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

2019 ◽  
Vol 127 (6) ◽  
pp. 1511-1518 ◽  
Author(s):  
Justin S. Lawley ◽  
Hannes Gatterer ◽  
Katrin A. Dias ◽  
Erin J. Howden ◽  
Satyam Sarma ◽  
...  

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 ~3 h.

2012 ◽  
Vol 113 (3) ◽  
pp. 434-441 ◽  
Author(s):  
K. A. Zuj ◽  
H. Edgell ◽  
J. K. Shoemaker ◽  
M. A. Custaud ◽  
P. Arbeille ◽  
...  

This study tested the hypothesis that cardiovascular effects of sublingual nitroglycerin (NG) would be exaggerated after 56 days of 6° head-down bed rest (HDBR) in women, and that an aerobic and resistive exercise countermeasure (EX, n = 8) would reduce the effect compared with HDBR without exercise (CON, n = 7). Middle cerebral artery maximal blood flow velocity (CBFV), cardiac stroke volume (SV), and superficial femoral artery blood flow (Doppler ultrasound) were recorded at baseline rest and for 5 min following 0.3 mg sublingual NG. Post-HDBR, NG caused greater increases in heart rate (HR) in CON compared with EX (+24.9 ± 7.7 and +18.8 ± 6.6 beats/min, respectively, P < 0.0001). The increase in HR combined with reductions in SV to maintain cardiac output. Systolic, mean, and pulse pressures were reduced 5–10 mmHg by NG, but total peripheral resistance was only slightly reduced at 3 min after NG. Reductions in CBFV of −12.5 ± 3.8 cm/s were seen after NG, but a reduction in the Doppler resistance index suggested dilation of the middle cerebral artery with no differences after HDBR. The femoral artery dilated with NG and blood flow was reduced ∼50% with the appearance of large negative waves suggesting a marked increase in downstream resistance, but there were no effects of HDBR. In general, responses of women to NG were not altered by HDBR; the greater increase in HR in CON but not EX was probably a consequence of cardiovascular deconditioning. These results contrast with the hypothesis and a previous investigation of men after HDBR by revealing no change in cardiovascular responses to exogenous nitric oxide.


2011 ◽  
Vol 110 (3) ◽  
pp. 670-680 ◽  
Author(s):  
Nan Liang ◽  
Tomoko Nakamoto ◽  
Seina Mochizuki ◽  
Kanji Matsukawa

To examine whether central command contributes differently to the cardiovascular responses during voluntary static exercise engaged by different muscle groups, we encouraged healthy subjects to perform voluntary and electrically evoked involuntary static exercise of ankle dorsal and plantar flexion. Each exercise was conducted with 25% of the maximum voluntary force of the right ankle dorsal and plantar flexion, respectively, for 2 min. Heart rate (HR) and mean arterial blood pressure (MAP) were recorded, and stroke volume, cardiac output (CO), and total peripheral resistance were calculated. With voluntary exercise, HR, MAP, and CO significantly increased during dorsal flexion (the maximum increase, HR: 12 ± 2.3 beats/min; MAP: 14 ± 2.0 mmHg; CO: 1 ± 0.2 l/min), whereas only MAP increased during plantar flexion (the maximum increase, 6 ± 2.0 mmHg). Stroke volume and total peripheral resistance were unchanged throughout the two kinds of voluntary static exercise. With involuntary exercise, there were no significant changes in all cardiovascular variables, irrespective of dorsal or plantar flexion. Furthermore, before the force onset of voluntary static exercise, HR and MAP started to increase without muscle contraction, whereas they had no significant changes with involuntary exercise at the moment. The present findings indicate that differential contribution of central command is responsible for the different cardiovascular responses to static exercise, depending on the strength of central control of the contracting muscle.


2011 ◽  
Vol 89 (9) ◽  
pp. 639-646 ◽  
Author(s):  
Ahmmed Ally ◽  
Timothy J. Maher

