http://journal.frontiersin.org/article/10.3389/fnagi.2016.00184/full
- Department of Kinesiology, University of Maryland, College Park, MD, USA
Introduction
Endurance exercise training (exercise) produces physiological adaptations that enhance aerobic fitness and cardiovascular health (Brooks et al., 1996). Consistent exercise effectively augments the maximal rate of oxygen consumption (V⋅
O2max) centrally, by increasing cardiac output, and/or peripherally by widening the arterial-venous oxygen (A-V⋅
O2) difference (Seals et al., 1981). V⋅
O2max is the gold-standard index of cardiorespiratory fitness and is highly correlated with both morbidity and mortality (Hoekstra et al., 2008; Sawada et al., 2012), with greater fitness status associated with a reduced risk of chronic disease and a longer lifespan. In addition to enhancing the function of the cardiovascular system, exercise has been shown to increase bone density, improve muscle quality, and protect against metabolic dysfunction (Brooks et al., 1996). Conversely, when the exercise stimulus is removed many of these systemic adaptations rapidly dissipate (Mujika and Padilla, 2000a, 2001a,b), thereby increasing the potential for adverse health effects. For example, 20 days of bed rest immobilization resulted in a substantial 28% decrease in V⋅
O2max (Saltin et al., 1968); a prolonged detraining period reduced muscle fiber capillarization and oxidative enzyme activity (Klausen et al., 1981); and a 10-day period of physical inactivity was related to the development of impaired glucose tolerance and insulin resistance (Rogers et al., 1990).
A growing body of empirical evidence supports the notion that exercise also robustly affects the human brain. Multimodal neuroimaging studies, including both structural and functional MRI, have helped elucidate the brain's complex neurobiological response to exercise. These exercise-induced effects include cytoarchitectonic modifications (Erickson et al., 2009; Smith et al., 2014; ten Brinke et al., 2015); altered patterns of neural activity (Smith et al., 2013); and improved performance across the cognitive domains (Tomporowski, 2003; Kramer et al., 2005; Davranche and McMorris, 2009; Chapman et al., 2013). The hippocampus, a subcortical brain structure well known for its role in learning and memory, has shown neurotrophic effects as the result of exercise training in humans and animal models (van Praag et al., 1999; Pereira et al., 2007; Erickson et al., 2009). Exercise interventions in humans have been shown to affect hippocampal-dependent cognition and to increase hippocampal blood perfusion (Pereira et al., 2007) and volume (Erickson et al., 2009). While the effects of detraining have been reported in peripheral physiological systems, the effects of detraining on brain function, and on cortical and hippocampal blood flow, have not been reported.
A key unanswered question, and the primary aim of this study, was to determine how short-term exercise cessation impacts cerebrovascular function in healthy highly physically active and physically fit older adults. To accomplish this goal we measured the resting cerebral blood flow (rCBF) of master athletes both before and immediately after 10 days of exercise cessation. To quantify rCBF we employed pseudo-continuous arterial spin labeling (pCASL), a perfusion-weighted MRI technique. Our hypotheses were twofold. We predicted (1) that 10 days of physical inactivity would alter rCBF in areas known to be susceptible to age-related decline (Greicius et al., 2004; Buckner et al., 2005), and (2) that detraining would decrease hippocampal blood flow, which we chose as an a priori region of interest (ROI).
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Results
The Master Athlete Profile
The master athletes who volunteered for this study are a unique population and should not be considered equivalent to older adults who engage in regular moderate to vigorous intensity leisure-time physical activity. Our participants had a mean continuous endurance training history of ~29 years, and on average were running 59 km per week and training 5 days per week just prior to the baseline testing. They also regularly participated in regional and national endurance competition. Moreover, as a group these master athletes had a
O2max above the 90th percentile for their age and sex.
Gray Matter rCBF
Results of the gray matter voxel-wise analysis demonstrated that the 10-day exercise cessation period significantly reduced absolute rCBF in eight brain regions (Figure 1). Of note are the Pre > Post comparisons, shown in blue on the Δ rCBF maps in Figure 1, revealing significantly decreased rCBF in each ROI (total volume = 5,640 mm3) that remained after correction for multiple comparisons using the False Discovery Rate (see Table 2). These regions included: (L) inferior temporal gyrus, fusiform gyrus, inferior parietal lobule, (R) cerebellar tonsil, lingual gyrus, precuneus, and (L/R) cerebellum. No statistically significant change in whole brain absolute CBF in gray matter was detected [mean (±SD) baseline = 69.4 (±10.4 ml/100g/min), post-cessation = 67.2 (±12.6 ml/100g/min)].
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