ABSTRACT
For often unclear reasons, the survival times of critically buried avalanche victims vary widely from minutes to hours. Individuals can survive and sustain organ function if they can breathe under the snow and maintain sufficient delivery of oxygen and efflux of carbon dioxide. We review the physiological responses of humans to critical avalanche burial, a model which shares similarities and differences with apnoea and accidental hypothermia. Within a few minutes of burial, an avalanche victim is exposed to hypoxaemia and hypercapnia, which have important effects on the respiratory and cardiovascular systems and pose a major threat to the central nervous system. As burial time increases, an avalanche victim also develops hypothermia. Despite progressively reduced metabolism, reduced oxygen and increased carbon dioxide tensions may exacerbate the pathophysiological consequences of hypothermia. Hypercapnia seems to be the main cause of cardiovascular instability, which, in turn, is the major reason for reduced cerebral oxygenation despite reductions in cerebral metabolic activity caused by hypothermia. 'Triple H syndrome' refers to the interaction of hypoxia, hypercapnia and hypothermia in a buried avalanche victim. Future studies should investigate how the respiratory gases entrapped in the porous snow structure influence the physiological responses of buried individuals and how haemoconcentration, blood viscosity and cell deformability affect blood flow and oxygen delivery. Attention should also be devoted to identifying strategies to prolong avalanche survival by either mitigating hypoxia and hypercapnia or reducing core temperature so that neuroprotection occurs before the onset of cerebral hypoxia.
ABSTRACT
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.
Subject(s)
Baroreflex , Exercise , Heart Rate , Hypoxia , Rest , Humans , Baroreflex/physiology , Male , Hypoxia/physiopathology , Exercise/physiology , Adult , Heart Rate/physiology , Rest/physiology , Blood Pressure/physiology , Female , Cardiac Output/physiologyABSTRACT
Inefficient ventilatory response during cardiopulmonary exercise testing (CPET) has been suggested as a cause of post-COVID-19 dyspnea. It has been described in hospitalized patients (HOSP) with lung parenchymal sequelae but also after mild infection in ambulatory patients (AMBU). We hypothesize that AMBU and HOSP have different ventilatory responses to exercise, due to different etiologies. We analyzed CPET realized between July 2020 and May 2022 of patients with persisting respiratory symptoms 3 mo after COVID-19. Chest computed tomography (CT) scan, pulmonary function tests, quality of life, and respiratory questionnaires were collected. CPET data were specifically explored as a function of ventilation (VÌe) and time. Seventy-nine consecutive patients were included (42 AMBU and 37 HOSP, median: 54 [44-60] yr old, 57% female). Patients were hospitalized for a median of 20 [8-34] days, with pneumonia (41%) or acute respiratory distress syndrome (ARDS; 30%). Among HOSP, 12(32%) patients had abnormal values for spirometry and 18(51%) for carbon monoxide diffusing capacity (P < 0.001). CPET showed no differences between AMBU and HOSP in peak absolute O2 uptake (VÌo2) (1.59 [1.22-2.11] mL·min-1; P = 0.65). Tidal volume (VT) as a function of VÌe, was lower in AMBU than in HOSP (P < 0.01) toward the end of exercise. The slope of the VÌe-CO2 production was higher than normal in both groups (30.9 [26.1-34.3]; P = 0.96). In conclusion, the severity of COVID-19 did not influence the exercise capacity, but AMBU demonstrated a less efficient ventilatory response to exercise as compared with HOSP. CPET with exploration of data as a function of VÌe and throughout the exercise better unveil ventilatory inefficiency.NEW & NOTEWORTHY We evaluated the exercise ventilatory response in patients with persisting dyspnea after severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection. We found that despite similar peak power and peak absolute O2 uptake, tidal volume as a function of ventilation was lower in ambulatory than in hospitalized patients toward the end of exercise, reflecting ventilatory inefficiency. We call for evaluation of minute ventilation with the exploration of data throughout the exercise and not only peak data to better unveil ventilatory inefficiency.
Subject(s)
COVID-19 , Quality of Life , Humans , Female , Male , COVID-19/complications , SARS-CoV-2 , Exercise Test/adverse effects , Exercise Test/methods , Dyspnea/etiology , Respiration , Exercise Tolerance/physiology , Oxygen ConsumptionABSTRACT
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 (VÌO2) and carbon dioxide production (VÌCO2) at different inspired fractions of oxygen (FiO2). METHODS: 27 mechanically ventilated ICU patients were enrolled. VÌO2 and VÌCO2 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: VÌO2 was 233.0 (95.2) ml/min and 217.5 (89.8) ml/min at FiO2 40% and 60%, respectively (NS). VÌCO2 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 VÌO2 and VÌCO2 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.
Subject(s)
Critical Illness , Respiration, Artificial , Humans , Calorimetry, Indirect , Energy Metabolism , Critical Care , Basal MetabolismABSTRACT
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.
