Effects of periodic breathing on sleep at high altitude: a randomized, placebo-controlled, crossover study using inspiratory CO2.

Hypoxia at high altitude facilitates changes in ventilatory control that can lead to nocturnal periodic breathing (nPB). Here, we introduce a placebo-controlled approach to prevent nPB by increasing inspiratory CO2 and used it to assess whether nPB contributes to the adverse effects of hypoxia on sleep architecture. In a randomized, single-blinded, crossover design, 12 men underwent two sojourns (three days/nights each, separated by 4 weeks) in hypobaric hypoxia corresponding to 4000 m altitude, with polysomnography during the first and third night of each sojourn. During all nights, subjects' heads were encompassed by a canopy retaining exhaled CO2, and CO2 concentration in the canopy (i.e. inspiratory CO2 concentration) was controlled by adjustment of fresh air inflow. Throughout the placebo sojourn inspiratory CO2 was ≤0.2%, whereas throughout the other sojourn it was increased to 1.76% (IQR, 1.07%-2.44%). During the placebo sojourn, total sleep time (TST) with nPB was 54.3% (37.4%-80.8%) and 45.0% (24.5%-56.5%) during the first and the third night, respectively (P = 0.042). Increased inspiratory CO2 reduced TST with nPB by an absolute 38.1% (28.1%-48.1%), the apnoea-hypopnoea index by 58.1/h (40.1-76.1/h), and oxygen desaturation index ≥3% by 56.0/h (38.9.1-73.2/h) (all P < 0.001), whereas it increased the mean arterial oxygen saturation in TST by 2.0% (0.4%-3.5%, P = 0.035). Increased inspiratory CO2 slightly increased the percentage of N3 sleep during the third night (P = 0.045), without other effects on sleep architecture. Increasing inspiratory CO2 effectively prevented hypoxia-induced nPB without affecting sleep macro-architecture, indicating that nPB does not explain the sleep deterioration commonly observed at high altitudes. KEY POINTS: Periodic breathing is common during sleep at high altitude, and it is unclear how this affects sleep architecture. We developed a placebo-controlled approach to prevent nocturnal periodic breathing (nPB) with inspiratory CO2 administration and used it to assess the effects of nPB on sleep in hypobaric hypoxia. Nocturnal periodic breathing was effectively mitigated by an increased inspiratory CO2 fraction in a blinded manner. Prevention of nPB did not lead to relevant changes in sleep architecture in hypobaric hypoxia. We conclude that nPB does not explain the deterioration in sleep architecture commonly observed at high altitude.

Drones reduce the time to defibrillation in a highly visited non-urban area: A randomized simulation-based trial.

INTRODUCTION: Out-of-hospital cardiac arrest (OHCA) has a high global incidence and mortality rate, with early defibrillation significantly improving survival. Our aim was to assess the feasibility of autonomous drone delivery of automated external defibrillators (AED) in a non-urban area with physical barriers and compare the time to defibrillate (TTD) with bystander retrieval from a public access defibrillator (PAD) point and helicopter emergency medical services (HEMS) physician performed defibrillation. METHODS: This randomized simulation-based trial with a cross-over design included bystanders performing AED retrievals either delivered by automated drone flight or on foot from a PAD point, and simulated HEMS interventions. The primary outcome was the time to defibrillation, with secondary outcomes comparing workload, perceived physical effort, and ease of use. RESULTS: Thirty-six simulations were performed. Drone-delivered AED intervention had a significantly shorter TTD [2.2 (95 % CI 2.0-2.3) min] compared to PAD retrieval [12.4 (95 % CI 10.4-14.4) min] and HEMS [18.2 (95 % CI 17.1-19.2) min]. The self-reported physical effort on a visual analogue scale for drone-delivered AED was significantly lower versus PAD [2.5 (1 - 22) mm vs. 81 (65-99) mm, p = 0.02]. The overall mean workload measured by NASA-TLX was also significantly lower for drone delivery compared to PAD [4.3 (1.2-11.7) vs. 11.9 (5.5-14.5), p = 0.018]. CONCLUSION: The use of drones for automated AED delivery in a non-urban area with physical barriers is feasible and leads to a shorter time to defibrillation. Drone-delivered AEDs also involve a lower workload and perceived physical effort than AED retrieval on foot.

Baroreflex dynamics during the rest to exercise transient in acute normobaric hypoxia in humans.

