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1 Department of Anaesthesia, The Copenhagen Muscle Research Centre, Rigshospitalet 3 Department of Radiology, The Copenhagen Muscle Research Centre, Rigshospitalet 2 Department of Medical Biochemistry and Genetics, The Panum Institute, University of Copenhagen, Denmark
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Abstract |
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1.5 mM. The finding that an increase in lactate could not be detected in the CSF or within the brain rules out accumulation in a distribution volume and indicates that the lactate taken up by the brain is metabolized.
(Received 11 September 2003;
accepted after revision 3 November 2003;
first published online 7 November 2003)
Corresponding author M. Dalsgaard: Department of Anaesthesia, Rigshospitalet 2041, Blegdamsvej 9, DK-2100 Copenhagen Ø, Denmark. Email: madskda{at}tiscali.dk
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Introduction |
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Following exhaustive exercise, the large additional uptake of lactate and glucose relative to oxygen, as expressed in a decreasing cerebral metabolic ratio, indicates that glucose and lactate are either stored or metabolized since they are not released from the brain during a 1 h recovery period (Ide et al. 2000; Dalsgaard et al. 2002). Accumulation of lactate in its distribution volume for the brain would be expected to be communicated to the cerebrospinal fluid (CSF) while at the same time transport of substrates from blood to CSF is restricted (Plum & Posner, 1967; Nilsson et al. 1992). Building up of lactate in the brain would also be expected to be visible by magnetic resonance spectroscopy (1H-MRS; Dager et al. 1992). In two experiments this study demonstrated that, following exhaustive exercise, lactate does not accumulate in the CSF (Experiment I) or within the brain as determined by 1H-MRS (Experiment II).
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Methods |
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Experiment I. AV-differences over the brain and cerebrospinal fluid
Nine healthy subjects were studied after giving written informed consent (mean ±S.E.M.; 2 females and 7 males; age 25 ± 1 years; height 182 ± 3 cm; weight, 80 ± 2 kg).
Aiming to increase the arterial lactate level markedly, we used a cycle ergometer that allowed for simultaneous arm cranking. A pace of 60 revolutions per minute for both the arms and the legs was dictated by a metronome. The participants attended the laboratory twice. A minimum of 3 days prior to the main study, their work capacity was determined by incremental exercise for the arms (149 ± 12 W) and the legs (306 ± 16 W) separately, and the subjects were familiarized with combined arm and leg exercise.
On the morning of the main study the participants had been fasting for 8 h, although intake of water was permitted. Catheterization and a subsequent resting period were followed by combined arm and leg exercise until exhaustion. The work rate was increased 10% every 2 min from a warm up level 30% of the individually determined maximal capacity. As soon as possible, i.e. 2–3 min after termination of exercise when the blood lactate was still above 13 mM, CSF was drained through a lumbar puncture.
Arterio-venous differences over the brain (AV) were determined by means of a retrograde catheter (14 gauge; 2.2 mm) in the right internal jugular vein with the tip positioned below the basis of the skull and another catheter (20 gauge; 1.1 mm) in the radial artery of the non-dominant arm. The catheters were reported to neither inflict pain nor hamper the ability to exercise. Blood samples were drawn three times at rest, every 2 min during exercise and during the recovery at minutes 1, 2, 3, 5, 7, 10, 15, 20 and 30. Pre-heparinized syringes (Radiometer, Copenhagen, Denmark) were rotated for about 3 min and subsequently kept in ice water until analysis for lactate, glucose and blood gas variables (ABL 725, Radiometer).
To obtain CSF postexercise and following local anaesthesia (2% lidocaine), a 25 gauge pencil-point cannula (Braun, Melsungen, Germany) was advanced between the third and fourth lumbar vertebrae to the subdural space. Aiming to minimize the risk of spinal headache, isotonic saline (1 l) was administered intravenously during the first hour of the recovery. The procedure was well tolerated and did not cause headache or other adverse effects. The CSF concentration of lactate was determined (ABL 725). To avoid multiple lumbar punctures, resting values were determined similarly from six other healthy subjects (3 females and 3 males, age 25 ± 1 years, height 179 ± 2 cm, weight 73 ± 3 kg) and the average of three measurements is reported (YSI, Yellow Springs, OH, USA).
Mean arterial pressure (MAP) was measured through a transducer (Bentley, Uden, The Netherlands) connected to a patient monitor (Dialogue 2000, Danica Electronic, Copenhagen, Denmark). Subjects expressed their perceived exertion (RPE) on a scale ranging from rest, ‘6’, to the hardest imaginable exercise, ‘20’ (Borg, 1970).
