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The hypoxic chemoreflex and the arterial baroreflex are implicated in the ventilatory response to exercise. It is well known that long-term exercise training increases parasympathetic and decreases sympathetic tone, both processes influenced by the arterial baroreflex and hypoxic chemoreflex function. Hypobaric hypoxia (i.e., high altitude [HA]) markedly reduces exercise capacity associated with autonomic reflexes. Indeed, a reduced exercise capacity has been found, paralleled by a baroreflex-related parasympathetic withdrawal and a pronounced chemoreflex potentiation. Additionally, it is well known that the baroreflex and chemoreflex interact, and during activation by hypoxia, the chemoreflex is predominant over the baroreflex. Thus, the baroreflex function impairment may likely facilitate the exercise deterioration through the reduction of parasympathetic tone following acute HA exposure, secondary to the chemoreflex activation. Therefore, the main goal of this review is to describe the main physiological mechanisms controlling baro- and chemoreflex function and their role in exercise capacity during HA exposure.

Accurate short- and mid-term blood glucose predictions are crucial for patients with diabetes struggling to maintain healthy glucose levels, as well as for individuals at risk of developing the disease. Consequently, numerous efforts from the scientific community have focused on developing predictive models for glucose levels. This study harnesses physiological data collected from wearable sensors to construct a series of data-driven models based on deep learning approaches. We systematically compare these models to offer insights for practitioners and researchers venturing into glucose prediction using deep learning techniques. Key questions addressed in this work encompass the comparison of various deep learning architectures for this task, determining the optimal set of input variables for accurate glucose prediction, comparing population-wide, fine-tuned, and personalized models, and assessing the impact of an individual's data volume on model performance. Additionally, as part of our outcomes, we introduce a meticulously curated dataset inclusive of data from both healthy individuals and those with diabetes, recorded in free-living conditions. This dataset aims to foster research in this domain and facilitate equitable comparisons among researchers.

Purpose: This study investigated the impact of four weeks of age-dependent detraining on army soldiers’ cardiorespiratory fitness and maximal and explosive strength. Methods: Fourteen volunteer tactical athletes participated, divided into two age groups (20 to 29 and 30 to 40 years). Before and after the detraining period, we assessed their anthropometric measurements (weight, height, body mass index, fat mass, and fat-free mass), cardiorespiratory fitness (maximal oxygen uptake [VO2max] and ventilatory thresholds [VT1 and VT2]), and kinematic properties during a single-leg counter-moving jump (CMJ) test for both the dominant and non-dominant legs. Two-way ANOVA followed by the Holm–Sidak post hoc test was used. Results: The anthropometric and cardiovascular variables did not show significant differences between the groups. However, both groups exhibited a significantly reduced maximum time and speed at the VO2max. Furthermore, the flight time and maximum height during the CMJ significantly decreased in the non-dominant leg for both age groups. Notably, the dominant leg’s concentric impulse (CI) significantly reduced during the CMJ, but this effect was observed only in the 30–40 age group. There were significant differences between the two age groups. Conclusions: Our findings suggest that four weeks of detraining negatively impacts aerobic fitness and muscular strength, independently of age. However, the dominant leg may be more susceptible to detraining effects in army soldiers aged 30–40. Furthermore, as a perspective, our results strongly suggest that a detraining period could affect successful missions (aerobic performance deterioration), as well as promote a muscle imbalance between the legs, which could encourage muscle injuries and endanger combat missions.

Abstract Swimmer athletes showed a decreased ventilatory response and reduced sympathetic activation during peripheral hypoxic chemoreflex stimulation. Based on these observations, we hypothesized that swimmers develop a diminished cardiorespiratory coupling due to their decreased hypoxic peripheral response. To resolve this hypothesis, we conducted a study using coherence time‐varying analysis to assess the cardiorespiratory coupling in swimmer athletes. We recruited 12 trained swimmers and 12 control subjects for our research. We employed wavelet time‐varying spectral coherence analysis to examine the relationship between the respiratory frequency (Rf) and the heart rate (HR) time series during normoxia and acute chemoreflex activation induced by five consecutive inhalations of 100% N2. Comparing swimmers to control subjects, we observed a significant reduction in the hypoxic ventilatory responses to N2 in swimmers (0.012 ± 0.001 vs. 0.015 ± 0.001 ΔVE/ΔVO2, and 0.365 ± 0.266 vs. 1.430 ± 0.961 ΔVE/ΔVCO2/ΔSpO2, both p

