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We examined the extent to which apnoea‐induced extremes of oxygen demand/carbon dioxide production impact redox regulation of cerebral bioenergetic function. Ten ultra‐elite apnoeists (six men and four women) performed two maximal dry apnoeas preceded by normoxic normoventilation, resulting in severe end‐apnoea hypoxaemic hypercapnia, and hyperoxic hyperventilation designed to ablate hypoxaemia, resulting in hyperoxaemic hypercapnia. Transcerebral exchange of ascorbate radicals (by electron paramagnetic resonance spectroscopy) and nitric oxide metabolites (by tri‐iodide chemiluminescence) were calculated as the product of global cerebral blood flow (by duplex ultrasound) and radial arterial (a) to internal jugular venous (v) concentration gradients. Apnoea duration increased from 306 ± 62 s during hypoxaemic hypercapnia to 959 ± 201 s in hyperoxaemic hypercapnia (P ≤ 0.001). Apnoea generally increased global cerebral blood flow (all P ≤ 0.001) but was insufficient to prevent a reduction in the cerebral metabolic rates of oxygen and glucose (P = 0.015–0.044). This was associated with a general net cerebral output (v > a) of ascorbate radicals that was greater in hypoxaemic hypercapnia (P = 0.046 vs. hyperoxaemic hypercapnia) and coincided with a selective suppression in plasma nitrite uptake (a > v) and global cerebral blood flow (P = 0.034 to <0.001 vs. hyperoxaemic hypercapnia), implying reduced consumption and delivery of nitric oxide consistent with elevated cerebral oxidative–nitrosative stress. In contrast, we failed to observe equidirectional gradients consistent with S‐nitrosohaemoglobin consumption and plasma S‐nitrosothiol delivery during apnoea (all P ≥ 0.05). Collectively, these findings highlight a key catalytic role for hypoxaemic hypercapnia in cerebral oxidative–nitrosative stress. Key points: Local sampling of blood across the cerebral circulation in ultra‐elite apnoeists determined the extent to which severe end‐apnoea hypoxaemic hypercapnia (prior normoxic normoventilation) and hyperoxaemic hypercapnia (prior hyperoxic hyperventilation) impact free radical‐mediated nitric oxide bioavailability and global cerebral bioenergetic function.Apnoea generally increased the net cerebral output of free radicals and suppressed plasma nitrite consumption, thereby reducing delivery of nitric oxide consistent with elevated oxidative–nitrosative stress.The apnoea‐induced elevation in global cerebral blood flow was insufficient to prevent a reduction in the cerebral metabolic rates of oxygen and glucose.Cerebral oxidative–nitrosative stress was greater during hypoxaemic hypercapnia compared with hyperoxaemic hypercapnia and coincided with a lower apnoea‐induced elevation in global cerebral blood flow, highlighting a key catalytic role for hypoxaemia.This applied model of voluntary human asphyxia might have broader implications for the management and treatment of neurological diseases characterized by extremes of oxygen demand and carbon dioxide production. [ABSTRACT FROM AUTHOR]

