5.24 The Basal Ganglia: Action Selection, Gating, and Vigour

Right now, your brain is proposing dozens of movements you’re not making. Shift your weight. Scratch your nose. Walk out of the gym mid-set. Something has to pick one option — and veto all the rest.

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That something is the basal ganglia: a group of deep nuclei whose default answer, to every movement you could possibly make, is no. Cortex pitches the ideas. The basal ganglia release exactly one and sit on the others.

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Two parallel pathways share the work — a direct pathway that lifts the brake and an indirect pathway that presses it harder — with dopamine setting the balance between them. And the same circuit is copied three times over, serving movement, decision-making and motivation.

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Which is why this one structure sits behind so much of your training life: action selection, movement vigour, habit formation, and the willingness to spend effort at all. The effort you feel like giving today? That’s a physiological variable, not a character reference. The habits that outlive your motivation? Context-triggered, not goal-driven. And cueing the action you want beats fighting the one you don’t — for reasons we can point to on a wiring diagram.

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Key takeaways

1. The basal ganglia’s output nucleus, the internal globus pallidus, fires non-stop and inhibits the thalamus. Movement isn’t a signal being sent — it’s a brake being released.
2. The direct pathway (D1) releases the selected action. The indirect pathway (D2) suppresses the alternatives. Dopamine boosts the first and dampens the second.
3. Three parallel loops — sensorimotor, associative and limbic — run the same circuit from different parts of cortex. That’s why one structure handles movement, choice and motivation.
4. Movement vigour — amplitude and speed — is set here. Parkinson’s disease produces small, slow movements without weakness, because the vigour signal is degraded.
5. With repetition, control migrates from the dorsomedial striatum (goal-directed) to the dorsolateral striatum (habitual). The habit becomes context-triggered and stops tracking the reward.
6. The subthalamic nucleus is a fast, global stop switch — the substrate of reactive inhibition. It’s what you use to abort a movement you’ve already committed to.
7. Because the default is inhibition, coaching that names the desired action works better than coaching that names the fault. Suppression is a separate, more expensive operation than selection.

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Beginner section: The gate, not the engine

Meet the cast

Deep inside each hemisphere sit several large clumps of grey matter with names that sound like a law firm: the caudate and putamen (together, the striatum), plus the globus pallidus, the subthalamic nucleus and the substantia nigra.

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Here’s the surprise. None of them connects directly to the spinal cord, and not one of them can make a muscle contract. Their job isn’t to move you — it’s to decide what gets through.

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The default answer is no

The easiest way to understand the basal ganglia is to notice that their normal state is refusal. The output nucleus fires continuously, holding down the thalamus — which would otherwise excite motor cortex (Purves et al., 2018).

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So movement isn’t triggered. It’s permitted. That continuous inhibition lifts for one specific action, and only that action happens.

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Think bouncer holding a door shut, not starter firing a pistol. When you stand over a bar, set your grip and then pull, nothing “sent” that pull — a brake came off it.

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The direct pathway: lifting the brake

Walk the chain in Figure 1. Cortex tells the striatum which action it wants. The striatum inhibits the output nucleus. The brake on the thalamus lifts, and the movement is released.

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Notice what never happened: no go signal travelled anywhere. Inhibition of inhibition — that’s the whole trick.

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The indirect pathway: everyone else stays down

Running in parallel is the indirect pathway, which does the opposite. It adds brake.

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Why keep both? Because selection is a two-part job: permit one action, and suppress all the others.

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Stand at a free-throw line and dozens of possible movements are being proposed at once. Choosing the shot means releasing it while holding everything else back.

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Same story under a barbell. The lift you’re about to attempt is one motor plan among many candidates, and it only looks like the obvious choice because its rivals are being actively silenced.

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Dopamine is the dial

Dopamine is the variable that sets the balance. It excites the direct pathway and inhibits the indirect pathway (Albin et al., 1989).