Unique worldwide, nitrate/iodine deposits (NIDs) are located along a 700 km geological belt in the Atacama Desert, Chile. They serve as the primary source of mineral ores for the extraction of iodine, sodium, and potassium nitrates. NIDs have been relatively underexplored from a biological perspective. To address this, we collected sixteen soil samples from abandoned mines in Oficinas Pissis and Savona for chemical, mineralogical, and metagenomic analyses. The soils primarily consisted of halite and darapskite, with only one sample being predominantly composed of thenardite. Deliquescence and water activity measurements yielded values ranging from 0.02% to 0.40% and 0.47 to 0.62, respectively. To investigate the presence, identification, relative abundance, and diversity of microbial life in NID soils, we employed MiSeq high-throughput sequencing and bioinformatic tools. The dominant phyla observed were Firmicutes and Proteobacteria, with Actinobacteria and Cyanobacteria being predominant in two soil samples. Furthermore, we detected nitrate/perchlorate-reducing bacterial activity in enriched cultures from the soil samples. This study sheds light on the resilience of microbial life in the Atacama Desert NIDs, providing compelling evidence for its existence and offering insight into factors that could facilitate it within this unique environment.

Preclinical research has provided compelling evidence indicating that exposure to hypobaric hypoxia (HH) results in a deterioration of spermatogenesis. This adverse effect extends to the underlying molecular mechanisms, progressively leading to impairments in the seminiferous epithelium and germ cells and alterations in semen parameters. Indeed, several studies have demonstrated that animals exposed to HH, whether in natural high-altitude environments or under simulated hypoxic conditions, exhibit damage to the self-renewal and differentiation of spermatogenesis, an increase in germline cell apoptosis, and structural alterations in the seminiferous tubules. One of the primary mechanisms associated with the inhibition of differentiation and an increase in apoptosis among germ cells is an elevated level of oxidative stress, which has been closely associated with HH exposure. Human studies have shown that individuals exposed to HH, such as mountaineers and alpinists, exhibit decreased sperm count, reduced motility, diminished viability, and increased sperm with abnormal morphology in their semen. This evidence strongly suggests that exposure to HH may be considered a significant risk factor that could elevate the prevalence of male infertility. This literature review aims to provide a comprehensive description and propose potential mechanisms that could elucidate the infertility processes induced by HH. By doing so, it contributes to expanding our understanding of the challenges posed by extreme environments on human physiology, opening new avenues for research in this field.

Abstract Background Diabetes mellitus (DM) has glucose variability that is of such relevance that the appearance of vascular complications in patients with DM has been attributed to hyperglycemic and dysglycemic events. It is known that T1D patients mainly have glycemic variability with a specific oscillatory pattern with specific circadian characteristics for each patient. However, it has not yet been determined whether an oscillation pattern represents the variability of glycemic in T2D. This is why our objective is to determine the characteristics of glycemic oscillations in T2D and generate a robust predictive model. Results Showed that glycosylated hemoglobin, glycemia, and body mass index were all higher in patients with T2D than in controls (all p

Introduction: The cardiorespiratory optimal point (COP) represents the lowest minute ventilation to oxygen consumption ratio (VE/VO2) and can be estimated during a CPET at submaximal intensity when an exercise test until volitional fatigue is not always advisable (i.e., a conflict zone where you cannot be confident of the security because near-competition, off-season, among other). COP’s physiological components have not been wholly described yet. Therefore, this study seeks to identify the determinants of COP in highly trained athletes and its influence on maximum and sub-maximum variables during CPET through principal c omponent analysis (PCA) (explains the dataset’s variance).Methods: Female (n = 9; age, 17.4 ± 3.1 y; maximal VO2 [VO2max]), 46.2 ± 5.9 mL/kg/min) and male (n = 24; age, 19.7 ± 4.0 y; VO2max, 56.1 ± 7.6 mL/kg/min) athletes performed a CPET to determine the COP, ventilatory threshold 1 (VT1) and 2 (VT2), and VO2max. The PCA was used to determine the relationship between variables and COP, explaining their variance.Results: Our data revealed that females and males displayed different COP values. Indeed, males showed a significant diminished COP compared to the female group (22.6 ± 2.9 vs. 27.2 ±3.4 VE/VO2, respectively); nevertheless, COP was allocated before VT1 in both groups.Discussion: PC analysis revealed that the COP variance was mainly explained (75.6%) by PC1 (expired CO2 at VO2max) and PC2 (VE at VT2), possibly influencing cardiorespiratory efficiency at VO2max and VT2. Our data suggest that COP could be used as a submaximal index to monitor and assess cardiorespiratory system efficiency in endurance athletes. The COP could be particularly useful during the offseason and competitive periods and the return to the sports continuum.

