PCP topics Flashcards
What points support temperature is defended around a setpoint
- Direct measures (through experimental conditions) show that core temps for thermoregulatory responses (vasomotor control, sweating…) not to be significantly different suggesting its defended at a point, any deviation from this point results in TR responses
- indirect: use of a neural model. Summation of warm/cold signals in the hypothalamus the dominant will win
What are critiques on evidence supporting setpoint
- RCI: shows overlap in cold/warm neurons firing; but no overlap in the cold/heat response therefore null zone
- potential experimental error due to positive feedback & the anticipatory response
what points support temperature is defended about a null-zone
- null zone = range of temperatures in which no shivering or sweat response is seen; only vasomotion
- experiment looking @ this ( through cold exposure/rest/exercise) found significant differences for the onset of shivering and sweating
- forced warm air/cold lactate solution show core temp being defend in a zone
What are critiques on evidence supporting a null zone
- Evidence was found on patients with bacterial infections, menopausal women, hyperglycemia in diabetes; not in a general population.
- Issues with taking core temp @ rectum only (delay for a change in rectal temp compared to tympanic)
What are points supporting humans pant
- alteration in the sensitivity of central chemoreceptors or change in threshold of PCO2 increasing pulmonary ventilation lead to hyperpnea
- drop in MCA blood velocity due to hyper-ventilation induced drop in PACO2
What are critiques on evidence supporting human panting
- studies showing panting utilized impaired-sweat subjects
- panting = ineffective method of heat loss and may contribute to heat stress
what points support humans do not pant
- change in respiration only occurs once a core temp is exceeded, this threshold is far higher than it is for other TR responses
- heat loss from respiratory system contributed minimally to head loss and isn’t necessary
What are critiques on evidence supporting humans do not pant
- definitions used are “wrong” and not all encompassing
- panting is shown in those with impaired sweating, therefore stating panting doesn’t occur in humans isn’t applicable to all
what points support that humans selectively cool their brain
- patients w/ intubation removed show an increase in core temp, but brain/esophageal temp decreased (due to evaporation/conduction of mucous in the nasal cavity)
- face fanning/evaporation of head sweat resulted in cooling of the brain
What are critiques on evidence supporting SBC
- tympanic membrane temp doesn’t necessarily = brain temp
- i.e. this is an indirect measure that rather reflects cooler skin temp
- no carotid rete, no panting
- human airway isn’t long enough to provide effective heat loss
- actual brain cooling occurs only in clinical interventions (via perfusing cooling helmet)
What evidence supports that humans do not SBC
Rather than SBC, the body cools itself uniformly via sweating/vasodilation and counter current heat exchange
- CCHE: HE between cool venous blood and warm arterial blood
What are critiques on evidence supporting no SBC
- research stating tympanic membrane doesn’t = brain temp was done on a single subject
What evidence supports that glycogen is the rate limiting substrate for shivering
- studies show glycogen depletion during shivering
- proteins only decrease slightly, reduced availability of FFA doesn’t disrupt shivering therefore glycogen = rating limiting
What are critiques on evidence supporting glycogen = rate limiting step
- studies didn’t last long enough for lipid oxidation to kick in
- individual variation in muscle fibre type is not taken into account esp in small sample size
What evidence supports glycogen is not the rate limiting step
- when glycogen depleted, use lipid oxidation
- prolonged shivering uses more lipids
- glycolysis = anaerobic > lactic acid
- varying muscle fibre recruitment
What are critiques on evidence supporting glycogen isn’t the rate limiting factor
- lack of quantification of changes in fibre recruitment/lack of info on protein contribution = reason why G-depleted/G-loaded show different fuel mixtures
- study showing different fuel sources didn’t normalize age/diet
what evidence supports that aging affects temp reg
- older = decreased core temp threshold for cooling, max vasoconstriction, decreased O2 consumption
- heat acclimation: younger = lower Tc, Tsk, HR and increased sweating
- older have more limited secretory sensitivity
What are critiques on evidence supporting aging affects temp reg
- No documentation of hydration status - decreased hydration leads to decreased skin BF
- no standardization for %BF; impaired threshold for VC not age
What evidence supports that aging does not affect temp reg
- heating: no difference in therm reg responses in old/young women
- cooling: maintain Tc
What are critiques on evidence supporting aging does not affect temp reg
- studies showing no changes in temp reg responses btwn young/old were matched for aerobic capacity (therefore more fit elders)
- temperatures were not extreme enough to induce differences
- workload was not matched
- studies are done in different seasons
What evidence supports the idea that NST is seen in other tissues
- WAT involved in NST; “brite” cells originating from WAT express UPC1
- brite cells show similar respiration rate to BAT
Skeletal muscle contributes via UPC3
What are critiques on evidence supporting NST is seen in other tissues
- if BAT is inhibited animals rely on shivering
- Only BAT shows significant met. activity when exposed to cold when compared to muscle
- large increase in BF to BAT when cold than muscles
What evidence supports that NST is not seen in other tissue
- T3 from skeletal muscle actually affects control centers in the brain regulating BAT activity
- “brite” vells may actually be a subtype of BAT
What are critiques on evidence supporting NST is not seen in other tissues
- small sample sizes
- utilize mice rather than humans
- neglect the effects of T3
- doesn’t take into account the long acclimation time for NST in skeletal muscle