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More dopamine: an easier release, and bigger, faster movements. Less dopamine: a stickier gate, and smaller, slower ones.

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This is why Parkinson’s disease — caused by the loss of dopamine-producing cells in the substantia nigra — produces movements that are small and slow rather than weak (Kandel et al., 2021). The engine is fine. The gate is stiff.

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One-line recap: dopamine doesn’t create movement, it prices the release. Keep that in your pocket for the vigour discussion later, because “how hard you feel like going today” rides on this same chemistry.

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Six terms worth keeping. They’ll carry you through the rest of the article.

• Striatum — the caudate plus the putamen. The basal ganglia’s input structure: the front desk where cortical proposals arrive.
• Globus pallidus internal segment (GPi) — the main output nucleus. Fires tonically and inhibits the thalamus.
• Subthalamic nucleus (STN) — a small excitatory nucleus that can rapidly crank up basal ganglia output. The substrate of fast, global stopping.
• Substantia nigra pars compacta — the midbrain source of dopamine to the striatum. Its degeneration causes Parkinson’s disease.
• Vigour — the amplitude and speed of a movement, as distinct from whether it happens at all. Set largely by basal ganglia output.
• Bradykinesia — slowness and shrinking of movement size. The core motor sign of dopamine depletion.

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One circuit, three loops

Now the reveal that makes the anatomy worth learning: the same circuit appears three times, fed by different parts of cortex.

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A sensorimotor loop handles movement. An associative loop handles decisions and rules. A limbic loop handles value and motivation (Alexander et al., 1986).

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That’s why a structure the textbooks file under “motor” turns out to be central to habit, effort and drive — all covered properly in articles 5.7, 5.14 and 5.15.

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Same machine, three customers. It’s also why effort, habit and movement quality keep turning up in the same conversation: they share hardware.

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One thing you can use today

Because the default state is inhibition, and selecting means releasing one option, telling an athlete what to do is computationally cheaper than telling them what not to do.

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“Do not drop your elbow” makes the brain represent the fault, then suppress it, then go hunting for a replacement. Three operations.

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“Drive the elbow through the line” is one selection. The gate opens, the movement runs.

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This is not a motivational point; it is a circuit point. And it applies just as much to the cues you mutter to yourself between reps as to anything a coach says out loud.

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Advanced section: Gating, vigour, stopping, and the striatal shift

Why a tonically inhibitory output is a good design

The architecture looks wasteful until you consider the problem it solves. A body with many effectors and a cortex generating many simultaneous proposals needs a mechanism that guarantees only one coherent action is executed at a time. A system that had to actively send a go signal would risk sending several at once. A system that holds everything down and selectively releases one channel cannot.

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Mink formalised this as the centre-surround or focused selection model: The direct pathway opens a narrow channel while the indirect pathway and the subthalamic nucleus broadly increase inhibition around it (Mink, 1996). Redgrave, Prescott and Gurney made the computational case that this is an efficient solution to the action selection problem, which is a genuine engineering difficulty rather than a philosophical one (Redgrave et al., 1999).

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The clinical evidence fits. Reduced basal ganglia output does not cause weakness; it causes unwanted movement to escape, as in Huntington’s disease and hemiballismus following subthalamic damage. Increased output causes difficulty releasing intended movement, as in Parkinson’s disease (Albin et al., 1989; DeLong, 1990). The failures are failures of gating in both directions.

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Vigour: Why the same movement can be big or small

Basal ganglia output does not only determine whether a movement occurs. It scales it. Turner and Desmurget reviewed the evidence that pallidal output relates to movement amplitude and speed, and that dopamine level correlates with the vigour with which a movement is performed (Turner & Desmurget, 2010). Mazzoni, Hristova and Krakauer showed something particularly informative in Parkinson’s patients: They could reach at normal speeds when explicitly required to, but required many more attempts to do so, suggesting the deficit is in the willingness to produce vigorous movement rather than the capacity for it (Mazzoni et al., 2007).