Abstract Background Chronic heart failure (CHF) is a global health problem. Increased sympathetic outflow, cardiac arrhythmogenesis and irregular breathing patterns have all been associated with poor outcomes in CHF. Several studies showed that activation of the renin-angiotensin system (RAS) play a key role in CHF pathophysiology. Interestingly, potassium (K+) supplemented diets showed promising results in normalizing RAS axis and autonomic dysfunction in vascular diseases, lowering cardiovascular risk. Whether subtle increases in dietary K+ consumption may exert similar effects in CHF has not been previously tested. Accordingly, we aimed to evaluate the effects of dietary K+ supplementation on cardiorespiratory alterations in rats with CHF. Methods Adult male Sprague–Dawley rats underwent volume overload to induce non-ischemic CHF. Animals were randomly allocated to normal chow diet (CHF group) or supplemented K+ diet (CHF+K+ group) for 6 weeks. Cardiac arrhythmogenesis, sympathetic outflow, baroreflex sensitivity, breathing disorders, chemoreflex function, respiratory–cardiovascular coupling and cardiac function were evaluated. Results Compared to normal chow diet, K+ supplemented diet in CHF significantly reduced arrhythmia incidence (67.8 ± 15.1 vs. 31.0 ± 3.7 events/hour, CHF vs. CHF+K+), decreased cardiac sympathetic tone (ΔHR to propranolol: − 97.4 ± 9.4 vs. − 60.8 ± 8.3 bpm, CHF vs. CHF+K+), restored baroreflex function and attenuated irregular breathing patterns. Additionally, supplementation of the diet with K+ restores normal central respiratory chemoreflex drive and abrogates pathological cardio-respiratory coupling in CHF rats being the outcome an improved cardiac function. Conclusion Our findings support that dietary K+ supplementation in non-ischemic CHF alleviate cardiorespiratory dysfunction.

Abstract Background Deep breathing (DB) and handgrip (HG) exercise -with and without circulatory occlusion (OC) in muscle-, have been shown to have beneficial effects on cardiovascular function; however, the combination of these maneuvers on heart rate (HR) and cardiac sympathovagal balance have not been previously investigated. Therefore, the aim of the present study was to evaluate the effect of simultaneous DB, HG, and OC maneuvers on the sympathovagal balance in healthy women and men subjects. Methods and results Electrocardiogram and ventilation were measured in 20 healthy subjects (Women: n = 10; age = 27 ± 4 years; weight = 67.1 ± 8.4 kg; and height = 1.6 ± 0.1 m. Men: n = 10; age = 27 ± 3 years; weight = 77.5 ± 10.1 kg; and height = 1.7 ± 0.1 m) at baseline and during DB, DB + HG, or DB + HG + OC protocols. Heart rate (HR) and respiratory rate were continuously recorded, and spectral analysis of heart rate variability (HRV) were calculated to indirectly estimate cardiac autonomic function. Men and women showed similar HR responses to DB, DB + HG and DB + HG + OC. Men exhibited a significant HR decrease following DB + HG + OC protocol which was accompanied by an improvement in cardiac autonomic control evidenced by spectral changes in HRV towards parasympathetic predominance (HRV High frequency: 83.95 ± 1.45 vs. 81.87 ± 1.50 n.u., DB + HG + OC vs. baseline; p

