Neuroplasticity of Dopamine Circuits After Exercise: Implications for Central Fatigue

Abstract

Habitual exercise increases plasticity in a variety of neurotransmitter systems. The current review focuses on the effects of habitual physical activity on monoamine dopamine (DA) neurotransmission and the potential implication of these changes to exercise-induced fatigue. Although it is clear that peripheral adaptations in muscle and energy substrate utilization contribute to this effect, more recently it has been suggested that central nervous system pathways "upstream" of the motor cortex, which initiate activation of skeletal muscles, are also important. The contribution of the brain to exercise-induced fatigue has been termed "central fatigue." Given the well-defined role of DA in the initiation of movement, it is likely that adaptations in DA systems influence exercise capacity. A reduction in DA neurotransmission in the substantia nigra pars compacta (SNpc), for example, could impair activation of the basal ganglia and reduce stimulation of the motor cortex leading to central fatigue. Here we present evidence that habitual wheel running produces changes in DA systems. Using in situ hybridization techniques, we report that 6 weeks of wheel running was sufficient to increase tyrosine hydroxylase mRNA expression and reduce D2 autoreceptor mRNA in the SNpc. Additionally, 6 weeks of wheel running increased D2 postsynaptic receptor mRNA in the caudate putamen, a major projection site of the SNpc. These results are consistent with prior data suggesting that habitually physically active animals may have an enhanced ability to increase DA synthesis and reduce D2 autoreceptor-mediated inhibition of DA neurons in the SNpc compared to sedentary animals. Furthermore, habitually physically active animals, compared to sedentary controls, may be better able to increase D2 receptor-mediated inhibition of the indirect pathway of the basal ganglia. Results from these studies are discussed in light of our understanding of the role of DA in the neurobiological mechanisms of central fatigue.

Altered reward anticipation: Potential explanation for weight gain in schizophrenia?

“…Mechanistically, acute physical exercise activates the dopaminergic reward pathway through increases in dopamine concentrations and dopamine receptor binding (Greenwood et al, 2011). Moreover, chronic voluntary and forced running increases dopamine levels in the brain (Foley and Fleshner, 2008;Greenwood et al, 2011;Sutoo and Akiyama, 1996). The ventral tegmental area shows stronger phasic dopamine spikes after voluntary wheel running in rats (Wang and Tsien, 2011), suggesting that neurons in the ventral tegmental area code motivational signals which trigger, sustain, or end movement.…”

Neurometaplasticity: Glucoallostasis control of plasticity of the neural networks of error commission, detection, and correction modulates neuroplasticity to influence task precision

“…[21][22][23][24][25][26][27]. Other factors such as electrical stimulation (transcranial direct current stimulation), habitual exercise, pharmacological agents, psycho-/behavioral therapy, stress as well as environmental factors also affect neurometaplasticity [28][29][30][31][32][33][34][35]. These factors affect neurometaplasticity by indirect influence on neurotransmitters, receptors, transporters, genome and epigenome of brain cells [29,30].…”

“…Other factors such as electrical stimulation (transcranial direct current stimulation), habitual exercise, pharmacological agents, psycho-/behavioral therapy, stress as well as environmental factors also affect neurometaplasticity [28][29][30][31][32][33][34][35]. These factors affect neurometaplasticity by indirect influence on neurotransmitters, receptors, transporters, genome and epigenome of brain cells [29,30]. The receptors implicated in LTP and LTD include N-methyl-D-aspartate receptor (NMDAR), metabotropic glutamate receptors (mGluRs), endocannabinoid receptors, ion channel receptors (e.g.…”

Role of Central Fatigue in Resistance and Endurance Exercises: An Emphasis on Mechanisms and Potential Sites

“…DA neurotransmitter levels increases in order to improve the performance in the case of amphetamine administration (Borg, Edström, Linderholm, & Marklund, 1972). However, there is evidence that brain dopamine level is similar to the resting condition during fatigue (Foley & Fleshner, 2008) and this creates the possibility that dopamine concentration in various groups differently increases during exercise. For instance, it has been reported that inhibition of DA reuptake, increases the core temperature at the end of exercise, but has no effect on the performance in normothermia (Watson et al, 2005).…”