Association of sleep and inflammation in law enforcement

The law enforcement profession has been associated with an increased risk for cardiovascular diseases (CVD), but the mechanisms are unclear. Previous research suggests a mechanism other than traditional CVD risk factors may be an underlying cause. Sleep health has been reported as an issue among LEO. Poor sleep health has been associated with increased CVD risk. Sleep disorders have been shown to increase biomarkers of inflammation. CVD is increasingly being recognized as an inflammatory disease. We sought to further investigate this issue by evaluating the sleep health, CVD risk, mental health, and inflammatory biomarkers of 133 LEO in the Iowa Department of Public Safety to determine if inflammation and sleep play a role in the occupational CVD risk in LEO. Officers were divided into three groups based on their sleep health (GOOD, BRDL, POOR). POOR reported significantly higher shiftwork disorder (P \u3c0.05) than GOOD or BRDL. POOR also had significantly higher depression (Center for Epidemiology Studies Depression Scale), life stress (Perceived Stress Scale), and occupational stress scores (Operational and Organizational Police Stress Questionnaires ) (P \u3c 0.05). No significant differences were found in inflammatory biomarkers or traditional CVD risk factors between GOOD, BRDL, or POOR. In conclusion, sleep disorders may contribute to unfavorable mental health disorders and predispose LEO to negative long-term health consequences including depression and neurodegenerative diseases

Association of sleep and inflammation in law enforcement

The law enforcement profession has been associated with an increased risk for cardiovascular diseases (CVD), but the mechanisms are unclear. Previous research suggests a mechanism other than traditional CVD risk factors may be an underlying cause. Sleep health has been reported as an issue among LEO. Poor sleep health has been associated with increased CVD risk. Sleep disorders have been shown to increase biomarkers of inflammation. CVD is increasingly being recognized as an inflammatory disease. We sought to further investigate this issue by evaluating the sleep health, CVD risk, mental health, and inflammatory biomarkers of 133 LEO in the Iowa Department of Public Safety to determine if inflammation and sleep play a role in the occupational CVD risk in LEO. Officers were divided into three groups based on their sleep health (GOOD, BRDL, POOR). POOR reported significantly higher shiftwork disorder (P <0.05) than GOOD or BRDL. POOR also had significantly higher depression (Center for Epidemiology Studies Depression Scale), life stress (Perceived Stress Scale), and occupational stress scores (Operational and Organizational Police Stress Questionnaires ) (P < 0.05). No significant differences were found in inflammatory biomarkers or traditional CVD risk factors between GOOD, BRDL, or POOR. In conclusion, sleep disorders may contribute to unfavorable mental health disorders and predispose LEO to negative long-term health consequences including depression and neurodegenerative diseases.</p

Safety, hemodynamic effects, and detection of acute xenon inhalation: rationale for banning xenon from sport

This study aimed to quantify the sedative effects, detection rates, and cardiovascular responses to xenon. On 3 occasions, participants breathed xenon (FiXe 30% for 20 min; FiXe 50% for 5 min; FiXe 70% for 2 min) in a nonblinded design. Sedation was monitored by a board-certified anesthesiologist. During 70% xenon, participants were also verbally instructed to operate a manual value with time-to-task failure being recorded. Beat-by-beat hemodynamics were measured continuously by ECG, photoplethysmography, and transcranial Doppler. Over 48 h postadministration, xenon was measured in blood and urine by gas chromatography-mass spectrometry. Xenon caused variable levels of sedation and restlessness. Task failure of the self-operating value occurred at 60-90 s in most individuals. Over the first minute, 50% and 70% xenon caused a substantial reduction in total peripheral resistance (P < 0.05). All dosages caused an increase in cardiac output (P < 0.05). By the end of xenon inhalation, slight hypertension was observed after all three doses (P < 0.05), with an increase in middle cerebral artery velocity (P < 0.05). Xenon was consistently detected, albeit in trace amounts, up to 3 h after all three doses of xenon inhalation in blood and urine with variable results thereafter. Xenon inhalation caused sedation incompatible with self-operation of a breathing apparatus, thus causing a potential life-threatening condition in the absence of an anesthesiologist. Yet, xenon can only be reliably detected in blood and urine up to 3 h postacute dosing. NEW & NOTEWORTHY Breathing xenon in dosages conceivable for doping purposes (FiXe 30% for 20 min; FiXe 50% for 5 min; FiXe 70% for 2 min) causes an initial rapid fall in total peripheral resistance with tachycardia and thereafter a mild hypertension with elevated middle cerebral artery velocity. These dose duration intervals cause sedation that is incompatible with operating a breathing apparatus and can only be detected in blood and urine samples with a high probability for up to similar to 3 h

Effect of acute and chronic xenon inhalation on erythropoietin, hematological parameters, and athletic performance

This study aimed to assess the efficacy of acute subanesthetic dosages of xenon inhalation to cause erythropoiesis and determine the effect of chronic xenon dosing on hematological parameters and athletic performance. To assess the acute effects, seven subjects breathed three subanesthetic concentrations of xenon: 30% fraction of inspired xenon (FIXe) for 20 min, 50% FIXe for 5 min, and 70% FIXe for 2 min. Erythropoietin (EPO) was measured at baseline, during, and after xenon inhalation. To determine the chronic effects, eight subjects breathed 70% FIXe for 2 min on 7 consecutive days, and EPO, total blood, and plasma volume were measured. Phase II involved assessment of 12 subjects for EPO, total blood volume, maximal oxygen uptake, and 3-km time before and after random assignment to 4 wk of xenon or sham gas inhalation. FIXe 50% and 70% stimulated an increase in EPO at 6 h [+2.3 mIU/mL; 95% confidence interval (CI) 0.1-4.5; P = 0.038] and at 192 h postinhalation (+2.9 mIU/mL; 95% CI 0.6-5.1; P = 0.017), respectively. Seven consecutive days of dosing significantly elevated plasma volume (+491 mL; 95% CI 194-789; P = 0.002). Phase II showed no significant effect on EPO, hemoglobin mass, plasma volume, maximal oxygen uptake, or 3-km time. Acute exposure to subanesthetic doses of xenon caused a consistent increase in EPO, and 7 consecutive days of xenon inhalation significantly expanded plasma volume. However, this physiological response appeared to be transient, and 4 wk of xenon inhalation did not stimulate increases in plasma volume or erythropoiesis, leaving cardiorespiratory fitness and athletic performance unchanged. NEW & NOTEWORTHY This is the first study to examine each element of the cascade by which xenon inhalation is purported to take effect, starting with measurement of the hypoxia-inducible factor effector, erythropoietin, to hemoglobin mass and blood volume and athletic performance. We found that acute exposure to xenon increased serum erythropoietin concentration, although major markers of erythropoiesis remained unchanged. While daily dosing significantly expanded plasma volume, no physiological or performance benefits were apparent following 4 wk of dosing