scholarly journals Acute Moderate Hypoxia Reduces One-Legged Cycling Performance Despite Compensatory Increase in Peak Cardiac Output: A Pilot Study

Author(s):  
Hannes Gatterer ◽  
Verena Menz ◽  
Martin Burtscher

In severe hypoxia, single-leg peak oxygen uptake (VO2peak) is reduced mainly due to the inability to increase cardiac output (CO). Whether moderate altitude allows CO to increase during single-leg cycling, thereby restoring VO2peak, has not been extensively investigated. Five healthy subjects performed an incremental, maximal, two-legged cycle ergometer test, and on separate days a maximal incremental one-leg cycling test in normoxia and in moderate hypoxia (fraction of inspired oxygen (FiO2) = 15%). Oxygen uptake, heart rate, blood pressure responses, power output, and CO (PhysioFlow) were measured during all tests. Moderate hypoxia lowered single-leg peak power output (154 ± 31 vs. 128 ± 26 watts, p = 0.03) and oxygen uptake (VO2) (36.8 ± 6.6 vs. 33.9 ± 6.9 mL/min/kg, p = 0.04), despite higher peak CO (16.83 ± 3.10 vs. 18.96 ± 3.59 L/min, p = 0.04) and systemic oxygen (O2) delivery (3.37 ± 0.84 vs. 3.47 ± 0.89 L/min, p = 0.04) in hypoxia compared to normoxia. Arterial–venous O2 difference (a–vDO2) was lower in hypoxia (137 ± 21 vs. 112 ± 19 mL/l, p = 0.03). The increases in peak CO from normoxia to hypoxia were negatively correlated with changes in mean arterial pressure (MABP) (p < 0.05). These preliminary data indicate that the rise in CO was not sufficient to prevent single-leg performance loss at moderate altitude and that enhanced baroreceptor activity might limit CO increases in acute hypoxia, likely by reducing sympathetic activation. Since the systemic O2 delivery was enhanced and the calculated a–vDO2 reduced in moderate hypoxia, a potential diffusion limitation cannot be excluded.

PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0242439
Author(s):  
Andreas Breenfeldt Andersen ◽  
Jacob Bejder ◽  
Thomas Bonne ◽  
Niels Vidiendal Olsen ◽  
Nikolai Nordsborg

Sprint-interval training (SIT) is efficient at improving maximal aerobic capacity and anaerobic fitness at sea-level and may be a feasible training strategy at altitude. Here, it was evaluated if SIT intensity can be maintained in mild to moderate hypoxia. It was hypothesized that 6 x 30 s Wingate sprint performance with 2 min active rest between sprints can be performed in hypoxic conditions corresponding to ~3,000 m of altitude without reducing mean power output (MPO). In a single-blinded, randomized crossover design, ten highly-trained male endurance athletes with a maximal oxygen uptake (V˙O2max) of 68 ± 5 mL O2 × min-1 × kg-1 completed 6 x 30 s all-out Wingate cycling sprints separated by two-minute active recovery on four separate days in a hypobaric chamber. The ambient pressure within the chamber on each experimental day was 772 mmHg (~0 m), 679 mmHg (~915 m), 585 mmHg (~ 2,150 m), and 522 mmHg (~3,050 m), respectively. MPO was not different at sea-level and up to ~2,150 m (~1% and ~3% non-significant decrements at ~915 and ~2,150 m, respectively), whereas MPO was ~5% lower (P<0.05) at ~3,050 m. Temporal differences between altitudes was not different for peak power output (PPO), despite a main effect of altitude. In conclusion, repeated Wingate exercise can be completed by highly-trained athletes at altitudes up to ~2,150 m without compromising MPO or PPO. In contrast, MPO was compromised in hypobaric hypoxia corresponding to ~3,050 m. Thus, SIT may be an efficient strategy for athletes sojourning to moderate altitude and aiming to maintain training quality.


2014 ◽  
Vol 39 (12) ◽  
pp. 1345-1351 ◽  
Author(s):  
Michael Price ◽  
Christopher Beckford ◽  
Adam Dorricott ◽  
Cameron Hill ◽  
Megan Kershaw ◽  
...  

