Developing the catecholamines hypothesis for the acute exercise-cognition interaction in humans: Lessons from animal studies

The catecholamines hypothesis for the acute exercise-cognition interaction in humans fails to adequately explain the interaction between peripherally circulating catecholamines and brain concentrations; how different exercise intensities × durations affect different cognitive tasks; and how brain catecholamines, glucocorticoids, BDNF and 5-hydroxytryptamine interact. A review of the animal literature was able to clarify many of the issues. Rodent studies showed that facilitation of cognition during short to moderate duration (SMD), moderate exercise could be accounted for by activation of the locus coeruleus via feedback from stretch reflexes, baroreceptors and, post-catecholamines threshold, β-adrenoceptors on the vagus nerve. SMD, moderate exercise facilitates all types of task by stimulation of the reticular system by norepinephrine (NE) but central executive tasks are further facilitated by activation of α2A-adrenoceptors and D1-dopaminergic receptors in the prefrontal cortex, which increases the signal to ‘noise’ ratio. During long-duration, moderate exercise and heavy exercise, brain concentrations of glucocorticoids and 5-hydroxytryptamine, the latter in moderate exercise only, also increase. This further increases catecholamines release. This results in increased activation of D1-receptors and α1-adrenoceptors, in the prefrontal cortex, which dampens all neural activity, thus inhibiting central executive performance. However, activation of β- and α1-adrenoceptors can positively affect signal detection in the sensory cortices, hence performance of perception/attention and autonomous tasks can be facilitated. Animal studies also show that during long-duration, moderate exercise and heavy exercise, NE activation of β-adrenoceptors releases cAMP, which modulates the signaling and trafficking of the BDNF receptor Trk B, which facilitates long-term potentiation

Past, present and future in exercise-cognition research

Early research into the effects of acute exercise on cognition were atheoretical and of poor design. In the 1990s and 2000s, cognitive-energetical theories and the catecholamines hypothesis have been developed as rationales for effects of acute exercise on cognition. It was claimed that acute exercise was a stressor and as such would affect cognition in an inverted-U manner, the same as other stressors. However, the inverted-U effect was rarely supported. Later research has somewhat consistently shown that moderate intensity, short to moderate duration exercise induces improved cognitive performance. However, the effects of heavy exercise and long-duration, moderate intensity exercise treatments remain somewhat equivocal, except for autonomous tasks which are facilitated. Recent research suggests that undertaking exercise, while simultaneously carrying out a motor task, is more beneficial than simply exercising before undertaking the cognitive tasks. Research examining the effect of chronic exercise on cognition was also originally atheoretical and poorly designed. Improved research designs have led to some consistency in findings and the evidence for chronic exercise having a facilitative effect on cognition is fairly consistent but only a small to moderate improvement has been demonstrated. Human studies provide a prima facie case for brain derived neurotrophic factor being a mediator in the chronic exercise-cognition interaction and evidence from animal studies strongly supports this. Recent work provides support for claims that exercise, while simultaneously undertaking a motor task, is more beneficial than simply exercising

The acute exercise-cognition interaction: From the catecholamines hypothesis to an interoception model

An interoception model for the acute exercise-cognition interaction is presented. During exercise following the norepinephrine threshold, interoceptive feedback induces increased tonic release of extracellular catecholamines, facilitating phasic release hence better cognitive performance of executive functions. When exercise intensity increases to maximum, the nature of task-induced norepinephrine release from the locus coeruleus is dependent on interaction between motivation, perceived effort costs and perceived availability of resources. This is controlled by interaction between the rostral and dorsolateral prefrontal cortices, orbitofrontal cortex, anterior cingulate cortex and anterior insula cortex. If perceived available resources are sufficient to meet predicted effort costs and reward value is high, tonic release from the locus coeruleus is attenuated thus facilitating phasic release, therefore cognition is not inhibited. However, if perceived available resources are insufficient to meet predicted effort costs or reward value is low, tonic release from the locus coeruleus is induced, attenuating phasic release. As a result, cognition is inhibited, although long-term memory and tasks that require switching to new stimuli-response couplings are probably facilitated

