The Influence of Cerebral Blood Flow and PETCO2 on Neuromuscular Function During Passive Heat Stress
Status:
Completed
Trial end date:
2016-12-01
Target enrollment:
Participant gender:
Summary
Increased core temperature (hyperthermia) has been associated with impaired neuromuscular
performance; however, the mechanisms associated with these performance decrements and their
potential synergies remain unclear. While the majority of research suggests that the observed
fatigue is related to the central nervous system, the influence of changes in cerebral blood
flow (CBF) and associated changes in cerebral alkalosis (estimated by end-tidal partial
pressure of carbon dioxide; PETCO2) remains unexamined. In response to hyperthermia, humans
hyperventilate as means of heat dissipation, resulting in a hypocapnia (reduced PETCO2)
mediated decrease in CBF and consequently, cerebral alkalosis (increased cerebral pH).
Previous research suggests that hyperventilation induces changes in neural excitability and
synaptic transmission; however, it remains unclear if these changes are related to hypocapnia
mediated decrease in CBF or decreased PETCO2 or both.
The purpose of the proposed research program is to examine the influence of changes in CBF
and cerebral alkalosis on neuromuscular function during passive heat stress. The research
project will consist of 3 separate experimental trials: (a) poikilocapnic hyperthermia
(increased core temperature; decrease CBF; decrease PETCO2), (b) isocapnic hyperthermia
(increased core temperature; no change CBF; no change PETCO2) and (c) isocapnic hyperthermia
+ indomethacin (increased core temperature; decrease CBF; no change PETCO2). During each
manipulation, neuromuscular function will be evaluated and compared to baseline
(normothermic) conditions using a repeated measures design.
It is hypothesized that changes in PETCO2 and therefore, changes in cerebral alkalosis will
contribute to neuromuscular fatigue independent of changes in CBF or increases in core
temperature.