Lactate is a potential energy source for the brain. The aim of this study was to establish whether systemic lactate is a brain energy source. We measured in vivo cerebral lactate kinetics and oxidation rates in 6 healthy individuals at rest with and without 90 mins of intravenous lactate infusion (36 mumol per kg bw per min), and during 30 mins of cycling exercise at 75% of maximal oxygen uptake while the lactate infusion continued to establish arterial lactate concentrations of 0.89+/-0.08, 3.9+/-0.3, and 6.9+/-1.3 mmol/L, respectively. At rest, cerebral lactate utilization changed from a net lactate release of 0.06+/-0.01 to an uptake of 0.16+/-0.07 mmol/min during lactate infusion, with a concomitant decrease in the net glucose uptake. During exercise, the net cerebral lactate uptake was further increased to 0.28+/-0.16 mmol/min. Most (13)C-label from cerebral [1-(13)C]lactate uptake was released as (13)CO(2) with 100%+/-24%, 86%+/-15%, and 87%+/-30% at rest with and without lactate infusion and during exercise, respectively. The contribution of systemic lactate to cerebral energy expenditure was 8%+/-2%, 19%+/-4%, and 27%+/-4% for the respective conditions. In conclusion, systemic lactate is taken up and oxidized by the human brain and is an important substrate for the brain both under basal and hyperlactatemic conditions.

We sought to quantify the contribution of cardiac output (Q) and total vascular conductance (TVC) to carotid baroreflex (CBR)‐mediated changes in mean arterial pressure (MAP) during mild to heavy exercise. CBR function was determined in eight subjects (25 ± 1 years) at rest and during three cycle exercise trials at heart rates (HRs) of 90, 120 and 150 beats min−1 performed in random order. Acute changes in carotid sinus transmural pressure were evoked using 5 s pulses of neck pressure (NP) and neck suction (NS) from +40 to −80 Torr (+5.33 to −10.67 kPa). Beat‐to‐beat changes in HR and MAP were recorded throughout. In addition, stroke volume (SV) was estimated using the Modelflow method, which incorporates a non‐linear, three‐element model of the aortic input impedance to compute an aortic flow waveform from the arterial pressure wave. The application of NP and NS did not cause any significant changes in SV either at rest or during exercise. Thus, CBR‐mediated alterations in Q were solely due to reflex changes in HR. In fact, a decrease in the carotid‐HR response range from 26 ± 7 beats min−1 at rest to 7 ± 1 beats min−1 during heavy exercise (P= 0.001) reduced the contribution of Q to the CBR‐mediated change in MAP. More importantly, at the time of the peak MAP response, the contribution of TVC to the CBR‐mediated change in MAP was increased from 74 ± 14 % at rest to 118 ± 6 % (P= 0.017) during heavy exercise. Collectively, these findings indicate that alterations in vasomotion are the primary means by which the CBR regulates blood pressure during mild to heavy exercise.

Middle cerebral artery flow velocity and pulse pressure during dynamic exercise in humans. Am J Physiol Heart Circ Physiol 288: H1526 -H1531, 2005. First published December 9, 2004; doi:10.1152/ajpheart. 00979.2004.-Exercise challenges cerebral autoregulation (CA) by a large increase in pulse pressure (PP) that may make systolic pressure exceed what is normally considered the upper range of CA. This study examined the relationship between systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) and systolic (V s), diastolic (Vd). and mean (Vm) middle cerebral artery (MCA) blood flow velocity during mild, moderate, and heavy cycling exercise. Dynamic CA and steady-state changes in MCA V in relation to changes in arterial pressure were evaluated using transfer function analysis. PP increased by 37% and 57% during moderate and heavy exercise, respectively (P Ͻ 0.05), and the pulsatility of MCA V increased markedly. Thus exercise increased MCA V m and Vs (P Ͻ 0.05) but tended to decrease MCA V d (P ϭ 0.06). However, the normalized low-frequency transfer function gain between MAP and MCA V m and between SBP and MCA Vs remained unchanged from rest to exercise, whereas that between DBP and MCA V d increased from rest to heavy exercise (P Ͻ 0.05). These findings suggest that during exercise, CA is challenged by a rapid decrease rather than by a rapid increase in blood pressure. However, dynamic CA remains able to modulate blood flow around the exercise-induced increase in MCA V m, even during high-intensity exercise. cerebral circulation; diastolic velocity; systolic velocity CEREBRAL AUTOREGULATION (CA) maintains steady-state cerebral blood flow relatively stable over a range of perfusion pressures from 60 to 150 mmHg (21), but it takes ϳ3 s for CA to be established (1), explaining why the velocity (V) in basal cerebral arteries fluctuates in parallel with blood pressure throughout the cardiac cycle. Thus exercise presents a challenge to CA by the rapid and large increases in pulse pressure (PP). This is exemplified during rowing where the rapid fluctuations in blood pressure associated with each stroke result in similar fluctuations in middle cerebral artery (MCA) mean blood flow velocity (V m ) (17). Equally, during rhythmic resistance exercise fluctuations in arterial pressure with each muscle contraction are too rapid to be countered by CA (9). Despite such large changes in the MCA V waveforms with exercise, the averaged MCA V m remains unchanged (9), slightly decreased (7), or increased when exercise does not cause large fluctuations in blood pressure (3,16,17). However, the MCA V m may not fully reflect the dynamic control of CA (15,24,26,27), and this may be relevant especially when PP increases systolic pressure beyond the CA range.Dynamic CA is frequency dependent (10,15,24,26,27), and frequency-domain analyses of CA allows for evaluation of the influence of exercise-induced changes in arterial blood pressure on MCA V. Brys et al. (3) used frequency-domain analysis to ev...

Preoperative anemia in elective fast-track THA and TKA is independently associated with transfusion and increased postoperative morbidity, supporting the need for preoperative evaluation and treatment.