PURPOSE: We hypothesised that during a rest-to-exercise transient in hypoxia (H), compared to normoxia (N), (i) the initial baroreflex sensitivity (BRS) decrease would be slower and (ii) the fast heart rate (HR) and cardiac output (CO) response would have smaller amplitude (A1) due to lower vagal activity in H than N. METHODS: Ten participants performed three rest-to-50 W exercise transients on a cycle-ergometer in N (ambient air) and three in H (inspired fraction of O2 = 0.11). R-to-R interval (RRi, by electrocardiography) and blood pressure profile (by photo-plethysmography) were recorded non-invasively. Analysis of the latter provided mean arterial pressure (MAP) and stroke volume (SV). CO = HR·SV. BRS was calculated by modified sequence method. RESULTS: Upon exercise onset in N, MAP fell to a minimum (MAPmin) then recovered. BRS decreased immediately from 14.7 ± 3.6 at rest to 7.0 ± 3.0 ms mmHg-1 at 50 W (p < 0.01). The first BRS sequence detected at 50 W was 8.9 ± 4.8 ms mmHg-1 (p < 0.05 vs. rest). In H, MAP showed several oscillations until reaching a new steady state. BRS decreased rapidly from 10.6 ± 2.8 at rest to 2.9 ± 1.5 ms mmHg-1 at 50 W (p < 0.01), as the first BRS sequence at 50 W was 5.8 ± 2.6 ms mmHg-1 (p < 0.01 vs. rest). CO-A1 was 2.96 ± 1.51 and 2.31 ± 0.94 l min-1 in N and H, respectively (p = 0.06). HR-A1 was 7.7 ± 4.6 and 7.1 ± 5.9 min-1 in N and H, respectively (p = 0.81). CONCLUSION: The immediate BRS decrease in H, coupled with similar rapid HR and CO responses, is compatible with a withdrawal of residual vagal activity in H associated with increased sympathetic drive.

Modeling the Power-Duration Relationship in Professional Cyclists During the Giro d'Italia.

ABSTRACT: Vinetti, G, Pollastri, L, Lanfranconi, F, Bruseghini, P, Taboni, A, and Ferretti, G. Modeling the power-duration relationship in professional cyclists during the Giro d'Italia. J Strength Cond Res 37(4): 866-871, 2023-Multistage road bicycle races allow the assessment of maximal mean power output (MMP) over a wide spectrum of durations. By modeling the resulting power-duration relationship, the critical power ( CP ) and the curvature constant ( W' ) can be calculated and, in the 3-parameter (3-p) model, also the maximal instantaneous power ( P0 ). Our aim is to test the 3-p model for the first time in this context and to compare it with the 2-parameter (2-p) model. A team of 9 male professional cyclists participated in the 2014 Giro d'Italia with a crank-based power meter. The maximal mean power output between 10 seconds and 10 minutes were fitted with 3-p, whereas those between 1 and 10 minutes with the 2- model. The level of significance was set at p < 0.05. 3-p yielded CP 357 ± 29 W, W' 13.3 ± 4.2 kJ, and P0 1,330 ± 251 W with a SEE of 10 ± 5 W, 3.0 ± 1.7 kJ, and 507 ± 528 W, respectively. 2-p yielded a CP and W' slightly higher (+4 ± 2 W) and lower (-2.3 ± 1.1 kJ), respectively ( p < 0.001 for both). Model predictions were within ±10 W of the 20-minute MMP of time-trial stages. In conclusion, during a single multistage racing event, the 3-p model accurately described the power-duration relationship over a wider MMP range without physiologically relevant differences in CP with respect to 2-p, potentially offering a noninvasive tool to evaluate competitive cyclists at the peak of training.

Dynamics of cardiovascular and baroreflex readjustments during a light-to-moderate exercise transient in humans.