The pathogenesis of predominantly neurological decompression sickness (DCS) is multifactorial. In SCUBA diving, besides gas bubbles, DCS has been linked to microparticle release, impaired endothelial function, and platelet activation. This study focused on vascular damage and its potential role in the genesis of DCS in breath-hold diving. Eleven breath-hold divers participated in a field study comprising eight deep breath-hold dives with short surface periods and repetitive breath-hold dives lasting for 6 h. Endothelium-dependent vasodilation of the brachial artery, via flow-mediated dilation (FMD), and the number of microparticles (MPs) were assessed before and after each protocol. All measures were analyzed by two-way within-subject ANOVA (2 * 2 ANOVA; factors: time and protocol). Absolute FMD was reduced following both diving protocols (p < 0.001), with no interaction (p = 0.288) or main effect of protocol (p = 0.151). There was a significant difference in the total number of circulating MPs between protocols (p = 0.007), where both increased post-dive (p = 0.012). The number of CD31+/CD41- and CD66b+ MP subtypes, although different between protocols (p < 0.001), also increased by 41.0% [+ or -] 56.6% (p = 0.050) and 60.0% [+ or -] 53.2% (p = 0.045) following deep and repetitive breath-hold dives, respectively. Both deep and repetitive breath-hold diving lead to endothelial dysfunction that may play an important role in the genesis of neurological DCS. Key words: endothelial function, flow-mediated dilation, microparticles, venous gas emboli, repetitive breath-hold dive, apnea. La pathogenese du mal de decompression, neurologique de facon predominante, est multifactorielle. En plongee sous-marine, hormis les bulles de gaz, on a lie le mal de decompression a la liberation de microparticules, a un mauvais fonctionnement de l'endothelium, ainsi qu'a l'activation des plaquettes. Cette etude etait centree sur les lesions vasculaires et leur role eventuel dans la genese du mal de decompression pendant la plongee en apnee. Onze plongeurs en apnee ont participe a une etude de terrain comprenant huit plongees en apnee en profondeur avec de courtes periodes a la surface, ainsi que des plongees en apnee repetitives pour une duree totale de 6 h. Nous avons evalue la vasodilatation dependante de l'endothelium de l'artere brachiale par la vasodilatation mediee par le flux et le nombre de MP avant et apres chaque protocole. Nous avons etudie toutes les mesures a l'aide d'une analyse de variance bidirectionnelle avec facteurs << within >> (ANOVA 2 * 2; facteurs : duree et protocole). La vasodilatation mediee par le flux absolue diminuait apres les deux protocoles de plongee (p < 0,001), sans interaction (p = 0,288) ni effet principal du protocole (p = 0,151). Nous avons observe une difference notable dans le nombre de MP en circulation d'un protocole a l'autre (p = 0,007), avec une augmentation post-plongee dans les deux cas (p = 0,012). Les nombres de sous-types CD31+/CD41- et CD66b+ de microparticules, bien que differents d'un protocole a l'autre (p < 0,001), augmentaient aussi de 41,0 % [+ or -] 56,6 % (p = 0,050) et de 60,0 % [+ or -] 53,2 % (p = 0,045) a la suite des plongees en profondeur et repetitives, respectivement. Les plongees en apnee en profondeur et repetitives menent toutes deux a un dysfonctionnement de l'endothelium, lequel pourrait jouer un role important dans la genese du mal de decompression neurologique. [Traduit par la Redaction] Mots-cles : fonction endotheliale, vasodilatation mediee par le flux, microparticules, embolies gazeuses veineuses, plongee en apnee repetitive, apnee., Introduction Decompression sickness (DCS) in SCUBA diving was related to gas bubbles created in tissues, in venous blood (venous gas emboli (VGE) or arterialized gas emboli (AGE)), arising from the [...]

Spinal cord injury (SCI) is associated with an increased risk and prevalence of cardiopulmonary and cerebrovascular disease-related morbidity and mortality. The factors that initiate, promote, and accelerate vascular diseases and events in SCI are poorly understood. Clinical interest in circulating endothelial cell-derived microvesicles (EMVs) and their microRNA (miRNA) cargo has intensified due to their involvement in endothelial dysfunction, atherosclerosis, and cerebrovascular events. The aim of this study was to determine whether a subset of vascular-related miRNAs is differentially expressed in EMVs isolated from adults with SCI. We assessed eight adults with tetraplegia (7 male/1 female; age: 46±4 years; time since injury: 26±5 years) and eight uninjured (6 male/2 female; age: 39±3 years). Circulating EMVs were isolated, enumerated, and collected from plasma by flow cytometry. The expression of vascular-related miRNAs in EMVs was assessed by RT-PCR. Circulating EMV levels were significantly higher (~130%) in adults with SCI compared with uninjured adults. The expression profile of miRNAs in EMVs from adults with SCI were significantly different than uninjured adults and were pathologic in nature. Expression of miR-126, miR-132, and miR-Let-7a were lower (~100–150%; p <.05), whereas miR-30a, miR-145, miR-155, and miR-216 were higher (~125–450%; p <.05) in EMVs from adults with SCI. This study is the first examination of EMV miRNA cargo in adults with SCI. The cargo signature of vascular-related miRNAs studied reflects a pathogenic EMV phenotype prone to induce inflammation, atherosclerosis, and vascular dysfunction. EMVs and their miRNA cargo represent a novel biomarker of vascular risk and a potential target for intervention to alleviate vascular-related disease after SCI. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the values of anaerobic energetic capacity variables in athletes engaged in different sport disciplines and to compare them in relation to specific demands of each sport. Wingate anaerobic tests were conducted on 145 elite athletes (14 boxers, 17 wrestlers, 27 hockey players, 23 volleyball players, 20 handball players, 25 basketball players, and 19 soccer players). Three variables were measured as markers of anaerobic capacity: peak power, mean power, and explosive power. The highest values of peak power were measured in volleyball 11.71 [+ or -] 1.56 W x [kg.sup.-1] and basketball players 10.69 [+ or -] 1.67 W. [kg.sup.-1], and the difference was significant compared with the other athletes (p [greater than or equal to] 0.05). The lowest value of peak power (8.58 [+ or-] 1.56 W.[kg.sup.-1]) was registered in handball players. The mean power variable showed a similar distribution as peak power among groups. The highest values of explosive power were also registered in volleyball 1.75 [+ or -] 0.33 W x [s.sup.-1] x 1.[kg.sup.-1] and basketball players 1.64 [+ or -] 0.35 W x [s.sup.-1] x 1.[kg.sup.-1], but there was no significant difference in values between volleyball players and wrestlers, between boxers and wrestlers, between boxers and basketball players, and between volleyball and hockey players (p > 0.05). The measured results show the influence of anaerobic capacity in different sports and the referral values of these variables for the elite male athletes. Explosive power presented a new dimension of anaerobic power, i.e., how fast maximal energy for power development can be obtained, and its values are high in all sports activities that demand explosiveness and fast maximal energy production. Coaches or other experts in the field could, in the future, find useful to follow and improve, through training process, one of the variables that is most informative for that sport. KEY WORDS explosive power, muscle energetics, wingate test

