The therapeutic potential of exercise and caffeine on attention-deficit/hyperactivity disorder in athletes

Abstract

Attention-deficit/hyperactivity disorder (ADHD) is characterized by evident and persistent inattention, hyperactivity, impulsivity, and social difficulties and is the most common childhood neuropsychiatric disorder, and which may persist into adulthood. Seventy to 80% of children and adults with ADHD are treated with stimulant medication, with positive response rates occurring for both populations. Medicated ADHD individuals generally show sustained and improved attention, inhibition control, cognitive flexibility, on-task behavior, and cognitive performance. The ethics of ADHD medication use in athletics has been a debated topic in sport performance for a long time. Stimulants are banned from competition in accordance with World Anti-Doping Association and National Collegiate Athletic Association regulations, due to their ability to not only enhance cognitive performance but also exercise performance. Limited research has been conducted looking at the differences in exercise performance variables in unmedicated ADHD verses medicated ADHD. Not all ADHD athletes choose stimulant medication in their treatment plan due to personal, financial, or other reasons. Non-stimulant treatment options include non-stimulant medication and behavioral therapy. However, the use of caffeinated compounds and exercise has both independently been shown to be effective in the management of ADHD symptoms in human studies and animal models. This mini review will discuss the effect of exercise and caffeine on neurobehavioral, cognitive, and neurophysiological factors, and exercise performance in ADHD athletes, and whether exercise and caffeine should be considered in the treatment plan for an individual with ADHD.

Keywords: adult ADHD; attention-deficit/hyperactivity disorder; caffeine; exercise; performance.

FIGURE 1

Effects of methylphenidate (MPH) and amphetamine (A) on neurotransmitter (NT) reuptake. (A) MPH inhibits NT transporters from reuptake into the presynaptic cell, increasing extracellular concentrations and increasing possible receptor binding. MPH treatment is shown to decrease NT transporter density in the striatum, thereby increasing the transportation of vesicular NT via vesicular monoamine transporter-2 (VMAT-2), leading to more NT within the synapse. (B) Amphetamine inhibits NT transporters in the reuptake of NT into the presynaptic cell and increases extracellular concentrations of NT in multiple brain regions. The increase in NT like dopamine concentrations within the synapse increases the incidence of receptor binding. Amphetamine is distinct from MPH in two ways: the inhibition of VMAT-2 results in the release if dopamine into the presynaptic terminal by presynaptic vesicles, and the internalization of a dopamine transporter resulting in the reversal of the transporter from in-flow to dual-flow of dopamine reuptake (Smith, 2003; Minzenberg, 2012; Volkow and Swanson, 2013; Chabreck, 2015; Stewman et al., 2018; Berezanskaya et al., 2022).

FIGURE 2

The effects of caffeine on adenosine receptors. (A) Adenosine binds to adenosine receptors and inhibits dopamine activity. (B) Caffeine acts as an antagonist where it blocks adenosine binding to adenosine receptors, enhancing dopamine activity. The mechanism increases neuron excitability, promotes neurotransmitter release, increase brain activity, and may improve spinal and supraspinal excitability (Fredholm et al., 1999; Smith, 2003; Hogervorst et al., 2008; Connell et al., 2016; Pires et al., 2018; Saville et al., 2018; Shabir et al., 2018; Franco-Alvarenga et al., 2019; Huertas et al., 2019; Cipollone et al., 2020; Machado et al., 2020; Sanchis et al., 2020; Wang et al., 2020; Lorenzo Calvo et al., 2021; Vázquez et al., 2022; Ágoston et al., 2022).