Subject(s)
Bicycling , Methamphetamine , Humans , Male , Bicycling/physiology , Oxygen Consumption/physiology , Physical Endurance/physiology , Exercise Test/methodsABSTRACT
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 lâmin-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.
Subject(s)
Baroreflex , Heart , Arteries , Baroreflex/physiology , Blood Pressure/physiology , Heart Rate/physiology , HumansABSTRACT
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.
Subject(s)
Carbon Dioxide , Oxygen Consumption , Carbon Dioxide/metabolism , Humans , Lactic Acid , Muscles/metabolism , Oxygen/metabolism , Oxygen Consumption/physiologyABSTRACT
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.
Subject(s)
Arterial Pressure , Baroreflex , Cardiovascular System/innervation , Exercise/physiology , Heart Rate , Posture , Rest/physiology , Sympathetic Nervous System/physiology , Vagus Nerve/physiology , Adult , Bicycling , Exercise Test , Female , Humans , Kinetics , Male , Supine Position , Tilt-Table Test , Young AdultABSTRACT
PURPOSE: We tested the vagal withdrawal concept for heart rate (HR) and cardiac output (CO) kinetics upon moderate exercise onset, by analysing the effects of vagal blockade on cardiovascular kinetics in humans. We hypothesized that, under atropine, the φ1 amplitude (A1) for HR would reduce to nil, whereas the A1 for CO would still be positive, due to the sudden increase in stroke volume (SV) at exercise onset. METHODS: On nine young non-smoking men, during 0-80 W exercise transients of 5-min duration on the cycle ergometer, preceded by 5-min rest, we continuously recorded HR, CO, SV and oxygen uptake ([Formula: see text]O2) upright and supine, in control condition and after full vagal blockade with atropine. Kinetics were analysed with the double exponential model, wherein we computed the amplitudes (A) and time constants (τ) of phase 1 (φ1) and phase 2 (φ2). RESULTS: In atropine versus control, A1 for HR was strongly reduced and fell to 0 bpm in seven out of nine subjects for HR was practically suppressed by atropine in them. The A1 for CO was lower in atropine, but not reduced to nil. Thus, SV only determined A1 for CO in atropine. A2 did not differ between control and atropine. No effect on τ1 and τ2 was found. These patterns were independent of posture. CONCLUSION: The results are fully compatible with the tested hypothesis. They provide the first direct demonstration that vagal blockade, while suppressing HR φ1, did not affect φ1 of CO.
Subject(s)
Cardiac Output/physiology , Exercise/physiology , Heart Rate/physiology , Nerve Block/methods , Oxygen Consumption/physiology , Vagus Nerve/physiology , Humans , Male , Young AdultABSTRACT
Objective. Total lung capacity (TLC) assessment outside of a research laboratory is challenging. We describe a novel method for measuring TLC that is both simple and based only on portable equipment, and report preliminary data in healthy subjects.Approach. We developed an open circuit system to administer a known amount of oxygen to a subject in a single maximal inspiratory maneuver. Oxygen fraction, expired and inspired flows were continuously monitored to allow a precise computation of the mass balance. Values of TLC and functional residual capacity (FRC) were compared with standard methods (body plethysmography and multiple-breath helium dilution). Twenty healthy subjects participated to the study, eleven of which performed the maneuver twice to assess test-retest reliability.Main results.There was high agreement in TLC between the proposed method and the two standard methods (R2 > 0.98, bias not different from 0, and 95% limits of agreements <± 0.4 l for both). Test-retest reliability was high (intraclass correlation coefficient >0.99 and no bias). Results were similar for FRC, with a slightly higher variability due its sensitivity to changes in posture or breathing pattern.Significance.Single-breath oxygen dilution is accurate and reliable in assessing TLC and FRC in healthy subjects. The technique is appealing for time- or resource-limited settings, such as field physiological research expeditions or mass screenings.
Subject(s)
Lung , Oxygen , Functional Residual Capacity , Healthy Volunteers , Humans , Lung Volume Measurements , Reproducibility of Results , Total Lung CapacityABSTRACT
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.
Subject(s)
Apnea/physiopathology , Baroreflex/physiology , Exercise/physiology , Rest/physiology , Adult , Apnea/metabolism , Blood Pressure/physiology , Female , Heart Rate/physiology , Humans , Male , Oxygen/metabolism , Vagus Nerve/metabolism , Vagus Nerve/physiologyABSTRACT
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.