Cardiovascular diseases (CVD) are highly prevalent in spinal cord injury (SCI), and peripheral vascular dysfunction might be a contributing factor. Recent evidence demonstrates that exposure to heat stress can improve vascular function and reduce the risk of CVD in uninjured populations. We therefore aimed to examine the extent of vascular dysfunction in SCI and the acute effects of passive heating. Fifteen participants with cervical SCI and 15 uninjured control (CON) participants underwent ultrasound assessments of vascular function and venous blood sampling for biomarkers of endothelial activation (i.e., CD62e+) and apoptosis (i.e., CD31+/42b−) before and after a 60-min exposure to lower limb hot water immersion (40°C). In SCI, macrovascular endothelial function was reduced in the brachial artery [SCI: 4.8 (3.2)% vs. CON: 7.6 (3.4)%, P = 0.04] but not the femoral artery [SCI: 3.7 (2.6)% vs. CON: 4.0 (2.1)%, P = 0.70]. Microvascular function, via reactive hyperemia, was ~40% lower in SCI versus CON in both the femoral and brachial arteries (P < 0.01). Circulating concentrations of CD62e+ were elevated in SCI versus CON [SCI: 152 (106) microparticles/µl vs. CON: 58 (24) microparticles/µl, P < 0.05]. In response to heating, macrovascular and microvascular function remained unchanged, whereas increases (+83%) and decreases (−93%) in antegrade and retrograde shear rates, respectively, were associated with heat-induced reductions of CD62e+ concentrations in SCI to levels similar to CON (P = 0.05). These data highlight the potential of acute heating to provide a safe and practical strategy to improve vascular function in SCI. The chronic effects of controlled heating warrant long-term testing.NEW & NOTEWORTHY Individuals with cervical level spinal cord injury exhibit selectively lower flow-mediated dilation in the brachial but not femoral artery, whereas peak reactive hyperemia was lower in both arteries compared with uninjured controls. After 60 min of lower limb hot water immersion, femoral artery blood flow and shear patterns were acutely improved in both groups. Elevated biomarkers of endothelial activation in the spinal cord injury group decreased with heating, but these biomarkers remained unchanged in controls. [ABSTRACT FROM AUTHOR]

The capacity of the cerebrovasculature to buffer changes in blood pressure (BP) is crucial to prevent stroke, the incidence of which is three- to fourfold elevated after spinal cord injury (SCI). Disruption of descending sympathetic pathways within the spinal cord due to cervical SCI may result in impaired cerebrovascular buffering. Only linear analyses of cerebrovascular buffering of BP, such as transfer function, have been used in SCI research. This approach does not account for inherent nonlinearity and nonstationarity components of cerebrovascular regulation, often depends on perturbations of BP to increase the statistical power, and does not account for the influence of arterial CO2 tension. Here, we used a nonlinear and nonstationary analysis approach termed wavelet decomposition analysis (WDA), which recently identified novel sympathetic influences on cerebrovascular buffering of BP occurring in the ultra-low-frequency range (ULF; 0.02-0.03Hz). WDA does not require BP perturbations and can account for influences of CO2 tension. Supine resting beat-by-beat BP (Finometer), middle cerebral artery blood velocity (transcranial Doppler), and end-tidal CO2 tension were recorded in cervical SCI (n = 14) and uninjured (n = 16) individuals. WDA revealed that cerebral blood flow more closely follows changes in BP in the ULF range (P = 0.0021, Cohen's d = 0.89), which may be interpreted as an impairment in cerebrovascular buffering of BP. This persisted after accounting for CO2. Transfer function metrics were not different in the ULF range, but phase was reduced at 0.07-0.2 Hz (P = 0.03, Cohen's d = 0.31). Sympathetically mediated cerebrovascular buffering of BP is impaired after SCI, and WDA is a powerful strategy for evaluating cerebrovascular buffering in clinical populations. [ABSTRACT FROM AUTHOR]