PURPOSE: We hypothesised that, during a light-to-moderate exercise transient, compared to an equivalent rest-to-exercise transient, (1) a further baroreflex sensitivity (BRS) decrease would be slower, (2) no rapid heart rate (HR) response would occur, and (3) the rapid cardiac output (CO) response would have a smaller amplitude (A1). Hence, we analysed the dynamics of arterial baroreflexes and the HR and CO kinetics during rest-to-50 W (0-50 W) and 50-to-100 W (50-100 W) exercise transients. METHODS: 10 subjects performed three 0-50 W and three 50-100 W on a cycle ergometer. We recorded arterial blood pressure profiles (photo-plethysmography) and R-to-R interval (RRi, electrocardiography). The former were analysed to obtain beat-by-beat mean arterial pressure (MAP) and stroke volume (SV). CO was calculated as SV times HR. BRS was measured by modified sequence method. RESULTS: During 0-50 W, MAP transiently fell (- 9.0 ± 5.7 mmHg, p < 0.01) and BRS passed from 15.0 ± 3.7 at rest to 7.3 ± 2.4 ms mmHg-1 at 50 W (p < 0.01) promptly (first BRS sequence: 8.1 ± 4.6 ms mmHg-1, p < 0.01 vs. rest). During 50-100 W, MAP did not fall and BRS passed from 7.2 ± 2.6 at 50 W to 3.3 ± 1.3 ms mmHg-1 at 100 W (p < 0.01) slowly (first BRS sequence: 5.3 ± 3.1 ms mmHg-1, p = 0.07 vs. 50 W). A1 for HR was 9.2 ± 6.0 and 6.0 ± 4.5 min-1 in 0-50 W and 50-100 W, respectively (p = 0.19). The corresponding A1 for CO were 2.80 ± 1.54 and 0.91 ± 0.55 l∙min-1 (p < 0.01). CONCLUSION: During 50-100 W, with respect to 0-50 W, BRS decreased more slowly, in absence of a prompt pressure decrease. BRS decrease and rapid HR response in 50-100 W were unexpected and ascribed to possible persistence of some vagal tone at 50 W.

A century of exercise physiology: key concepts on coupling respiratory oxygen flow to muscle energy demand during exercise.

After a short historical account, and a discussion of Hill and Meyerhof's theory of the energetics of muscular exercise, we analyse steady-state rest and exercise as the condition wherein coupling of respiration to metabolism is most perfect. The quantitative relationships show that the homeostatic equilibrium, centred around arterial pH of 7.4 and arterial carbon dioxide partial pressure of 40 mmHg, is attained when the ratio of alveolar ventilation to carbon dioxide flow ([Formula: see text]) is - 21.6. Several combinations, exploited during exercise, of pertinent respiratory variables are compatible with this equilibrium, allowing adjustment of oxygen flow to oxygen demand without its alteration. During exercise transients, the balance is broken, but the coupling of respiration to metabolism is preserved when, as during moderate exercise, the respiratory system responds faster than the metabolic pathways. At higher exercise intensities, early blood lactate accumulation suggests that the coupling of respiration to metabolism is transiently broken, to be re-established when, at steady state, blood lactate stabilizes at higher levels than resting. In the severe exercise domain, coupling cannot be re-established, so that anaerobic lactic metabolism also contributes to sustain energy demand, lactate concentration goes up and arterial pH falls continuously. The [Formula: see text] decreases below - 21.6, because of ensuing hyperventilation, while lactate keeps being accumulated, so that exercise is rapidly interrupted. The most extreme rupture of the homeostatic equilibrium occurs during breath-holding, because oxygen flow from ambient air to mitochondria is interrupted. No coupling at all is possible between respiration and metabolism in this case.

A closed-loop approach to the study of the baroreflex dynamics during posture changes at rest and at exercise in humans.

We hypothesized that during rapid uptilting at rest, due to vagal withdrawal, arterial baroreflex sensitivity (BRS) may decrease promptly and precede the operating point (OP) resetting, whereas different kinetics are expected during exercise steady state, due to lower vagal activity than at rest. To test this, eleven subjects were rapidly (<2 s) tilted from supine (S) to upright (U) and vice versa every 3 min, at rest and during steady-state 50 W pedaling. Mean arterial pressure (MAP) was measured by finger cuff (Portapres) and R-to-R interval (RRi) by electrocardiography. BRS was computed with the sequence method both during steady and unsteady states. At rest, BRS was 35.1 ms·mmHg-1 (SD = 17.1) in S and 16.7 ms·mmHg-1 (SD = 6.4) in U (P < 0.01), RRi was 901 ms (SD = 118) in S and 749 ms (SD = 98) in U (P < 0.01), and MAP was 76 mmHg (SD = 11) in S and 83 mmHg (SD = 8) in U (P < 0.01). During uptilt, BRS decreased promptly [first BRS sequence was 19.7 ms·mmHg-1 (SD = 5.0)] and was followed by an OP resetting (MAP increase without changes in RRi). At exercise, BRS and OP did not differ between supine and upright positions [BRS was 7.7 ms·mmHg-1 (SD = 3.0) and 7.7 ms·mmHg-1 (SD = 3.5), MAP was 85 mmHg (SD = 13) and 88 mmHg (SD = 10), and RRi was 622 ms (SD = 61) and 600 ms (SD = 70), respectively]. The results support the tested hypothesis. The prompt BRS decrease during uptilt at rest may be ascribed to a vagal withdrawal, similarly to what occurs at exercise onset. The OP resetting may be due to a slower control mechanism, possibly an increase in sympathetic activity.