Is there an acute exercise-induced physiological/biochemical threshold which triggers increased speed of cognitive functioning? A meta-analytic investigation

Purpose: The purpose of this study was to examine, using meta-analytic measures, the evidence regarding the optimal exercise intensity at which improvements in speed of cognitive function are triggered. Specifically, it was hypothesized that the catecholamine, lactate, and ventilatory thresholds is the point at which significant improvements in speed of cognitive function are observed. Methods: We compared mean effect sizes for threshold studies and for those studies where exercise intensity was classed as moderate (40%–79% VO2max or equivalent) but in which the thresholds were not measured. Results: Random effects meta-analysis showed significant, moderate, mean effect sizes for studies at the threshold (g = 0.58, Z = 2.98, p < 0.003) and for those during moderate intensity exercise but in which the threshold was not measured (g = 0.54, Z = 5.01, p < 0.001). There was no significant difference between mean effect sizes, which suggests that the thresholds are unlikely to represent a trigger point. Conclusion: Moderate intensity exercise, even below the thresholds, can induce improved speed of cognition, possibly due to a combination of increased peripheral catecholamine concentrations inducing vagal/nucleus tractus solitarii pathway activation and central increases due to perceptions of stress

Does acute exercise affect the performance of whole-body, psychomotor skills in an inverted-U fashion?:a meta-analytic investigation

The primary purpose of this study was to examine, using meta-analytical measures, whether research into the performance of whole-body, psychomotor tasks following moderate and heavy exercise demonstrates an inverted-U effect. A secondary purpose was to compare the effects of acute exercise on tasks requiring static maintenance of posture versus dynamic, ballistic skills. Moderate intensity exercise was determined as being between 40% and 79% maximum power output (ẆMAX) or equivalent, while ≥ 80% ẆMAX was considered to be heavy. There was a significant difference (Zdiff = 4.29, p = 0.001, R2 = 0.42) between the mean effect size for moderate intensity exercise (g = 0.15) and that for heavy exercise size (g = − 0.86). These data suggest a catastrophe effect during heavy exercise. Mean effect size for static tasks (g = − 1.24) was significantly different (Zdiff = 3.24, p = 0.001, R2 = 0.90) to those for dynamic/ballistic tasks (g = − 0.30). The result for the static versus dynamic tasks moderating variables point to perception being more of an issue than peripheral fatigue for maintenance of static posture. The difference between this result and those found in meta-analyses examining the effects of acute exercise on cognition shows that, when perception and action are combined, the complexity of the interaction induces different effects to when cognition is detached from motor performance

Acute anxiety predicts components of the cold shock response on cold water immersion:toward an integrated psychophysiological model of acute cold water survival

