Impact of moderate isocapnic hyperthermia on dynamic cerebral autoregulation and its directional sensitivity
Mahmoudreza Taghizadeh, Marc-Antoine Roy, Shahrzad Soleimani Dehnavi, Daniel Gagnon, Patrice BrassardThe effects of heat exposure on dynamic cerebral autoregulation (dCA), the capacity of the cerebrovasculature to buffer rapid changes in arterial pressure, and its directional sensitivity, defined as the asymmetric cerebrovascular response to increases versus decreases in mean arterial pressure (MAP), remain incompletely understood. This uncertainty is largely attributable to concomitant heat-induced reductions in arterial carbon dioxide. We hypothesized that moderate isocapnic hyperthermia would impair dCA, particularly at higher frequencies of MAP oscillations, while preserving directional sensitivity across thermal conditions. Twenty healthy young participants (9 females, age: 24 ± 5 yrs) completed oscillatory lower body negative pressure trials at 0.05 and 0.10 Hz under normothermic and hyperthermic (core temperature +1.0°C) conditions. End-tidal carbon dioxide partial pressure (P ET CO 2 ) was clamped at baseline using a computer-controlled gas delivery system. Middle cerebral artery mean blood velocity (MCAvmean), MAP, P ET CO 2 , heart rate, and core temperature were continuously recorded. dCA was assessed using transfer function analysis (TFA), and directional sensitivity was quantified using time-adjusted absolute (∆MCAvmean T /∆MAP T ) and relative (RelMCAvmean T /RelMAP T ) metrics. Moderate isocapnic hyperthermia increased TFA coherence at both frequencies and selectively impaired dCA at 0.10 Hz, as evidenced by increased TFA gain and normalized gain. Directional sensitivity was present at 0.05 Hz, indicated by higher ∆MCAvmean T /∆MAP T and RelMCAvmean T /RelMAP T during MAP decreases compared with increases, but was absent at 0.10 Hz. These findings demonstrate that isocapnic hyperthermia impairs dCA at higher frequency while preserving directional sensitivity at lower frequency, suggesting that distinct physiological mechanisms govern these components of cerebrovascular regulation beyond the influence of carbon dioxide.