Early and late stimulus-evoked cortical hemodynamic responses provide insight into the neurogenic nature of neurovascular coupling

Understanding neurovascular coupling is a prerequisite for the interpretation of results obtained from modern neuroimaging techniques. This study investigated the hemodynamic and neural responses in rat somatosensory cortex elicited by 16 seconds electrical whisker stimuli. Hemodynamics were measured by optical imaging spectroscopy and neural activity by multichannel electrophysiology. Previous studies have suggested that the whisker-evoked hemodynamic response contains two mechanisms, a transient ‘backwards’ dilation of the middle cerebral artery, followed by an increase in blood volume localized to the site of neural activity. To distinguish between the mechanisms responsible for these aspects of the response, we presented whisker stimuli during normocapnia (‘control’), and during a high level of hypercapnia. Hypercapnia was used to ‘predilate’ arteries and thus possibly ‘inhibit’ aspects of the response related to the ‘early’ mechanism. Indeed, hemodynamic data suggested that the transient stimulus-evoked response was absent under hypercapnia. However, evoked neural responses were also altered during hypercapnia and convolution of the neural responses from both the normocapnic and hypercapnic conditions with a canonical impulse response function, suggested that neurovascular coupling was similar in both conditions. Although data did not clearly dissociate early and late vascular responses, they suggest that the neurovascular coupling relationship is neurogenic in origin.

Negative blood oxygen level dependence in the rat: a model for investigating the role of suppression in neurovascular coupling

Modern neuroimaging techniques rely on neurovascular coupling to show regions of increased brain activation. However, little is known of the neurovascular coupling relationships that exist for inhibitory signals. To address this issue directly we developed a preparation to investigate the signal sources of one of these proposed inhibitory neurovascular signals, the negative blood oxygen level-dependent (BOLD) response (NBR), in rat somatosensory cortex. We found a reliable NBR measured in rat somatosensory cortex in response to unilateral electrical whisker stimulation, which was located in deeper cortical layers relative to the positive BOLD response. Separate optical measurements (two-dimensional optical imaging spectroscopy and laser Doppler flowmetry) revealed that the NBR was a result of decreased blood volume and flow and increased levels of deoxyhemoglobin. Neural activity in the NBR region, measured by multichannel electrodes, varied considerably as a function of cortical depth. There was a decrease in neuronal activity in deep cortical laminae. After cessation of whisker stimulation there was a large increase in neural activity above baseline. Both the decrease in neuronal activity and increase above baseline after stimulation cessation correlated well with the simultaneous measurement of blood flow suggesting that the NBR is related to decreases in neural activity in deep cortical layers. Interestingly, the magnitude of the neural decrease was largest in regions showing stimulus-evoked positive BOLD responses. Since a similar type of neural suppression in surround regions was associated with a negative BOLD signal, the increased levels of suppression in positive BOLD regions could importantly moderate the size of the observed BOLD response.

A dynamic model of neurovascular coupling: Implications for blood vessel dilation and constriction

Neurovascular coupling in response to stimulation of the rat barrel cortex was investigated using concurrent multichannel electrophysiology and laser Doppler flowmetry. The data were used to build a linear dynamic model relating neural activity to blood flow. Local field potential time series were subject to current source density analysis, and the time series of a layer IV sink of the barrel cortex was used as the input to the model. The model output was the time series of the changes in regional cerebral blood flow (CBF). We show that this model can provide excellent fit of the CBF responses for stimulus durations of up to 16 s. The structure of the model consisted of two coupled components representing vascular dilation and constriction. The complex temporal characteristics of the CBF time series were reproduced by the relatively simple balance of these two components. We show that the impulse response obtained under the 16-s duration stimulation condition generalised to provide a good prediction to the data from the shorter duration stimulation conditions. Furthermore, by optimising three out of the total of nine model parameters, the variability in the data can be well accounted for over a wide range of stimulus conditions. By establishing linearity, classic system analysis methods can be used to generate and explore a range of equivalent model structures (e.g., feed-forward or feedback) to guide the experimental investigation of the control of vascular dilation and constriction following stimulation.

