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Hemodynamic response to work at simuated altitude
... Above this altitude, the body undergoes a series of pulmonary and cardiovascular adaptations to maintain adequate oxygenation. These adaptations involve increased pulmonary ventilation and cardiac output, primarily driven by a higher heart rate [2][3][4][5]. The cave of Baba Amarnath Ji, standing at 130 ft and 13,000 ft (3,882 meters) in the north Indian state of Jammu and Kashmir, is visited by thousands of devotees each year for a six-week period starting in June, in a pilgrimage known as the Amarnath pilgrimage. ...
... This observation led to the initiation of our study. Despite research on high-altitude medicine that has investigated these adaptations [2][3][4][5], there are still gaps in comprehending ACS among Amarnath pilgrims. Previous research on ACS among Hajj pilgrims has revealed a correlation with an increased incidence of complications and adverse results. ...
... Lors de la première phase d'exposition à l'altitude, le Q c au repos ne semble pas affecté (Hopkins et al. 2003;Wagner et al. 1987;Wolfel et al. 1991) ou seulement faiblement augmenté (Wagner et al. 1986). Lors d'un exercice sous-maximal, il est maintenant bien établi que le Q c en altitude est augmenté par rapport à la plaine pour une même intensité d'exercice (Stenberg et al. 1966;Wagner 2000;Boos et al. 2016). Pour un exercice maximal, certains auteurs ont montré que le Q cmax n'est pas diminué mais apparaît à une intensité d'exercice maximale inférieure en altitude comparée à celle de la plaine (Horstman et al. 1980;Hughes et al. 1968;Wagner et al. 1987;Stenberg et al. 1966;Wagner et al. 1986). ...
... Lors d'un exercice sous-maximal, il est maintenant bien établi que le Q c en altitude est augmenté par rapport à la plaine pour une même intensité d'exercice (Stenberg et al. 1966;Wagner 2000;Boos et al. 2016). Pour un exercice maximal, certains auteurs ont montré que le Q cmax n'est pas diminué mais apparaît à une intensité d'exercice maximale inférieure en altitude comparée à celle de la plaine (Horstman et al. 1980;Hughes et al. 1968;Wagner et al. 1987;Stenberg et al. 1966;Wagner et al. 1986). Ces mêmes auteurs ont observé que le Q cmax reste identique pour des altitudes jusqu'à 4 500 m que ce soit chez des sédentaires ou des sportifs. ...
A l’heure actuelle aucun consensus n’existe sur l’utilisation des substrats énergétiques lors d’un exercice en altitude. Certaines études ont montré une utilisation accrue des glucides en altitude comparée à la plaine mais les intensités d’exercices utilisées sont discutables et l’utilisation de méthodes biochimiques traditionnelles ont permis de doser qu’un nombre restreint de molécules. Aujourd’hui grâce à la métabolomique, il est possible d’analyser les variations d’un grand nombre de métabolites simultanément. Le but de cette thèse est d’étudier l’incidence de l’altitude modérée sur l’utilisation des substrats énergétiques à l’effort à l’aide de la métabolomique par résonnance magnétique nucléaire du proton. Des échantillons de plasmas et d’urines ont été collectés lors d’exercices d’endurance en plaine et en altitude modérée chez des sujets non acclimatés. Nos premiers résultats, dans les plasmas, ont montré une baisse de la glycémie et une utilisation accrue des acides aminés ramifiés entre avant et après un exercice d’endurance en altitude, ce qui n’a pas été observé en plaine. Ces résultats ont ensuite été confirmé lors d’un exercice d’endurance jusqu’à épuisement. De plus, nous avons montré que l’utilisation des urines permet de mettre en avant les résultats obtenus dans les plasmas, ce qui est très encourageant pour la compréhension des adaptations métaboliques en altitude par des méthodes non invasives. Pour finir, nous avons utilisé une méthode statistique innovante appelée « analyse en composantes communes et poids spécifiques ». Les résultats ont permis d’observer les variabilités communes entre les paramètres physiologiques mesurés et les variations des métabolites plasmatiques.