Subject(s)
Hypoventilation/physiopathology , Lung/physiology , Pulmonary Gas Exchange/physiology , Adult , Breath Holding , Carbon Dioxide/metabolism , Exercise/physiology , Female , Humans , Hypoventilation/metabolism , Lung/metabolism , Male , Oxygen/metabolism , Oxygen Consumption/physiology , Partial Pressure , Respiration , RestABSTRACT
INTRODUCTION: Measuring physiological parameters at depth is an emergent challenge for athletic training, diver's safety and biomedical research. Recent advances in wearable sensor technology made this challenge affordable; however, its impact on breath-hold diving has never been comprehensively discussed. METHODS: We performed a systematic review of the literature in order to assess what types of sensors are available or suitable for human breath-hold diving, within the two-fold perspective of safety and athletic performance. RESULTS: In the 52 studies identified, sensed physiological variables were: electrocardiogram, body temperature, blood pressure, peripheral oxygen saturation, interstitial glucose concentration, impedance cardiography, heart rate, body segment inertia and orientation. CONCLUSIONS: Limits and potential of each technology are separately reviewed. Inertial sensor technology and transmission pulse oximetry could produce the greatest impact on breath-hold diving performances in the future.
Subject(s)
Diving , Wearable Electronic Devices , Breath Holding , Heart Rate , Humans , Pulmonary Gas ExchangeABSTRACT
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.
Subject(s)
Physiology/methods , Regression AnalysisABSTRACT
To check whether the evolution of alveolar pressures of O2 (PAO2) and CO2 (PACO2) explains the cardiovascular responses to apnoea, eight divers performed resting apnoeas of increasing duration in air and in O2. We measured heart rate (fH), arterial pressure (AP), and peripheral resistances (TPR) beat-by-beat, PAO2 and PACO2 at the end of each apnoea. The three phases of the cardiovascular response to apnoea were observed. In O2, TPR increase (9⯱â¯4â¯mmHg min l-1) and fH decrease (-11⯱â¯8 bpm) were lower than in air (15⯱â¯5â¯mmHgâ¯minâ¯l-1 and -28⯱â¯13 bpm, respectively). At end of maximal apnoeas in air, PAO2 and PACO2 were 50⯱â¯9 and 48⯱â¯5â¯mmHg, respectively; corresponding values in O2 were 653⯱â¯8â¯mmHg and 55⯱â¯5â¯mmHg. At end of phase II, PAO2 and PACO2 in air were 90⯱â¯13â¯mmHg and 42⯱â¯4â¯mmHg respectively; corresponding values in O2 were 669⯱â¯7â¯mmHg and 47⯱â¯6â¯mmHg. The PACO2 increase may trigger the AP rise in phase III.
Subject(s)
Blood Pressure/physiology , Breath Holding , Diving/physiology , Heart Rate/physiology , Pulmonary Gas Exchange/physiology , Adult , Humans , MaleABSTRACT
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.
Subject(s)
Energy Metabolism/physiology , Exercise Test , Exercise/physiology , Physical Endurance/physiology , Adult , Humans , Male , Oxygen Consumption/physiology , Task Performance and Analysis , Young AdultABSTRACT
If, as postulated, the end of the steady state phase (φ2) of cardiovascular responses to apnoea corresponds to the physiological breaking point, then we may hypothesize that φ2 should become visible if exercise apnoeas are performed in pure oxygen. We tested this hypothesis on 9 professional divers by means of continuous recording of blood pressure (BP), heart rate (fH), stroke volume (QS), and arterial oxygen saturation (SpO2) during dry maximal exercising apnoeas in ambient air and in oxygen. Apnoeas lasted 45.0⯱â¯16.9â¯s in air and 77.0⯱â¯28.9â¯s in oxygen (pâ¯<â¯0.05). In air, no φ2 was observed. Conversely, in oxygen, a φ2 of 28⯱â¯5â¯s duration appeared, during which systolic BP (185⯱â¯29â¯mmHg), fH (93⯱â¯16 bpm) and QS (91⯱â¯16â¯ml) remained stable. End-apnoea SpO2 was 95.5⯱â¯1.9% in air and 100% in oxygen. The results support the tested hypothesis.
Subject(s)
Air , Apnea/physiopathology , Cardiovascular System/physiopathology , Exercise/physiology , Oxygen , Adult , Blood Pressure/physiology , Diving , Heart Rate/physiology , Humans , Male , Oxygen/metabolism , Stroke Volume/physiologyABSTRACT
The steady state concept implies that the oxygen flow is invariant and equal at each level along the respiratory system. The same is the case with the carbon dioxide flow. This condition has several physiological consequences, which are analysed. First, we briefly discuss the mechanical efficiency of exercise and the energy cost of human locomotion, as well as the roles played by aerodynamic work and frictional work. Then we analyse the equations describing the oxygen flow in lungs and in blood, the effects of ventilation and of the ventilation - perfusion inequality, and the interaction between diffusion and perfusion in the lungs. The cardiovascular responses sustaining gas flow increase in blood are finally presented. An equation linking ventilation, circulation and metabolism is developed, on the hypothesis of constant oxygen flow in mixed venous blood. This equation tells that, if the pulmonary respiratory quotient stays invariant, any increase in metabolic rate is matched by a proportional increase in ventilation, but by a less than proportional increase in cardiac output.
Subject(s)
Exercise/physiology , Oxygen Consumption/physiology , Respiration , Carbon Dioxide/metabolism , Cardiac Output/physiology , HumansABSTRACT
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.