Hi there young man - this question and its possible answers are NOT "simply wrong" BUT RATHER "highly complex and confusing" - let me try to explain as empirically as I can:-
Yes you are right that catecholamines can cause vasoconstriction by stimulating alpha-1 adrenoceptors, but there are several other factors that interplay to result in variable effects on b.p.
Firstly, adrenaline has both alpha and beta adrenergic effects, so that yes it can cause vasoconstriction via the alpha-1 effect, but the alpha-2 effect [on presynaptic receptors] tends to block the release of NA hence dampening the vasoconstrictive effect. Secondly, one of the [diverse] actions of adrenaline on beta-2 receptors is to cause vasodilatation of muscular arterioles [medium-sized arteries], which adds to the vasodilatory effect of the action of adrenaline on alpha-2 receptors, so the situation is highly complex NOT "simple" at all!
In conclusion, what will happen to b.p. during exercise will depend on various factors, far beyond what you need to know at A level - if you are studying at degree level, particularly in medicine or pharmacology, then try to grasp the above; if at school/college, I would stick to the basics in my previous post in order to avoid confusion to OP and others, which I tried to keep simple for OP, who I assume is doing A level biology.
If at medical school or PG level, it might also help to know that neurotransmitters are not pure agonists or antagonists - there is a continuum [kinda spectrum] between agonist activity and antagonistic activity, so that an agonist will have some blocking activity and vice versa, hence the corollary that some beta-adrenoceptor antagonists have a noticeable ISA [Intrinsic Sympathomimetic Activity] e.g. pindolol, so will cause less bradycardia and a weaker negative inotropic effect than other beta-blockers without significant ISA.
If you need more detail, you know where to find me.