Anna Taboni

We found that a single night spent at simulated moderate altitude (1,900 m) prompts measurable ventilatory acclimatization when ascending to simulated high altitude (3,000 m) in males with coronary artery disease. We also found that, although sleeping at 1,900 m increases the occurrence of apneas and/or hypopneas, this did not modify heart rate variability and baroreflex sensitivity responses at 3,000 m.

Purpose: Dynamic apnea with fins (DYN) involves swimming the longest distance relying solely on the body’s oxygen and anaerobic energy stores. The energy cost per unit distance ( C ) is therefore an important determinant of DYN performance, yet it has never been measured. This study aimed to assess the C of DYN and its aerobic (EO ₂ ), anaerobic lactic (ELa), and alactic (EPCr) energy contributions. Methods: In a 50-m swimming pool, 22 freedivers (3 females; 10 using bi-fins, 6 using monofin, 6 using both) performed a 50-m DYN, and 7 performed a 100-m DYN. Net C (above resting) was calculated from the O ₂ debt measured at emersion plus ELa (calculated from the blood lactate increase). In nine subjects (six of whom performed also the 100-m DYN), determination of hemoglobin mass and total lung capacity allowed the estimation of EO ₂ and, by subtraction, EPCr. Results: C was unchanged between the 100-m and the 50-m DYN ( P = 0.81) and resulted higher with bi-fins than with the monofin (7.4 ± 2.2 vs 5.5 ± 1.6 J·kg ⁻¹ ·m ⁻¹ , P = 0.02) due to a higher O ₂ debt and ELa. DYN personal best correlated better with the distance swum per unit of EO ₂ at 50 m ( R ² = 0.70) than with C ( R ² = 0.25). From 50 to 100 m, fractional EO ₂ decreased (58% ± 19% to 47% ± 13%, P = 0.02), ELa increased (10% ± 5% to 21% ± 5%, P < 0.001), and EPCr was unchanged (31% ± 20% to 32% ± 15%, P = 0.83). Conclusions: The C of DYN seems compatible with published values for surface swimming with fins at the same speed. At 100 m, ELa and EPCr were disproportionately high for the exercise intensity, possibly due to a diving response. Sparing EO ₂ is at least as important as C in determining DYN performance.

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 (V̇_Emax), peripheral oxygen saturation (SpO₂) and maximal oxygen consumption (V̇O_2max) 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). V̇_Emax and V̇O_2max were 11% and 6% higher in HH, respectively (p < 0.01 for both). SpO₂ at maximal exercise was positively correlated with V̇_Emax, V̇_Emax/V̇O_2max and V̇O_2max. Conclusions: The higher V̇O_2max found in HH than in NH can be attributed to the higher V̇_Emax 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.

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. image

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.

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 (Ve) 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 O-2 uptake (Vo(2)) (1.59 [1.22-2.11] mL center dot min(-1); P = 0.65). Tidal volume (VT) as a function of Ve, was lower in AMBU than in HOSP (P < 0.01) toward the end of exercise. The slope of the Ve-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 Ve and throughout the exercise better unveil ventilatory inefficiency.

Vinetti, G, Rossi, H, Bruseghini, P, Corti, M, Ferretti, G, Piva, S, Taboni, A, and Fagoni, N. The functional threshold power field test exceeds laboratory performance in junior road cyclists. J Strength Cond Res 37(9): 1815–1820, 2023—The functional threshold power (FTP) field test is appealing for junior cyclists, but it was never investigated in this age category, and even in adults, there are few data on FTP collected in field conditions. Nine male junior road cyclists (16.9 ± 0.8 years) performed laboratory determination of maximal aerobic power (MAP), 4-mM lactate threshold (P_4mM), critical power (CP), and the curvature constant (W′), plus a field determination of FTP as 95% of the average power output during a 20-minute time trial in an uphill road. The level of significance was set at p < 0.05. Outdoor FTP (269 ± 34 W) was significantly higher than CP (236 ± 24 W) and P_4mM (233 ± 23 W). The of the field FTP test (66.9 ± 4.4 ml·kg⁻¹·min⁻¹) was significantly higher than the assessed in the laboratory (62.7 ± 3.7 ml·kg⁻¹·min⁻¹). Functional threshold power was correlated, in descending order, with MAP (r = 0.95), P_4mM (r = 0.94), outdoor and indoor (r = 0.93 and 0.93, respectively), CP (r = 0.84), and W′ (r = 0.66). It follows that in junior road cyclists, the FTP field test was feasible and related primarily to aerobic endurance parameters and secondarily, but notably, to W′. However, the FTP field test significantly exceeded all laboratory performance tests. When translating laboratory results to outdoor uphill conditions, coaches and sport scientists should consider this discrepancy, which may be particularly enhanced in this cycling age category.