Peak cardiac power output and cardiac reserve in sedentary men and women

Background and Purpose: Cardiac power output (CPO) and cardiac reserve (CR) are novel parameters of overall cardiac function. The purpose of this study was to determine differences in values of the CPO at rest and peak exercise and CR in sedentary men and women. Material and Methods: Thirty healthy men (age 21.2±0.7 years, body mass 63±6.3 kg, height 168.3±5.1 cm) and thirty healthy women (age 21.3±1.9 years, mass 82.5±7.9 kg, height 181.9±4.9 cm) were included in this study. Echocardiography was used to assess cardiac and hemodynamic parameters. CPO was calculated, at rest and after performed maximal bicycle test, as the product of cardiac output and mean arterial pressure, and CR as the difference of CPO value measured at peak exercise and at rest. Results: At rest, the two groups had similar values of cardiac power output (1.04±0.3W versus 1.14±0.25W, p>0.05). CPO after peak exercise was higher in men (5.1±0.72W versus 3.9±0.58W, p<0.05), as was cardiac reserve (3.96±0.64W versus 2.86±0.44W, p<0.05), respectively. After allometric scaling method was used to decrease the effect of body size on peak CPO, men still had significantly higher peak CPO (2.79±0.4 W m-2 versus 2.46±0.32 W m-2, p<0.05). At peak exercise, a significant positive relationship was found between cardiac power output and end diastolic volume (r=0.60), end diastolic left ventricular internal dimension (r=0.58), stroke volume (r=0.86) and cardiac output (r=0.87). Conclusion: The study showed that men had higher CPO after peak exercise and greater cardiac reserve than women, even after decreasing body size effect

Peak cardiac power output and cardiac reserve in sedentary men and women

Background and Purpose: Cardiac power output (CPO) and cardiac reserve (CR) are novel parameters of overall cardiac function. The purpose of this study was to determine differences in values of the CPO at rest and peak exercise and CR in sedentary men and women. Material and Methods: Thirty healthy men (age 21.2±0.7 years, body mass 63±6.3 kg, height 168.3±5.1 cm) and thirty healthy women (age 21.3±1.9 years, mass 82.5±7.9 kg, height 181.9±4.9 cm) were included in this study. Echocardiography was used to assess cardiac and hemodynamic parameters. CPO was calculated, at rest and after performed maximal bicycle test, as the product of cardiac output and mean arterial pressure, and CR as the difference of CPO value measured at peak exercise and at rest. Results: At rest, the two groups had similar values of cardiac power output (1.04±0.3W versus 1.14±0.25W, p>0.05). CPO after peak exercise was higher in men (5.1±0.72W versus 3.9±0.58W, p<0.05), as was cardiac reserve (3.96±0.64W versus 2.86±0.44W, p<0.05), respectively. After allometric scaling method was used to decrease the effect of body size on peak CPO, men still had significantly higher peak CPO (2.79±0.4 W m-2 versus 2.46±0.32 W m-2, p<0.05). At peak exercise, a significant positive relationship was found between cardiac power output and end diastolic volume (r=0.60), end diastolic left ventricular internal dimension (r=0.58), stroke volume (r=0.86) and cardiac output (r=0.87). Conclusion: The study showed that men had higher CPO after peak exercise and greater cardiac reserve than women, even after decreasing body size effect

STARENJE, VARIJABILNOST SRČANE FREKVENCIJE I METABOLIČKI UTJECAJ PRETILOSTI

The relationship between aging and changes in heart rate variability (HRV) could depend on the metabolic profile of obese people, i.e. metabolically healthy obese (MHO) and metabolically unhealthy obese (MUO). We aimed to determine the age at which obesity related autonomic dysfunction becomes significant and whether it decreases differently according to metabolic profile. We analyzed HRV in 99 adults using Wildman’s criteria for metabolic profile and 5-minute HRV for autonomic nervous system. In MHO, high frequency (HF) decreased in the 4th decade of life. In MUO, standard deviation of R-R intervals (SDNN), root mean square of successive differences of all R-R intervals (RMSSD), number of adjacent intervals differing by more than 50 ms expressed as percentage of all intervals in the collecting period (pNN50), HF, low frequency (LF), LF/HF (LF divided by HF) and total power (TP) decreased in the 4th decade of life (partial shared variance 28%-36%). In conclusion, an age dependent decrease of HRV occurs in MUO between the third and fifth decade of life. In MHO, HF significantly decreases around the age of 40 years. Cardiometabolic profile influences metabolic aging, altering the autonomic nervous system.Dobne promjene u varijabilnosti srčane frekvencije (HRV) mogu zavisiti o metaboličkom profilu pretilih osoba, tj. metaboličkin zdrave (MHO) i metabolički rizične pretile osobe (MUO). Željeli smo utvrditi dob u kojoj nastupa autonomna disfunkcija povezana s pretilošću te opada li HRV različito kod osoba različitog metaboličkog profila. Analizirali smo HRV kod 99 odraslih osoba uz primjenu Wildmanovih kriterija metaboličkog profila i HRV kao aktivnosti autonomnog živčanog sustava. Kod MHO, visoka frekvencija (HF) opadala je u 4. desetljeću života. Kod MUO su standardna devijacija svih R-R intervala (SDNN), kvadratni korijen srednje razlike između sukcesivnih normalnih R-R intevala (RMSSD), postotak sukcesivnih R-R intervala vrijednost kojih prelazi 50 ms (pNN50), HF, niska frekvencija (LF), omjer LF i HF (LF/HF) i ukupna spektralna snaga (TP) opadali u 4. desetljeću života (parcijalna podijeljena varijanca 28%-36%). U zaključku, utvrđen je od dobi zavisan pad HRV kod MUO između trećeg i petog desetljeća života. Kod MHO osoba HF je značajno opala oko 40. godine života. Kardiometabolički profil utječe na starenje remeteći funkcije autonomnog živčanog sustava