Baroreflex responses during dry resting and exercise apnoeas in air and pure oxygen.

PURPOSE: We analysed the characteristics of arterial baroreflexes during the first phase of apnoea (φ1). METHODS: 12 divers performed rest and exercise (30 W) apnoeas (air and oxygen). We measured beat-by-beat R-to-R interval (RRi) and mean arterial pressure (MAP). Mean RRi and MAP values defined the operating point (OP) before (PRE-ss) and in the second phase (φ2) of apnoea. Baroreflex sensitivity (BRS, ms·mmHg-1) was calculated with the sequence method. RESULTS: In PRE-ss, BRS was (median [IQR]): at rest, 20.3 [10.0-28.6] in air and 18.8 [13.8-25.2] in O2; at exercise 9.2[8.4-13.2] in air and 10.1[8.4-13.6] in O2. In φ1, during MAP decrease, BRS was lower than in PRE-ss at rest (6.6 [5.3-11.4] in air and 7.7 [4.9-14.3] in O2, p < 0.05). At exercise, BRS in φ1 was 6.4 [3.9-13.1] in air and 6.7 [4.1-9.5] in O2. After attainment of minimum MAP (MAPmin), baroreflex resetting started. After attainment of minimum RRi, baroreflex sequences reappeared. In φ2, BRS at rest was 12.1 [9.6-16.2] in air, 12.9 [9.2-15.8] in O2. At exercise (no φ2 in air), it was 7.9 [5.4-10.7] in O2. In φ2, OP acts at higher MAP values. CONCLUSION: In apnoea φ1, there is a sudden correction of MAP fall via baroreflex. The lower BRS in the earliest φ1 suggests a possible parasympathetic mechanism underpinning this reduction. After MAPmin, baroreflex resets, displacing its OP at higher MAP level; thus, resetting may not be due to central command. After resetting, restoration of BRS suggests re-establishment of vagal drive.

Follow-up of Acute Respiratory Disorders in Cyclists Competing in the 100th Giro d'Italia.

Acute respiratory disorder is a common sub-clinical condition affecting elite cyclists. Monitoring the perturbations of the immunological cells in the respiratory tract, indicative of a likely proinflammatory state, during an International Cycling Union world tour is a challenging task. The aim of this study was to follow up on the sign and symptoms of upper way respiratory infections with or without asthma, using non-invasive methods, during a 21-day race (100° Giro d'Italia, 2017). Nine male elite cyclists of the Bahrain Merida Team were evaluated before the training season and daily during the race. Clinical history, skin prick and spirometric test, acute respiratory symptoms were measured using validated questionnaires, and values of fraction of exhaled nitric oxide were collected longitudinally. Four of the 9 athletes had allergies with/or consistent abnormal spirometric curves before the race. During the race, 5 athletes had a fraction of exhaled nitric oxide values >20 ppb which correlated with respiratory symptoms collected through questionnaires. These were related to the environmental characteristics of the places travelled through in the race. The athletes with a predisposition to chronic respiratory inflammation in the pre-competitive season were more likely to develop acute respiratory symptoms during the race.

Breath holding as an example of extreme hypoventilation: experimental testing of a new model describing alveolar gas pathways.

