Anouk Schrantee1,2,3, Jannie Wijnen4, Michelle M Solleveld1,3, Aart J Nederveen1, Serge Dumoulin2,5, Dennis WJ Klomp4, Liesbeth Reneman1, and Paul J Lucassen3
1Department of Radiology and Nuclear Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands, 2Spinoza Centre for Neuroimaging, Royal Netherlands Academy of Arts and Sciences (KNAW), Amsterdam, Netherlands, 3Swammerdam Institute for Life Sciences, Center for Neurosciences, University of Amsterdam, Amsterdam, Netherlands, 4Department of Radiology, University Medical Center Utrecht, Utrecht, Netherlands, 5Department of Experimental Psychology, Helmholtz Institute, Utrecht University, Utrecht, Netherlands
Synopsis
Prolonged exercise has beneficial
effects on cognition, which could be mediated by changes in neuronal
metabolism. We present the first 7T MRS exercise study investigating neurometabolite concentrations before and after randomization
to aerobic exercise or toning exercise in a large sample of healthy volunteers.
We found that change in cardiovascular fitness was positively associated with
changes in hippocampus glutamine, and negatively associated with change in glutamate
in the anterior cingulate cortex; regardless of exercise group.
This suggests that exercise-induced metabolic changes might not specific to the
hippocampus, and that exercise likely has widespread effects on brain
metabolism.
Introduction
Prolonged aerobic exercise has beneficial
effects on cognition, but the underlying mechanisms are still unclear. Recent
studies have pointed to an important role for neuronal metabolism. For example,
high-intensity exercise has been associated with decreased Glx (glutamate+glutamine
(Glu+Gln)) in the hippocampus1,2, a brain area characterized by prominent
plasticity which plays an important role in cognition. So far, it is unknown
whether these changes are limited to the hippocampus and whether only aerobic
exercise can induce such changes. In this work, we present the first 7T MRS
exercise study investigating neurometabolite
concentrations before and after randomization to an aerobic exercise or resistance
training in a large sample of healthy volunteers. We focused on Glu,
Gln, glutathione (GSH) and N-acetyl
aspartate (NAA) as metabolites of interest due to their role in neuronal
activity and viability3.Methods
Fifty-two sedentary volunteers were randomized
to 12 weeks of high or low intensity exercise (Figure 1)4. Before
and after the intervention, subjects performed a maximal exercise test to
obtain VO2max (reflecting cardiovascular fitness), and underwent MR
and cognitive measurements. Single-voxel spectra were collected from the left
hippocampus and dorsal anterior cingulate cortex (dACC) (Figure 2). Subjects
were scanned on a 7T whole-body MR system (Philips) using a dual-channel
transmit coil in combination with a 32-channel receive coil (Nova Medical) with
a sLASER sequence using FOCI pulses5. Other sequence parameters
were: TR/TE=5000/36ms; bandwidth=4kHz; 2048 data-points; voxel-size=30x15x15mm,
NSAdACC=64 NSAhippocampus=128, B1>17µT. Non-water
suppressed spectra were obtained for quantification and eddy-current
correction. T1-weighted scans (0.83x0.83x0.9mm) were acquired and segmented
using SPM to determine the contribution of gray matter, white matter and CSF to
each voxel. Spectral fitting was performed using LCModel6. Metabolite
concentrations were calculated using water-scaling and were corrected for
partial volume effects using the tissue volume fractions7: $$[metabolite]=\frac{\frac{signal_{metabolite}}{signal_{H_{2}O}}*(volGM*[{H_{2}O}_{GM}]+volWM*[{H_{2}O}_{WM}]+volCSF*[{H_{2}O}_{CSF}])}{volGM+volWM}$$ Spectral quality measures, i.e. signal-to-noise ratio (SNRhippocampus>15;
SNRACC>30) and Cramér–Rao lower bounds (CRLBGln≤40, CRLBGlu≤15,
CRLBGSH≤15, CRLBNAA≤5) were used to
exclude poor quality spectra. Repeated-measures ANOVA was used to test the
interaction of exercise group and time. Pearson’s correlation coefficient was
used to assess the association between VO2max and neurometabolite
changes.Results
In total, 47 subjects (90%) successfully completed
the intervention. We found a main effect of time on VO2max (p=0.04),
but the high-intensity group did not show a larger increase than the
low-intensity group (p=0.53) (despite having spent significantly more time in
the target heart-rate zone (p<0.001)) (Figure 3). For the hippocampus (mean
SNR=28) and ACC (mean SNR=44), respectively, 13 and 6 subjects had to be
removed from the analysis due to 1 or 2 sessions having poor quality spectra. No
significant interaction effect was found between time and group for any of the
metabolites in the hippocampus. A main effect of time was found for Gln
(p=0.02), GSH (p<0.01) and NAA (p<0.01), but not for Glu (p=0.22) (Figure
4). Additionally, when combining both exercise groups, the change in VO2max
correlated with Gln change (r=0.36, p=0.03). For the ACC, we did not
find an interaction or main effect (Figure 5). However,
when combining both exercise groups, the VO2max
change showed a trend-significant association with Glu (r=-0.29, p=0.07).Discussion
In
contrast to some prior studies8, aerobic exercise did not induce
significantly higher changes in VO2max than toning exercise. This might be
due to the general fitness of young healthy volunteers compared to previously
studied elderly populations. This might partially explain the lack of effect of
exercise group on neurometabolites. When combining both groups, we showed a
significant positive association between changes in cardiovascular fitness (VO2max)
and Gln levels in the hippocampus, but a trend towards a negative association
between changes in cardiovascular fitness and Glu in the ACC. Total Glu and Gln
tend to be strongly coupled in healthy tissue3, and this correlation
was stronger in the ACC (r=0.65, p<0.01) than the hippocampus (r=0.20, p=0.25) (Figure 4 and 5). This could
either be due to true biological differences between the hippocampus and ACC,
or this discrepancy could be due to lower SNR and higher CRLB’s
in hippocampus than ACC. However, the exact meaning of increased
Gln and decreased Glx in relation to exercise is difficult to interpret. In conclusion,
we here presented the largest human exercise MRS study so far, showing the
possibility to resolve both Glu and Gln using 7T MRS. Our results suggest that
exercise-induced metabolic changes might not specific to the hippocampus, and
that exercise likely has a widespread effect on brain metabolism. Acknowledgements
No acknowledgement found.References
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