Exercise; CNS control of electrolyte and water balance

Question 1

Things that change with increasing exercise intensity

Answer 1

everything (CO, HR, MAP, systolic BP, pulse pressure, Plasma lactate, PaO2 and Ventilation) except PaCO2, pH and diastolic BP

Question 2

Why would alveolar CO2 an O2 decrease and increase, respectively, during heavy exercise? what else increasing to match the increase in CO? T/F: the lung is rate limiting for gas transfer during exercise

Answer 2

Alveolar CO2 falls with maximal exercise; alveolar O2 is high with maximal exercise (mild hyperoxia) because your lungs just increase ventilation; Increase in Co is met with an increase in HR (HR = 220-age) Falsehood. It isn’t. what is rate limiting is the heart

Question 3

what happens to the arterial - venous gradient for oxygen with increasing exercise intensity?

Answer 3

Arterial venous gradient for oxygen gets bigger b/c more of the O2 gets sucked out of the arterial system into venous system (I think)

Question 4

relationship between exercise and oxygen consumption explain why it is this way

Answer 4

Linear relationship between exercise intensity and O2 consumption basically there’s more work required for your heart to deliver O2 to your muscles/tissues as you increase exercise intensity

Question 5

Relationship between Oxygen Consumption, Ventilation and Blood Lactate

Answer 5

Linear relationship between ventilation and oxygen usage; further increase in blood lactate (i.e. metabolic acidosis) causes steeper relationship between ventilation and O2 because you’re undergoing respiratory compensation

Question 6

except in cases of intense exercise, what happens to the levels of alveolar PO2 and PCO2?

Answer 6

Alveolar PO2 and alveolar PCO2 stay relatively constant except in cases of intense exercise

Question 7

relationship between maximal CO and O2 consumption what does this say about who determines max O2 consumption/muscle work?

Answer 7

O2 is has a linear relationship with maximal cardiac output Maximal Oxygen Consumption (and hence muscle work) is determined primarily by Cardiac Performance

Question 8

describe the curve below

what happens at rest vs w/ exercise

Answer 8

Basically both your venous and cardiac function curves rise

At rest, CO output is ltd by venous return, and vasculature presents high resistance to blood flow

W/ exercise, there’s an increase in venous return, and increased sympathetic return to heart, which raises CO

Question 9

what’s the bohr shift? why’s it important?

Answer 9

But as the blood passes across the capillary,the driving gradient for O2 diffusion gets smaller and the PCO2 increases so that the blood pH will fall. The increase in PCO2 causes the red cells to acidify

Bohr effect greatly improves the ability to unload O2
and hence helps maintain the gradient for O2 diffusion out of the capillary

Question 10

to which organs does blood flow/CO increase/decrease during max exercise?

Answer 10

At rest, cardiac output to major organs is normal/high ish

With increasing exercise, there’s increased CO to muscle; CO decreases to everything else

The ABSOLUTE amount of blood going to the brain is the same, even though the CO has decreased

Question 11

which hormones/proteins are increasingly secreted with increasing exercise intensity? (what do you want when you exercise; which hormones help you get there?)

what happens in the brain?

Answer 11

Key things you want: glucose, and increased blood pressure/cardiac output

Ang 2

ADH

Aldosterone

ACTH

Cortisol

Catecholamines

Increased sympathetic nerve activity

Question 12

How would you get hyponatremia during excessive exercise?

what happens to blood glucose levels with prolonged intense exercise? what’s a potential downstream effect?

Answer 12

Drinking water with augmented water retention when combined with salt loss via sweat can lead to to hyponatremia, then CNS swelling and confusion.

**Prolonged intense exercise may further depress blood glucose and lead to fatigue.

Question 13

describe the graph below

what accounts for the rapid vs slow changes? how would you prove this?

Answer 13

Rapid increase in ventilation w/in first 40 mins, then gradual increase between time 40 and 80, then rapid decrease, and gradual decrease

Rapid vs gradual phases are due to neural and chemical inputs respectively

(chemical inputs: you can prove it based on the fact that for example, people on the back of a tandem bike will be sweating and getting tired but their legs are actually being moved passively on the bike)

Question 14

When skin temperature > external temperature, the body loses heat by both ___ and __.