The aim of this study was to determine the aerobic contribution to upper body and lower body Wingate Anaerobic tests (WAnT). Eight nonspecifically trained males volunteered to take part in this study. Participants undertook incremental exercise tests for peak oxygen uptake and two 30-s WAnT (habituation and experimental) for both the upper and lower body. The resistive loadings used were 0.040 and 0.075 kg·kg body mass−1, respectively. Peak power output (PPO) and mean power output (MPO) were calculated for each WAnT. The aerobic contribution of each WAnT was assessed using breath by breath expired gas analysis. Peak oxygen uptake was lower for the upper body when compared with the lower body (P = 0.001). Similarly, PPO and MPO were greater for the lower body (both P < 0.001). Absolute oxygen uptake during the upper body WAnT was lower than for the lower body (P = 0.013), whereas relative oxygen uptake (% peak oxygen uptake) was similar (P = 0.997). The mean aerobic contribution for the upper body WAnT (43.5% ± 29.3%) was greater than for the lower body (29.4% ± 15.8%; P < 0.001). The greater aerobic contribution to the WAnT observed for the upper body in comparison with the lower body is likely due to methodological differences in upper and lower body WAnT protocols and potentially differences in anaerobic power production and exercise efficiency. The results of this study suggest that differences may exist for the aerobic contribution of upper and lower body Wingate anaerobic tests.


2016 ◽  
Vol 41 (1) ◽  
pp. 20-25 ◽  
Author(s):  
Jonathan Ache-Dias ◽  
Rodolfo A. Dellagrana ◽  
Anderson S. Teixeira ◽  
Juliano Dal Pupo ◽  
Antônio R.P. Moro

This study analyzed the effect of 4 weeks of jumping interval training (JIT), included in endurance training, on neuromuscular and physiological parameters. Eighteen recreational runners, randomized in control and experimental groups, performed 40 min of running at 70% of velocity at peak oxygen uptake, for 3 times per week. Additionally, the experimental group performed the JIT twice per week, which consisted of 4 to 6 bouts of continuous vertical jumps (30 s) with 5-min intervals. Three days before and after the training period, the countermovement (CMJ) and continuous jump (CJ30), isokinetic and isometric evaluation of knee extensors/flexors, progressive maximal exercise, and submaximal constant-load exercise were performed. The JIT provoked improvement in neuromuscular performance, indicated by (i) increased jump height (4.7%; effect size (ES) = 0.99) and power output (≈3.7%; ES ≈ 0.82) of CMJ and rate of torque development of knee extensors in isometric contraction (29.5%; ES = 1.02); (ii) anaerobic power and capacity, represented by the mean of jump height (7.4%; ES = 0.8), and peak power output (PPO) (5.6%; ES = 0.73) of the first jumps of CJ30 and the mean of jump height (10.2%, ES = 1.04) and PPO (9.5%, ES = 1.1), considering all jumps of CJ30; and (iii) aerobic power and capacity, represented by peak oxygen uptake (9.1%, ES = 1.28), velocity at peak oxygen uptake (2.7%, ES = 1.11), and velocity corresponding to the onset of blood lactate accumulation (9.7%, ES = 1.23). These results suggest that the JIT included in traditional endurance training induces moderate to large effects on neuromuscular and physiological parameters.


1994 ◽  
Vol 77 (3) ◽  
pp. 1403-1410 ◽  
Author(s):  
R. Callister ◽  
A. V. Ng ◽  
D. R. Seals