... Several studies have established that ambient hypoxia negatively affects performance as a result of impaired oxygen delivery to the working skeletal muscles (7,38,63,72) and accelerates the development of central and peripheral fatigue (1,20,28). However, in a recent meta-analysis including 51 studies, Mallette et al. (42) showed that acute exposure to normobaric hyperoxic (with more than 21% O 2 ) gas mixtures (NBO) during exercise had a moderate positive effect on performance in comparison to exercise in NBA, acutely improving exercise performance in time trials, time-toexhaustion (TTE) tests, graded-exercise tests, and dynamic muscle function tests. ...
Šet, V, and Lenasi, H. Does hyperbaric oxygenation improve athletic performance? J Strength Cond Res XX(X): 000-000, 2022-Hyperbaric oxygen (HBO) has been suggested to affect oxygen availability and performance, and delay the onset of fatigue. Many mechanisms of HBO-induced alterations have been proposed, including modulation of various metabolic pathways, and the antioxidant defense mechanisms. As exercise per se affects similar aspects, it is tempting to speculate that simultaneous application of both, exercise and HBO might have synergistic effects. The aim of this review was to search through the currently available literature and evaluate the effect of acute exposure to HBO on exercise performance, potential effects of a combination of HBO and physical training, and to elucidate some possible mechanisms behind. We conducted searches in the PubMed and Scopus databases (search term: "hyperbaric" AND "oxygen" AND "exercise") and in relevant hyperbaric textbook and assessed potentially eligible full texts for details. Meta-analysis could not be performed because of a few available and rather heterogeneous studies. Twenty-seven studies were included in the final assessment (14 on exercise during HBO, 9 on exercise following HBO, 4 on applying HBO during recovery and rest between exercise bouts, and 3 on a combination of HBO and training). The results are contradictory, showing either positive or none ergogenic effects. There is some risk of bias and placebo effect. Discrepant findings of the available studies might partly be explained by different protocols applied, both regarding HBO and exercise intensity and regimen. There is a need for further research with well-designed trials to evaluate the effect of HBO on performance before recommending it to routine use in athletes.
... Several studies have established that ambient hypoxia negatively affects performance as a result of impaired oxygen delivery to the working skeletal muscles (7,38,63,72) and accelerates the development of central and peripheral fatigue (1,20,28). However, in a recent meta-analysis including 51 studies, Mallette et al. (42) showed that acute exposure to normobaric hyperoxic (with more than 21% O 2 ) gas mixtures (NBO) during exercise had a moderate positive effect on performance in comparison to exercise in NBA, acutely improving exercise performance in time trials, time-toexhaustion (TTE) tests, graded-exercise tests, and dynamic muscle function tests. ...
Šet, V, and Lenasi, H. Does hyperbaric oxygenation improve athletic performance? J Strength Cond Res XX(X): 000-000, 2022-Hyperbaric oxygen (HBO) has been suggested to affect oxygen availability and performance, and delay the onset of fatigue. Many mechanisms of HBO-induced alterations have been proposed, including modulation of various metabolic pathways, and the antioxidant defense mechanisms. As exercise per se affects similar aspects, it is tempting to speculate that simultaneous application of both, exercise and HBO might have synergistic effects. The aim of this review was to search through the currently available literature and evaluate the effect of acute exposure to HBO on exercise performance, potential effects of a combination of HBO and physical training, and to elucidate some possible mechanisms behind. We conducted searches in the PubMed and Scopus databases (search term: "hyperbaric" AND "oxygen" AND "exercise") and in relevant hyperbaric textbook and assessed potentially eligible full texts for details. Meta-analysis could not be performed because of a few available and rather heterogeneous studies. Twenty-seven studies were included in the final assessment (14 on exercise during HBO, 9 on exercise following HBO, 4 on applying HBO during recovery and rest between exercise bouts, and 3 on a combination of HBO and training). The results are contradictory, showing either positive or none ergogenic effects. There is some risk of bias and placebo effect. Discrepant findings of the available studies might partly be explained by different protocols applied, both regarding HBO and exercise intensity and regimen. There is a need for further research with well-designed trials to evaluate the effect of HBO on performance before recommending it to routine use in athletes.
