Physiological responses in a simulated canarian wrestling contest

La Lucha Canaria (LC) ha sido recientemente reconocida como deporte por el Consejo Superior de Deportes, aunque su origen se pierde en el tiempo. Sin embargo, no hay ningún trabajo en la bibliografía científica que describa qué ocurre fisiológicamente durante la competición en esta modalidad de lucha, y éste es el objetivo del presente trabajo. Con una muestra de 12 luchadores de alto nivel (puntales) simulamos el sistema de competición actual en Lucha Canaria. Se estudió la frecuencia cardiaca, la tensión arterial y la concentración de lactato en sangre en diferentes momentos de la simulación. Los patrones observados de respuesta de FC, TA y lactato, caracterizan a la competición en LC como un ejercicio intermitente, con picos de intensidad que superan el umbral láctico y determinan incrementos importantes de FC y TA sistólica. Este estudio es el primero en que se valora la respuesta fisiológica del luchador canario en competición.The aim of this article is to describe what happens from a physiological point of view in a Canarian Wrestling (CW) contest. The Spanish National Sports Council recognized Canarian Wrestling as a sport on June 1st, 2009, although its origin is not very well documented. No scientific article exists in the scientific literature to describe what happens physiologically during a CW contest. Twelve high level wrestlers were recruited to simulate a CW match. The study involved data about heart rate (HR), blood pressure (BP) and blood lactate levels (L) at different moments of the combat. The conclusions of the data observed concerning HR, BP and L classify Canarian Wrestling as an intermittent exercise, with intensity peaks that exceed the lactic threshold and high levels of HR and systolic BP. This is the first paper in which the physiological responses in a Canarian Wrestling competition are reported

Incidence, clinical characteristics and management of inflammatory bowel disease in Spain: large-scale epidemiological study

(1) Aims: To assess the incidence of inflammatory bowel disease (IBD) in Spain, to describe the main epidemiological and clinical characteristics at diagnosis and the evolution of the disease, and to explore the use of drug treatments. (2) Methods: Prospective, population-based nationwide registry. Adult patients diagnosed with IBD—Crohn’s disease (CD), ulcerative colitis (UC) or IBD unclassified (IBD-U)—during 2017 in Spain were included and were followed-up for 1 year. (3) Results: We identified 3611 incident cases of IBD diagnosed during 2017 in 108 hospitals covering over 22 million inhabitants. The overall incidence (cases/100, 000 person-years) was 16 for IBD, 7.5 for CD, 8 for UC, and 0.5 for IBD-U; 53% of patients were male and median age was 43 years (interquartile range = 31–56 years). During a median 12-month follow-up, 34% of patients were treated with systemic steroids, 25% with immunomodulators, 15% with biologics and 5.6% underwent surgery. The percentage of patients under these treatments was significantly higher in CD than UC and IBD-U. Use of systemic steroids and biologics was significantly higher in hospitals with high resources. In total, 28% of patients were hospitalized (35% CD and 22% UC patients, p < 0.01). (4) Conclusion: The incidence of IBD in Spain is rather high and similar to that reported in Northern Europe. IBD patients require substantial therapeutic resources, which are greater in CD and in hospitals with high resources, and much higher than previously reported. One third of patients are hospitalized in the first year after diagnosis and a relevant proportion undergo surgery. © 2021 by the authors. Licensee MDPI, Basel, Switzerland

Effect of hypertension on the angiotensin II fibres arriving at the posterior lobe of the hypophysis of the rat. An immunohistochemical study

We studied immunohistochemically the posterior lobe of the hypophysis (PL) of 15-week-old spontaneously hypertensive rats (SHR) and of matched normotensive Wistar Kyoto rats (WKY), by using our own polyclonal antibody raised in mice against Angiotensin I1 (mouse-antiangiotensin 11, MAAII). The blood pressure, water intake and volume of the PL were also recorded. The SHR rats were hypertensive, drank more water and showed a clear hypertrophy of their hypophysial PL. Also the PL of the SHR animals showed an increase in the immunoreactivity to the antiangiotensin I1 antibody in the fibres arriving at the PL, with respect to the PL of WKY rats. This increase is compatible with the hyperactivity of the brain RAS, depletion of vasopressin content in the PL and increase in plasmatic levels of vasopressin described in SHR rats with respect to normotensive animals, as angiotensin I1 could locally stimulate vasopressin release to plasma from the neurohypophysis

Effects of alcohol and aging on the cingular (area 24) and frontal (area 6) cortical areas of the mouse