NEW FINDINGS: What is the central question of this study? We modelled the alveolar pathway during breath holding on the hypothesis that it follows a hypoventilation loop on the O2 -CO2 diagram. What is the main finding and its importance? Validation of the model was possible within the range of alveolar gas compositions compatible with consciousness. Within this range, the experimental data were compatible with the proposed model. The model and its characteristics might allow predictions of alveolar gas composition whenever the alveolar ventilation goes to zero; for example, static and dynamic breath holding at the surface or during ventilation/intubation failure in anaesthesia. ABSTRACT: According to the hypothesis that alveolar partial pressures of O2 and CO2 during breath holding (BH) should vary following a hypoventilation loop, we modelled the alveolar gas pathways during BH on the O2 -CO2 diagram and tested it experimentally during ambient air and pure oxygen breathing. In air, the model was constructed using the inspired and alveolar partial pressures of O2 ( PIO2 and PAO2 , respectively) and CO2 ( PICO2 and PACO2 , respectively) and the steady-state values of the pre-BH respiratory exchange ratio (RER). In pure oxygen, the model respected the constraint of PACO2=-PAO2+PIO2 . To test this, 12 subjects performed several BHs of increasing duration and one maximal BH at rest and during exercise (30 W cycling supine), while breathing air or pure oxygen. We measured gas flows, PAO2 and PACO2 before and at the end of all BHs. Measured data were fitted through the model. In air, PIO2  = 150 ± 1 mmHg and PICO2  = 0.3 ± 0.0 mmHg, both at rest and at 30 W. Before BH, steady-state RER was 0.83 ± 0.16 at rest and 0.77 ± 0.14 at 30 W; PAO2  = 107 ± 7 mmHg at rest and 102 ± 8 mmHg at 30 W; and PACO2  = 36 ± 4 mmHg at rest and 38 ± 3 mmHg at 30 W. By model fitting, we computed the RER during the early phase of BH: 0.10 [95% confidence interval (95% CI) = 0.08-0.12] at rest and 0.13 (95% CI = 0.11-0.15) at 30 W. In oxygen, model fitting provided PIO2 : 692 (95% CI = 688-696) mmHg at rest and 693 (95% CI = 689-698) mmHg at 30 W. The experimental data are compatible with the proposed model, within its physiological range.

A regression method for the power-duration relationship when both variables are subject to error.

PURPOSE: The power-duration relationship has been variously modelled, although duration must be acknowledged as the dependent variable and is supposed to represent the only source of experimental error. However, there are certain situations, namely extremely high power outputs or outdoor field conditions, in which the error in power output measurement may not remain negligible. The geometric mean (GM) regression method deals with the assumption that also the independent variable is subject to a certain amount of experimental error, but has never been utilized in this context. METHODS: We applied the GM regression method for the two- and three-parameter critical power models and tested it against the usual weighted least square (WLS) procedure with our previous published data. RESULTS: There were no significant differences between parameter estimates of WLS and GM. Bias and limit of agreements between the two methods were low, while correlation coefficients were high (0.85-1.00). CONCLUSIONS: GM provided equivalent results with respect to WLS in fitting the critical power model to experimental data and for its conceptual characteristics must be preferred wherever concerns on the precision of P measurement are present, such as for in-field power meters.

Experimental validation of the 3-parameter critical power model in cycling.

PURPOSE: The three-parameter model of critical power (3-p) implies that in the severe exercise intensity domain time to exhaustion (Tlim) decreases hyperbolically with power output starting from the power asymptote (critical power, wcr) and reaching 0 s at a finite power limit (w0) thanks to a negative time asymptote (k). We aimed to validate 3-p for short Tlim and to test the hypothesis that w0 represents the maximal instantaneous muscular power. METHODS: Ten subjects performed an incremental test and nine constant-power trials to exhaustion on an electronically braked cycle ergometer. All trials were fitted to 3-p by means of non-linear regression, and those with Tlim greater than 2 min also to the 2-parameter model (2-p), obtained constraining k to 0 s. Five vertical squat jumps on a force platform were also performed to determine the single-leg (i.e., halved) maximal instantaneous power. RESULTS: Tlim ranged from 26 ± 4 s to 15.7 ± 4.9 min. In 3-p, with respect to 2-p, wcr was identical (177 ± 26 W), while curvature constant W' was higher (17.0 ± 4.3 vs 15.9 ± 4.2 kJ, p < 0.01). 3-p-derived w0 was lower than single-leg maximal instantaneous power (1184 ± 265 vs 1554 ± 235 W, p < 0.01). CONCLUSIONS: 3-p is a good descriptor of the work capacity above wcr up to Tlim as short as 20 s. However, since there is a discrepancy between estimated w0 and measured maximal instantaneous power, a modification of the model has been proposed.