... P eak oxygen uptake ( _ VO 2peak ) and exercise performance are lower at high altitude than at sea level due to the reduction in inspired oxygen (Stenberg et al., 1966;Lawler et al., 1988;Martin and O'Kroy, 1993;Ferretti et al., 1997). In addition, it has been shown that ventilatory responses to hypoxia are important determinants of _ VO 2peak and exercise performance at high altitude (Gavin et al., 1998;Chapman, 2013). ...
Cao, Yinhang, Naoto Fujii, Tomomi Fujimoto, Yin-Feng Lai, Takeshi Ogawa, Tsutomu Hiroyama, Yasushi Enomoto, and Takeshi Nishiyasu. CO2-enriched air inhalation modulates the ventilatory and metabolic responses of endurance runners during incremental running under hypobaric hypoxia. High Alt Med Biol. 00:000-000, 2022. Aim: We measured the effects of breathing CO2-enriched air on ventilatory and metabolic responses during incremental running exercise under moderately hypobairc hypoxic (HH) conditions. Materials and Methods: Ten young male endurance runners [61.4 ± 6.0 ml/(min·kg)] performed incremental running tests under three conditions: (1) normobaric normoxia (NN), (2) HH (2,500 m), and (3) HH with 5% CO2 inhalation (HH+CO2). The test under NN was always performed first, and then, the two remaining tests were completed in random and counterbalanced order. Results: End-tidal CO2 partial pressure (55 ± 3 vs. 35 ± 1 mmHg), peak ventilation (163 ± 14 vs. 152 ± 12 l/min), and peak oxygen uptake [52.3 ± 5.5 vs. 50.5 ± 4.9 ml/(min·kg)] were all higher in the HH+CO2 than HH trial (all p < 0.01), respectively. However, the duration of the incremental test did not differ between HH+CO2 and HH trials. Conclusion: These data suggest that chemoreflex activation by breathing CO2-enriched air stimulates breathing and aerobic metabolism during maximal intensity exercise without affecting exercise performance in male endurance runners under a moderately hypobaric hypoxic environment.
... Notwithstanding, there are two conditions in which the Q versus V R O 2 relationship appears to be shifted upwards with respect to that observed at sea level: acute hypoxia (Hartley et al. 1973;Hughes et al. 1968;Roca et al. 1989;Stenberg et al. 1966) and moderate carbon monoxide poisoning (Ekblom et al. 1975;Vogel and Gleser 1972). Both these conditions lead to a reduction of C a O 2 . ...
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 (V˙A/V˙RCO2) 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 V˙A/V˙RCO2 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.
... Mean values (± 95% confidence limits, where available) of systemic oxygen extraction fraction vs maximal oxygen uptake from studies using the direct (pulmonary artery catheter) or the modified (right atrium catheter) Fick method, 4,9,30,48,52,56,60,[114][115][116][117] the indicator dilution method 5,11,16,17,21,22,24,29,39,[49][50][51]54,83,106,108,118,119 and the transpulmonary thermodilution method. 53 Broken line is the regression equation obtained from Fig. 1d. ...
This thesis includes four research papers, based on four separate studies aiming to elucidate the importance of O2 extraction and blood volume (BV) for maximal O2 uptake (VO2max).