The resting-state neurovascular coupling relationship: rapid changes in spontaneous neural activity in the somatosensory cortex are associated with haemodynamic fluctuations that resemble stimulus-evoked haemodynamics

Although promise exists for patterns of resting-state blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) brain connectivity to be used as biomarkers of early brain pathology, a full understanding of the nature of the relationship between neural activity and spontaneous fMRI BOLD fluctuations is required before such data can be correctly interpreted. To investigate this issue, we combined electrophysiological recordings of rapid changes in multi-laminar local field potentials from the somatosensory cortex of anaesthetized rats with concurrent two-dimensional optical imaging spectroscopy measurements of resting-state haemodynamics that underlie fluctuations in the BOLD fMRI signal. After neural ‘events’ were identified, their time points served to indicate the start of an epoch in the accompanying haemodynamic fluctuations. Multiple epochs for both neural ‘events’ and the accompanying haemodynamic fluctuations were averaged. We found that the averaged epochs of resting-state haemodynamic fluctuations taken after neural ‘events’ closely resembled the temporal profile of stimulus-evoked cortical haemodynamics. Furthermore, we were able to demonstrate that averaged epochs of resting-state haemodynamic fluctuations resembling the temporal profile of stimulus-evoked haemodynamics could also be found after peaks in neural activity filtered into specific electroencephalographic frequency bands (theta, alpha, beta, and gamma). This technique allows investigation of resting-state neurovascular coupling using methodologies that are directly comparable to that developed for investigating stimulus-evoked neurovascular responses.

Corticosterone Treatment Results in Enhanced Release of Peptidergic Vesicles in Astrocytes via Cytoskeletal Rearrangements

While the effect of stress on neuronal physiology is widely studied, its effect on the functionality of astrocytes is not well understood. We studied the effect of high doses of stress hormone corticosterone, on two physiological properties of astrocytes, i.e., gliotransmission and interastrocytic calcium waves. To study the release of peptidergic vesicles from astrocytes, hippocampal astrocyte cultures were transfected with a plasmid to express pro-atrial natriuretic peptide (ANP) fused with the emerald green fluorescent protein (ANP.emd). The rate of decrease in fluorescence of ANP.emd on application of ionomycin, a calcium ionophore was monitored. Significant increase in the rate of calcium-dependent exocytosis of ANP.emd was observed with the 100 nM and 1 M corticosterone treatments for 3 h, which depended on the activation of the glucocorticoid receptor. ANP.emd tagged vesicles exhibited increased mobility in astrocyte culture upon corticosterone treatment. Increasing corticosterone concentrations also resulted in concomitant increase in the calcium wave propagation velocity, initiated by focal ATP application. Corticosterone treatment also resulted in increased GFAP expression and F-actin rearrangements. FITC-Phalloidin immunostaining revealed increased formation of cross linked F-actin networks with the 100 nM and 1 M corticosterone treatment. Alternatively, blockade of actin polymerization and disruption of microtubules prevented the corticosterone-mediated increase in ANP.emd release kinetics. This study reports for the first time the effect of corticosterone on gliotransmission via modulation of cytoskeletal elements. As ANP acts on both neurons and blood vessels, modulation of its release could have functional implications in neurovascular coupling under pathophysiological conditions of stress.

Altération du couplage neurovasculaire par l'angiotensine II : évaluation du rôle de la signalisation calcique astrocytaire

Le couplage neurovasculaire (CNV) est un mécanisme d’homéostasie cérébrale régulant le débit sanguin cérébral (CBF) en fonction de l’activité neuronale. La manière dont il est altéré par l’angiotensine II (Ang II), une hormone synthétisée et relâchée dans la circulation systémique ou, alternativement, produite dans le cerveau grâce aux astrocytes, demeure à élucider. Ces cellules expriment le récepteur AT1 (rAT1) et participent à l’orchestration du CNV en relâchant des agents vasoactifs suivant la réponse calcique astrocytaire. Nous avons donc étudié le rôle de cette réponse dans l’altération du CNV induite par l’Ang II. Nous avons trouvé par fluxmétrie par laser Doppler que l’Ang II atténue (p<0.05) la réponse du CBF engendrée par l’activation des récepteurs métabotropes du glutamate du groupe I (mGluRI) du cortex chez la souris C57BL/6. De manière similaire, l’Ang II diminue l'élévation du CBF induite par la stimulation des vibrisses (p<0.05). Sur tranches de cerveaux en aiguë, la polarité de la réponse vasculaire induite par un agoniste mGluRI dans les artérioles parenchymateuses a été significativement renversée par l’Ang II de la vasodilatation vers la vasoconstriction. En parallèle, l’Ang II a augmenté les niveaux de calcium astrocytaire basaux et l’amplitude des réponses calciques (p<0.05). L’altération des réponses vasculaires et calciques maximales a été prévenue par le candesartan, antagoniste des rAT1. Nos résultats suggèrent que l’Ang II potentialise via les rAT1 la réponse calcique qui atteint un seuil favorisant la vasoconstriction par rapport à la vasodilatation, altérant ainsi l’augmentation du CBF en réponse à l’activité neuronale.