Introduction: Arterialization of venous gas emboli (VGE) formed after surfacing from SCUBA diving can become arterial gas emboli (AGE) through intrapulmonary arterial-venous anastomoses that open with exercise. Methods: We recmited twenty patent foramen ovale-negative SCUBA divers and conducted a field and a laboratory study with the aim of investigating the appearance of AGE in intracranial vessels. At the field, they performed a single dive to a depth of 18-m sea water with a 47-min bottom time and a direct ascent to the surface. Transthoracic echocardiography was used to score VGE and AGE, and transcranial Doppler was used to visualize middle and posterior cerebral arteries with automated objective bubble detection. Observations were conducted for 45-min after dive at rest and at the laboratory after agitated saline injection at rest and throughout an incremental cycle supine exercise test until exhaustion and for 10 min of recovery. Results: After resurfacing, all divers presented endogenous VGE and arterialization was present in three divers. Saline contrast injection led to AGE in nine of 19 subjects at rest. AGE that reached the cerebral arteries after dive were recorded in two divers at 60 W, three at 90 W, five at 120 W, six at 150 W, and four at 180 W and in three, four, five, nine, and nine, respectively, after saline contrast injection in the laboratory. All divers had AGE grades of 1 or 2, and only single AGE reached the cerebral vasculature. Conclusions: These data suggest that few emboli of venous origin reach the brain through exercise-induced intrapulmonary arterial-venous anastomoses but cerebral embolization is not high risk in the studied population. [ABSTRACT FROM AUTHOR]

Predicated on evidence that diving-related microparticle generation is an oxidative stress response, this study investigated the role that oxygen plays in augmenting production of annexin V-positive microparticles associated with open-water SCUBA diving and whether elevations can be abrogated by ascorbic acid. Following a cross-over study design, 14 male subjects ingested placebo and 2-3 wk later ascorbic acid (2 g) daily for 6 days prior to performing either a 47-min dive to 18 m of sea water while breathing air (~222 kPa N2/59 kPa O2) or breathing a mixture of 60% O2/balance N2 from a tight-fitting face mask at atmospheric pressure for 47 min (~40 kPa N2/59 kPa O2). Within 30 min after the 18-m dive in the placebo group, neutrophil activation, and platelet-neutrophil interactions occurred, and the total number of microparticles, as well as subgroups bearing CD66b, CD41, CD31, CD142 proteins or nitrotyrosine, increased approximately twofold. No significant elevations occurred among divers after ingesting ascorbic acid, nor were elevations identified in either group after breathing 60% O2. Ascorbic acid had no significant effect on post-dive intravascular bubble production quantified by transthoracic echocardiography. We conclude that high-pressure nitrogen plays a key role in neutrophil and microparticle-associated changes with diving and that responses can be abrogated by dietary ascorbic acid supplementation. [ABSTRACT FROM AUTHOR]

The effects of different recovery protocols on heart rate recovery (HRR) trend through fitted heart rate (HR) decay curves were assessed. Twenty one trained male athletes and 19 sedentary male students performed a submaximal cycle exercise test on four occasions followed by 5 min: 1) inactive recovery in the upright seated position, 2) active (cycling) recovery in the upright seated position, 3) supine position, and 4) supine position with elevated legs. The HRR was assessed as the difference between the peak exercise HR and the HR recorded following 60 seconds of recovery (HRR60). Additionally the time constant decay was obtained by fitting the 5 minute post-exercise HRR into a first-order exponential curve. Within-subject differences of HRR60 for all recovery protocols in both groups were significant (p < 0.001) except for the two supine positions (p > 0.05). Values of HRR60 were larger in the group of athletes for all conditions (p < 0.001). The time constant of HR decay showed within-subject differences for all recovery conditions in both groups (p < 0.01) except for the two supine positions (p > 0.05). Between group difference was found for active recovery in the seated position and the supine position with elevated legs (p < 0.05). We conclude that the supine position with or without elevated legs accelerated HRR compared with the two seated positions. Active recovery in the seated upright position was associated with slower HRR compared with inactive recovery in the same position. The HRR in athletes was accelerated in the supine position with elevated legs and with active recovery in the seated position compared with non-athletes. [ABSTRACT FROM AUTHOR]