Values are presented as means ±S.E.M. Changes with time were detected by Friedman's test and located using Wilcoxon's signed test by rank. The CSF lactate was compared using the Mann–Whitney test. A P-value < 0.05 was considered significant.
Experiment II. Magnetic resonance spectroscopy
The 1H-MRS of the brain was performed on another five volunteers before, during and after exhaustive exercise to determine the cerebral lactate concentration. In order to estimate the detection limit for lactate, seven basketballs (15 cm diameter) were measured containing buffered (pH 7) solutions of 100 mM NaCl, 50 mM phosphate, 5 mM NaN3, 10 mM creatine, and varying concentrations of sodium lactate (Fig. 1). Each ball was replaced and measured five times by sampling of 20 averages using the same acquisition parameters and the same sized volume of interest (VOI) as in vivo. From these experiments the detection limit was estimated conservatively as 0.75 mM. The in vivo detection limit for lactate was assessed individually. The concentration of total creatine in vivo was assumed to remain stable and therefore the reduction in percentage from baseline was used to estimate the signal loss due to respiratory movement. If the creatine concentration, say, was halved postexercise the detection limit was set twice as high (1.5 mM). In most of the volunteers the spectral resolution was maintained postexercise and their detection limits for lactate became 1.5 mM or less. In one subject, however, the spectral resolution dropped postexercise (the full width at half maximum, FWHM, increased from 0.052 to 0.109 p.p.m). Therefore, the 1.0 and 2.0 mM lactate phantoms were measured in deliberately misadjusted magnetic fields, deteriorating resolution to the same extent as in vivo (FWHM, 0.092 and 0.114 p.p.m.; 1.0 and 2.0 mM phantoms, respectively). Based on these measurements the detection limit for lactate became 2.0 mM for this volunteer.
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Spectra were processed for graphical display using the scanner's software applying eddy current correction, zero filling, filtering (Gaussian 512 ms), and filtering of the residual water signal. Quantification of the data used the fully automated LCModel (Provencher, 1993) and the principle of reciprocity (Michaelis et al. 1993). Absence or presence of lactate was determined using the Cramér-Rao lower bound (CRLB) as calculated by the LCModel quantification program. The CRLB is the estimated standard deviation expressed as a percentage of the estimated concentration. For a CRLB less than 20%, detection and quantification of lactate were considered reliable.
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Results |
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Exercise increased MAP from 89 ± 3 at rest to 112 ± 4 mmHg (P < 0.05). Exhaustion was on average reached after 12 ± 1 min and all subjects reported RPE to be ‘20’. Also, the arterial and venous content of O2, glucose and lactate all increased compared to rest with lactate reaching 14.5 ± 0.9 mM in the immediate recovery (Fig. 2).
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In response to exercise peak blood lactate was 6.7 ± 0.7 and 13.4 ± 1.3 mM for in- and out-magnet exercise, respectively. The 1H-MRS spectra were obtained at rest and during the interval from 0.5 to 5.0 min postexercise, which coincides with a high cerebral lactate uptake, the lowest cerebral metabolic ratio, and the time of the lumbar puncture in Experiment I. There was no significant difference in the cerebral lactate concentration between exercise and rest in these spectra (Fig. 5).
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Discussion |
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5.7 and a discrete lactate efflux from the brain (AVlac with two decimals –0.03 ± 0.01) confirming previous reports (Avogaro et al. 1990; Madsen et al. 1995b; Sandström et al. 1999; Dalsgaard et al. 2002, 2003; Nybo et al. 2003). In response to exhaustive exercise, the brain took up lactate in molar amounts similar to that of glucose. Integrating the AVlac curve during exercise and for the first 5 min of the recovery in Experiment I, and assuming a global CBF of 0.7 l min--1 (Nybo et al. 2002), the lactate uptake was 8 mmol (the mean lactate uptake in the two subjects in Experiment II who exercised inside the magnet would be 4 mmol if AVlac is assumed to be proportional to the blood concentration). Taking the estimated distribution volume for lactate in the CNS to be of a size comparable to that of glucose in the rat (0.77 ml g-1; Choi et al. 2001), the resulting concentration would be 8 mM. Such a high concentration of lactate in the brain would be expected to increase the CSF lactate concentration (Plum & Posner, 1967; Nilsson et al. 1992) but no increase was observed. Also, it is reasonable to assume that the subjects in Experiment II had an equivalent cerebral lactate uptake, with the potential of increasing lactate concentration within the brain at least 4-fold (2-fold for two subjects) the estimated detection limit of the MRS lactate measurements. However, the 1H-MRS signal from lactate was not detectable in the brain following exercise. Such calculations indicate that the lactate taken up by the brain does not accumulate in a distribution volume. The lactate taken up by the brain is likely to be metabolized (Smith et al. 2003). The necessary transporters for the blood–brain barrier, neurones and astrocytes have been characterized (Dringen et al. 1995; Koehler-Stec et al. 1998). Lactate is oxidized by neuronal tissue in vitro (Larrabee, 1995, 1996) and is of importance for synaptic function (Schurr et al. 1988; Brown et al. 2003). The ‘lactate shuttle’ hypothesis incorporates such findings by linking neuronal activity with glycolysis and glycogenolysis in astrocytes. Lactate is then released into the interstitium and subsequently taken up and oxidized by neurones (Pellerin & Magistretti, 1994; Tsacopoulos & Magistretti, 1996). Engagement of a lactate shuttle during cerebral activation is supported by a more than twofold increase of lactate in the visual cortex with photic stimulation (Sappey-Marinier et al. 1992). Equally, in the rat extracellular lactate increases in motor control areas (striatum) during exercise (De Bruin et al. 1990). In the present study, the high lactate influx to the brain could attenuate such intercellular trafficking of lactate.