Strategies for revascularizing the ischemic retina

Les rétinopathies ischémiques (RI) sont la cause majeure de cécité chez les personnes âgées de moins de 65 ans. Il existe deux types de RIs soit la rétinopathie du prématuré (ROP) ainsi que la rétinopathie diabétique (RD). Les RIs sont décrites en deux phases soit la phase de vasooblitération, marquée par une perte importante de vaisseaux sanguins, et une phase de néovascularisation secondaire à lʼischémie menant à une croissance pathologique de vaisseaux. Cette seconde phase peut générer des complications cliniques telles quʼun oedème dans lʼhumeur vitré ainsi que le détachement de la rétine chez les patients déjà atteints dʼune RI. Les traitements approuvés pour les RIs visent à réduire la formation des vaisseaux pathologiques ou lʼoedème; mais ceux-ci malheureusement ne règlent pas les problèmes sous-jacents tels que la perte vasculaire et lʼischémie. La rétine est un tissu hautement vascularisé qui contribue à lʼirrigation et à lʼhoméostasie des neurones. Lʼinteraction neurovasculaire, comprenant de neurones, vaisseaux et cellules gliales, contribue au maintien de cette homéostasie. Durant le développement, les neurones et les cellules gliales jouent un rôle important dans la vascularisation de la rétine en sécrétant des facteurs qui stimulent l'angiogenèse. Cependant, nos connaissances sur lʼinteraction neurovasculaire dans les RIs sont limitées. En identifiant les interactions importantes entre les cellules composant cette unité neurovasculaire dans la rétine, nous pourrons viser des cibles qui engendreront une revascularisation seine afin de diminuer les signes pathologiques chez les patients atteints dʼune RI. Les travaux présentés dans cette thèse visent à mieux expliquer cette interaction neurovasculaire en soulignant des concepts importants propres aux RIs. En utilisant un modèle de rétinopathie induite par lʼoxygène chez la souris, qui reproduit les caractéristiques importantes de la ROP (et en certaines instances, la RD), nous identifions quelques molécules clés jouant un rôle significatif dans les RIs soit la sémaphorine 3A (sema3A), lʼIL-1β, ainsi que le récepteur PAR2. Nos résultats démontrent que Sema3A, sécrétée par les cellules ganglionnaires rétiniennes (CGRs) durant une ischémie, empêche la revascularisation normale et que cette expression est induite par lʼIL-1β provenant des microglies activées. En bloquant Sema3A directement ou via lʼinhibition de lʼIL- 1β, nous remarquons une revascularisation seine ainsi quʼune diminution importante des vaisseaux pathologiques. Cela nous indique que Sema3A est impliquée dans la guidance vasculaire et quʼelle contribue à la pathogenèse des RIs. Lʼactivation de façon exogène de PAR2, identifié aussi comme régulateur du récepteur de lʼIL-1β (IL- 1RI) sur les CGRs, se traduit par une diminution séquentielle de lʼIL-1RI et de Sema3A ce qui mène également à une revascularisation seine. En conclusion, ces travaux soulignent lʼimportance de lʼinteraction neurovasculaire ainsi que la guidance vasculaire dans les RIs. Ils renforcent lʼimportance de la communication entre neurone, vaisseau et microglie dans la pathogenèse des RIs. Finalement, nous identifions quelques molécules clés qui pourront servir comme cibles afin de lutter contre lʼischémie qui cause des problèmes vasculaires chez les patients atteints dʼune RI.

