I like to think about the equations as well as what's been discussed. First though a quick note though. Diastolic blood pressure does not significantly change in normotensive people due to a decreasing TPR but increasing CO (more "volume" in the arterial side if you will conceptually). Interestingly in hypertensives this isn't true and their diastolic pressure does increase with exercise due to inability to drop TPR down as well which I think highlights the principle of if you can't drop TPR diastolic increases, meaning something is increasing it but TPR balances it, more on this later. So anyway diastolic pressure tends not to change much, more in that later.
Now some general things to keep in mind as exercise level increases oxygen demand increases thus more blood must be supplied, the cardiac output/delivery oxygen is the rate limiting step if you will of oxygen delivery to the muscle. So with this in mind a look at the differences. So MAP=COxTPR, CO=SVxHR, SV=EDV-ESV, pulse pressure= systolic pressure-diastolic, and pulse pressure is proportional to SV and inversely proportional to arterial compliance. So now
So with those in mind lets go through exercise. The responses is mediated by both central and local processes. The central processes act in anticipation to exercise (from brain) and increase sympathetic output to the heart and blood vessels and decrease parasympathetic output to the heart. This increases the CO by increasing the heart rate, but also the SV (the end systolic pressure will be less due to more contraction and ejection of more of the EDV). This is essential and really provides the extra O2 needed. Now remember back to the cardiac function curves, what is needed to increase the CO? An increase in venous return! (On these graphs, exercise moves straight up I.e both the venous return and CO increase so that RAP stays the same). The increase in venous return is mediated by contraction of the skeletal muscle squeezing the veins more and increased sympathetic activity produces venous construction. So this decreased the unstressed volume (venous side) and means that more of that volume that is being put out on the arterial side gets back to the heart or doesn't pool in the veins as much. So now the other effect of sympathetic activation: arterioles constrict, except at the muscles which is mediated mostly by local metabolites, these dilate thus assuring that blood flow gets to the muscles that need it. Since the muscles are huge and heavily supplied by blood this leads to a decrease in TPR as discussed.
So now let's look back at the heart. So CO increased via increase in HR (major factor in sustained exercise as SV can only increase so much) and SV. The increase in SV is seen by increase in pulse pressure (they are proportional remember since you are pumping out a larger volume into the lower compliance arteries). This increased stroke volume with an increased HR is possible due to increased venous return as mentioned earlier. All together than this increased stroke volume and HR will generate a higher systolic pressure and increase the MAP since CO went up more than TPR went down thinking back to that equation. Diastolic doesn't change and indeed may even drop just a tad in some people due to the decrease in TPR (which could depend on how man muscle groups you are activating ostensibly).
So to answer your question directly: the diastolic is maintained because the volume of the system is not changing (which can effect mean systemic filling pressure which I like to think of as somewhat related to diastolic pressure) you have relatively more volume in the arterial side due to venous construction and CO and the TPR has conceivably gone down less than those other forces (CO) leading to a regulation of diastolic pressure. Although, it is possible to see a slight decrease.
The rise in systolic pressure on the other hand is due to increased CO, especially from the increased SV. Said another way the MAP=COxTPR (again showing the relationship between the two) so we know MAP increases in exercise this we know that the CO had to go up more than the TPR went down (the counteracting effects) otherwise we wouldn't see an increase.
Anyway sorry about the crazy long post hopefully it is somewhat helpful and clear (done on my phone quickly so apologies in advance for typos and such) , if it is still confusing constanzo (full version) has a nice explanation of it.
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