A major cause of stroke is cerebral ischemia in regions supplied by the middle cerebral artery (MCA). In this study, we hypothesized that compromised cardiovascular function during static exercise may involve altered expression of inducible NOS (iNOS) protein within the rostral ventrolateral medulla (RVLM) and caudal ventrolateral medulla (CVLM). We compared cardiovascular responses and iNOS protein expression within the left and right sides of both RVLM and CVLM in sham-operated rats and in rats with a 90 min left-sided MCA occlusion (MCAO) followed by 24 h of reperfusion. Increases in blood pressure during a static muscle contraction were attenuated in MCAO rats compared with sham-operated rats. Also, iNOS expression within the left RVLM was augmented compared with the right RVLM in MCAO rats and compared with both RVLM quadrants in sham-operated rats. In contrast, compared with sham-operated rats and the right CVLM of MCAO rats, iNOS expression was attenuated in the left CVLM in left-sided MCAO rats. These data suggest that the attenuation of pressor responses during static exercise in MCAO rats involves overexpression of iNOS within the ipsilateral RVLM and attenuation in iNOS within the ipsilateral CVLM. Differential expression of iNOS within the medulla plays a role in mediating cardiovascular responses during static exercise following stroke.


Cephalalgia ◽  
2019 ◽  
Vol 40 (3) ◽  
pp. 266-277
Author(s):  
Willebrordus PJ van Oosterhout ◽  
Guus G Schoonman ◽  
Dirk P Saal ◽  
Roland D Thijs ◽  
Michel D Ferrari ◽  
...  

Introduction Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. Methods In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg−1·min−1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. Results Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls ( p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. Discussion Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.


1992 ◽  
Vol 262 (6) ◽  
pp. H1802-H1808 ◽  
Author(s):  
M. Huang ◽  
R. L. Hester ◽  
A. C. Guyton ◽  
R. A. Norman

We determined the cardiovascular responses in normal and deoxycorticosterone acetate (DOCA)-salt hypertensive rats with reduced total peripheral resistance due to an arteriovenous (a-v) fistula. Animals were divided into four groups: control, fistula, DOCA-salt, and DOCA-salt fistula. The fistula was made by anastomosing the aorta and vena cava below the renal arteries. Four weeks after the creation of the fistula both DOCA-salt and DOCA-salt fistula animals received DOCA and salt for 6–8 wk. At the end of 10–12 wk we measured mean arterial pressure, cardiac output, tissue flows, and right atrial pressure. Flow measurements using radioactive microspheres were made in anesthetized animals. Cardiac index (CI) was 202% higher in the fistula group than in the control animals and 165% higher in the DOCA-salt fistula than in the DOCA-salt animals. There was no difference in cardiac output between the control and DOCA-salt animals. The increase in cardiac output was due to the fistula flow as evidenced by a significant increase in the number of microspheres in the lung. Mean arterial pressure was 115 +/- 4 mmHg (control) and 108 +/- 5 mmHg (fistula) in non-DOCA rats but increased in both DOCA groups, 159 +/- 3 mmHg (DOCA-salt) and 145 +/- 5 mmHg (DOCA-salt fistula). Right atrial pressure was increased above control in both fistula animals but was normal in DOCA-salt animals. Total peripheral resistance (TPR) was higher than control in DOCA-salt animals, but TPR in both the fistula and DOCA-salt fistula animals was lower than control.(ABSTRACT TRUNCATED AT 250 WORDS)


1965 ◽  
Vol 209 (6) ◽  
pp. 1069-1074 ◽  
Author(s):  
V. P. Popovic ◽  
Kenneth M. Kent

Rats cooled to a body temperature of 15 C live for 9–10 hr. However, they do not survive the rewarming if the hypothermia has lasted more than 5 hr. Neither the cause of death in hypothermia after 10 hr, nor the cause of resuscitation failure of animals rewarmed after 5 hr in hypothermia is known. In 31 rats cooled to and maintained at a body temperature of 15 C, cardiac output decreased continually during the entire period of hypothermia, having by the end of hypothermic survival the value of only 25% of output at the beginning of the hypothermic period. The arteriovenous differences of O2 content increased, while total peripheral resistance increased continuously during this time. During the 10 hr of hypothermic survival the hematocrit ratio rose from 42 to 65–70 vol %. Because of these changes it is suggested here that the failure of circulation is the probable cause of death in hypothermia.


2008 ◽  
Vol 33 (2) ◽  
pp. 246-253 ◽  
Author(s):  
Jessica M. Scott ◽  
Ben T.A. Esch ◽  
Sarah-Jane C. Lusina ◽  
Donald C. McKenzie ◽  
Michael S. Koehle ◽  
...  

