Zoran Valic

The research questions in this study were to examine the contribution of negative automatic thoughts and negative emotions, measured by two newly-constructed questionnaires, to psychophysiological stress responses among more experienced military and less experienced recreational divers. Further, we examined whether daily variations in cortisol levels could be attributed to the impact of negative thoughts/emotions rather than diving experience. Altogether 15 recreational and 14 military male divers participated in the dive wherein stress responses were measured by anxiety measures (DASS-21 and STAI) and cortisol salivary concentrations. The results of factor analysis and principal component analysis demonstrated acceptable construct validity and internal consistency of both questionanires. Recreational and military divers did not differ significantly in the proportion of negative thoughts and emotions, while recreational divers had significantly higher levels of cortisol release after awakening and immediately before/after diving, indicating their more intense stress responses. A significant interaction between daily variations in cortisol secretion and negative emotions indicated a greater importance of emotions in response to diving stress rather than diving experience. Accordingly, using a multiple regression analysis showed that more pre-diving negative emotions predicted higher levels of pre-diving anxiety and depression as well as more cortisol release. More negative thoughts predicted higher levels of depressive symptoms, while belonging to a group of recreational divers was a significant predictor of higher pre-diving anxiety. This study points to the importance of considering cognitive and emotional experiences, particularly in recreational divers, for the purpose of prevention of negative psychophysiological stress responses prior to diving.

This manuscript quantified spleen volume changes and examined the relationship between those changes and oxygen uptake kinetics during supine cycling. Ten volunteers (age = 22 ± 3), completed 3 step transitions from 20 W to their power output at 90% gas exchange threshold. Ultrasonic measurements of the spleen were performed each minute. The largest spleen volume reduction was 105 mL (p = 0.001). No associations existed between i) spleen volumes at rest; and ii) spleen volume changes (%) and tau pulmonary oxygen uptake (τV̇O_2p). Larger resting spleen volume and greater emptying do not correlate with a faster τV̇O_2p. Novelty: Greater splenic contractions do not augment τV̇O_2p, irrespective of spleen emptying and subsequent erythrocyte release.

We studied the effects of age on different physiological parameters, including those derived from (i) maximal cardiopulmonary exercise testing (CPET), (ii) moderate-intensity step transitions, and (iii) tensiomyography (TMG)-derived variables in moderately active women. Twenty-eight women (age, 19 to 53 years), completed 3 laboratory visits, including baseline data collection, TMG assessment, maximal oxygen uptake test via CPET, and a step-transition test from 20 W to a moderate-intensity cycling power output (PO), corresponding to oxygen uptake at 90% gas exchange threshold. During the step transitions, breath-by-breath pulmonary oxygen uptake, near infrared spectroscopy derived muscle deoxygenation (ΔHHb), and beat-by-beat cardiovascular response were continuously monitored. There were no differences observed between the young and middle-aged women in their maximal oxygen uptake and peak PO, while the maximal heart rate (HR) was 12 bpm lower in middle-aged compared with young (p = 0.016) women. Also, no differences were observed between the age groups in τ pulmonary oxygen uptake, ΔHHb, and τHR during on-transients. The first regression model showed that age did not attenuate the maximal CPET capacity in the studied population (p = 0.638), while in the second model a faster τ pulmonary oxygen uptake, combined with shorter TMG-derived contraction time (Tc) of the vastus lateralis (VL), were associated with a higher maximal oxygen uptake (∼30% of explained variance, p = 0.039). In conclusion, long lasting exercise involvement protects against a maximal oxygen uptake and τpulmonary oxygen uptake deterioration in moderately active women. Novelty: Faster τ pulmonary oxygen uptake and shorter Tc of the VL explain 33% of the variance in superior maximal oxygen uptake attainment. No differences between age groups were found in τ pulmonary oxygen uptake, τΔHHb, and τHR during on-transients.

To assess the effect of air, gas mixture composed of 50% nitrogen and 50% oxygen (nitrox 50), or gas mixture composed of 1% nitrogen and 99% oxygen (nitrox 99) on bubble formation and vascular/endothelial function during decompression after self-contained ...

Obstructive sleep apnea (OSA) has been associated with dysregulation of the hypothalamic–pituitary–adrenal axis and alterations in glucose metabolism with increased risk for type 2 diabetes. The aim of the current study was to compare morning plasma cortisol levels and glucose metabolism parameters between moderate (apnea–hypopnea index (AHI): 15–30 events/h) and severe OSA patients (AHI >30 events/h), with respective controls. A total of 56 male OSA patients, 24 moderate (AHI = 21.1 ± 5.3) and 32 severe (AHI = 49.7 ± 18.1), underwent a full-night polysomnography, oral glucose tolerance test (OGTT), and measurement of morning plasma cortisol levels. These groups were compared to 20 matched subjects in a control group. Morning plasma cortisol levels were statistically lower in severe OSA group than in moderate OSA and control groups (303.7 ± 93.5 vs. 423.9 ± 145.1 vs. 417.5 ± 99.8 pmol/L, P < 0.001). Significant negative correlations were found between morning plasma cortisol levels and AHI (r = −0.444, P = 0.002), as well as oxygen desaturation index (r = −0.381, P = 0.011). Fasting plasma glucose (5.0 ± 0.5 vs. 5.4 ± 0.7 vs. 4.9 ± 0.6 mmol/L, P = 0.009) was higher in the severe OSA group compared to moderate OSA and controls. Homeostasis model assessment insulin resistance (HOMA-IR) was higher in the severe OSA group compared to moderate OSA and controls (4.6 ± 3.7 vs. 2.7 ± 2.0 and 2.2 ± 1.8, respectively, P = 0.006). In conclusion, our study showed that morning plasma cortisol levels measured at 8 a.m. were significantly lower in severe OSA patients than those in moderate OSA group and controls. Morning plasma cortisol levels showed a negative correlation with AHI and oxygen desaturation index. Additionally, this study confirmed the evidence of glucose metabolism impairment in moderate and severe OSA patients, with more pronounced effect in the severe OSA patients group.