Effects of recovery interval duration on the parameters of the critical power model for incremental exercise.

INTRODUCTION: We tested the linear critical power ([Formula: see text]) model for discrete incremental ramp exercise implying recovery intervals at the end of each step. METHODS: Seven subjects performed incremental (power increment 25 W) stepwise ramps to subject's exhaustion, with recovery intervals at the end of each step. Ramps' slopes (S) were 0.83, 0.42, 0.28, 0.21, and 0.08 W s-1; recovery durations (t r) were 0 (continuous stepwise ramps), 60, and 180 s (discontinuous stepwise ramps). We determined the energy store component (W'), the peak power ([Formula: see text]), and [Formula: see text]. RESULTS: When t r = 0 s, [Formula: see text] and W' were 187 ± 26 W and 14.5 ± 5.8 kJ, respectively. When t r = 60 or 180 s, the model for ramp exercise provided inconsistent [Formula: see text] values. A more general model, implying a quadratic [Formula: see text] versus [Formula: see text] relationship, was developed. This model yielded, for t r = 60 s, [Formula: see text] = 189 ± 48 W and W' = 18.6 ± 17.8 kJ, and for t r = 180 s, [Formula: see text] = 190 ± 34 W, and W' = 16.4 ± 16.7 kJ. These [Formula: see text] and W' did not differ from the corresponding values for t r = 0 s. Nevertheless, the overall amount of energy sustaining work above [Formula: see text], due to energy store reconstitution during recovery intervals, was higher the longer t r, whence higher [Formula: see text] values. CONCLUSIONS: The linear [Formula: see text] model for ramp exercise represents a particular case (for t r = 0 s) of a more general model, accounting for energy resynthesis following oxygen deficit payment during recovery.

Cardiorespiratory Responses to Exercise in Hypobaric versus Normobaric Hypoxia: A Randomized, Single-Blind, Crossover Study.

PURPOSE: There is controversy whether there are meaningful physiological differences between hypobaric (HH) and normobaric hypoxia (NH). This study aimed to compare the cardiorespiratory responses to acute HH and NH under strictly controlled conditions. We hypothesized no differences at rest and during submaximal exercise, whereas during maximal exercise, a higher maximal ventilation (V̇Emax), peripheral oxygen saturation (SpO2) and maximal oxygen consumption (V̇O2max) in HH than in NH. METHODS: In a randomized, single-blind, crossover design, eight young healthy subjects (three females) were studied in an environmental chamber in which either the barometric pressure (HH) or the inspired oxygen fraction (NH) was reduced to the equivalent of ~4000 m altitude. Measurements were taken at rest, during submaximal (moderate and high intensity) and maximal cycling exercise. RESULTS: All resting parameters were similar between HH and NH, except for a lower root mean square of the successive R-R interval differences in HH (p < 0.05). SpO2 was 2% higher in HH at all exercise intensities (p < 0.05). During submaximal exercise, minute ventilation was similar between HH and NH. However, HH yielded a 7% lower tidal volume during moderate-intensity exercise (p < 0.05) and a lower respiratory exchange ratio during high-intensity exercise (p < 0.01). V̇Emax and V̇O2max were 11% and 6% higher in HH, respectively (p < 0.01 for both). SpO2 at maximal exercise was positively correlated with V̇Emax, V̇Emax/V̇O2max and V̇O2max. CONCLUSIONS: The higher V̇O2max found in HH than in NH can be attributed to the higher V̇Emax counteracting desaturation at maximal exercise. Conversely, submaximal SpO2 improved in HH through mechanisms other than increased ventilation. These findings are likely due to respiratory muscle unloading in HH, which operated through different mechanisms depending on exercise intensity.

T-wave axis deviation and left ventricular hypertrophy interaction in diabetes and hypertension.

