterload can cause longer isovolumetric contraction and decreased cardiac output. In exercise, would afterload be reduced due to fall in TPR?
Afrerload is the TPR as far as we're concerned, really. For moderate exercise, afterload decrease contributes to increased CO. In things like weightlifting, afterload is increased, but there's an increased drive (beat harder) and you get increased CO anyway (this is likely why weightlifter's hearts undergo a different type of hypertrophy from endurance athlete's hearts).

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