Gender differences in parasympathetic reactivation during recovery from Wingate anaerobic test

Background and Purpose: We wanted to investigate gender differences in parasympathetic reactivation from supramaximal exercise. Materials and methods: Parasympathetic reactivation from a Wingate anaerobic test was investigated in 16 male and 15 female volunteers. Heart rate recovery was assessed as the difference between peak exercise heart rate and heart rate recorded following 60 seconds of recovery (HRR60 ). The time constant of the first 30 s post-exercise HR (T30) was determined as a negative reciprocal of the slope of the regression line. Another time constant decay (T) was obtained by fitting the 5 minute post-exercise HRR into a first-order exponential curve. Measures of heart rate variability (HRV) were used to describe the changes in autonomic cardiac regulation following exercise. Results: Post exercise heart rate recovery was faster in male participants, demonstrated through HRR60 (29.5±8.9 vs. 23.4±9.8 seconds respectively) and T30 (292.4±88.7 vs. 409.2±138.3 seconds respectively), but the time constant of the exponential heart rate decay (T) did not differ between the two genders (140.4±55.7 in males and 130.3±49.7seconds in females). The present study demonstrated similar RMSSD, lnHF and HFnu at rest in male and female participants. The time course of RMSSD30 recovery was impaired immediately after exercise. None of the observed vagal HRV indices have restored after five minutes of recovery following the 30-s Wingate test, but the post-exercise lnHF2-5min was significantly smaller in females (3.3±0.9 ms 2 in males vs. 2.5±1.0 ms 2 in females). Conclusion: The immediate HRR and parasympathetic reactivation was affected by gender and was attenuated in female participants

Ventilation inhibits sympathetic action potential recruitment even during severe chemoreflex stress

© 2017 the American Physiological Society. This study investigated the influence of ventilation on sympathetic action potential (AP) discharge patterns during varying levels of high chemoreflex stress. In seven trained breath-hold divers (age 33 ± 12 yr), we measured muscle sympathetic nerve activity (MSNA) at baseline, during preparatory rebreathing (RBR), and during 1) functional residual capacity apnea (FRCApnea) and 2) continued RBR. Data from RBR were analyzed at matched (i.e., to FRCApnea) hemoglobin saturation (HbSat) levels (RBRMatched) or more severe levels (RBREnd). A third protocol compared alternating periods (30 s) of FRC and RBR (FRC-RBRALT). Subjects continued each protocol until 85% volitional tolerance. AP patterns in MSNA (i.e., providing the true neural content of each sympathetic burst) were studied using wavelet-based methodology. First, for similar levels of chemoreflex stress (both HbSat: 71 ± 6%; P = NS), RBRMatched was associated with reduced AP frequency and APs per burst compared with FRCApnea (both P _ 0.001). When APs were binned according to peak-to-peak amplitude (i.e., into clusters), total AP clusters increased during FRCApnea (+10 ± 2; P \u3c 0.001) but not during RBRMatched (+1 ± 2; P = NS). Second, despite more severe chemoreflex stress during RBREnd (Hb-Sat: 56 ± 13 vs. 71 ± 6%; P = 0.001), RBREnd was associated with a restrained increase in the APs per burst (FRCApnea: +18 ± 7; RBREnd: +11 ± 5) and total AP clusters (FRCApnea: +10 ± 2; RBREnd: +6 ± 4) (both P \u3c 0.01). During FRC-RBRALT, all periods of FRC elicited sympathetic AP recruitment (all P \u3c 0.001), whereas all periods of RBR were associated with complete withdrawal of AP recruitment (all P = NS). Presently, we demonstrate that ventilation per se restrains and/or inhibits sympathetic axonal recruitment during high, and even extreme, chemoreflex stress. NEW & NOTEWORTHY The current study demonstrates that the sympathetic neural recruitment patterns observed during chemoreflex activation induced by rebreathing or apnea are restrained and/or inhibited by the act of ventilation per se, despite similar, or even greater, levels of severe chemoreflex stress. Therefore, ventilation modulates not only the timing of sympathetic bursts but also the within-burst axonal recruitment normally observed during progressive chemoreflex stress