We have studied the morphometric changes of the neurons of the cingular area 24 and frontal area 6 of the mouse, produced by age andlor chronic alcohol intake. The parameters analyzed were nuclear area of these cortical neurons and cellular density (celllneuropil coefficient). Wc dctccted a decrease in the number of neurons with age in practically al1 layers of the control animals. In the animals that chronically ingested the alcoholic solution, we also detected a decrease in the number of neurons with age, but only in layer V of the frontal cortex and in layer VI of the cingular area 24. The comparison between the control and the alcoholic group showed that alcohol intake caused an incrcasc in the nuclear area of the neurons in layer 11-111 of the frontal cortcx at 180 days, while in the cingular cortex the increase in nuclear area of its neurons was significative at 180 days in layer 11-111 and at 35 and 180 days in layers V and VI. We think that these changes are the expression of the neurona1 plasticity in both cortical areas in response to the alcohol exposure

The effects of chronic administration of captopril on the mouse median eminence

The effects of Captopril (an angiotensinconverting enzyme inhibitor) on the median eminence (ME) of the male albino mouse have been examined using morphometric and immunohistochemical procedures. We measured the nuclear area of the ependymocytes of the ME and of the glial cells of the reticular external zone of the ME. We also determined the cell/neuropil coefficient (CNC), which expreses the relation between cellular area and neuropil of the ME, and the global volume of the ME in each animal. For the immunohistochemical study we used rabbit antiarginine- vasopressin, and compared the results in the different groups of mice. We detected an increase in the immunoreactive material (arginine-vasopressin, A-V) and an increase in the global volume of the organ and also an increase of the neuropil of the ME after the longest exposure to the drug. These alterations could be related to the inhibition of the brain angiotensin 11 by captopril and the accumulation of vasopressin in the fibrous tract that runs from the paraventricular nucleus (PVN) to the neurohypophysis

Effect of hypertension on the angiotensin II fibres arriving at the posterior lobe of the hypophysis of the rat. An immunohistochemical study

We studied immunohistochemically the posterior lobe of the hypophysis (PL) of 15-week-old spontaneously hypertensive rats (SHR) and of matched normotensive Wistar Kyoto rats (WKY), by using our own polyclonal antibody raised in mice against Angiotensin I1 (mouse-antiangiotensin 11, MAAII). The blood pressure, water intake and volume of the PL were also recorded. The SHR rats were hypertensive, drank more water and showed a clear hypertrophy of their hypophysial PL. Also the PL of the SHR animals showed an increase in the immunoreactivity to the antiangiotensin I1 antibody in the fibres arriving at the PL, with respect to the PL of WKY rats. This increase is compatible with the hyperactivity of the brain RAS, depletion of vasopressin content in the PL and increase in plasmatic levels of vasopressin described in SHR rats with respect to normotensive animals, as angiotensin I1 could locally stimulate vasopressin release to plasma from the neurohypophysis

The effects of chronic administration of captopril on the mouse median eminence

The effects of Captopril (an angiotensinconverting enzyme inhibitor) on the median eminence (ME) of the male albino mouse have been examined using morphometric and immunohistochemical procedures. We measured the nuclear area of the ependymocytes of the ME and of the glial cells of the reticular external zone of the ME. We also determined the cell/neuropil coefficient (CNC), which expreses the relation between cellular area and neuropil of the ME, and the global volume of the ME in each animal. For the immunohistochemical study we used rabbit antiarginine- vasopressin, and compared the results in the different groups of mice. We detected an increase in the immunoreactive material (arginine-vasopressin, A-V) and an increase in the global volume of the organ and also an increase of the neuropil of the ME after the longest exposure to the drug. These alterations could be related to the inhibition of the brain angiotensin 11 by captopril and the accumulation of vasopressin in the fibrous tract that runs from the paraventricular nucleus (PVN) to the neurohypophysis

Effects of alcohol and aging on the cingular (area 24) and frontal (area 6) cortical areas of the mouse

We have studied the morphometric changes of the neurons of the cingular area 24 and frontal area 6 of the mouse, produced by age andlor chronic alcohol intake. The parameters analyzed were nuclear area of these cortical neurons and cellular density (celllneuropil coefficient). Wc dctccted a decrease in the number of neurons with age in practically al1 layers of the control animals. In the animals that chronically ingested the alcoholic solution, we also detected a decrease in the number of neurons with age, but only in layer V of the frontal cortex and in layer VI of the cingular area 24. The comparison between the control and the alcoholic group showed that alcohol intake caused an incrcasc in the nuclear area of the neurons in layer 11-111 of the frontal cortcx at 180 days, while in the cingular cortex the increase in nuclear area of its neurons was significative at 180 days in layer 11-111 and at 35 and 180 days in layers V and VI. We think that these changes are the expression of the neurona1 plasticity in both cortical areas in response to the alcohol exposure