Electrocardiographic signs of left ventricular hypertrophy (ECG-LVH) and T-wave axis (TA) deviation are independent predictors of fatal and non fatal events. We assessed the prevalence of ECG-LVH, TA abnormalities and their combination according to the presence or absence of diabetes and/or hypertension in a large sample of the adult general Italian population. Data from 10,184 women (54 ± 11 years) and 8775 men (54 ± 11 years) were analyzed from the Moli-sani cohort, a database of randomly recruited adults (age >35) from the general population of Molise, a central region of Italy that includes collection of standard 12-lead resting ECG. Subjects with previous myocardial infarction, angina, cerebrovascular disease or left bundle brunch block or missing values for TA or ECG-LVH have been excluded. TA was measured from the standard 12-lead ECG and it was defined as the rotation of the T wave in the frontal plane as computed by a proprietary algorithm (CalECG/Bravo, AMPS-LLC, NY). ECG-LVH was defined as Sokolow Lyon voltage (SLv) >35 mm or Cornell voltage duration Product (CP) >= 2440 mm*ms. Among subjects with ECG-LVH, prevalence of hypertension was 59.0% and 49.7%, respectively for men and women, whereas that of diabetes was 10.7% and 5.7%. In hypertensives, TA was normal in 72.3% of subjects, borderline in 24.8% and abnormal in 2.9%. In diabetics, TA was normal in 70.4% of subjects, borderline in 26.5% and abnormal in 3.1%. In both hypertensive and diabetic subjects, the prevalence of ECG-LVH, was significantly greater in subjects with borderline or abnormal TA. Hypertension was an independent predictor of abnormal TA (odd ratio: 1.38, P = .025). These results suggest that hypertension might play a relevant role in the pathogenesis of TA deviation.

Comparison of resting energy expenditure measured with metabolic cart and calculated with predictive formulas in critically ill patients on mechanical ventilation.

INTRODUCTION: The purpose was to compare the resting energy expenditure (REE) measured with the Q-NRG™+ metabolic-cart (MREE) with REE predicted by equations (the Harris-Benedict formula and an equation developed in ward, REE-HB and REE-W, respectively). We also aimed to assess the agreement of the measurements of oxygen consumption (V̇O2) and carbon dioxide production (V̇CO2) at different inspired fractions of oxygen (FiO2). METHODS: 27 mechanically ventilated ICU patients were enrolled. V̇O2 and V̇CO2 were measured by Q-NRG™+ during breathing 40% and 60% FiO2. MREE was compared with REE-W and REE-HB normalized for body weight. RESULTS: V̇O2 was 233.0 (95.2) ml/min and 217.5 (89.8) ml/min at FiO2 40% and 60%, respectively (NS). V̇CO2 was 199.0 (91.7) ml/min at FiO2 40%, and 197.5 (85.5) ml/min at FiO2 60% (NS). The REE estimated from the equations was significantly different from the MREE. The best agreement was found for the Harris-Benedict equation without correction for stress-factors. Harris-Benedict equation corrected overestimates REE. CONCLUSIONS: This new metabolic cart Q-NRG™+ provides a concordance of values for V̇O2 and V̇CO2 when measured at different FiO2, and is a reliable tool for estimating energy expenditure and assessing the nutritional needs of the patient. This study demonstrates that the estimation of REE using predictive formulas does not allow accurate calculation of metabolic demands in ventilated intensive care patient. However, predictive equations allow for a rapid assessment of REE and calculation of the amount of energy derived from different substrates.

Changes in body mass, appetite-related hormones, and appetite sensation in women during 4 days of hypobaric hypoxic exposure equivalent to 3,500-m altitude.

Altitude exposure may suppress appetite and hence provide a viable weight-loss strategy. While changes in food intake and availability as well as physical activity may contribute to altered appetite at altitude, herein we aimed to investigate the isolated effects of hypobaric hypoxia on appetite regulation and sensation. Twelve healthy women (age: 24.0 ± 4.2 years, body mass: 60.6 ± 7.0 kg) completed two 4-day sojourns in a hypobaric chamber, one in normoxia [PB = 761 mmHg, 262 m (NX)] and one in hypobaric hypoxia [PB = 493 mmHg (HH)] equivalent to 3,500-m altitude. Energy intake was standardized 4 days prior and throughout both sojourns. Plasma concentrations of leptin, acylated ghrelin, cholecystokinin (CCK), and cytokine growth differentiation factor 15 (GDF15) were determined every morning. Before and after breakfast, lunch, and dinner, appetite was assessed using visual analog scales. Body mass was significantly decreased following HH but not NX (-0.71 ± 0.32 kg vs. -0.05 ± 0.54 kg, condition: P < 0.001). Compared to NX, acylated ghrelin decreased throughout the HH sojourn (condition × time: P = 0.020), while leptin was higher throughout the entire HH sojourn (condition: P < 0.001). No differences were observed in CCK and GDF15 between the sojourns. Feelings of satiety and fullness were higher (condition: P < 0.001 and P = 0.013, respectively), whereas prospective food consumption was lower in HH than in NX (condition: P < 0.001). Our findings suggest that hypoxia exerts an anorexigenic effect on appetite-regulating hormones, suppresses subjective appetite sensation, and can induce weight loss in young healthy women. Among the investigated hormones, acylated ghrelin and leptin most likely explain the observed HH-induced appetite suppression.NEW & NOTEWORTHY This study investigated the effects of hypoxia on appetite regulation in women while strictly controlling for diet, physical activity, menstrual cycle, and environmental conditions. In young women, 4 days of altitude exposure (3,500 m) decreases body weight and circulating acylated ghrelin levels while preserving leptin concentrations. In line with the hormonal changes, altitude exposure induces alterations in appetite sensation, consisting of a decreased feeling of hunger and prospective food intake and an increased feeling of fullness and satiety.

