The absolute requirement for reproduction implies that the hypothalamo-pituitary-gonadal axis, controlling fertility, is an evolutionary robust mechanism. The GnRH neurons of the hypothalamus represent the key cell type within the body dictating fertility. However, the level of functional redundancy within the GnRH neuron population is unknown. As a result of a fortuitous transgene insertion event, GNR23 mice exhibit a marked allele-dependent reduction in GnRH neuron number within their brain. Wild-type mice have approximately 600 GnRH neurons, compared with approximately 200 (34%) and approximately 70 (12%) in GNR23(+/-) and GNR23(-/-) mice, respectively. Using these mice, we examined the minimal GnRH neuron requirements for fertility. Male GNR23(-/-) mice exhibited normal fertility. In contrast, female GNR23(-/-) mice were markedly subfertile, failing to produce normal litters, have estrous cycles, or ovulate. The failure of ovulation resulted from an inability of the few existing GnRH neurons to generate the LH surge. This was not the case, however, for the first cycle at puberty that appeared normal. Together, these observations demonstrate that 12% of the GnRH neuron population is sufficient for pulsatile gonadotropin secretion and puberty onset, whereas between 12 and 34% are required for cyclical control in adult female mice. This indicates that substantial redundancy exists within the GnRH neuronal population and suggests that the great majority of GnRH neurons must be dysfunctional before fertility is affected.

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The aim of this review was to determine the magnitude of the placebo and nocebo effect on sport performance. Articles published before March 2019 were located using Medline, Web of Science, PubMed, EBSCO, Science Direct, and Scopus. Studies that examined placebo and nocebo effects of an objective dependent variable on sports performance, which included a control or baseline condition, were included in the analysis. Studies were classified into two categories of ergogenic aids: 1) nutritional and 2) mechanical. Cohen's d effect sizes were calculated from 32 studies involving 1,513 participants. Small to moderate placebo effects were found for both placebo (d = 0.36) and nocebo (d = 0.37) effects and when separated by nutritional (d = 0.35) and mechanical (d = 0.47) ergogenic aids. The pooled effect size revealed a small to moderate effect size across all studies (d = 0.38). Results suggest that placebo and nocebo effects can exert a small to moderate effect on sports performance.

In June 2017 a group of experts in anthropology, biology, kinesiology, neuroscience, physiology, and psychology convened in Canterbury, UK, to address questions relating to the placebo effect in sport and exercise. The event was supported exclusively by Quality Related (QR) funding from the Higher Education Funding Council for England (HEFCE). The funder did not influence the content or conclusions of the group. No competing interests were declared by any delegate. During the meeting and in follow-up correspondence, all delegates agreed the need to communicate the outcomes of the meeting via a brief consensus statement. The two specific aims of this statement are to encourage researchers in sport and exercise science to 1. Where possible, adopt research methods that more effectively elucidate the role of the brain in mediating the effects of treatments and interventions. 2. Where possible, adopt methods that factor for and/or quantify placebo effects that could explain a percentage of inter-individual variability in response to treatments and intervention.

Oestrogen plays an important role in testicular function. This study used mice null for oestrogen receptor a (ERa) or b (ERb) to investigate which receptor mediates the effects of oestrogen within the testis. Groups of ERa knockout mice (aERKO) and ERb knockout mice (bERKO) and wild-type littermates (nZ5-8) were killed at 11 weeks post partum. One testis was fixed in Bouin's fluid for stereology and the other frozen for testosterone measurement. Trunk blood was collected for testosterone RIA. The optical disector combined with the fractionator methodology was used to estimate Leydig, Sertoli and germ cell numbers. At all times, the knockout animals were compared with their wild-type littermates. The physical disector quantified cells stained immunohistochemically for the apoptotic marker active caspase-3 and Hoechst staining was used to identify nuclear fragmentation. The mean Leydig cell volume was measured using the point sampled intercept method. The Leydig cell number per testis was significantly increased in bERKO mice but not in aERKO mice. Plasma and testicular testosterone concentrations were increased in aERKO mice but no changes were observed in bERKO mice. Hypertrophic Leydig cell changes were observed in aERKO mice, and a decreased mean cell volume was seen in bERKO mice. No difference in Sertoli cell number per testis was observed in any of the groups. The spermatogonial cell number per testis was increased in bERKO mice. Immunohistochemistry identified increased numbers of active caspase-3-labelled germ cells per testis in aERKO mice but not bERKO mice. Hoechst staining supported these findings. There was significant germ cell loss in aERKO mice. This study suggests that ERb may be involved in regulation of Leydig cell proliferation and testosterone production in the adult mouse testis.

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Information about a harmful supplement worsened repeat sprint performance (a mean nocebo effect), whereas information about a beneficial supplement did not improve performance (no mean placebo effect was observed). However, participants' intention to use sport supplements influenced the direction and magnitude of subsequent placebo responses, with participants intending to use supplements more likely to respond to the positive intervention.