In study I, twelve untrained subjects (VO2max: 44 ml · kg-1 · min-1) completed ten weeks of supervised endurance training (three sessions per week). VO2max and maximal cardiac output (Qmax) were measured during upright and supine cycling before and after training, as well as immediately after the training-induced gain in BV was reversed by blood withdrawal. The supine position increases venous return to the heart and may thus counteract potential adverse effects of blood withdrawal. The BV increased by 4% (~2 dl) with training. After reversing BV to the pre-training level, VO2max and Qmax remained 11% and 9% higher than before training, respectively, regardless of exercise position. By using the Fick principle (VO2 = Q × a-v ̅O2diff), it was calculated that 30% and 70% of the increase in VO2max was attributed to increased O2 content difference between arterial and mixed venous blood (a-v ̅O2diff) and increased Qmax, respectively. These improvements coincided with increased protein content of mitochondrial enzymes, a small increase in the capillary-to-fibre ratio (m. vastus lateralis) and an increased left ventricular mass (echocardiography). Thus, VO2max may increase with endurance training independent of BV expansion, caused by combined central and peripheral adaptations.
In study II, thirteen subjects (VO2max: 63 ml · kg-1 · min-1) performed maximal exercise on a cycle ergometer in three experimental conditions: with normal BV and immediately after acute BV reductions of 150 ml and 450 ml, representing 2.5% and 7.6% of the total BV (6.0 l), respectively. After the 150 ml reduction, VO2max was preserved compared with the control test (non-significant reduction of 1%), likely caused by a rapid plasma volume (PV) restoration (calculated from changes in haematocrit and haemoglobin concentration). After the 450 ml BV reduction, VO2max was reduced by 7% despite partial PV restoration, increased maximal heart rate and increased leg O2 extraction as indicated by near-infrared spectroscopy. The reduction in VO2max was 2.5-fold larger after withdrawing 450 compared with 150 ml blood after normalising to the BV removed. Therefore, the body may cope with small but not moderate blood loss to preserve VO2max. These data may enhance our understanding regarding the impact of, e.g., acute BV manipulations, PV reduction following dehydration induced by prolonged exercise or hyperthermia, or daily oscillations of PV.
In study III, the muscle oxidative capacity in one leg was increased by six weeks of one-legged endurance training (3-4 sessions per week) in nine subjects (VO2max: 56 ml · kg-1 · min-1). The impact on leg O2 extraction fraction (arterial and femoral venous catheters) vs the untrained control leg was investigated during dynamic two-legged knee extension exercise with both legs performing the same power output. This exercise model involves a small muscle mass, does not tax Qmax and is thus not perfusion limited. Therefore, the muscle oxidative capacity may potentially be the principal limiting factor for O2 extraction and VO2 before training. At low to moderate exercise intensities, O2 extraction fraction was similar in both legs. At higher exercise intensities, which are associated with greater mitochondrial activation and lower time for haemoglobin-O2 off-loading, the O2 extraction fraction was increased in the trained leg. The between-leg difference in O2 extraction correlated with the between-leg difference in mitochondrial protein content (m. vastus lateralis). Therefore, our data suggest that endurance training improves O2 extraction in exercise models where the mitochondria do not possess an apparent excess oxidative capacity over O2 delivery, particularly when the exercise intensity is close to maximal.
In study IV, the relationships between pulmonary VO2max and systemic and leg O2 extraction fractions were investigated by statistically analysing data from 43 previously published catheterisation studies, comprising 377 subjects. It was observed that a-v ̅O2diff (mostly calculated by the Fick principle, and Qmax measured by the indicator-dilution method) increased curvilinearly and reached its maximum at ~4.5 l · min-1 in VO2max (moderately trained subjects), and was, if anything, slightly lower in those subjects with the highest VO2max (> 5 l · min-1). However, after accounting for the hypoxemia-induced lowering of arterial O2 content (CaO2) with increasing VO2max, the calculated systemic O2 extraction fraction (a-v ̅O2diff / CaO2) increased with VO2max up to ~4.5-5.0 l · min-1 and approached a plateau at ~90%. This pattern was strengthened by the direct measurements using arterial and femoral venous catheters, with leg O2 extraction fraction increasing progressively with VO2max until reaching ~90-95%. These analyses emphasise that a-v ̅O2diff and systemic O2 extraction fraction cannot be used interchangeably, and that the systemic and peripheral O2 extraction fractions improves with increasing VO2max and training status. By using the theoretical model of Piiper and Scheid, it appeared that the limiting factors to VO2max change with increasing VO2max: untrained, but healthy individuals display mixed perfusion-diffusion limitations, and this diffusion limitation reduces as VO2max increase.