Realistic mean field forward predictions for the integration of co-registered EEG/fMRI

Brain activity can be measured non-invasively with functional imaging techniques. Each pixel in such an image represents a neural mass of about 105 to 107 neurons. Mean field models (MFMs) approximate their activity by averaging out neural variability while retaining salient underlying features, like neurotransmitter kinetics. However, MFMs incorporating the regional variability, realistic geometry and connectivity of cortex have so far appeared intractable. This lack of biological realism has led to a focus on gross temporal features of the EEG. We address these impediments and showcase a "proof of principle" forward prediction of co-registered EEG/fMRI for a full-size human cortex in a realistic head model with anatomical connectivity, see figure 1. MFMs usually assume homogeneous neural masses, isotropic long-range connectivity and simplistic signal expression to allow rapid computation with partial differential equations. But these approximations are insufficient in particular for the high spatial resolution obtained with fMRI, since different cortical areas vary in their architectonic and dynamical properties, have complex connectivity, and can contribute non-trivially to the measured signal. Our code instead supports the local variation of model parameters and freely chosen connectivity for many thousand triangulation nodes spanning a cortical surface extracted from structural MRI. This allows the introduction of realistic anatomical and physiological parameters for cortical areas and their connectivity, including both intra- and inter-area connections. Proper cortical folding and conduction through a realistic head model is then added to obtain accurate signal expression for a comparison to experimental data. To showcase the synergy of these computational developments, we predict simultaneously EEG and fMRI BOLD responses by adding an established model for neurovascular coupling and convolving "Balloon-Windkessel" hemodynamics. We also incorporate regional connectivity extracted from the CoCoMac database [1]. Importantly, these extensions can be easily adapted according to future insights and data. Furthermore, while our own simulation is based on one specific MFM [2], the computational framework is general and can be applied to models favored by the user. Finally, we provide a brief outlook on improving the integration of multi-modal imaging data through iterative fits of a single underlying MFM in this realistic simulation framework.

Complex spatiotemporal haemodynamic response following sensory stimulation in the awake rat

Detailed understanding of the haemodynamic changes that underlie non-invasive neuroimaging techniques such as blood oxygen level dependent functional magnetic resonance imaging is essential if we are to continue to extend the use of these methods for understanding brain function and dysfunction. The use of animal and in particular rodent research models has been central to these endeavours as they allow in-vivo experimental techniques that provide measurements of the haemodynamic response function at high temporal and spatial resolution. A limitation of most of this research is the use of anaesthetic agents which may disrupt or mask important features of neurovascular coupling or the haemodynamic response function. In this study we therefore measured spatiotemporal cortical haemodynamic responses to somatosensory stimulation in awake rats using optical imaging spectroscopy. Trained, restrained animals received non-noxious stimulation of the whisker pad via chronically implanted stimulating microwires whilst optical recordings were made from the contralateral somatosensory cortex through a thin cranial window. The responses we measure from un-anaesthetised animals are substantially different from those reported in previous studies which have used anaesthetised animals. These differences include biphasic response regions (initial increases in blood volume and oxygenation followed by subsequent decreases) as well as oscillations in the response time series of awake animals. These haemodynamic response features do not reflect concomitant changes in the underlying neuronal activity and therefore reflect neurovascular or cerebrovascular processes. These hitherto unreported hyperemic response dynamics may have important implications for the use of anaesthetised animal models for research into the haemodynamic response function.

Is optical imaging spectroscopy a viable measurement technique for the investigation of the negative BOLD phenomenon? A concurrent optical imaging spectroscopy and fMRI study at high field (7T)

Traditionally functional magnetic resonance imaging (fMRI) has been used to map activity in the human brain by measuring increases in the Blood Oxygenation Level Dependent (BOLD) signal. Often accompanying positive BOLD fMRI signal changes are sustained negative signal changes. Previous studies investigating the neurovascular coupling mechanisms of the negative BOLD phenomenon have used concurrent 2D-optical imaging spectroscopy (2D-OIS) and electrophysiology (Boorman et al., 2010). These experiments suggested that the negative BOLD signal in response to whisker stimulation was a result of an increase in deoxy-haemoglobin and reduced multi-unit activity in the deep cortical layers. However, Boorman et al. (2010) did not measure the BOLD and haemodynamic response concurrently and so could not quantitatively compare either the spatial maps or the 2D-OIS and fMRI time series directly. Furthermore their study utilised a homogeneous tissue model in which is predominantly sensitive to haemodynamic changes in more superficial layers. Here we test whether the 2D-OIS technique is appropriate for studies of negative BOLD. We used concurrent fMRI with 2D-OIS techniques for the investigation of the haemodynamics underlying the negative BOLD at 7 Tesla. We investigated whether optical methods could be used to accurately map and measure the negative BOLD phenomenon by using 2D-OIS haemodynamic data to derive predictions from a biophysical model of BOLD signal changes. We showed that despite the deep cortical origin of the negative BOLD response, if an appropriate heterogeneous tissue model is used in the spectroscopic analysis then 2D-OIS can be used to investigate the negative BOLD phenomenon.

