Abstract
Recent studies have reported that acute aerobic exercise modulates intracortical excitability in the primary motor cortex (M1). However, whether acute low-intensity aerobic exercise can also modulate M1 intracortical excitability, particularly intracortical excitatory circuits, remains unclear. In addition, no previous studies have investigated the effect of acute aerobic exercise on short-latency afferent inhibition (SAI). The aim of this study was to investigate whether acute low-intensity aerobic exercise modulates intracortical circuits in the M1 hand and leg areas. Intracortical excitability of M1 (Experiments 1, 2) and spinal excitability (Experiment 3) were measured before and after acute low-intensity aerobic exercise. In Experiment 3, skin temperature was also measured throughout the experiment. Transcranial magnetic stimulation was applied over the M1 non-exercised hand and exercised leg areas in Experiments 1, 2, respectively. Participants performed 30 min of low-intensity pedaling exercise or rested while sitting on the ergometer. Short- and long-interval intracortical inhibition (SICI and LICI), and SAI were measured to assess M1 inhibitory circuits. Intracortical facilitation (ICF) and short-interval intracortical facilitation (SICF) were measured to assess M1 excitatory circuits. We found that acute low-intensity aerobic exercise decreased SICI and SAI in the M1 hand and leg areas. After exercise, ICF in the M1 hand area was lower than in the control experiment, but was not significantly different to baseline. The single motor-evoked potential, resting motor threshold, LICI, SICF, and spinal excitability did not change following exercise. In conclusion, acute low-intensity pedaling modulates M1 intracortical circuits of both exercised and non-exercised areas, without affecting corticospinal and spinal excitability.
Highlights
Regular physical activity or aerobic exercise is well-known to increase brain plasticity (Cotman and Berchtold, 2002; Cotman and Engesser-Cesar, 2002; Kramer and Erickson, 2007; Hillman et al, 2008), which is a process indispensable to learning and memory
This study was conducted in accordance with the Declaration of Helsinki, and was approved by the ethics committee of Niigata University of Health and Welfare
Our results suggest that low-intensity aerobic exercise does not modulate corticospinal and spinal excitability, which we evaluated using single-pulse motor-evoked potential (MEP), Resting motor threshold (RMT) and the F/M ratio
Summary
Regular physical activity or aerobic exercise is well-known to increase brain plasticity (Cotman and Berchtold, 2002; Cotman and Engesser-Cesar, 2002; Kramer and Erickson, 2007; Hillman et al, 2008), which is a process indispensable to learning and memory. Previous animal studies have demonstrated that physical activity upregulates the secretion of growth factors including brain-derived neurotrophic factor (BDNF) (Neeper et al, 1995, 1996), insulin-like growth factor 1 (Trejo et al, 2001; Cetinkaya et al, 2013), vascular endothelial growth factor (Latimer et al, 2011) and nerve growth factor (Ding et al, 2004) The effects of these factors involve angiogenesis (Kleim et al, 2002) and neurogenesis (van Praag et al, 1999; Inoue et al, 2015) in the brain, and these molecular and cellular mechanisms contribute to facilitate brain plasticity. Late cortical disinhibition did not change after moderate intensity exercise as shown by Mooney et al (2016)
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