... For example, athletes can expect a 7-9% decrease in their maximal aerobic capacity for every 1,000 m above 1,000 m altitude that they travel (Balke et al., 1965). A drop in atmospheric PO 2 leads to decreased arterial PO 2 due to a decrease in pressure gradient, resulting in a proportional decrease in oxygen delivery to the muscle and brain during exercise (Decroix et al., 2018;Stenberg et al., 1966). This decrease in O 2 delivery leads to the development of reactive oxygen species, contributing to the development of both central and peripheral fatigue (Decroix et al., 2018). ...
Dark chocolate (DC) is high in flavonoids and has been shown to increase nitric oxide in the blood. Increased nitric oxide has the potential to improve delivery of oxygen to muscle, especially in hypoxic conditions, such as altitude. Our aim was to assess the impact of DC supplementation on cycling performance at altitude. Twelve healthy, trained cyclists (n = 2 females, n = 10 males; age = 35 [12] years; height = 177 [7] cm; mass = 75.2 [11.0] kg; VO2max = 55 [6] ml·kg-1·min-1) were randomized to supplement with 60 g of DC or placebo twice per day for 14 days in a double-blind crossover study. After the 2 weeks of supplementation, the participants attended a laboratory session in which they consumed 120 g of DC or placebo and then cycled for 90 min at 50% peak power output, followed immediately by a 10-km time trial (TT) at simulated altitude (15% O2). The plasma concentration of blood glucose and lactate were measured before and at 15, 30, 60, and 90 min during the steady-state exercise and post TT, while muscular and prefrontal cortex oxygenation was measured continuously throughout exercise using near-infrared spectroscopy. DC resulted in a higher concentration of blood glucose (5.5 [0.5] vs. 5.3 [0.9] mmol/L) throughout the trial and lower blood lactate concentration following the TT (7.7 [1.92] vs. 10.0 [4.6] mmol/L) compared with the placebo. DC had no effect on the TT performance (19.04 [2.16] vs. 19.21 ± 1.96 min) or oxygenation status in either the prefrontal cortex or muscle. The authors conclude that, although it provided some metabolic benefit, DC is not effective as an ergogenic aid during TT cycling at simulated altitude.
... This is because the altitude increase decreases the oxygen uptake (Kang and Sapoval 2016;Woorons et al. 2005) due to a fall in the partial pressure of atmospheric oxygen at higher altitudes, which in turn leads to the decrease in the oxygen level in the arteries. As a result, the amount of oxygen reaching the muscles during activity relatively decreases Stenberg et al. 1966). In contrast, for the absolute work rate, the O 2 consumption is independent of the altitude (Saltin et al. 1968;Pugh et al. 1964). ...
This study aimed to determine the influence of intermittent hypoxia and the days required for a worker to be acclimatized in high-altitude countries. We conducted an experimental study. Ten nonsmoking male students were randomly recruited from King Saud University. Fourteen days of exposure to intermittent normobaric hypoxia (15%) was the independent variable. Heart rate (HR), respiratory frequency (RF), minute ventilation (VE), respiratory exchange ratio (RER), tidal volume (VT), oxygen uptake (VO2),VO2/kg, VO2/HR, VE/VO2, and VE/VCO2 were the dependent variables. Our results showed that 12 days of exposure to intermittent hypoxia were sufficient for workers to acclimatize to hypoxia based on their respiratory responses (i.e., HR, RF, VE). This type of acclimatization session is very important for workers who are suddenly required to work in such an environment, because prolonged exposure to high altitude without acclimatization leads to cell death due to a lack of oxygen, and this, in turn, puts workers’ lives at risk.