Background: Postexercise hypotension (PEH) is a common physiological phenomenon occurring immediately after endurance training (ET), resistance training (RT), and ET plus RT, also termed concurrent training (CT); however, there is little knowledge about the interindividual and magnitude response of PEH in morbidly obese patients.Aim: The aims of this study were (1) to investigate the effect of CT order (ET + RT vs. RT + ET) on the blood pressure responses; 2) characterize these responses in responders and nonresponders, and 3) identify potential baseline outcomes for predicting blood pressure decreases as responders.Methods: A quasi-experimental study developed in sedentary morbidly obese men and women (age 43.6 ± 11.3 years; body mass index [BMI] ≥40 kg/m2) was assigned to a CT group of ET plus RT (ET + RT; n = 19; BMI 47.8 ± 16.7) or RT plus ET order group (RT + ET; n = 17; BMI 43.0 ± 8.0). Subjects of both groups received eight exercise sessions over four weeks. Primary outcomes include systolic (SBP), diastolic (DBP), mean arterial pressure [MAP], heart rate at rest [HR], and pulse pressure [PP] measurements before and after 10 min post-exercise. Secondary outcomes were other anthropometric, body composition, metabolic, and physical fitness parameters. Using the delta ∆SBP reduction, quartile categorization (Q) in “high” (Rs: quartile 4), “moderate” (MRs: quartile 3), “low” (LRs: quartile 2), and “nonresponders” (NRs: quartile 1) was reported.Results: Significant pre–post changes were observed in ET + RT in session 2 for SBP (131.6 vs. 123.4 mmHg, p = 0.050) and session 4 (131.1 vs. 125.2 mmHg, p = 0.0002), while the RT + ET group showed significant reductions in session 4 (134.2 vs. 125.3 mmHg, p < 0.001). No significant differences were detected in the sum of the eight sessions for SBP (∑∆SBP) between ET + RT vs. RT + ET (−5.7 vs. −4.3 mmHg, p = 0.552). Interindividual analyses revealed significant differences among frequencies comparing Q1 “NRs” (n = 8; 22.2%), Q2 “LRs” (n = 8; 22.2%), Q3 “MRs” (n = 9; 25.0%), and Q4 “HRs” (n = 11; 30.5%), p < 0.0001. Quartile comparisons showed significant differences in SBP changes (p = 0.035). Linear regression analyses revealed significant association between ∑∆SBP with body fat % (β –3.826, R2 0.211 [21.1%], p = 0.031), skeletal muscle mass [β –2.150, R2 0.125 (12.5%), p = 0.023], fasting glucose [β 1.273, R2 0.078 (7.8%), p = 0.003], triglycerides [β 0.210, R2 0.014 (1.4%), p = 0.008], and the 6-min walking test [β 0.183, R2 0.038 (3.8%), p = 0.044].Conclusion: The CT order of ET + RT and RT + ET promote a similar ‘magnitude’ in the postexercise hypotensive effects during the eight sessions of both CT orders in 4 weeks of training duration, revealing “nonresponders” and ‘high’ responders that can be predicted from body composition, metabolic, and physical fitness outcomes.

The non-responders (NRs) after exercise training have been poorly studied in populations with morbid obesity. The purpose of this study was to determine the NR prevalence after 20 weeks of concurrent training of morbidly obese women with a high or low number of metabolic syndrome (MetS) risk factors. Twenty-eight women with morbid obesity participated in an exercise training intervention and were allocated into two groups distributed based on a high (≥3, n = 11) or low number (

Abstract Mounting an appropriate ventilatory response to exercise is crucial to meeting metabolic demands, and abnormal ventilatory responses may contribute to exercise-intolerance (EX-inT) in heart failure (HF) patients. We sought to determine if abnormal ventilatory chemoreflex control contributes to EX-inT in volume-overload HF rats. Cardiac function, hypercapnic (HCVR) and hypoxic (HVR) ventilatory responses, and exercise tolerance were assessed at the end of a 6 week exercise training program. At the conclusion of the training program, exercise tolerant HF rats (HF + EX-T) exhibited improvements in cardiac systolic function and reductions in HCVR, sympathetic tone, and arrhythmias. In contrast, HF rats that were exercise intolerant (HF + EX-inT) exhibited worse diastolic dysfunction, and showed no improvements in cardiac systolic function, HCVR, sympathetic tone, or arrhythmias at the conclusion of the training program. In addition, HF + EX-inT rats had impaired HVR which was associated with increased arrhythmia susceptibility and mortality during hypoxic challenges (~ 60% survival). Finally, we observed that exercise tolerance in HF rats was related to carotid body (CB) function as CB ablation resulted in impaired exercise capacity in HF + EX-T rats. Our results indicate that: (i) exercise may have detrimental effects on cardiac function in HF-EX-inT, and (ii) loss of CB chemoreflex sensitivity contributes to EX-inT in HF.