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That distinction — capacity versus willingness — is directly relevant to athletes. Effort is not simply a psychological attitude sitting on top of a physical system; it is partly a physiological variable determined by dopaminergic signalling and effort-cost computation, as described in 5.7. An athlete who is producing small, slow, tentative movements despite intact strength is not necessarily lacking character. Low sleep, illness, chronic overload and monotony all reduce dopaminergic tone and therefore reduce vigour.

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The practical version is that vigour responds to things other than exhortation: Novelty, competition, music, stakes, adequate sleep, and reduced monotony. It also responds to explicit instruction, but at a higher cost in attention, which is why athletes who have to consciously drive intent every rep fatigue faster mentally.

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Stopping: The subthalamic nucleus and reactive inhibition

Aborting a movement already underway is a separate operation from choosing not to start one. The hyperdirect pathway, running from cortex straight to the subthalamic nucleus, bypasses the striatum entirely and can raise basal ganglia output within about 10 to 15 ms of a cortical signal (Nambu et al., 2002). Aron and Poldrack and subsequent work with the stop-signal task implicate a right inferior frontal to pre-supplementary motor to subthalamic circuit in reactive stopping (Aron & Poldrack, 2006).

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A crucial feature is that this stop signal is global rather than selective (Verbruggen & Logan, 2008). When you abort one action, everything is transiently suppressed, which is why an athlete who checks a committed movement typically loses postural control and rhythm as well, not just the intended action. Coaches see this constantly: The player who half-commits to a tackle or a swing and ends up doing nothing well.

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Two training implications follow. First, stopping is trainable, and stop-signal reaction time improves with practice, but it remains fundamentally slower than going, which is why baiting an opponent into commitment is so effective in every sport. Second, it is better to design decisions that avoid the need for late aborts — delaying commitment, keeping options open longer, using footwork that preserves both choices — than to train the abort itself.

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The dorsomedial to dorsolateral shift, and what it costs

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Early in learning, control sits in the dorsomedial striatum and is genuinely goal-directed: If you change the value of the outcome, behaviour changes immediately. With extended practice, control migrates to the dorsolateral striatum and becomes habitual: Behaviour is triggered by context and continues even when the outcome no longer justifies it (Graybiel, 2008). Yin and Knowlton reviewed the lesion and behavioural evidence for this dissociation, and human imaging shows a comparable shift in activation as tasks become automatic (Yin & Knowlton, 2006; Ashby et al., 2010).

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This has an underappreciated cost. Automaticity buys speed, low attentional demand and resistance to pressure. It sells flexibility. A deeply habitual technique is exactly what you want under fatigue and in competition, and it is exactly what makes technical change difficult, because the old habit is not deleted — it is outcompeted. This is the mechanism behind the regression discussed in 5.14 and 5.16, where a corrected technique reverts under stress.

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The programming implication is to time automatisation deliberately. Technical changes belong in the phase of the year where the old pattern can be de-emphasised and the new one built with high attention and low competitive stakes. Late-season technical rebuilds fail not because athletes lack discipline but because a habitual controller has priority and stress increases its priority further.

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Reinforcement learning and the striatum as a value store

Dopamine release into the striatum carries a reward prediction error, as described in detail in 5.7, and the striatum uses it to update the strength of cortico-striatal synapses. Frank’s modelling work suggests an asymmetry that matters practically: D1-expressing direct-pathway neurons learn preferentially from better-than-expected outcomes, while D2-expressing indirect-pathway neurons learn preferentially from worse-than-expected outcomes (Frank & Seeberger, 2004). Learning from success and learning from failure are handled by partly separate populations.

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Individual differences follow from this. Some athletes are markedly better at consolidating what worked, others at avoiding what did not, and dopaminergic genotype has been associated with the balance in laboratory tasks. The applied version does not require genetics: Coaches can observe which type of feedback actually changes a given athlete’s behaviour, and weight their feedback accordingly.