... At high altitude, peak oxygen uptake ( _ VO 2peak ) is lower than at sea level due to a reduction in the amount of oxygen inspired (Stenberg et al. 1966;Lawler et al. 1988;Martin and O'Kroy 1993). However, this reduction in _ VO 2peak is characterized by large interindividual variations (Young et al. 1985;Fulco et al. 1998;Chapman et al. 1999Chapman et al. , 2011Ogawa et al. 2007;Chapman 2013), with individuals showing greater reductions in _ VO 2peak exhibiting smaller increases in ventilation in response to hypoxia (Lawler et al. 1988;Gavin et al. 1998;Ogawa et al. 2007;Chapman 2013). ...
We tested whether expiratory flow limitation (EFL) occurs in endurance athletes in a moderately hypobaric hypoxic environment equivalent to 2500 m above sea level and, if so, whether EFL inhibits peak ventilation (_ VE peak), thereby exacerbating the hypoxia-induced reduction in peak oxygen uptake (_ VO 2peak). Seventeen young male endurance runners performed incremental exhaustive running on separate days under hypobaric hypoxic (560 mmHg) and normobaric normoxic (760 mmHg) conditions. Oxygen uptake (_ VO 2), minute ventilation (_ VE), arterial O 2 saturation (SpO 2), and operating lung volume were measured throughout the incremental exercise. Among the runners tested, 35% exhibited EFL (EFL group, n = 6) in the hypobaric hypoxic condition , whereas the rest did not (Non-EFL group, n = 11). There were no differences between the EFL and Non-EFL groups for _ VE peak and _ VO 2peak under either condition. Percent changes in _ VE peak (4 AE 4 vs. 2 AE 4%) and _ VO 2peak (À18 AE 6 vs. À16 AE 6%) from normobaric normoxia to hypobaric hypoxia also did not differ between the EFL and Non-EFL groups (all P > 0.05). No differences in maximal running velocity, SpO 2 , or operating lung volume were detected between the two groups under either condition. These results suggest that under the moderate hypobaric hypoxia (2500 m above sea level) frequently used for high-attitude training,~35% of endurance athletes may exhibit EFL, but their ventilatory and metabolic responses during maximal exercise are similar to those who do not exhibit EFL.
... At high altitude, peak oxygen uptake ( _ VO 2peak ) is lower than at sea level due to a reduction in the amount of oxygen inspired (Stenberg et al. 1966;Lawler et al. 1988;Martin and O'Kroy 1993). However, this reduction in _ VO 2peak is characterized by large interindividual variations (Young et al. 1985;Fulco et al. 1998;Chapman et al. 1999Chapman et al. , 2011Ogawa et al. 2007;Chapman 2013), with individuals showing greater reductions in _ VO 2peak exhibiting smaller increases in ventilation in response to hypoxia (Lawler et al. 1988;Gavin et al. 1998;Ogawa et al. 2007;Chapman 2013). ...
We tested whether expiratory flow limitation (EFL) occurs in endurance athletes in a moderately hypobaric hypoxic environment equivalent to 2500 m above sea level and, if so, whether EFL inhibits peak ventilation (_ VE peak), thereby exacerbating the hypoxia-induced reduction in peak oxygen uptake (_ VO 2peak). Seventeen young male endurance runners performed incremental exhaustive running on separate days under hypobaric hypoxic (560 mmHg) and normobaric normoxic (760 mmHg) conditions. Oxygen uptake (_ VO 2), minute ventilation (_ VE), arterial O 2 saturation (SpO 2), and operating lung volume were measured throughout the incremental exercise. Among the runners tested, 35% exhibited EFL (EFL group, n = 6) in the hypobaric hypoxic condition , whereas the rest did not (Non-EFL group, n = 11). There were no differences between the EFL and Non-EFL groups for _ VE peak and _ VO 2peak under either condition. Percent changes in _ VE peak (4 AE 4 vs. 2 AE 4%) and _ VO 2peak (À18 AE 6 vs. À16 AE 6%) from normobaric normoxia to hypobaric hypoxia also did not differ between the EFL and Non-EFL groups (all P > 0.05). No differences in maximal running velocity, SpO 2 , or operating lung volume were detected between the two groups under either condition. These results suggest that under the moderate hypobaric hypoxia (2500 m above sea level) frequently used for high-attitude training,~35% of endurance athletes may exhibit EFL, but their ventilatory and metabolic responses during maximal exercise are similar to those who do not exhibit EFL.