When the external temperature > skin temperature the body gains heat by radiation and conduction. ___ is the only means to lose heat

Answer 14

radiation

conduction

evaporation

Question 15

how do you maintain water balance?

describe the effect of each of the following:

water gain/loss to ECF compartment

adding impermeable solute like Na

adding permeant solute e.g. urea

Answer 15

water in = water out

Water gain: enters the ECF first, then moves into the ICF; if you add straight up water, you get cellular and extracellular overhydration (and hyposmolarity)

Losing water: from ICF and ECF; both of them shrink and become hyperosmolar

Adding Na expands ECF (not permeable), which draws water from ICF; so the ICF shrinks and the ECF has overhydration

adding permeant solute (urea): No changes (since urea is permeable, things will balance out) [osmolality does increase though]

**The osmoreceptors will drive thirst for this reason (increased ADH activity)

Question 16

what are osmoreceptors more sensitive to? na+ or osmolality? how would you prove this

effect of increasing osmolality on thirst

relationship of AVP to osmolality changes

Answer 16

osmolality

Sucrose increases thirst because its not membrane permeant; it’ll collect in the ECF and draw water from the ICF, which prompts thirst; that just shows that osmoreceptors are sensitive to osmolality period, not just Na+

Progressively increasing tonicity = increased thirst (increased osmolality)

AVP levels = linear relationship to changesin plasma osmolality

Question 17

what happens when there’s a lesion to the OVLT?

Answer 17

Response is still there but it takes so much longer

Question 18

describe the graph below

what’s the conclusion about the data (i.e. what turns off drinking?)

define rapid rehydration

T/F: humans and other mamammals are rapid rehydrators

Answer 18

Over time, as the dogs drank more water, AVP decreased but plasma osmolality didn’t change, which means that something else had to prompt the dogs to stop drinking​

Rapid rehydration – when mammals are dehydrated throughout the day and they want to replace that deficit very quickly

Apparently there’s sensors in the mouth that mediate this process (that’s in dogs though, don’t know about people)

Humans AREN’T rapid rehydrators, generally. They tend to take several sips

Question 19

describe Central diabetes insipidus

what is the relationship between the thirst response and AVP response when plasma osmolality increases?

Answer 19

central DI: no AVP being made

In DI, there is typically a thirst (Th) response to increased plasma Osm but no plasma AVP response.

So the osmosensitive magnocellular neurons in the SON make and release AVP and trigger thirst, but AVP itself is not the molecular mediator of the thirst drive.

Question 20

SIADH vs Primary polydipsia (define them)

what are the ADH levels in either case? what happens to plasma sodium concs? what’s the result of each?

Answer 20

SIADH (Syndrome of Inappropriate ADH)

Elevated plasma ADH (AVP)

Over secretion of ADH relative to plasma osmolality

Usually a centrally mediated disturbance –trauma, lesion, etc

Result: excess renal mediated water retention

Hyponatremia (below normal plasma Sodium concentration)

Overhydration tends to suppress normal thirst

Some cancers make and secrete excess ADH

Primary Polydipsia (Excess water intake)

Constant thirst

May drink 20 Liters of water/day

Hyponatremia

ADH secretion is almost completely suppressed.

Plasma ADH is very low (suppressed).

Thirst drive is independent of ADH in these pts

Question 21

what happens to ECF and ICF compartments when you have hermorrhage? what happens to AVP?

describe how baroreceptors respond to hemorrhage

how is the drop in blood pressure during hemorrhage related to thirst?

Answer 21

When you have hemorrhage, you have shrinkage of ECF Compartment but no change in intracellular volume, so no change in AVP

Baroreceptors will also respond to hemorrhage; they’ll sense drop in blood pressure and will prompt AVP secretion via their other receptors;

When you lose blood, your blood pressure will drop, which stimulates thirst, and activates the AVP response

Question 22

T/F: humans, like other animals, have a hard wired salt hunger

patients with what disease may have demonstratable salt hunger?

Answer 22

Falsehood. Normal humans DON’T have an acute salt drive. Salt desire is mainly hedonic

Patients with Addison’s disease (autoimmune cause of adrenal insufficiency) may have demonstratable salt hunger

Question 23

cerebral salt wasting (what is it, how does it develop and what are some symptoms?)

Answer 23

relatively rare endocrine syndrome associated with trauma/injury or tumors in or surrounding the CNS (especially the areas surrounding the third ventricle)

Primary signs and symptoms:

• Hyponatremia: secondary to excessive renal sodium excretion
• Dehydration and hypovolemia (cf SIADH)
• Polyuria due to inadequate sodium retention
• Polydipsia due to polyuria
• Extreme salt cravings – a pathological “salt hunger”
• Other late onset symptoms: muscle cramps, lightheadedness, dizziness or vertigo, feelings of anxiety or panic, tachycardia or bradycardia, hypotension sometimes resulting in cardiac syncope.