Immersion water sports involve long-term apneas; therefore, athletes must physiologically adapt to maintain muscle oxygenation, despite not performing pulmonary ventilation. Breath-holding (i.e., apnea) is common in water sports, and it involves a decrease and increases PaO2 and PaCO2, respectively, as the primary signals that trigger the end of apnea. The principal physiological O2 sensors are the carotid bodies, which are able to detect arterial gases and metabolic alterations before reaching the brain, which aids in adjusting the cardiorespiratory system. Moreover, the principal H+/CO2 sensor is the retrotrapezoid nucleus, which is located at the brainstem level; this mechanism contributes to detecting respiratory and metabolic acidosis. Although these sensors have been characterized in pathophysiological states, current evidence shows a possible role for these mechanisms as physiological sensors during voluntary apnea. Divers and swimmer athletes have been found to displayed longer apnea times than land sports athletes, as well as decreased peripheral O2 and central CO2 chemoreflex control. However, although chemosensitivity at rest could be decreased, we recently found marked sympathoexcitation during maximum voluntary apnea in young swimmers, which could activate the spleen (which is a reservoir organ for oxygenated blood). Therefore, it is possible that the chemoreflex, autonomic function, and storage/delivery oxygen organ(s) are linked to apnea in immersion water sports. In this review, we summarized the available evidence related to chemoreflex control in immersion water sports. Subsequently, we propose a possible physiological mechanistic model that could contribute to providing new avenues for understanding the respiratory physiology of water sports.

Summary: Background: Breathing disorders (BD) (apnoeas/hypopneas, periodic breathing) are highly prevalent in chronic heart failure (CHF) and are associated with altered central respiratory control. Ample evidence identifies the retrotrapezoid nucleus (RTN) as an important chemosensitivity region for ventilatory control and generation of BD in CHF, however little is known about the cellular mechanisms underlying the RTN/BD relationship. Within the RTN, astrocyte‐mediated purinergic signalling modulates respiration, but the potential contribution of RTN astrocytes to BD in CHF has not been explored. Methods: Selective neuron and/or astrocyte-targeted interventions using either optogenetic and chemogenetic manipulations in the RTN of CHF rats were used to unveil the contribution of the RTN on the development/maintenance of BD, the role played by astrocytes in BD and the molecular mechanism underpinning these alterations. Findings: We showed that episodic photo-stimulation of RTN neurons triggered BD in healthy rats, and that RTN neurons ablation in CHF animals eliminates BD. Also, we found a reduction in astrocytes activity and ATP bioavailability within the RTN of CHF rats, and that chemogenetic restoration of normal RTN astrocyte activity and ATP levels improved breathing regularity in CHF. Importantly, P''X/ P2X7 receptor (P2X7r) expression was reduced in RTN astrocytes from CHF rats and viral vector-mediated delivery of human P2X7 P2X7r into astrocytes increases ATP bioavailability and abolished BD. Interpretation: Our results support that RTN astrocytes play a pivotal role on BD generation and maintenance in the setting CHF by a mechanism encompassing P2X7r signalling. Funding: This study was funded by the National Research and Development Agency of Chile (ANID).

