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
