Analysis of In-Season External Load and Sport Performance in Women's Collegiate Basketball.

ABSTRACT: Brown, FSA, Fields, JB, Jagim, AR, Baker, RE, and Jones, MT. Analysis of in-season external load and sport performance in women's collegiate basketball. J Strength Cond Res 38(2): 318-324, 2024-Quantifying and monitoring athlete workload throughout a competitive season is a means to manage player readiness. Therefore, the purpose of the current study was to quantify practice and game external loads and to assess the relationship between such loads and basketball-specific performance metrics across a women's collegiate basketball season. Thirteen National Collegiate Athletic Association Division I women basketball athletes (age 20.08 ± 1.55 years) wore Global Positioning Systems sensors equipped with triaxial accelerometers for 29 games and 66 practices during the 2019-20 season. A multivariate analysis of variance was used to assess differences in external load between high- and low-minute players and across quarters within games ( p < 0.05). Bivariate Pearson correlation coefficients were run to determine relationships between external loads and metrics of basketball performance. Findings indicated that high- and low-minute athletes experienced different loads during games and practices ( p < 0.001). External loads differed by quarter, such that player load (PL) was highest in Q4 ( p = 0.007), PL·min -1 was highest in Q1 and lowest in Q4 ( p < 0.001), and explosive ratio (i.e., ratio of PL and explosive efforts) was lowest in Q3 ( p = 0.45). Relationships existed between PL·min -1 and field goals ( r = 0.41; p = 0.02) and between the explosive ratio and free throws ( r = 0.377 p = 0.04). These results can be used to inform design of training sessions with the intent to prepare athletes for the demands of the competitive season. It is recommended that future research continue to explore the relationship of sport-specific performance metrics and athlete external load.

Physiological consequences of selective suppression of synaptic transmission in developing cerebral cortical networks in vitro: differential effects on intrinsically generated bioelectric discharges in a living 'model' system for slow-wave sleep activity.

Within the context of an updated thorough review of the literature concerning activity-dependent cerebro-cortical development, a survey is made of recent experiments which utilize spontaneous spike-trains as the dependent variable in rodent neocortex cultures when synaptic transmission is interfered with during early ontogeny. Emphasis is placed on the complexity of homeostatic adaptations to reduced as well as intensified firing. Two kinds of adaptation are distinguished: (i) rapid recovery (within several hours) towards baseline levels despite sustained blockade of excitatory synaptic transmission, and (ii) the generation of essentially normal firing patterns in cultures assayed in control medium following development in the presence of excitatory receptor blockers. The former category of homeostatic responses is strongly dependent on the type of preparation, with isolated organotypic explants showing greatly limited plasticity in comparison with co-cultures of matching contralateral pieces of cortical tissue. In such co-cultures, compensatory excitatory drive manifests itself even when all three known types of ionotropic glutamate receptors are chronically blocked, and is then mediated by (muscarinic) cholinergic mechanisms which normally do not contribute measurably to spontaneous activity. The rapid return of high levels of spontaneous firing during sustained selective glutamatergic receptor blockade appears to protect neuronal cultures treated in this way from becoming hyperexcitable. In particular, quasi-epileptiform paroxysmal bursting upon return to control medium, such as appears in preparations where bioelectric activity has been totally suppressed during network formation, fails to appear in chronically receptor blocked cultures. On the contrary, desensitization of blocked glutamate receptors, as a physiological compensation for the up-regulation of non-blocked receptors, could be demonstrated for both the AMPA and the NMDA glutamate receptor sub-types. This wide range of homeostatic responses underscores the importance of spontaneous neuronal discharges for setting and maintaining an optimal balance between excitatory and inhibitory mechanisms in developing neocortical networks.

Spontaneous neuronal discharge patterns in developing organotypic mega-co-cultures of neonatal rat cerebral cortex.

Sagittal slices of neonatal rat neocortex, extending from the prefrontal to the occipital area, were cultured separately or in pairs, oriented in such a way that axons projecting from the ventricular surface of each explant could innervate the other one. Functional connections were made between as well as within the explants, and spontaneous field potentials and associated action potentials occurred in variable bursts, and with varying degrees of synchrony. Spike-train analysis revealed that the activity patterns seen in these 'mega' co-cultures closely mimic 'tracé alternant' patterns, consisting of trains of burst discharges recurring several times per minute, which are characteristic for the immature intact cerebral cortex during slow-wave sleep. The prefrontal region was consistently less active than the occipital area but the two were qualitatively similar with respect to their patterns of neuronal firing. Isolated mega-cultures, on the other hand, despite their large size, exhibited only intermittent brief bursts that closely resembled those observed both in occipital cortex tissue fragments and in dissociated cell cultures. The mega-co-culture preparation thus appears to give the best currently available approximation to intrinsic cerebral discharge patterns in vivo.

Homeostatically regulated spontaneous neuronal discharges protect developing cerebral cortex networks from becoming hyperactive following prolonged blockade of excitatory synaptic receptors.