Abstract Daily glucose variability is higher in diabetic mellitus (DM) patients which has been related to the severity of the disease. However, it is unclear whether glycemic variability displays a specific pattern oscillation or if it is completely random. Thus, to determine glycemic variability pattern, we measured and analyzed continuous glucose monitoring (CGM) data, in control subjects and patients with DM type-1 (T1D). CGM data was assessed for 6 days (day: 08:00–20:00-h; and night: 20:00–08:00-h). Participants (n = 172; age = 18–80 years) were assigned to T1D (n = 144, females = 65) and Control (i.e., healthy; n = 28, females = 22) groups. Anthropometry, pharmacologic treatments, glycosylated hemoglobin (HbA1c) and years of evolution were determined. T1D females displayed a higher glycemia at 10:00–14:00-h vs. T1D males and Control females. DM patients displays mainly stationary oscillations (deterministic), with circadian rhythm characteristics. The glycemia oscillated between 2 and 6 days. The predictive model of glycemia showed that it is possible to predict hyper and hypoglycemia (R2 = 0.94 and 0.98, respectively) in DM patients independent of their etiology. Our data showed that glycemic variability had a specific oscillation pattern with circadian characteristics, with episodes of hypoglycemia and hyperglycemia at day phases, which could help therapeutic action for this population.

Background The aim of this study is to conduct a systematic review with meta-analysis to explore the effects of plyometric jump training (PJT) on the physical fitness of individual sport athletes (ISA). Methods Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, we searched through PubMed, Web of Science, and SCOPUS electronic databases. We included controlled studies that incorporated a PJT intervention among ISA (with no restriction for age or sex), that included a pre-to-post intervention assessment of physical fitness (e.g., sprint; jump). From the included studies, relevant data (e.g., PJT and participants characteristics) was extracted. We assessed the methodological quality of the included studies using the PEDro scale. Using a random-effects model, meta-analyses for a given outcome was conducted. Means and standard deviations for a measure of pre-post-intervention physical fitness from the PJT and control groups were converted to Hedges’ g effect size (ES). Heterogeneity was assessed using the I2 statistic. The risk of bias was explored using the extended Egger’s test. The statistical significance threshold was set at p < 0.05. Moderator analyses were conducted according to the sex, age and sport background of the athletes. Results Twenty-six studies of moderate-high methodological quality were included (total participants, n = 667). Compared to controls, PJT improved vertical jump (ES = 0.49; p < 0.001; I = 0.0%), linear sprint (ES = 0.23; p = 0.032; I2 = 10.9%), maximal strength (ES = 0.50; p < 0.001; I2 = 0.0%) and endurance performance (ES = 0.30; p = 0.028; I2 = 11.1%). No significant effect was noted for sprint with change of direction (ES = 0.34; p = 0.205; I2 = 70.9%). Athlete’s sex, age and sport background had no modulator role on the effect of PJT on vertical jump, linear sprint, maximal strength and endurance performance. Among the included studies, none reported adverse effects related to the PJT intervention. Conclusions PJT induces small improvements on ISA physical fitness, including jumping, sprinting speed, strength and endurance.

During an apnea, changes in PaO2 activate peripheral chemoreceptors to increase respiratory drive. Athletes with continuous apnea, such as breath-hold divers, have shown a decrease in hypoxic ventilatory response (HVR), which could explain the long apnea times; however, this has not been studied in swimmers. We hypothesize that the long periods of voluntary apnea in swimmers is related to a decreased HVR. Therefore, we sought to determine the HVR and cardiovascular adjustments during a maximum voluntary apnea in young-trained swimmers. In fifteen trained swimmers and twenty-seven controls we studied minute ventilation (VE), arterial saturation (SpO2), heart rate (HR), and autonomic response [through heart rate variability (HRV) analysis], during acute chemoreflex activation (five inhalations of pure N2) and maximum voluntary apnea test. In apnea tests, the maximum voluntary apnea time and the end-apnea HR were higher in swimmers than in controls (p < 0.05), as well as a higher low frequency component of HRV (p < 0.05), than controls. Swimmers showed lower HVR than controls (p < 0.01) without differences in cardiac hypoxic response (CHR). We conclude that swimmers had a reduced HVR response and greater maximal voluntary apnea duration, probably due to decreased HVR.

