Resistance exercise acutely elevates dynamic cerebral autoregulation gain

This is the final version. Available on open access from Wiley via the DOI in this recordDynamic cerebral autoregulation (dCA) describes the regulation of cerebral blood flow (CBF) in response to fluctuations in systemic blood pressure (BP). Heavy resistance exercise is known to induce large transient elevations in BP, which are translated into perturbations of CBF, and may alter dCA in the immediate aftermath. This study aimed to better quantify the time course of any acute alterations in dCA after resistance exercise. Following familiarisation to all procedures, 22 (14 male) healthy young adults (22 ± 2 years) completed an experimental trial and resting control trial, in a counterbalanced order. Repeated squat-stand manoeuvres (SSM) at 0.05 and 0.10 Hz were used to quantify dCA before, and 10 and 45 min after four sets of ten repetition back squats at 70% of one repetition maximum, or time matched seated rest (control). Diastolic, mean and systolic dCA were quantified by transfer function analysis of BP (finger plethysmography) and middle cerebral artery blood velocity (transcranial Doppler ultrasound). Mean gain (p = 0.02; d = 0.36) systolic gain (p = 0.01; d = 0.55), mean normalised gain (p = 0.02; d = 0.28) and systolic normalised gain (p = 0.01; d = 0.67) were significantly elevated above baseline during 0.10 Hz SSM 10-min post resistance exercise. This alteration was not present 45 min post-exercise, and dCA indices were never altered during SSM at 0.05 Hz. dCA metrics were acutely altered 10 min post resistance exercise at the 0.10 Hz frequency only, which indicate changes in the sympathetic regulation of CBF. These alterations recovered 45 min post-exercise

Individualising thresholds of cerebral perfusion pressure using estimated limits of autoregulation

$\textbf{Objectives:}$ In severe traumatic brain injury (TBI), cerebral perfusion pressure (CPP) management based on cerebrovascular pressure reactivity (PRx) has the potential to provide a personalised treatment target to improve patient outcomes. So far, the methods have focused on identifying one autoregulation guided CPP target – called CPPopt. We investigated whether a CPP autoregulation range - which uses a continuous estimation of the ‘lower’ and ‘upper’ CPP limits of cerebrovascular pressure autoregulation (PRx) - has prognostic value. $\textbf{Design:}$ Single-centre retrospective analysis of prospectively collected data $\textbf{Setting:}$ The neurocritical care unit at a tertiary academic medical centre $\textbf{Patients:}$ Data from 729 severe TBI patients admitted between 1996 and 2016 were used. Treatment was guided by controlling intracranial pressure and CPP according to a local protocol. $\textbf{Interventions:}$ None $\textbf{Methods and Main Results:}$ CPP-PRx curves were fitted automatically using a previously published curve-fitting heuristic from the relationship between PRx and CPP. The CPP values at which this ‘U-shaped curve’ crossed the fixed threshold from intact to impaired pressure reactivity (PRx =0.3) were denoted automatically the ‘Lower’ and ‘Upper’ CPP Limits of Reactivity (LLR and ULR), respectively. The % of time with CPP below (%CPPULR) or within these reactivity limits (%CPP WLR) was calculated for each patient and compared across dichotomised Glasgow Outcome Scores. After adjusting for age, initial GCS, and mean ICP, %CPP<LLR was associated with unfavourable outcome (OR %CPP<LLR 1.04, 95%-CI 1.02-1.06, p <0.001) and mortality (OR 1.06 95%-CI 1.04-1.08, p<0.001). $\textbf{Conclusions:}$ Individualised autoregulation-guided CPP management may be a plausible alternative to fixed CPP threshold management in severe TBI patients. Prospective randomized research will help to define which autoregulation guided method is beneficial, safe and most practical.JD is support by a Woolf Fisher scholarship. PJH is supported by an NIHR Research Professorship, Academy of Medical Sciences/Health Foundation Senior Surgical Scientist Fellowship. DKM is funded by the NIHR Cambridge Biomedical Centre (RCZB/004), and an NIHR Senior Investigator Award (RCZB/014)