Introduction: Drowning is a leading cause of accidental death. In cold-water, sudden skin cooling triggers the life-threatening cold shock response (CSR). The CSR comprises tachycardia, peripheral vasoconstriction, hypertension, inspiratory gasp, and hyperventilation with the hyperventilatory component inducing hypocapnia and increasing risk of aspirating water to the lungs. Some CSR components can be reduced by habituation (i.e., reduced response to stimulus of same magnitude) induced by 3–5 short cold-water immersions (CWI). However, high levels of acute anxiety, a plausible emotion on CWI: magnifies the CSR in unhabituated participants, reverses habituated components of the CSR and prevents/delays habituation when high levels of anxiety are experienced concurrent to immersions suggesting anxiety is integral to the CSR.Purpose: To examine the predictive relationship that prior ratings of acute anxiety have with the CSR. Secondly, to examine whether anxiety ratings correlated with components of the CSR during immersion before and after induction of habituation.Methods: Forty-eight unhabituated participants completed one (CON1) 7-min immersion in to cold water (15°C). Of that cohort, twenty-five completed four further CWIs that would ordinarily induce CSR habituation. They then completed two counter-balanced immersions where anxiety levels were increased (CWI-ANX) or were not manipulated (CON2). Acute anxiety and the cardiorespiratory responses (cardiac frequency [fc], respiratory frequency [fR], tidal volume [VT], minute ventilation [E]) were measured. Multiple regression was used to identify components of the CSR from the most life-threatening period of immersion (1st minute) predicted by the anxiety rating prior to immersion. Relationships between anxiety rating and CSR components during immersion were assessed by correlation.Results: Anxiety rating predicted the fc component of the CSR in unhabituated participants (CON1; p &lt; 0.05, r = 0.536, r2= 0.190). After habituation immersions (i.e., cohort 2), anxiety rating predicted the fR component of the CSR when anxiety levels were lowered (CON2; p &lt; 0.05, r = 0.566, r2= 0.320) but predicted the fc component of the CSR (p &lt; 0.05, r = 0.518, r2= 0.197) when anxiety was increased suggesting different drivers of the CSR when anxiety levels were manipulated; correlation data supported these relationships.Discussion: Acute anxiety is integral to the CSR before and after habituation. We offer a new integrated model including neuroanatomical, perceptual and attentional components of the CSR to explain these data

Neuroscience of Exercise: Neuroplasticity and Its Behavioral Consequences

The human brain adapts to changing demands by altering itsfunctional and structural properties (neuroplasticity) whichresults in learning and acquiring skills. Convergent evidencefrom both human and animal studies suggests that enhancedphysical exercise facilitates neuroplasticity of certain brainstructures and as a result cognitive functions [1] as well asaffective [2] and behavioral responses [3].This special issue isbeing proposed at a very challenging time. There is evidencelinking increased physical exercise with an enhancement ofneurogenesis, synaptogenesis, angiogenesis, and the releaseof neurotrophins as well as neuroendocrinological changes,which are associated with benefits in cognitive and affectiveas well as behavioral functioning (such as fine motor functioning)

The effects of acute high-intensity aerobic exercise on cognitive performance: A structured narrative review

It is well established that acute moderate-intensity exercise improves cognitive performance. However, the effects of acute high-intensity aerobic exercise on cognitive performance have not been well characterized. In this review, we summarize the literature investigating the exercise-cognition interaction, especially focusing on high-intensity aerobic exercise. We discuss methodological and physiological factors that potentially mediate cognitive performance in response to high-intensity exercise. We propose that the effects of high-intensity exercise on cognitive performance are primarily affected by the timing of cognitive task (during vs. after exercise, and the time delay after exercise). In particular, cognitive performance is more likely to be impaired during high-intensity exercise when both cognitive and physiological demands are high and completed simultaneously (i.e., the dual-task paradigm). The effects may also be affected by the type of cognitive task, physical fitness, exercise mode/duration, and age. Second, we suggest that interactions between changes in regional cerebral blood flow (CBF), cerebral oxygenation, cerebral metabolism, neuromodulation by neurotransmitters/neurotrophic factors, and a variety of psychological factors are promising candidates that determine cognitive performance in response to acute high-intensity exercise. The present review has implications for recreational, sporting, and occupational activities where high cognitive and physiological demands are required to be completed concurrently

Creatine supplementation research fails to support the theoretical basis for an effect on cognition: Evidence from a systematic review

Creatine supplementation has been put forward as a possible aid to cognition, particularly for vegans, vegetarians, the elderly, sleep deprived and hypoxic individuals. However, previous narrative reviews have only provided limited support for these claims. This is despite the fact that research has shown that creatine supplementation can induce increased brain concentrations of creatine, albeit to a limited extent. We carried out a systematic review to examine the current state of affairs. The review supported claims that creatine supplementation can increases brain creatine content but also demonstrated somewhat equivocal results for effects on cognition. It does, however, provide evidence to suggest that more research is required with stressed populations, as supplementation does appear to significantly affect brain content. Issues with research design, especially supplementation regimens, need to be addressed. Future research must include measurements of creatine brain content