Cardiac arrythmias play a critical role in several pathological conditions. Importantly, increased arrhythmic risk is associated with systemic oxidative stress and activation of the autonomic nervous system. Thus, we hypothesized that dietary antioxidant supplementation may help in reducing cardiac stress-induced arrhythmias. Sulforaphane (SFN), an isothiocyanate present in Brassicaceaes, is recognized as a powerful health-promoting compound with known antioxidant properties. Then, we aimed to generate a broccoli extract (BE) enriched in SFN and determine whether oral BE supplementation induced cardio-protection during acute cardiac stress in rats. BE decreases cardiac sympathetic drive and increases parasympathetic cardiac modulation as evidenced by heart rate variability (HRV) shifts. In addition, isoproterenol-induced cardiac stress (a sympathomimetic agent) induced a ~ 4-fold increase in arrhythmia incidence and this effect was almost completely abolished by BE treatment. In conclusion, dietary supplementation with a BE regulates cardiac autonomic drive and protects the heart from acute cardiac stress.

Regular exercise training is a recognized lifestyle strategy to lower resting blood pressure (BP), but little is known about substrate metabolism in population with high BP. Thus, the purpose of this study was to investigate the effects of 16-weeks of HIIT on body composition, BP, cardiorespiratory fitness by V.O2max, and substrate utilization during exercise among prehypertensive and hypertensive patients with excessive adiposity. We also aimed to test the potential association between changes in cardiorespiratory fitness, substrate utilization during exercise and BP. Forty-two physically inactive overweight/obese participants participated in 16-weeks of HIIT intervention. The HIIT frequency was three times a week (work ratio 1:2:10, for interval cycling: rest period: repeated times; 80–100% of the maximum heart rate). Groups were distributed based on their baseline BP: HIIT-hypertensive (H-HTN: age 47.7 ± 12.0 years; body mass index [BMI] 30.3 ± 5.5 kg/m2; systolic [SBP]/diastolic BP [DBP] 151.6 ± 10/81.9 ± 4.2 mmHg), HIIT-pre-hypertensive (H-PreHTN: age 37.6 ± 12.0 years; BMI 31.9 ± 5.3 kg/m2; SBP/DBP 134.4 ± 3.2/74.9 ± 7.0 mmHg), and a normotensive control group (H-CG: age 40.7 ± 11.0 years; BMI 29.5 ± 4.2 kg/m2; SBP/DBP 117.0 ± 6.2/72.4 ± 4.1 mmHg). Anthropometry/body composition, BP, and metabolic substrate utilization during exercise (fat [FATox], carbohydrate [CHOox] oxidation, respiratory exchange ratio [RER], and V.O2max), were measured before and after the 16-week HIIT intervention. Adjusted mixed linear models revealed a significant improved in V.O2max were + 3.34 in the H-CG, + 3.63 in the H-PreHTN, and + 5.92 mL⋅kg–1⋅min–1, in the H-HTN group, however, the Time × Group interaction were not significant (p = 0.083). All the exercise types induced similar decreases on SBP (−8.70) in the H-HTN, (−7.14) in the H-CG, and (−5.11) mmHg in the H-PreHTN, as well as DBP levels (−5.43) mmHg in H-CG group (p = 0.032 vs. H-HTN group). At 16-week, no significant correlations were noted for the changes of blood pressure, cardiorespiratory fitness or exercise metabolism substrates outcomes. In conclusion, our results suggest that a 16-week HIIT-intervention improved V.O2max and blood pressure BP, but these changes are independent of substrate utilization during exercise in normotensive and hypertensive participants with excessive adiposity.

Baroreflex (BR) control is critically dependent of sympathetic and parasympathetic modulation. It has been documented that during acute hypobaric hypoxia there is a BR control impairment, however, the effect of a natural hypoxic environment on BR function is limited and controversial. Therefore, the aim of this study was to determine the effect of acute High-Altitude exposure on sympathetic/parasympathetic modulation of BR control in normal rats. Male Sprague Dawley rats were randomly allocated into Sea-Level (n = 7) and High-Altitude (n = 5) (3,270 m above sea level) groups. The BR control was studied using phenylephrine (Phe) and sodium nitroprusside (SNP) through sigmoidal analysis. The autonomic control of the heart was estimated using heart rate variability (HRV) analysis in frequency domain. Additionally, to determine the maximum sympathetic and parasympathetic activation of BR, spectral non-stationary method analysis, during Phe (0.05 μg/mL) and SNP administration (0.10 μg/mL) were used. Compared to Sea-Level condition, the High-Altitude group displayed parasympathetic withdrawal (high frequency, 0.6–2.4 Hz) and sympathoexcitation (low frequency, 0.04–0.6 Hz). Regarding to BR modulation, rats showed a significant decrease (p < 0.05) of curvature and parasympathetic bradycardic responses to Phe, without significant differences in sympathetic tachycardic responses to SNP after High-Altitude exposure. In addition, the non-stationary analysis of HRV showed a reduction of parasympathetic activation (Phe) in the High-Altitude group. Our results suggest that acute exposure to High-Altitude produces an autonomic and BR control impairment, characterized by parasympathetic withdrawal after 24 h of high-altitude exposure.