We tested the hypothesis that sympathetic vasoconstrictor nerve activity to nonactive skeletal muscle (MSNA) decreases immediately before and remains suppressed during initiation of conventional large muscle upright dynamic exercise in humans. In 11 healthy young subjects, adequate recordings of MSNA from the radial nerve in the arm were obtained during upright seated rest (control) and throughout 1 min of leg-cycling exercise at one or more submaximal workloads (range 33–266 W; approximately 10–80% of peak power output). MSNA was analyzed during four consecutive time intervals; control, preparation for cycling (end of control to onset of pedal movement), initiation of cycling (onset of pedal movement to attainment of target power output), and the initial 60 s of cycling at target power output. MSNA decreased (P < 0.05) abruptly and markedly in all subjects [to 19 +/- 4% (SE) of control levels] during the preparation period before the 33-W load and remained suppressed throughout the period of initiation of cycling in 8 of 11 subjects; MSNA increased during the initiation period in three subjects in whom diastolic arterial pressure fell below control levels. This general pattern was observed at all loads. MSNA remained at or below control levels throughout the 1 min of cycling exercise at 33–166 W. MSNA increased above control levels during the latter portion of the 1 min of cycling only at loads > or = 60% of peak power output.(ABSTRACT TRUNCATED AT 250 WORDS)


2003 ◽  
Vol 94 (2) ◽  
pp. 668-676 ◽  
Author(s):  
J. A. L. Calbet ◽  
J. A. De Paz ◽  
N. Garatachea ◽  
S. Cabeza de Vaca ◽  
J. Chavarren

The aim of this study was to evaluate the effects of severe acute hypoxia on exercise performance and metabolism during 30-s Wingate tests. Five endurance- (E) and five sprint- (S) trained track cyclists from the Spanish National Team performed 30-s Wingate tests in normoxia and hypoxia (inspired O2 fraction = 0.10). Oxygen deficit was estimated from submaximal cycling economy tests by use of a nonlinear model. E cyclists showed higher maximal O2 uptake than S (72 ± 1 and 62 ± 2 ml · kg−1 · min−1, P < 0.05). S cyclists achieved higher peak and mean power output, and 33% larger oxygen deficit than E ( P< 0.05). During the Wingate test in normoxia, S relied more on anaerobic energy sources than E ( P < 0.05); however, S showed a larger fatigue index in both conditions ( P < 0.05). Compared with normoxia, hypoxia lowered O2 uptake by 16% in E and S ( P < 0.05). Peak power output, fatigue index, and exercise femoral vein blood lactate concentration were not altered by hypoxia in any group. Endurance cyclists, unlike S, maintained their mean power output in hypoxia by increasing their anaerobic energy production, as shown by 7% greater oxygen deficit and 11% higher postexercise lactate concentration. In conclusion, performance during 30-s Wingate tests in severe acute hypoxia is maintained or barely reduced owing to the enhancement of the anaerobic energy release. The effect of severe acute hypoxia on supramaximal exercise performance depends on training background.


2008 ◽  
Vol 295 (2) ◽  
pp. R624-R632 ◽  
Author(s):  
Frédéric Lador ◽  
Enrico Tam ◽  
Marcel Azabji Kenfack ◽  
Michela Cautero ◽  
Christian Moia ◽  
...  

We tested the hypothesis that vagal withdrawal plays a role in the rapid (phase I) cardiopulmonary response to exercise. To this aim, in five men (24.6 ± 3.4 yr, 82.1 ± 13.7 kg, maximal aerobic power 330 ± 67 W), we determined beat-by-beat cardiac output (Q̇), oxygen delivery (Q̇aO2), and breath-by-breath lung oxygen uptake (V̇o2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O2 = 0.11), because the latter reduces resting vagal activity. We computed Q̇ from stroke volume (Qst, by model flow) and heart rate ( fH, electrocardiography), and Q̇aO2 from Q̇ and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state fH and Q̇ were higher, and Qst and V̇o2 were unchanged. Q̇aO2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A1) for V̇o2 was unchanged. For fH, Q̇ and Q̇aO2, A1 was lower. Phase I time constant (τ1) for Q̇aO2 and V̇o2 was unchanged. The same was the case for Q̇ at 100 W and for fH at 50 W. Qst kinetics were unaffected. In conclusion, the results do not fully support the hypothesis that vagal withdrawal determines phase I, because it was not completely suppressed. Although we can attribute the decrease in A1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Qst. Thus the dual origin of the phase I of Q̇ and Q̇aO2, neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed.


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