Surgical masks and filtering facepiece class 2 respirators (FFP2) have no major physiological effects at rest and during moderate exercise at 3000-m altitude: a randomised controlled trial.

BACKGROUND: During the COVID-19 pandemic, the use of face masks has been recommended or enforced in several situations; however, their effects on physiological parameters and cognitive performance at high altitude are unknown. METHODS: Eight healthy participants (four females) rested and exercised (cycling, 1 W/kg) while wearing no mask, a surgical mask or a filtering facepiece class 2 respirator (FFP2), both in normoxia and hypobaric hypoxia corresponding to an altitude of 3000 m. Arterialised oxygen saturation (SaO2), partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2), heart and respiratory rate, pulse oximetry (SpO2), cerebral oxygenation, visual analogue scales for dyspnoea and mask's discomfort were systematically investigated. Resting cognitive performance and exercising tympanic temperature were also assessed. RESULTS: Mask use had a significant effect on PaCO2 (overall +1.2 ± 1.7 mmHg). There was no effect of mask use on all other investigated parameters except for dyspnoea and discomfort, which were highest with FFP2. Both masks were associated with a similar non-significant decrease in SaO2 during exercise in normoxia (-0.5 ± 0.4%) and, especially, in hypobaric hypoxia (-1.8 ± 1.5%), with similar trends for PaO2 and SpO2. CONCLUSIONS: Although mask use was associated with higher rates of dyspnoea, it had no clinically relevant impact on gas exchange at 3000 m at rest and during moderate exercise, and no detectable effect on resting cognitive performance. Wearing a surgical mask or an FFP2 can be considered safe for healthy people living, working or spending their leisure time in mountains, high-altitude cities or other hypobaric environments (e.g. aircrafts) up to an altitude of 3000 m.

Effects of Water Immersion on the Internal Power of Cycling.

PURPOSE: Water immersion adds additional drag and metabolic demand for limb movement with respect to air, but its effect on the internal metabolic power (Eint) of cycling is unknown. We aimed at quantifying the increase in Eint during underwater cycling with respect to dry conditions at different pedaling rates. METHODS: Twelve healthy subjects (four women) pedaled on a waterproof cycle ergometer in an experimental pool that was either empty (DRY) or filled with tap water at 30.8°C ± 0.6°C (WET). Four different pedal cadences (fp) were studied (40, 50, 60, and 70 rpm) at 25, 50, 75, and 100 W. The metabolic power at steady state was measured via open circuit respirometry, and Eint was calculated as the metabolic power extrapolated for 0 W. RESULTS: The Eint was significantly higher in WET than in DRY at 50, 60, and 70 rpm (81 ± 31 vs 32 ± 30 W, 167 ± 35 vs 50 ± 29 W, 311 ± 51 vs 81 ± 30 W, respectively, all P < 0.0001), but not at 40 rpm (16 ± 5 vs 11 ± 17 W, P > 0.99). Eint increased with the third power of fp both in WET and DRY (R2 = 0.49 and 0.91, respectively). CONCLUSIONS: Water drag increased Eint, although limbs unloading via the Archimedes' principle and limbs shape could be potential confounding factors. A simple formula was developed to predict the increase in mechanical power in dry conditions needed to match the rate of energy expenditure during underwater cycling: 44 fp3 - 7 W, where fp is expressed in Hertz.