This study was undertaken to determine pattern sensitivity of phrenic nerve plasticity in respect to different respiratory challenges. We compared long-term effects of intermittent and continuous hypercapnic and hypoxic stimuli, and combined intermittent hypercapnia and hypoxia on phrenic nerve plasticity. Adult, male, urethane-anesthetized, vagotomized, paralyzed, mechanically ventilated Sprague-Dawley rats were exposed to: acute intermittent hypercapnia (AIHc or AIHcO2), acute intermittent hypoxia (AIH), combined intermittent hypercapnia and hypoxia (AIHcH), continuous hypercapnia (CHc), or continuous hypoxia (CH). Peak phrenic nerve activity (pPNA) and burst frequency were analyzed during baseline (T0), hypercapnia or hypoxia exposures, at 15, 30, and 60 min (T60) after the end of the stimulus. Exposure to acute intermittent hypercapnia elicited decrease of phrenic nerve frequency from 44.25±4.06 at T0 to 35.29±5.21 at T60, (P=0.038, AIHc) and from 45.5±2.62 to 37.17±3.68 breaths/min (P=0.049, AIHcO2), i.e. frequency phrenic long term depression was induced. Exposure to AIH elicited increase of pPNA at T60 by 141.0±28.2 % compared to baseline (P=0.015), i.e. phrenic long-term facilitation was induced. Exposure to AIHcH, CHc, or CH protocols failed to induce long-term plasticity of the phrenic nerve. Thus, we conclude that intermittency of the hypercapnic or hypoxic stimuli is needed to evoke phrenic nerve plasticity.

New Findings: What is the central question of this study? Intermittent hypercapnia is a concomitant feature of breathing disorders. Hypercapnic stimuli evoke a form of respiratory plasticity known as phrenic long‐term depression in experimental animals. This study was performed to investigate the putative role of serotonin receptors in the initiation of phrenic long‐term depression in anaesthetized rats. What is the main finding and its importance? Phrenic nerve long‐term depression was revealed in animals pretreated with the serotonin broad‐spectrum antagonist, methysergide. This study highlights that serotonin receptors modulate respiratory plasticity evoked by acute intermittent hypercapnia in anaesthetized rats. This study was performed to test the hypothesis that intermittent hypercapnia can evoke a form of respiratory plasticity known as long‐term depression of the phrenic nerve (pLTD) and that 5‐HT receptors play a role in the initiation of pLTD. Adult male urethane‐anaesthetized, vagotomized, paralysed, mechanically ventilated Sprague–Dawley rats were exposed to an acute intermittent hypercapnia protocol. One group received i.v. injection of the non‐selective 5‐HT receptor antagonist methysergide and another group received i.v. injection of the selective 5‐HT_1A receptor antagonist WAY‐100635 20 min before exposure to intermittent hypercapnia. A control group received i.v. injection of saline. Peak phrenic nerve activity and respiratory rhythm parameters were analysed at baseline (T0), during each of five hypercapnic episodes, and 15, 30 and 60 min (T60) after the last hypercapnia. Intravenous injection of methysergide before exposure to acute intermittent hypercapnia induced development of amplitude pLTD at T60 (decreased by 46.1 ± 6.9%, P = 0.003). Conversely, in control and WAY‐100635‐pretreated animals, exposure to acute intermittent hypercapnia did not evoke amplitude pLTD. However, a long‐term decrease in phrenic nerve frequency was evoked both in control (42 ± 4 breaths min⁻¹ at T0 versus 32 ± 5 breaths min⁻¹ at T60; P = 0.036) and in methysergide‐pretreated animals (42 ± 2 breaths min⁻¹ at T0 versus 32 ± 3 breaths min⁻¹ at T60; P = 0.028). In WAY‐100635 pretreated animals, frequency pLTD was prevented. These results suggest that 5‐HT receptors modulate respiratory plasticity induced by acute intermittent hypercapnia in anaesthetized rats.

Elevated levels of carbon dioxide (hypercapnia) and/or decreased level of oxygen (hypoxia) act through neural networks to influence ventilatory and cardiovascular function. Both hypercapnic and hypoxic stimuli can evoke increase in sympathetic nerve activity and it appears that hypoxia can evoke prolonged duration of this increase. The present study was performed to investigate the renal sympathetic nerve activity in urethane‐anesthetized, mechanically ventilated Sprague‐Dawley rats exposed to five hypercapnic stimuli each lasting 3 minutes. Blood pressure and renal sympathetic nerve activity were measured and recorded throughout the experiment. Analysis was performed in the period before and during hypercapnic exposures (15% of the CO ₂ in the air), as well as 15, 30 and 60 minutes after the last hypercapnic episode. Renal sympathetic nerve activity increased to 190.3±22.8% during hypercapnia when compared to baseline. At 15 minutes after the last hypercapnic exposure nerve activity remained elevated at 138.0±14.8%. At 30 and 60 minutes renal sympathetic nerve activity was 136.8±21.5% and 131.8±18.3%, respectively. Acute intermittent hypercapnia evoked increase in renal sympathetic nerve activity that lasted at least 60 minutes after cessation of stimulus. This study was supported by Croatian Science Foundation.