Abstract The aim of this study was to determine the acute effects of high‐intensity interval training (HIIT) exercise and endurance exercise (EE) on pulmonary function, sympathetic/parasympathetic balance, and cardiorespiratory coupling (CRC) in healthy participants. Using a crossover repeated‐measurements design, four females and four males were exposed to EE (20 min at 80% maximal heart rate [HR]), HIIT (1 min of exercise at 90% maximal HR per 1 min of rest, 10 times), or control condition (resting). Pulmonary function, HR, CRC, and heart rate variability (HRV) were assessed before and after the interventions. Results revealed no significant effects of EE or HIIT on pulmonary function. The EE, but not HIIT, significantly increased CRC. In contrast, HRV was markedly changed by HIIT, not by EE. Indeed, both the low‐frequency (LFHRV) and high‐frequency (HFHRV) components of HRV were increased and decreased, respectively, after HIIT. The increase in LFHRV was greater after HIIT than after EE. Therefore, a single bout of HIIT or EE has no effects on pulmonary function. Moreover, CRC and cardiac autonomic regulation are targeted differently by the two exercise modalities.

Abstract Enhanced carotid body (CB) chemoreflex function is strongly related to cardiorespiratory disorders and disease progression in heart failure (HF). The mechanisms underlying CB sensitization during HF are not fully understood, however previous work indicates blood flow per se can affect CB function. Then, we hypothesized that the CB-mediated chemoreflex drive will be enhanced only in low output HF but not in high output HF. Myocardial infarcted rats and aorto-caval fistulated rats were used as a low output HF model (MI-CHF) and as a high output HF model (AV-CHF), respectively. Blood flow supply to the CB region was decreased only in MI-CHF rats compared to Sham and AV-CHF rats. MI-CHF rats exhibited a significantly enhanced hypoxic ventilatory response compared to AV-CHF rats. However, apnea/hypopnea incidence was similarly increased in both MI-CHF and AV-CHF rats compared to control. Kruppel-like factor 2 expression, a flow sensitive transcription factor, was reduced in the CBs of MI-CHF rats but not in AV-CHF rats. Our results indicate that in the setting of HF, potentiation of the CB chemoreflex is strongly associated with a reduction in cardiac output and may not be related to other pathophysiological consequences of HF.

Obstructive sleep apnea (OSA) is the most common form of sleep disordered breathing and is associated with wide array of cardiovascular morbidities. It has been proposed that during OSA, the respiratory control center (RCC) is affected by exaggerated afferent signals coming from peripheral/central chemoreceptors which leads to ventilatory instability and may perpetuate apnea generation. Treatments focused on decreasing hyperactivity of peripheral/central chemoreceptors may be useful to improving ventilatory instability in OSA patients. Previous studies indicate that oxidative stress and inflammation are key players in the increased peripheral/central chemoreflex drive associated with OSA. Recent data suggest that erythropoietin (Epo) could also be involved in modulating chemoreflex activity as functional Epo receptors are constitutively expressed in peripheral and central chemoreceptors cells. Additionally, there is some evidence that Epo has anti-oxidant/anti-inflammatory effects. Accordingly, we propose that Epo treatment during OSA may reduce enhanced peripheral/central chemoreflex drive and normalize the activity of the RCC which in turn may help to abrogate ventilatory instability. In this perspective article we discuss the potential beneficial effects of Epo administration on ventilatory regulation in the setting of OSA.