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It also explains why punishment-heavy environments produce cautious, avoidance-shaped athletes. If nearly all of the prediction error an athlete receives is negative, the indirect pathway does most of the learning, and the resulting behaviour is optimised for not being wrong rather than for being good.

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Reading basal ganglia claims critically

The basal ganglia are invoked frequently in performance media, usually in one of three overreaching ways: That habits take a fixed number of days to form, that dopamine can be topped up to increase drive, or that deep brain stimulation findings imply consumer applications.

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• Habit formation timelines vary enormously between behaviours and people. Lally and colleagues found a median of about 66 days to reach an automaticity plateau with a range from 18 to well over 250 days, and simple behaviours automatised much faster than complex ones (Lally et al., 2010).
• Dopamine precursor supplementation does not reliably raise phasic striatal signalling in healthy people, and the tonic and phasic components have different functional roles. See 5.8 and 5.20.
• Deep brain stimulation of the subthalamic nucleus is a neurosurgical treatment with substantial side effect profiles including impulsivity. It is not a model for anything available to athletes.

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What is well supported and useful is the framework: Selection is a release from inhibition, vigour is a physiological variable, stopping is global and slower than going, and repetition shifts control from flexible to habitual. Every one of those has a concrete coaching consequence.

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Practical section: Coaching a gate

1. Cue the action you want, not the fault you want removed. Selection is one operation; suppression plus replacement is three. This single change makes most technical coaching more effective immediately.
2. Treat vigour as a trainable and monitorable variable. Jump height, throw distance or bar velocity on the first set of a session tells you what the gate is currently allowing. A drop of more than about 5 percent from an athlete’s norm is worth investigating before adding load.
3. Design to avoid late aborts. Teach delayed commitment, split-stance readiness and footwork that keeps two options live, rather than training athletes to stop faster. Stopping will always be slower than going.
4. Time technical change to the calendar. Build new patterns when stakes are low and attention is available. Under pressure and fatigue the habitual controller takes priority regardless of intention.
5. Vary the environment when you want flexibility and stabilise it when you want automaticity. These are opposite goals and cannot be pursued in the same block.
6. Match feedback style to the athlete. Some athletes change behaviour after being told what worked; others after being told what failed. Watch which one actually produces change rather than assuming.
7. Keep the reward structure positive enough that learning is not dominated by avoidance. An environment of constant correction produces athletes who are good at not being wrong.

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A note on monitoring. Because vigour is set by the same dopaminergic system that responds to sleep loss, illness, monotony and accumulated stress, simple output measures are unusually sensitive early warnings. A counter-movement jump takes thirty seconds, needs no equipment beyond a phone or a mat, and will often flag a problem several days before an athlete reports feeling flat.

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A note on habit. The striatal shift means that whatever you repeat becomes the default, including the technique you did not intend to teach. High-volume practice of a slightly wrong pattern is not neutral; it is training. This is the strongest argument for keeping technical volume low enough that quality can be maintained.

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Sport applications

In combat sports the stopping asymmetry is the basis of feinting. A feint forces the opponent to commit, and because aborting is globally suppressive and slower than initiating, the opponent loses not just the intended action but their balance and rhythm. Training should therefore emphasise delayed commitment rather than faster aborting.

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In team sports the same asymmetry is why a defender who stays square and slightly back is harder to beat than one who is fast but commits early. The skill being trained is deferral of selection, which is a basal ganglia function.

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In strength sports vigour is the practical currency. Bar velocity at a fixed load is a direct readout of how much the gate is allowing on that day, which is why velocity-based training works as a daily autoregulation tool rather than only as a load prescription method.

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In skill sports the habitual shift explains the off-season. Technical rebuilds work in the general preparation phase and fail in competition phases, because increased arousal biases control towards the habitual controller.