The purpose of this study was to assess the effect of three different body positions on HRV measures following short-term submaximal exercise. Thirty young healthy males performed submaximal cycling for five minutes on three different occasions. Measures of HRV were obtained from 5-min R to R wave intervals before the exercise (baseline) and during the last five minutes of a 15 min recovery (post-exercise) in three different body positions (seated, supine, supine with elevated legs). Measures of the mean RR normal-to-normal intervals (RRNN), the standard deviation of normal-to-normal intervals (SDNN), the root mean square of successive differences (RMSSD) and the low-frequency (LF) and the high-frequency (HF) spectral power were analyzed. Post-exercise RRNN, RMSSD were significantly higher in the two supine positions (p < 0.01) compared with seated body position. Post-exercise ln LF was significantly lower in the supine position with elevated legs than in the seated body position (p < 0.05). No significant difference was found among the three different body positions for postexercise ln HF (p > 0.05). Post-exercise time domain measures of HRV (RRNN, SDNN, RMSSD) were significantly lower compared with baseline values (p < 0.01) regardless body position. Post-exercise ln LF and ln HF in all three positions remained significantly reduced during recovery compared to baseline values (p < 0.01). The present study suggests that 15 minutes following short-term submaximal exercise most of the time and frequency domain HRV measures have not returned to pre-exercise values. Modifications in autonomic cardiac regulation induced by body posture present at rest remained after exercise, but the post-exercise differences among the three positions did not resemble the ones established at rest. [ABSTRACT FROM AUTHOR]

Key points Microneurographic recordings of the human cervical vagus nerve have revealed the presence of multi‐unit neural activity with measurable cardiac rhythmicity. This suggests that the physiology of vagal neurones with cardiovascular regulatory function can be studied using this method. Here, the activity of cardiac rhythmic single units was discriminated from human cervical vagus nerve recordings using template‐based waveform matching. The activity of 44 cardiac rhythmic neurones (22 with myelinated axons and 22 with unmyelinated axons) was isolated. By consideration of each unit's firing pattern with respect to the cardiac and respiratory cycles, the functional identification of each unit was attempted. Of note is the observation of seven cardiac rhythmic neurones with myelinated axons whose activity was recruited or enhanced by slow, deep breathing, was maximal during the nadir of respiratory sinus arrhythmia, and showed an expiratory peak. This is characteristic of cardioinhibitory efferent neurones, which are responsible for respiratory sinus arrhythmia. The remaining 15 cardiac rhythmic neurones with myelinated axons were categorised as cardiopulmonary receptors or arterial baroreceptors based on the position of their peak in firing with respect to the R‐wave of the cardiac cycle. This latter method is not viable for neurones with unmyelinated axons due to their slow and unknown conduction velocities. With the exception of three neurones whose expiratory modulation implicates them as cardiac‐projecting efferent neurones, this population is likely dominated by arterial baroreceptors. In conclusion, the activity of single units with cardiovascular function has been discriminated within the human cervical vagus, enabling their systematic study. Recordings of the electrical activity of the vagus nerve have recently been made at the level of the neck in humans. Examination of the gross activity of this nerve reveals subpopulations of neurones whose activity fluctuates in time with the heart's beat, suggesting that the neurones that monitor or modify cardiac function can be studied using this method. Here, the activity of individual cardiac rhythmic neurones was isolated from human vagus nerve recordings using template‐based spike sorting. The relationship between this activity and the cardiac and respiratory cycles was used as a means of classifying each neurone. Neuronal firing patterns that are consistent with that of neurones that modify cardiac function, including heart‐slowing ‘cardioinhibitory’ neurones, as well as neurones that inform the brain of cardiovascular status were observed. This approach enables, for the first time, the systematic study of the function of these neurones in humans in both health and disease. [ABSTRACT FROM AUTHOR]