Response to Exercise and Stress Flashcards
Neural regulation - even anticipation of exercise elicits____. This will continue increasing as exercise begins and increases.
- Increased sympathetic activity –> increase blood flow
- Increased HR
- Increased contractility
- Venoconstriction to increase resistance in the inactive regional vascular beds
- Decreased parasympathetic activity
As you increase exercise, cardiac output, bp, and oxygen consumption also increase.
Total peripheral resistance _creases
Despite systemic vasoconstriction, total peripheral resistance decreases as local factors promote vasodilation in the active muscles and heart.
During exercise, skeletal muscle beds that are active will see a dramatic vasodilation as what metabolic factors build up locally?
K+
adenosine
H+
Mechanisms are in place to maintain proper supply to ___ during exercise. This occurs via a weak ___ and a strong ___.
Brain and other critical organs (like heart)
Weak sympathetic response
Strong myogenic response
Exercise has what impact on the vascular function curve?
UPWARDS because of net vasodilation and net decrease in total peripehral resistance.
Ultimately, cardiac output is increased
Describe what happens to blood flow to the skin during exercise.
- Increased sympathetic activity reduces blood flow to the skin.
- As body temp rises, cutaneous blood flow increases to perform heat exchange.
- As you then approach max O2 uptake, cutaneous blood flow is reduced again to shunt O2 to the active muscles.
bradykinin is associated with
mediating cutaneous circulation
2 aspects of the venous system that enhance blood flow during exercise
Sympathetic activation –> venoconstriction of capacitance vessels increases preload
Skeletal muscle contraction & deeper respiration compresses veins to pump it forward
What impact does exercise have on the baroreceptor reflex?
Exercise increases bp -> baroreceptor maintains blood pressure at the new “exercise induced” set-point
Ex) Increasing exercise will cause vasodilation –> drops total peripheral resistance –> baroreceptor reflex keeps the bp up despite this
How does severe exercise cause acute distress?
- Heart rate maxes out (~180bpm) and stroke volume plateaus
- Sympathetic vasoconstriction dominates over temperature regulation –> reduced skin circulation --> you overheat
Post exercise
Sympathetic drive drops, returning cardiac output to normal
Total peripheral resistance stays low as vasodilators take longer to wash out
Bp drops and the baroreceptor reflex stabilizes it.
Two factors that limit exercise performance (training & conditioning)
O2 utilization & O2 supply*
The skeletal muscles of athletes have better O2 utlization because
- increased capillary density
- mitochondria
- ATPase activity
Describe autonomci tone in highly trained athletes
High parasympathetic tone
Low sympathetic tone
–> lower resting heart rate & lower peripheral resistance
What allows athletes to achieve greater O2 delivery to tissues with smaller increases in heart rate?
Greater stroke volume –> better O2 delivery
Hemorrhagic Shock is the body’s response to rapid blood loss, which causes
decreased cardiac output and blood pressure
–> activates compensatory mechanisms to raise the bp
If prolonged (3-4hrs), decompensatory mechanisms cause further drops in bp and ultimately death
Compensatory mechanisms of hemorrhagic shock include
- baroreceptor reflexes - 1st to activate
- chemoreceptor reflexes
- criculating vasoconstrictors
- reabsorption of tissue fluid
- renal salt & water conservation
- cerebral ischemia responses
Hemorrhagic shock’s impact on baroreceptor reflex
-
Drop in pressure causes a drop in baroreceptor activity
- –> increased sympathetic tone
- –> increase in HR, contractility (CO), vasoconstriction, and venoconstriction.
- Kidneys override the vasoconstriction to maintain blood flow, but in severe hemorrhage, renal blood flow may be blocked –> kidney failure
When does the baroreceptor mechanism stop working?
This mechanism will cease functioning below ~60mmHg
Hemorrhage drops blood volume, which causes a __ward shift in the ascular function curve.
The baroreceptor responds by increasing sympathetic activity, causinga __ward shift in the cardiac function curve
downward shift in vascular fxn
upward shift in cardiac fxn
Renal compensation / circulating vasoconstrictors as a reponse to hemorrhagic shock
- Epinephrine & norepinephrine from adrenal medulla
- Decreased renal perfusion –> renin secretion –> RAAS promotes water retention & vasocosntriction:
- –> vasopressin/ADH from pituitary
- –> aldosterone from adrenal gland
Chemoreceptor reflex can operate below ~60mmHg.
Describe what it responds to and what it does
- Responds to hypoxia & acidic pH due to poor tissue perfusion
- Promotes increased CO & vasoconstriction:
- Increased respiration
- Incrased sympathetic activity
Tissue fluid reabsorption/capillary fluid shift as a response to hemorragic shock
Arterial hypotension, vasoconstriction, and reduced venous pressure –> lower hydrostatic pressure in capillaries
–> increased fluid rebabsorption
–> increased blood volume
Cerebral ischemia picks up around ~40mmHg after the chemoreceptor reflexbegins to decline
The brain is now experiencing ischemia –> increase sympathetics much higher than baroreceptor
Decompensatory mechanisms occurs a result of ___
the compensatory mechanisms activated during hemorrhage fail –> decompensatory mechanisms exaggerate itse ffects in positive feedback.
DECREASES bp
What are the decompensatory mechanisms?
- cardiogenic shock
- sympathetic escape
- CNS depression
- metabolic acidosis
- aberrations in clotting
- systemic inflammatory response
-
Cardiogenic shock: myocardium becomes hypoxic & acidotic,
- Reducing cardiac function
- Promoting arrhythmias
-
Sympathetic escape: without perfusion, there is no washout of vasodilators in the peripheral tissue –> vasodilation reduces TPR
- –> bp drops & increases hydrostatic pressure
- –> filtration and reducing blood volume
- –> bp drops & increases hydrostatic pressure
- CNS depression declines sympathetic activity
- Metabolic acidosis from lactic acid not being washed out –> depress CO and vascular smooth muscle contraction needed for vasoconstriction
- Clotting problems: blood viscosity increases without flow –> clotting factors create a hypercoagulability state
-
Systemic inflammatory response: release endotoxins and cytokines
- –> increased NO and ROS that promote vasodilation and decreased cardiac output