The cerebral metabolic ratio
Brain activity increases in proportion to exercise intensity as illustrated by a local increase in blood flow to brain areas responsible for initiation, integration and coordination of exercise (Williamson et al. 1999; Delp et al. 2001). Accordingly, the whole-brain metabolic response to exercise (Dalsgaard et al. 2003) matches that of stimulated brain regions (Fox et al. 1988). Following exercise in this study, the reduction in the cerebral ratio of O2/glucose reflects a large increase in AVglc as opposed to a moderate increase in AVO2. This differs from situations of less intense physical activity where the decrease in O2/glucose is associated with a stable AVO2 (Schmalbruch et al. 2002), or with a 20% increase in AVO2 only after brain activation (Ide et al. 2000; Schmalbruch et al. 2002). The reduction in the cerebral metabolic ratio by almost 40% is provoked otherwise only during maximal leg exercise in hyperthermia (Nybo et al. 2003) or if the cerebral lactate uptake is included in the equation (Ide et al. 2000). An additive effect of superimposing arm exercise on leg exercise may contribute to the increase in AVO2. When AVlac was taken into account, the cerebral metabolic ratio decreased further to 50% of control by the end of exercise. It is a consistent observation that the cerebral metabolic ratio reaches the nadir 1–2 min into the recovery rather than at the peak of exercise where brain activity would be assumed to be highest (Ide et al. 2000; Dalsgaard et al. 2002; Nybo et al. 2003). Perhaps at cessation of exercise CBF mirrors the drop in MAP and cardiac output whilst cerebral metabolism remains high, or the relatively higher arterial concentration of glucose (47%) and lactate (14%) allows for a larger cerebral uptake.
The cerebral metabolic ratio stayed low during the first minutes of the recovery to return to baseline over the 30 min observation period. Since this ratio does not appear to overshoot, the surplus glucose plus lactate taken up during and after exercise is not oxidized within the time frame of the experiment. Thus, it is either oxidized later, stored in the brain, or released in a different form than glucose or lactate.
Glucose can provide the carbon skeleton for neurotransmitters as glutamate and 
-aminobutyric acid (GABA) and enhanced production may contribute to the reduction in the cerebral metabolic ratio (Cruz & Dienel, 2002). However, enlargement of glutamate and glutamine pools after exhaustive exercise in humans is not communicated as a release from the brain (Dalsgaard et al. 2002). Alternatively, restoration of brain glycogen may play a role for the surplus of glucose taken up in response to cerebral activation (Madsen et al. 1995a, 1999) and perhaps even during activation (Shulman et al. 2001; Schmalbruch et al. 2002). In the latter case lactate may efflux from the brain when the plasma concentration is low (Madsen et al. 1995b) but that is not confirmed during exercise. However, AVlac represents a net balance between the cerebral uptake and a potential release. Moreover, repletion of large brain glycogen stores may require more than three times the period that leads to its depletion (Dienel et al. 2002) and could continue to a level even higher than at rest (Choi et al. 2003). The fate of the additional glucose and lactate taken up by the brain remains speculative. We can only conclude that the uptake seems directed in that there is no accumulation of these substances within the brain.
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); see below. Data are means of five measurements with S.E.M. too small to be visible on the graph. The CRLB was calculated by the LCModel quantification program and is the estimated standard deviation expressed as a percentage of the estimated concentration. In all five measurements of the 0.2 mM phantom, CRLB was > 31%. Even though for this phantom the LCModel estimated the lactate concentration consistently to an average of 0.29 mM, the large CRLB (> 20%) by definition renders the detection of lactate at this level unreliable.
P < 0.01.
P < 0.05.
