Paridad de género y formación académica en el Poder Judicial

Physical activity and exercise result in a significant elevation in metabolic rate which can as a consequence elevate total body heat accumulation. Thermoregulatory mechanisms are therefore essential to dissipate this accumulated heat load and maintain normal physiological function (Crandall & Gonzalez-Alonso, 2010). Under both passive and active conditions body core temperature is maintained within tight boundaries through complex neurological and hormonal negative feedback mechanisms (Gonzalez-Alonso et al., 2008; Pires et al., 2016). Increases in core temperature elicit specific countermeasures which involve the induction of a sweating response to facilitate evaporative heat loss and via peripheral cutaneous vasodilation. However, these responses may induce significant cardiovascular/haemodynamic challenges that impair central venous return and reduce splanchnic blood flow in line with increases in exercise intensity (Rowell, 2004; Van Wijck et al., 2011).

Mechanistic links between the presentation of gastrointestinal symptoms, and disruption to gut mucosa have been partially ascribed to both passive and exertional tissue hyperthermia (Pals et al.1997). Where exercise occurs under different ambient conditions this may mediate secondary to the thermoregulatory challenge imposed reductions in splanchnic blood flow of up to 80%, due to sympathetic mediated vasoconstriction of the splanchnic vascular bed (Crandall & Gonzalez-Alonso, 2010; van Wijck et al., 2011). Briefly, during moderate to strenuous exercise, the release of noradrenaline and its binding to α-adreno- receptors of the sympathetic nervous system, induces a splanchnic vasoconstriction. Such responses result in an increase in the total splanchnic vascular resistance whilst, at the same time, leading to a reduction in vascular resistance in skeletal muscle and skin. The reduction in splanchnic blood flow being inversely proportional to the percentage of maximal oxygen consumption (V̇O2 max) achieved during exercise performance (Ashton et al., 2003; de Oliveira et al., 2014; Gutekunst et al., 2013). As a result, when blood flow is redirected from the splanchnic region to the skeletal muscle and other active tissues GI ischemia and hypoxia may also result (ter Steege et al., 2012b). Elevations in oxidative stress and nitrosative stress in the GI barrier are considered to be causally associated ( Lambert et al., 2002; Dokladny et al., 2016). These physiological responses have been associated with several frequently expressed GI symptomology such as nausea, vomiting, abdominal pain, and diarrhea although the strength of association is weak to moderate at best (ter Steege et al., 2012a).

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Impairments in splanchnic blood flow under passive, exertional and additional heat stress models seen in literature; may predispose toward build-up of heat in the GI wall and heat mediated disruption to epithelial, mucus and smooth muscle barriers in the (GI) wall (Lambert, 2009; Pires et al., 2016; Selkirk et al., 2008; Zuhl et al., 2014). Mechanistically, hyperthermia-induced morphological disruption of enterocytes and tight junction protein function is noted in rodent models at high gut wall temperatures (≥46 °C) (Lambert et al., 2002). In vitro, temperatures of 38.3°C have been demonstrated to cause damage to Madin- Darby canine kidney epithelial cells (Moseley et al., 1994). Temperature increases in the physiological range from 37 to 41°C also are reported to cause increased permeability in an in vitro intestinal epithelial model through enterocyte cell death, tissue oxidative and nitrosative stress (Bulkley, 1987; Hall et al., 2001; Hayashi et al., 2012; Lambert et al., 2002; Machado et al., 2017; Taylor & Colgan, 2007). However, these responses may be accentuated or attenuated depending upon the athlete’s acclimation to and the severity of the environmental conditions in which exercise is undertaken as well as fluid loss (Costa et al., 2017; Guy et al., 2016; Lambert et al., 2001; Pires et al., 2016).

van Wijck et al. (2011) recently discussed that when exercising in the heat there is an extra loss of the total body water and a decrease in plasma volume due to inadequate fluid intake, which can impair cardiac output, further reducing the blood flow to the gut resulting in intestinal hypoxia. Dehydration levels approximating 2 % of body mass may be sufficient to increase GI permeability (Lambert et al., 2008). Through a process of down regulation of Na+/K+ -ATPase which contributes to normal intestinal fluid balance; fluid balance may be compromised (Lambert et al., 2008). Subsequently, an increased chloride secretion in the enterocyte crypts and decreased sodium absorption in the villus tips [likely due to transient ischemic damage] can lead to a net fluid loss from the small intestine. As noted by others by ensuring the athletes remain relatively hydrated with regular water replacement may mitigate the risk of fluid imbalance effecting intestinal absorption (Costa et al. 2017; de Oliveria et al., 2014; Lambert et al., 2008).

Where core temperature and permeability increase combined with bacterial translocation several authors have ascribed this as a putative mechanism in exertional heat illness and heat stroke, which can in turn result in damage to the organs (Fehrenbach and Schneider, 2006; Selkirk et al., 2008). Marchbank et al. (2010) have indicated that running for as little as 20 minutes at 80 % of V̇O2 max elevates core temperature by ~ 2oC and increases gut permeability by ~250 %. Similarly during longer distance exercise intestinal permeability has been increased after the completion of extended duration runs > 2 h (Snipe et al., 2017),

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half, full and ultra-marathons marathon (Oktedalen et al., 1992; Gill et al., 2015; Stuempfle et al., 2016).

Pires et al. (2016) in a recent systematic review on in vivo alterations to GI permeability suggest that impariements in GI barrier dysfunction may be subject to a ‘critical threshold’ whereby core temperatures of up to 38.0°C ‘may likely facilitate’ increased permeability, whereas temperatures of above 39.0°C ‘definitely induce’ GI permeability (Pires et al., 2016). Although others, have examined GI permeability in the heat and found GI permeability to remain unaffected (Snipe, 2017; Yeh et al., 2013). It should be remembered the hyperthermia reported is a function of the core temperature assessment methods which may influence reported values. Rectal thermometry may underestimate the temperature observed in the small intestine GI wall by up to 0.5-20C due to location difference between rectum and small intestine. Pearson et al. (2012) have suggest a ‘temporal lagging’ with rectal GI measure of temperature relative to pulmonary artery temperature. The implication that the GI tract may be slower to increase in temperature but also slower to cool down upon exercise cessation. As such the rate and extent of small intestine wall temperature changes may precede the core temperature rise and then likely lag behind in terms of enterocyte heat exposure reduction (Pearson et al., 2012).

Figure 2.6 Schematic representation (modified) of the potential contributory factory to GI mediated dysfunction and its potential impact. [After van Wijck et al. (2012) American Journal of Physiology-Gastrointestinal and Liver Physiology 2012, 303, G155-G168].

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