Does neural input or processing play a greater role in the magnitude of neuroimaging signals?

An important constraint on how hemodynamic neuroimaging signals such as fMRI can be interpreted in terms of the underlying evoked activity is an understanding of neurovascular coupling mechanisms that actually generate hemodynamic responses. The predominant view at present is that the hemodynamic response is most correlated with synaptic input and subsequent neural processing rather than spiking output. It is still not clear whether input or processing is more important in the generation of hemodynamics responses. In order to investigate this we measured the hemodynamic and neural responses to electrical whisker pad stimuli in rat whisker barrel somatosensory cortex both before and after the local cortical injections of the GABAA agonist muscimol. Muscimol would not be expected to affect the thalamocortical input into the cortex but would inhibit subsequent intra-cortical processing. Pre-muscimol infusion whisker stimuli elicited the expected neural and accompanying hemodynamic responses to that reported previously. Following infusion of muscimol, although the temporal profile of neural responses to each pulse of the stimulus train was similar, the average response was reduced in magnitude by ∼79% compared to that elicited pre-infusion. The whisker-evoked hemodynamic responses were reduced by a commensurate magnitude suggesting that, although the neurovascular coupling relationships were similar for synaptic input as well as for cortical processing, the magnitude of the overall response is dominated by processing rather than from that produced from the thalamocortical input alone.

Funktionelle Magnetresonanztomographie mittels simultaner EEG-Registrierung interiktaler Spikes bei fokaler Epilepsie: Vergleich der on-, off- mit der häufigkeitskorrelierten Datenanalyse

Obwohl die funktionelle Magnetresonanztomographie (fMRI) interiktaler Spikes mit simultaner EEG-Ableitung bei Patienten mit fokalen Anfallsleiden seit einigen Jahren zur Lokalisation beteiligter Hirnstrukturen untersucht wird, ist sie nach wie vor eine experimentelle Methode. Um zuverlässig Ergebnisse zu erhalten, ist insbesondere die Verbesserung des Signal-zu-Rausch-Verhältnisses in der statistischen Bilddatenauswertung von Bedeutung. Frühere Untersuchungen zur sog. event-related fMRI weisen auf einen Zusammenhang zwischen Häufigkeit von Einzelreizen und nachfolgender hämodynamischer Signalantwort in der fMRI hin. Um einen möglichen Einfluss der Häufigkeit interiktaler Spikes auf die Signalantwort nachzuweisen, wurden 20 Kinder mit fokaler Epilepsie mit der EEG-fMRI untersucht. Von 11 dieser Patienten konnten die Daten ausgewertet werden. In einer zweifachen Analyse mit dem Softwarepaket SPM99 wurden die Bilddaten zuerst ausschließlich je nach Auftreten interiktaler Spikes der „Reiz“- oder „Ruhe“-Bedingung zugeordnet, unabhängig von der jeweiligen Anzahl der Spikes je Messzeitpunkt (on/off-Analyse). In einem zweiten Schritt wurden die „Reiz“- Bedingungen auch differenziert nach jeweiliger Anzahl einzelner Spikes ausgewertet (häufigkeitskorrelierte Analyse). Die Ergebnisse dieser Analysen zeigten bei 5 der 11 Patienten eine Zunahme von Sensitivität und Signifikanzen der in der fMRI nachgewiesenen Aktivierungen. Eine höhere Spezifität konnte hingegen nicht gezeigt werden. Diese Ergebnisse weisen auf eine positive Korrelation von Reizhäufigkeit und nachfolgender hämodynamischer Antwort auch bei interiktalen Spikes hin, welche für die EEG-fMRI nutzbar ist. Bei 6 Patienten konnte keine fMRI-Aktivierung nachgewiesen werden. Mögliche technische und physiologische Ursachen hierfür werden diskutiert.

