Juan José Pérez Díaz

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Can’t Hold any More! A Large Survey on Cycling Subjective Experience at the Limit of Effort

Juan José Pérez Díaz Isabel Benítez José-Antonio Salas-Montoro Míkel Zabala Daniel Sanabria

Cycling challenges athletes to their physiological and psychological limits, often culminating in task failure: an abrupt reduction in intensity or cessation of effort. While physiological mechanisms such as metabolic acidosis and oxygen supply have been widely studied, less is known about the subjective experience associated with task failure. In this study, a survey of 2,818 licensed cyclists provided novel insights into the subjective dimensions of task failure. Participants reported that physical sensations, especially breathing and muscle pain, were the most prominent cues at the limit of effort. Notably, 60.5% indicated they do not always reach their maximum perceived effort before task failure, suggesting a significant psychological component. Age, experience, and the use of feedback tools like powermeters influenced whether task failure was perceived as voluntary or involuntary. Cyclists in higher age categories more frequently perceived reaching their limits as voluntary, while younger or less experienced athletes reported involuntary task failure. Furthermore, strategies such as self-motivation, focusing on goals, and regulating breathing were commonly employed to sustain performance. Altered time perception during maximum effort was also a notable finding, with most cyclists perceiving time as passing more slowly. These results underline the multifactorial nature of task failure, involving complex interactions between physiological, psychological, and perceptual factors. Understanding these dynamics could inform targeted training approaches, enabling athletes to better manage effort and delay task failure, thereby optimizing performance.

Cycling

10.31234/osf.io/j7nq4_v1

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Supplementary Material for: Calbindin-1 Expression in the Hippocampus following Neonatal Hypoxia-Ischemia and Therapeutic Hypothermia and Deficits in Spatial Memory

Figshare (2019)

Janasha Goffigan‐Holmes D Sanabria Juan José Pérez Díaz D. K. Flock Raul Chavez‐Valdez

Hippocampal injury following neonatal hypoxia-ischemia (HI) leads to memory impairments despite therapeutic hypothermia (TH). In the hippocampus, the expression of calbindin-1 (Calb1), a Ca²⁺-buffering protein, increases during postnatal development and decreases with aging and neurodegenerative disorders. Since persistent Ca²⁺ dysregulation after HI may lead to ongoing injury, persistent changes in hippocampal expression of Calb1 may contribute to memory impairments after neonatal HI. We hypothesized that, despite TH, neonatal HI persistently decreases Calb1 expression in the hippocampus, a change associated with memory deficits in the mouse. We induced cerebral HI in C57BL6 mice at postnatal day 10 (P10) with right carotid ligation and 45 min of hypoxia (FiO₂ = 0.08), followed by normothermia (36°C, NT) or TH (31°C) for 4 h with anesthesia-shams as controls. Nissl staining and glial fibrillary acidic protein (GFAP) immunohistochemistry (IHC) were used to grade brain injury and astrogliosis at P11, P18, and P40 prior to the assessment of Calb1 expression by IHC. The subset of mice followed to P40 also performed a memory behavior task (Y-maze) at P22–P26. Nonparametric statistics stratified by sex were applied. In both anterior and posterior coronal brain sections, hippocampal Calb1 expression doubled between P11 and P40 due to an increase in the cornus ammonis (CA) field (Kruskal-Wallis [KW] p < 0.001) and not the dentate gyrus (DG). Neonatal HI produced delayed (P18) and late (P40) deficits in the expression of Calb1 exclusively in the CA field (KW p = 0.02) in posterior brain sections. TH did not attenuate Calb1 deficits after HI. Thirty days after HI injury (at P40), GFAP scores in the hippocampus (p < 0.001, r = –0.47) and CA field (p < 0.001, r = –0.39) of posterior brain sections inversely correlated with their respective Calb1 expression. Both sexes demonstrated deficits in Y-maze testing, including approximately 40% lower spontaneous alterations performance and twice as much total impairment compared to sham mice (KW p < 0.001), but it was only in females that these deficits correlated with the Calb1 expression in the hippocampal CA field (p < 0.05) of the posterior sections. Hippocampal atrophy after neonatal HI also correlated with worse deficits in Y-maze testing, but it did not predict Calb1 deficits. Neonatal HI produces a long-lasting Calb1 deficit in the hippocampal CA field during development, which is not mitigated by TH. Late Calb1 deficit after HI may be the result of persistent astrogliosis and can lead to memory impairment, particularly in female mice.

Hypoxia

10.6084/m9.figshare.7831544

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Orthostatic Hypotension and Syncope in a Patient with Pheochromocytoma

Syncope Cases (2006)

B. Daga Calejero Ethel Ibáñez-Echevarría A. Carmona Ainat A. Sánchez Val Juan José Pérez Díaz

10.1002/9780470995013.ch52

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CARDIAC PERFORMANCE PRESERVED IN SPITE OF THIOPENTAL LOADING

Anesthesiology (1992)