We tested the hypothesis that following an acute bout of exercise cardiovascular and cerebrovascular responses to lower-body negative pressure (LBNP) would be altered due to post-exercise hypotension (PEH). Ten healthy, male, endurance-trained athletes (mean age ± SD = 29.6 ± 5) were assessed for cardiovascular and cerebrovascular responses to LBNP following acute bouts of interval and continuous exercise. Mean arterial pressure (MAP), cardiac output, total peripheral resistance, heart rate variability, and total cerebral oxygen index were determined during a baseline LBNP session. These indices were also determined during two other LBNP sessions: following an acute bout of interval exercise, and following an acute bout of continuous exercise. Compared with baseline, MAP was reduced after both exercise conditions, similar to values previously reported (10 mmHg; p < 0.05 vs. pre-exercise). Total peripheral resistance was significantly reduced following both exercise bouts, and heart rate was significantly increased post-exercise (rest: 59.6 ± 11.2; interval: 77.8 ± 12.8; continuous: 80.3 ± 15.2 beats·min–1). Both cardiac output and stroke volume responses to LBNP following exercise were not altered when compared with baseline measurements. Tissue oxygenation during –40 mmHg (interval: 74.31% ± 7.82% vs. continuous: 69.13% ± 5.23%) was significantly lower than during normobaric pressure (interval: 77.14% ± 1.30% vs. continuous: 74.41% ± 0.94%). It appears from these observations that although young, endurance-trained males experience PEH following acute bouts of interval or continuous exercise, this hypotension does not alter the cardiovascular and cerebrovascular responses to a moderate orthostatic stress.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Mark Willems ◽  
Pelin Bilgic ◽  
Stefano Montanari ◽  
Mehmet Sahin

Abstract Objectives New Zealand blackcurrant (NZBC) is an anthocyanin-rich berry with potential effects on cardiovascular health (e.g., 7-day NZBC extract lowered total peripheral resistance at rest). We examined effects of 7- and 14-day intake of NZBC extract on cardiovascular responses during moderate intensity exercise. Methods Fifteen healthy men (mean ± SD, age: 24 ± 6 yr, body mass: 79 ± 16 kg, height: 178 ± 6 cm, BMI: 24.7 ± 4.3 kg·m−2, IPAQ score: 4534 ± 1576 MET·week−1) volunteered. Resting metabolic equivalent (1-MET) was measured using Douglas bags (1-MET: 3.97 ± 0.66 ml·kg−1·min−1) with an incremental walking test to determine the relationship between walking speed and MET. A randomised, cross-over experimental design was used for baseline, 7-day and 14-day intake. Participants consumed 2 capsules of NZBC extract (600 mg and containing 210 mg of anthocyanins, CurraNZ™ Health Currancy Ltd., UK) with breakfast with a 14-day washout. On the morning of testing, the final 2 capsules were ingested 2-hr before the 30-min walk at 4 (n = 3) or 5 (n = 12) METs (speed: 5.68 ± 0.67 km·hr−1). Cardiovascular responses were measured at 7–10, 17–20 and 27–30 min during the walk (Portapres Model 2), averaged and analysed (ANOVA and post-hoc t-tests). Results Intake duration had no effect on heart rate (e.g., baseline: 102 ± 18 beats·min−1), systolic blood pressure (e.g., baseline 158 ± 18 mm Hg) and ejection time (e.g., baseline: 0.28 ± 0.03 s). Cardiac output (baseline: 11.7 ± 2.0, 7-day: 12.7 ± 2.5, 14-day: 12.7 ± 2.1 L·min−1, P = 0.012) and stroke volume (baseline: 114 ± 13, 7-day: 123 ± 22, 14-day: 126 ± 21 mL·min−1, P = 0.017) were increased, and total peripheral resistance (baseline: 0.51 ± 0.11, 7-day: 0.46 ± 0.17, 14-day: 0.44 ± 0.12 mmHg·L−1·min−1, P = 0.018) and diastolic blood pressure (baseline 71 ± 9, 7-day: 66 ± 10, 14-day: 63 ± 11 mm Hg, P = 0.002) were lower for 7- and 14-day intake. Only 14-day intake resulted in lower mean arterial pressure (baseline: 93 ± 10, 7-day: 89 ± 9, 14-day: 87 ± 11 mm Hg, P = 0.034). Conclusions Beneficial effects of anthocyanin-rich NZBC extract intake on cardiovascular responses during moderate intensity exercise do not require long-duration intake. Funding Sources Health Currancy (UK) Ltd and CurraNZ (NZ) Ltd provided supplements and support for conference attendance with Blackcurrant New Zealand Inc. (NZ).


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