Changes in cerebral hemodynamics and oxygenation induced by different speech tasks – an assessment by combining functional near‐infrared spectroscopy and capnography

Introduction In several studies, we found that during guided rhythmic speech exercises, a decrease in cerebral hemodynamics and oxygenation occurred as the result of a decrease in the partial pressure of carbon dioxide in the arterial blood (PaCO2) during speaking. To further explore the effect of PaCO2 variations on cerebral hemodynamics and oxygenation, the aim of the present study was to investigate the impact of spoken, inner and heard speech tasks on these parameters. Material and Methods Speech tasks included recitation or inner recitation or listening to hexameter, alliteration, prose, or performing mental arithmetic. The following physiological parameters were measured: tissue oxygen saturation (StO2) and absolute concentrations of oxyhemoglobin, deoxyhemoglobin, total hemoglobin (over the left and right anterior prefrontal cortex, using an ISS OxiplexTS frequency domain near-infrared spectrometer) and end-tidal CO2 (PETCO2; using Nellcor N1000 and Datex NORMOCAP capnographs). Statistical analysis was applied to the differences between baseline, 2 tasks, and 3 post-baseline periods. Data of 3 studies with 24, 7 and 29 healthy subjects, respectively, were combined, and linear regression analyses were calculated. Results Linear regression analyses revealed significant relations between changes in oxyhemoglobin, deoxyhemoglobin, total hemoglobin or StO2 and the participants’ age, the baseline PETCO2 or certain speech tasks. While hexameter verses affected changes during the tasks, alliteration verses only affected changes during the recovery phase. Discussion and Conclusion The observed effects in hemodynamics and oxygenation indicate a combination of neurovascular coupling (increased neuronal activity leading to an increase in the cerebral metabolic rate of oxygen resulting in an increase in cerebral flood flow/volume) and CO2 reactivity (increased breathing during speech tasks causing a decrease in PaCO2 leading to vasoconstriction and decrease in cerebral blood flow). The neurovascular coupling characteristics are task-dependent. References Scholkmann F, Gerber U, Wolf M, Wolf U. End-tidal CO2: An important parameter for a correct interpretation in functional brain studies using speech tasks. Neuroimage 2013;66:71-79. Scholkmann F, Wolf M, Wolf U. The effect of inner speech on arterial CO2, cerebral hemodynamics and oxygenation – A functional NIRS study. Adv Exp Med Biol 2013;789:81-87.

Retinal vessel analysis:flicker reproducibility, methodological standardisations and practical limitations

The Retinal Vessel Analyser (RVA) is a commercially available ophthalmoscopic instrument capable of acquiring vessel diameter fluctuations in real time and in high temporal resolution. Visual stimulation by means of flickering light is a unique exploration tool of neurovascular coupling in the human retina. Vessel reactivity as mediated by local vascular endothelial vasodilators and vasoconstrictors can be assessed non-invasively, in vivo. In brief, the work in this thesis • deals with interobserver and intraobserver reproducibility of the flicker responses in healthy volunteers • explains the superiority of individually analysed reactivity parameters over vendorgenerated output • links in static retinal measures with dynamic ones • highlights practical limitations in the use of the RVA that may undermine its clinical usefulness • provides recommendations for standardising measurements in terms of vessel location and vessel segment length and • presents three case reports of essential hypertensives in a -year follow-up. Strict standardisation of measurement procedures is a necessity when utilising the RVA system. Agreement between research groups on implemented protocols needs to be met, before it could be considered a clinically useful tool in detecting or predicting microvascular dysfunction.

Information–movement coupling in developing cricketers under changing ecological practice constraints

Changing informational constraints of practice, such as when using ball projection machines, has been shown to significantly affect movement coordination of skilled cricketers. To date, there has been no similar research on movement responses of developing batters, an important issue since ball projection machines are used heavily in cricket development programmes. Timing and coordination of young cricketers (n = 12, age = 15.6 ± 0.7 years) were analyzed during the forward defensive and forward drive strokes when facing a bowling machine and bowler (both with a delivery velocity of 28.14 ± 0.56 m s−1). Significant group performance differences were observed between the practice task constraints, with earlier initiation of the backswing, front foot movement, downswing, and front foot placement when facing the bowler compared to the bowling machine. Peak height of the backswing was higher when facing the bowler, along with a significantly larger step length. Altering the informational constraints of practice caused major changes to the information–movement couplings of developing cricketers. Data from this study were interpreted to emanate from differences in available specifying variables under the distinct practice task constraints. Considered with previous findings, results confirmed the need to ensure representative batting task constraints in practice, cautioning against an over-reliance on ball projection machines in cricket development programmes.