Exercise; CNS control of electrolyte and water balance Flashcards
Things that change with increasing exercise intensity
everything (CO, HR, MAP, systolic BP, pulse pressure, Plasma lactate, PaO2 and Ventilation) except PaCO2, pH and diastolic BP
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
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
what happens to the arterial - venous gradient for oxygen with increasing exercise intensity?
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)
relationship between exercise and oxygen consumption explain why it is this way
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
Relationship between Oxygen Consumption, Ventilation and Blood Lactate
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
except in cases of intense exercise, what happens to the levels of alveolar PO2 and PCO2?
Alveolar PO2 and alveolar PCO2 stay relatively constant except in cases of intense exercise
relationship between maximal CO and O2 consumption what does this say about who determines max O2 consumption/muscle work?
O2 is has a linear relationship with maximal cardiac output Maximal Oxygen Consumption (and hence muscle work) is determined primarily by Cardiac Performance
describe the curve below
what happens at rest vs w/ exercise
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
what’s the bohr shift? why’s it important?
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
to which organs does blood flow/CO increase/decrease during max exercise?
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
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?
Key things you want: glucose, and increased blood pressure/cardiac output
Ang 2
ADH
Aldosterone
ACTH
Cortisol
Catecholamines
Increased sympathetic nerve activity
How would you get hyponatremia during excessive exercise?
what happens to blood glucose levels with prolonged intense exercise? what’s a potential downstream effect?
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.
describe the graph below
what accounts for the rapid vs slow changes? how would you prove this?
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)
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
radiation
conduction
evaporation
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
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)
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
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
what happens when there’s a lesion to the OVLT?
Response is still there but it takes so much longer
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
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
describe Central diabetes insipidus
what is the relationship between the thirst response and AVP response when plasma osmolality increases?
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.
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?
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
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?
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
T/F: humans, like other animals, have a hard wired salt hunger
patients with what disease may have demonstratable salt hunger?
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
cerebral salt wasting (what is it, how does it develop and what are some symptoms?)
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.
