High-altitude exposures and intestinal barrier dysfunction.

Gastrointestinal complaints are often reported during ascents to high altitude (>2,500 m), though their etiology is not known. One potential explanation is injury to the intestinal barrier which has been implicated in the pathophysiology of several diseases. High-altitude exposures can reduce splanchnic perfusion and blood oxygen levels causing hypoxic and oxidative stress. These stressors might injure the intestinal barrier leading to consequences such as bacterial translocation and local/systemic inflammatory responses. The purpose of this mini-review is to 1) discuss the impact of high-altitude exposures on intestinal barrier dysfunction and 2) present medications and dietary supplements which may have relevant impacts on the intestinal barrier during high-altitude exposures. There is a small but growing body of evidence which shows that acute exposures to high altitudes can damage the intestinal barrier. Initial data also suggest that prolonged hypoxic exposures can compromise the intestinal barrier through alterations in immunological function, microbiota, or mucosal layers. Exertion may worsen high-altitude-related intestinal injury via additional reductions in splanchnic circulation and greater hypoxemia. Collectively these responses can result in increased intestinal permeability and bacterial translocation causing local and systemic inflammation. More research is needed to determine the impact of various medications and dietary supplements on the intestinal barrier during high-altitude exposures.

Insulin resistance is improved in high-fat fed mice by photobiomodulation therapy at 630 nm.

Photobiomodulation therapy (PBMT) in the infrared spectrum exerts positive effects on glucose metabolism, but the use of PBMT at the red spectrum has not been assessed. Male Swiss albino mice were divided into low-fat control and high-fat diet (HFD) for 12 weeks and were treated with red (630 nm) PBMT or no treatment (Sham) during weeks 9 to 12. PBMT was delivered at 31.19 J/cm2 , 60 J total dose per day for 20 days. In HFD-fed mice, PBMT improved glucose tolerance, insulin resistance and fasting hyperinsulinemia. PBMT also reduced adiposity and inflammatory infiltrate in adipose tissue. Phosphorylation of Akt in epididymal adipose tissue and rectus femoralis muscle was improved by PBMT. In epididymal fat PBMT reversed the reduced phosphorylation of AS160 and the reduced Glut4 content. In addition, PBMT reversed the alterations caused by HFD in rectus femoralis muscle on proteins involved in mitochondrial dynamics and ß-oxidation. In conclusion, PBMT at red spectrum improved insulin resistance and glucose metabolism in HFD-fed mice.

The Effect of Acute Glutamine Supplementation on Markers of Inflammation and Fatigue During Consecutive Days of Simulated Wildland Firefighting.

OBJECTIVE: To examine the effect of oral glutamine supplementation on inflammation and fatigue during and after simulated wildland firefighting (WLFF) tasks in hot conditions over 2 consecutive days. METHODS: Eleven men and women ingested a glutamine supplement or a placebo before and after simulated wildland firefighting in an environmental chamber (38 °C, 35% relative humidity). Subjective fatigue, markers of inflammation, and cellular stress were measured pre, post and 4 hours post-exercise on both days. RESULTS: Gastrointestinal damage, subjective fatigue, and ratings of perceived exertion were lower after glutamine supplementation compared with placebo. Heat shock protein 70 (HSP70) and nuclear factor kappa-inhibitor alpha (IκBα) levels were higher on both days of the glutamine trial compared with placebo. CONCLUSIONS: Glutamine supplementation may improve recovery after fire suppression in WLFFs. This may result from the upregulation of HSP70 which inhibits inflammation and protects against gastrointestinal (GI) barrier damage.

Association Between Exercise-Induced Hyperthermia and Intestinal Permeability: A Systematic Review.

BACKGROUND: Prolonged and strenuous physical exercise increases intestinal permeability, allowing luminal endotoxins to translocate through the intestinal barrier and reach the bloodstream. When recognized by the immune system, these endotoxins trigger a systemic inflammatory response that may affect physical performance and, in severe cases, induce heat stroke. However, it remains to be elucidated whether there is a relationship between the magnitude of exercise-induced hyperthermia and changes in intestinal permeability. OBJECTIVE: In this systematic review, we evaluated whether an exercise-induced increase in core body temperature (T Core) is associated with an exercise-induced increase in intestinal permeability. METHODS: The present systematic review screened the MEDLINE/PubMed and Web of Science databases in September 2016, without any date restrictions. Sixteen studies that were performed in healthy participants, presented original data, and measured both the exercise-induced changes in T Core and intestinal permeability were selected. These studies assessed intestinal permeability through the measurement of sugar levels in the urine and measurement of intestinal fatty acid binding protein or lipopolysaccharide levels in the blood. RESULTS: Exercise increased both T Core and intestinal permeability in most of the 16 studies. In addition, a positive and strong correlation was observed between the two parameters (r = 0.793; p < 0.001), and a T Core exceeding 39 °C was always associated with augmented permeability. CONCLUSION: The magnitude of exercise-induced hyperthermia is directly associated with the increase in intestinal permeability.

Palm cooling does not reduce heat strain during exercise in a hot, dry environment.

To compare the effectiveness of the rapid thermal exchange device (RTX) in slowing the development of hyperthermia and associated symptoms among hand immersed in water bath (WB), water-perfused vest (WPV), and no cooling condition (NC). Ten subjects performed 4 heat stress trials. The protocol consisted of 2 bouts of treadmill walking, separated by a cooling-rehydration period. The times to reach the predetermined rectal temperature in the first (38.5 degrees C) and second bouts (39 degrees C) were not different among RTX, NC, and WB, but was longer for the WPV in both bouts (p<0.05). Heat storage was significantly lower for WPV only in the first bout vs. the other conditions (p<0.05). Heart rate (HR) was not different at 10, 20, and 30 min during the first bout among RTX, NC, and WB, but was lower for WPV (p<0.05). HR was not different among conditions during the second bout. The RTX was not effective in slowing the development of hyperthermia.