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In endurance sport the willingness-versus-capacity distinction matters most. An athlete who has stopped producing vigorous efforts in training despite intact physiology is showing a dopaminergic and effort-cost problem, and the correct interventions are recovery, novelty and reduced monotony rather than more volume.

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Common mistakes

• Coaching in negatives. Do not lean forward requires representing and suppressing the fault. Name the intended action instead.
• Reading low vigour as low character. Movement amplitude and speed are physiologically set. Check sleep, illness, monotony and accumulated load first.
• Training athletes to abort faster. Stopping is globally suppressive and inherently slower than going. Train delayed commitment instead.
• Attempting technical rebuilds in competition phases. Stress and fatigue give priority to the habitual controller, so the old pattern will win.
• Believing habits form in 21 days. Reported medians are closer to two months with a very wide range, and complex behaviours take considerably longer.
• Accumulating high-volume sloppy repetitions. The striatum stores whatever is repeated. Volume without quality is training the fault.
• Running a punishment-dominated environment. When almost all feedback is negative, the avoidance pathway does the learning and athletes optimise for not being wrong.
• Chasing dopamine with supplements to increase drive. Precursor loading does not reliably change phasic striatal signalling in healthy people. See 5.20.

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Coaching cues

• Say what you want, not what you do not want.
• Check the first jump or the first rep velocity before deciding how hard today should be.
• Stay long, decide late.
• Rebuild technique in the quiet part of the year.
• Vary the drill when you want adaptability; repeat it when you want automaticity.
• Find out whether this athlete learns from what worked or from what failed.
• If the movement is small and slow but the strength is there, the problem is upstream.

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FAQs

Are the basal ganglia the habit centre of the brain?

They are a necessary part of the habit system rather than its location. Habit formation requires cortex to supply the context and the action, the striatum to store the association, and dopamine to signal when it should be strengthened. The dorsolateral striatum becomes the dominant controller for well-practised behaviours, but calling it the habit centre implies a modularity that does not exist. Article 5.14 covers the full circuit.

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Why do Parkinson’s patients move normally in an emergency?

This phenomenon, sometimes called paradoxical kinesia, is well documented and not fully explained. The most plausible accounts involve brainstem pathways, particularly reticulospinal drive released by high arousal, bypassing the degraded basal ganglia gate. It supports the general picture that the vigour deficit is a problem of gating and willingness rather than of motor capacity.

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Does this mean intent and effort are not under my control?

They are under your control, but at a cost. You can consciously override low vigour by explicitly driving intent, and it works. What the physiology adds is that doing so consumes attention and is fatiguing, which is why athletes cannot maintain forced intent across long sessions. Managing the inputs that set vigour, particularly sleep, monotony and accumulated stress, is more sustainable than overriding them.

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Is bar velocity actually a useful daily measure?

Yes, within limits. Mean concentric velocity at a fixed submaximal load is reasonably reliable and sensitive to daily readiness, and it correlates with relative intensity closely enough to guide load selection. What it cannot do is replace a training plan, and the measurement error of cheap devices is large enough that only meaningful changes, generally above about 5 percent, should alter decisions.

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Why is it so hard to change a technique I have used for years?

Because the old pattern still exists and has priority. Learning a new technique creates a competing representation rather than overwriting the old one, and the older, more practised, more habitual pattern is favoured under fatigue, arousal and time pressure. The practical consequences are that technical change needs low-pressure repetitions in large numbers, and that partial change is worse than either state because it leaves two patterns competing.

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What is the difference between not starting a movement and stopping one?

Anatomically and functionally, quite a lot. Withholding an action is proactive and can be set up in advance by biasing the indirect pathway. Aborting an action already released is reactive, uses the fast hyperdirect route to the subthalamic nucleus, and suppresses everything rather than just the target action. That is why a late abort tends to cost balance and rhythm as well.

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Do the basal ganglia have anything to do with the yips or choking?