In order to further examine the role of spontaneous action potential (SAP) discharges in neocortical development, amino-acid-mediated synaptic transmission was selectively blocked in an improved organotypic neocortex culture preparation. Contralateral occipital cortex slices from neonatal rats were co-cultured for several weeks in a ventricle-to-ventricle orientation known to greatly enhance cyto-morphological and electrophysiological maturation. Such preparations are highly resistant to attempts to suppress neuronal firing by blocking ionotropic glutamate receptors: not only can kainate receptors partly substitute for NMDA- and AMPA-mediated neurotransmission when these receptors are pharmacologically blocked, but (muscarinic) cholinergic receptors also begin to drive SAP activity when the kainate receptors, too, are chronically blocked. Only tetrodotoxin proved able to eliminate SAPs altogether in these co-cultures, while GABAergic receptor blockade (using bicucculine) led to persistent epileptiform discharges. Treatment effects were assayed upon transfer to control medium by means of a quantitative analysis of spontaneously occurring polyneuronal spike trains. Total suppression of action potentials for several weeks (by tetrodotoxin treatment) led, as in earlier experiments, to strongly intensified burst firing upon transfer to control medium. Chronic glutamate receptor blocked cultures, on the other hand, showed only minor deviations from control firing levels and patterns when assayed in normal medium. Protection against the development of hyperactivity despite partial blockade of synaptic transmission was roughly proportional to the degree to which spontaneous firing during the treatment period approximated normal SAP levels. This homeostatic response to chronically reduced excitatory drive thus differs from earlier results using isolated organotypic cortex cultures, in which the restoration of SAP activity failed to prevent the development of network hyperactivity. Chronic bicucculine treatment, in contrast, had little or no homeostatic effect on SAP firing patterns; on the contrary, opposite to earlier findings using isolated occipital cortex explants, paroxysmal discharges persisted even after transfer to control medium.

Compensatory physiological responses to chronic blockade of amino acid receptors during early development in spontaneously active organotypic cerebral cortex explants cultured in vitro.

Paired organotypic explants from rat occipital cortex were cultured for up to three weeks in the presence of selective blockers of amino acid receptor blockers, during which period spontaneous action potential generation was monitored electrophysiologically. In contrast to isolated explants (Corner, M.A., van Pelt, J., Wolters, P.S., Baker, R.E.and Nuytinck, R.H. (2002) Physiological e.ects of sustained blockade of excitatory synaptic transmission on spontaneously active developing neuronal networks--an inquiry into the reciprocal linkage between intrinsic biorhythms and neuroplasticity in early ontogeny. Neurosci. Biobehav. Rev., 26: 127-185), which upregulated their initially depressed spontaneous bursting activity only under conditions of N-methyl D-aspartate (NMDA) receptor blockade, cross-innervated co-cultures showed a large degree of functional recovery even when combined NMDA and AMPA receptor blockade was carried out. This compensatory activity could be eliminated by acute addition of a selective kainate receptor blocker to the medium. When kainate along with AMPA and NMDA receptor mediated activity was chronically suppressed, however, considerable functional recovery--in the form of recurrent burst discharges--took place gradually over a period of three weeks in vitro. These spontaneous bursts disappeared rapidly upon treatment with the muscarinic receptor blocker, atropine, but continuous low-level firing emerged at the same time. Similar "tonic" background activity was induced in control cultures as well, but without any noticeable reduction in burst discharges. Co-cultured neocortex explants, in which cyto-morphological maturation proceeds to a far greater degree than in isolated explants (Baker, R.E.and van Pelt, J. (1997) Co-cultured but not isolated cortical explants display normal dendritic development: a longterm quantitative study. Dev. Brain Res., 98: 21-27) are evidently capable of an astonishing degree of functional compensation for loss of excitatory synaptic drive during development. It could be shown, furthermore, that such homeostatic responses are not mediated largely by a weakening of inhibitory mechanisms in the absence of spontaneous firing. Chronic inhibitory synaptic blockade, on the other hand, led to intensified bursting activity which gradually normalized over a 3-week culture period. The cellular basis for this reversal of the disinhibited state, as well as for the residual neuronal firing even after cholinergic mechanisms have been largely eliminated, is at present unknown. The degree to which immature cortical networks attempt to compensate for altered levels of physiological activity, as documented in the present report, is another indication of how important such activity can be for normal development (see Corner, M.A., van Pelt, J., Wolters, P.S., Baker, R.E. and Nuytinck, R.H. (2002) Physiological e.ects of sustained blockade of excitatory synaptic transmission on spontaneously active developing neuronal networks-an inquiry into the reciprocal linkage between intrinsic biorhythms and neuroplasticity in early ontogeny. Neurosci. Biobehav. Rev., 26: 127-185).. At the same time, the large variations in overall firing levels and "macro-scale" temporal patterns from culture to culture within a given series, despite all attempts at identical preparation of the explants, can only mean that the "set-points" for such regulation are themselves subject to unknown ontogenetic factors which, apparently, are nonuniformly distributed even within a restricted region of the neocortex. On the other hand, it was striking to note that, regardless of age or treatment, an unexpected degree of consistency in temporal patterning existed at "mini-" and "micro-" time-scales (viz., EEG delta and beta frequency ranges, respectively) even when network bursting tendencies became greatly reduced in favor of tonic firing.

Cells in human postmortem brain tissue slices remain alive for several weeks in culture.

Animal models for human neurological and psychiatric diseases only partially mimic the underlying pathogenic processes. Therefore, we investigated the potential use of cultured postmortem brain tissue from adult neurological patients and controls. The present study shows that human brain tissue slices obtained by autopsy within 8 h after death can be maintained in vitro for extended periods (up to 78 days) and can be manipulated experimentally. We report for the first time that 1) neurons and glia in such cultures could be induced to express the reporter gene LacZ after transduction with adeno-associated viral vectors and 2) cytochrome oxidase activity could be enhanced by the addition of pyruvate to the medium. These slice cultures offer new opportunities to study the cellular and molecular mechanisms of neurological and psychiatric diseases and new therapeutic strategies.