Severe hypoxaemic hypercapnia compounds cerebral oxidative–nitrosative stress during extreme apnoea: Implications for cerebral bioenergetic function

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 &gt; 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 &gt; v) and global cerebral blood flow (P = 0.034 to &lt;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

Impaired dynamic cerebral autoregulation in trained breath-hold divers

Breath-hold divers (BHD) experience repeated bouts of severe hypoxia and hypercapnia with large increases in blood pressure. However, the impact of long-term breath-hold diving on cerebrovascular control remains poorly understood. The ability of cerebral blood vessels to respond rapidly to changes in blood pressure represents the property of dynamic autoregulation. The current investigation tested the hypothesis that breathhold diving impairs dynamic autoregulation to a transient hypotensive stimulus. Seventeen BHD (3 women, 11 ± 9 yr of diving) and 15 healthy controls (2 women) completed two or three repeated sit-tostand trials during spontaneous breathing and poikilocapnic conditions. Heart rate (HR), finger arterial blood pressure (BP), and cerebral blood flow velocity (BFV) from the right middle cerebral artery were measured continuously with three-lead electrocardiography, finger photoplethysmography, and transcranial Doppler ultrasonography, respectively. End-tidal carbon dioxide partial pressure was measured with a gas analyzer. Offline, an index of cerebrovascular resistance (CVRi) was calculated as the quotient of mean BP and BFV. The rate of the drop in CVRi relative to the change in BP provided the rate of regulation [RoR; (δCVRi/δT)/δBP]. The BHD demonstrated slower RoR than controls (P ≤ 0.001, d = 1.4). Underlying the reduced RoR in BHD was a longer time to reach nadir CVRi compared with controls (P = 0.004, d = 1.1). In concert with the longer CVRi response, the time to reach peak BFV following standing was longer in BHD than controls (P = 0.01, d = 0.9). The data suggest impaired dynamic autoregulatory mechanisms to hypotension in BHD. NEW & NOTEWORTHY Impairments in dynamic cerebral autoregulation to hypotension are associated with breath-hold diving. Although weakened autoregulation was observed acutely in this group during apneic stress, we are the first to report on chronic adaptations in cerebral autoregulation. Impaired vasomotor responses underlie the reduced rate of regulation, wherein breath-hold divers demonstrate a prolonged dilatory response to transient hypotension. The slower cerebral vasodilation produces a longer perturbation in cerebral blood flow velocity, increasing the risk of cerebral ischemia

TLR2 Mediates Recognition of Live Staphylococcus epidermidis and Clearance of Bacteremia

Background: Staphylococcus epidermidis (SE) is a nosocomial pathogen that causes catheter-associated bacteremia in the immunocompromised, including those at the extremes of age, motivating study of host clearance mechanisms. SE-derived soluble components engage TLR2; but additional signaling pathways have also been implicated, and TLR2 can play complex, at times detrimental, roles in host defense against other Staphylococcal spp. The role of TLR2 in responses of primary blood leukocytes to live SE and in clearance of SE bacteremia, the most common clinical manifestation of SE infection, is unknown. Methodology/Principal Findings: We studied TLR2-mediated recognition of live clinical SE strain 1457 employing TLR2- transfected cells, neutralizing anti-TLR antibodies and TLR2-deficient mice. TLR2 mediated SE-induced cytokine production in human embryonic kidney cells, human whole blood and murine primary macrophages, in part via recognition of a soluble TLR2 agonist. After i.v. challenge with SE, early (1 h) cytokine/chemokine production and subsequent clearance of bacteremia (24-48 h) were markedly impaired in TLR2-deficient mice. Conclusions/Significance: TLR2 mediates recognition of live SE and clearance of SE bacteremia in vivo

Les droits disciplinaires des fonctions publiques : « unification », « harmonisation » ou « distanciation ». A propos de la loi du 26 avril 2016 relative à la déontologie et aux droits et obligations des fonctionnaires

The production of tt‾ , W+bb‾ and W+cc‾ is studied in the forward region of proton–proton collisions collected at a centre-of-mass energy of 8 TeV by the LHCb experiment, corresponding to an integrated luminosity of 1.98±0.02 fb−1 . The W bosons are reconstructed in the decays W→ℓν , where ℓ denotes muon or electron, while the b and c quarks are reconstructed as jets. All measured cross-sections are in agreement with next-to-leading-order Standard Model predictions.The production of $t\overline{t}$, $W+b\overline{b}$ and $W+c\overline{c}$ is studied in the forward region of proton-proton collisions collected at a centre-of-mass energy of 8 TeV by the LHCb experiment, corresponding to an integrated luminosity of 1.98 $\pm$ 0.02 \mbox{fb}^{-1}. The $W$ bosons are reconstructed in the decays $W\rightarrow\ell\nu$, where $\ell$ denotes muon or electron, while the $b$ and $c$ quarks are reconstructed as jets. All measured cross-sections are in agreement with next-to-leading-order Standard Model predictions