Probably, though the evidence is not settled. Task-specific dystonias, of which the yips in golf may be one variant in some athletes, involve abnormal basal ganglia function and abnormal surround inhibition. Choking under pressure is better explained by attentional and prefrontal mechanisms, as discussed in 5.3. The two are frequently conflated and should not be, because the management differs substantially.

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Recommended videos

Each video below was chosen because it covers a specific part of this article in more depth than text alone allows.

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Related reading on FitXplor

• 5.7 The Dopamine System: Reward Prediction, Motivation, and Effort
• 5.14 The Neuroscience of Habit Formation
• 5.22 The Motor Cortex and the Descending Motor Pathways
• 5.23 The Cerebellum: Timing, Internal Models, and Error-Driven Learning
• 5.15 Behaviour Change: From Intention to Automaticity

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References

Albin, R. L., Young, A. B., & Penney, J. B. (1989). The functional anatomy of basal ganglia disorders. Trends in Neurosciences, 12(10), 366–375.

Alexander, G. E., DeLong, M. R., & Strick, P. L. (1986). Parallel organization of functionally segregated circuits linking basal ganglia and cortex. Annual Review of Neuroscience, 9, 357–381.

Aron, A. R., & Poldrack, R. A. (2006). Cortical and subcortical contributions to stop signal response inhibition: role of the subthalamic nucleus. Journal of Neuroscience, 26(9), 2424–2433.

DeLong, M. R. (1990). Primate models of movement disorders of basal ganglia origin. Trends in Neurosciences, 13(7), 281–285.

Frank, M. J., Seeberger, L. C., & O’Reilly, R. C. (2004). By carrot or by stick: cognitive reinforcement learning in Parkinsonism. Science, 306(5703), 1940–1943.

Graybiel, A. M. (2008). Habits, rituals, and the evaluative brain. Annual Review of Neuroscience, 31, 359–387.

Lally, P., van Jaarsveld, C. H. M., Potts, H. W. W., & Wardle, J. (2010). How are habits formed: modelling habit formation in the real world. European Journal of Social Psychology, 40(6), 998–1009.

Mazzoni, P., Hristova, A., & Krakauer, J. W. (2007). Why don’t we move faster? Parkinson’s disease, movement vigor, and implicit motivation. Journal of Neuroscience, 27(27), 7105–7116.

Mink, J. W. (1996). The basal ganglia: focused selection and inhibition of competing motor programs. Progress in Neurobiology, 50(4), 381–425.

Nambu, A., Tokuno, H., & Takada, M. (2002). Functional significance of the cortico-subthalamo-pallidal hyperdirect pathway. Neuroscience Research, 43(2), 111–117.

Redgrave, P., Prescott, T. J., & Gurney, K. (1999). The basal ganglia: a vertebrate solution to the selection problem? Neuroscience, 89(4), 1009–1023.

Turner, R. S., & Desmurget, M. (2010). Basal ganglia contributions to motor control: a vigorous tutor. Current Opinion in Neurobiology, 20(6), 704–716.

Yin, H. H., & Knowlton, B. J. (2006). The role of the basal ganglia in habit formation. Nature Reviews Neuroscience, 7(6), 464–476.

Verbruggen, F., & Logan, G. D. (2008). Response inhibition in the stop-signal paradigm. Trends in Cognitive Sciences, 12(11), 418–424.

Ashby, F. G., Turner, B. O., & Horvitz, J. C. (2010). Cortical and basal ganglia contributions to habit learning and automaticity. Trends in Cognitive Sciences, 14(5), 208–215.

Purves, D., Augustine, G. J., Fitzpatrick, D., Hall, W. C., LaMantia, A.-S., Mooney, R. D., Platt, M. L., & White, L. E. (2018). Neuroscience (6th ed.). Oxford University Press.

Kandel, E. R., Koester, J. D., Mack, S. H., & Siegelbaum, S. A. (Eds.). (2021). Principles of Neural Science (6th ed.). McGraw Hill.