Abstract
During strenuous exercise there is a progressive increase in lactate uptake and metabolism into the brain as workload and plasma lactate levels increase. Although it is now widely accepted that the brain can metabolize lactate, few studies have directly measured brain lactate following vigorous exercise. Here, we used ultra-high field magnetic resonance spectroscopy of the brain to obtain static measures of brain lactate, as well as brain glutamate and glutamine after vigorous exercise. The aims of our experiment were to (a) track the changes in brain lactate following recovery from exercise, and (b) to simultaneously measure the signals from brain glutamate and glutamine. The results of our experiment showed that vigorous exercise resulted in a significant increase in brain lactate. Furthermore, both glutamate and glutamine were successfully resolved, and as expected, although contrary to some previous reports, we did not observe any significant change in either amino acid after exercise. We did however observe a negative correlation between glutamate and a measure of fitness. These results support the hypothesis that peripherally derived lactate is taken up by the brain when available. Our data additionally highlight the potential of ultra-high field MRS as a non-invasive way of measuring multiple brain metabolite changes with exercise.
Highlights
IntroductionThe brain has been shown to be capable of using substrates other than glucose when they are available to support activity, including lactate (Schurr et al, 1997; Bouzier-Sore et al, 2003; Overgaard et al, 2012; Schurr, 2014), pyruvate (Cruz et al, 2001; Sharma et al, 2003), and ketone bodies (Nybo et al, 2003; Chowdhury et al, 2014)
In the non-activated state, the brain’s energy needs are met primarily by glucose
Using the same Linear Mixed Effects (LME) approach described above, we found that the model including the post-exercise variable (0 or 1) explained significantly more of the variance than the null model demonstrating that brain lactate was significantly increased from baseline after exercise but not after the control intervention (Figure 4A)
Summary
The brain has been shown to be capable of using substrates other than glucose when they are available to support activity, including lactate (Schurr et al, 1997; Bouzier-Sore et al, 2003; Overgaard et al, 2012; Schurr, 2014), pyruvate (Cruz et al, 2001; Sharma et al, 2003), and ketone bodies (Nybo et al, 2003; Chowdhury et al, 2014). It has even been suggested that lactate may be preferred to glucose, possibly ‘sparing’ brain glucose metabolism during exercise (Quistorff et al, 2008; van Hall, 2010; Schurr, 2014). Whilst persistently elevated brain lactate may indicate pathology, transient increases are normal consequences of the energetic processes involved in vigorous exercise and are believed to be complimentary to healthy brain processes (Schurr, 2008; Dienel, 2012) and brain recovery (Bouzat et al, 2014; Brooks and Martin, 2015; Glenn et al, 2015)
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