... This pattern was confirmed in the leg when measured using catheters, with the O 2 extraction fraction increasing progressively with leg and pulmonary V O 2max until reaching ~90 to 95%. Therefore, the calculated systemic O 2 extraction fraction (Fick equation) is supported by direct measurements via arterial and femoral venous blood sampling and strongly F I G U R E 3 Mean values (±95% confidence limits, where available) of systemic oxygen extraction fraction versus maximal oxygen uptake from studies using the direct (pulmonary artery catheter) or the modified (right atrium catheter) Fick method, 4,9,28,32,51,55,61,[121][122][123][124][125][126][127] the indicator dilution method 5,11,16,17,21,22,24,31,42,[52][53][54]57,85,112,114,[128][129][130] and the transpulmonary thermodilution method. 56 Broken line is the regression equation obtained from Figure 1D In most endurance training studies investigating the interplay between central and peripheral adaptations in improving V O 2max , Q max was measured by non-invasive methods (such as inert-gas rebreathing techniques, impedance cardiography and bioreactance) and the Fick equation was used to derive the a-vO 2 difference (for references, see the meta-analysis by Montero et al 44 ). ...
We analysed the importance of systemic and peripheral arteriovenous O2 difference (a‐vO2 and a‐vfO2 difference, respectively) and O2 extraction fraction for maximal oxygen uptake (VO2max). Fick law of diffusion and the Piiper and Scheid model were applied to investigate whether diffusion vs perfusion limitations vary with VO2max. Articles (n=17) publishing individual data (n=154) on VO2max, maximal cardiac output (Qmax; indicator‐dilution or Fick method), a‐vO2 difference (catheters or Fick equation) and systemic O2 extraction fraction were identified. For the peripheral responses, group‐mean data (articles: n=27; subjects: n=234) on leg blood flow (LBF; thermodilution), a‐vfO2 difference and O2 extraction fraction (arterial and femoral venous catheters) were obtained. Qmax and two‐LBF increased linearly by 4.9‐6.0 L·min‐1 per 1 L·min‐1 increase in VO2max (R²=0.73 and R²=0.67, respectively; both P<0.001). The a‐vO2 difference increased from 118‐168 mL·L‐1 from a VO2max of 2‐4.5 L·min‐1 followed by a reduction (second‐order polynomial: R²=0.27). After accounting for a hypoxemia‐induced decrease in arterial O2 content with increasing VO2max (R²=0.17; P<0.001), systemic O2 extraction fraction increased up to ~90% (VO2max: 4.5 L·min‐1) with no further change (exponential decay model: R²=0.42). Likewise, leg O2 extraction fraction increased with VO2max to approach a maximal value of ~90‐95% (R²=0.83). Muscle O2 diffusing capacity and the equilibration index Y increased linearly with VO2max (R²=0.77 and R²=0.31, respectively; both P<0.01), reflecting decreasing O2 diffusional limitations and accentuating O2 delivery limitations. In conclusion, although O2 delivery is the main limiting factor to VO2max, enhanced O2 extraction fraction (≥90%) contributes to the remarkably high VO2max in endurance‐trained individuals.
... At high altitude, peak oxygen uptake ( _ VO 2peak ) is lower than at sea level due to a reduction in the amount of oxygen inspired (Stenberg et al. 1966;Lawler et al. 1988;Martin and O'Kroy 1993). However, this reduction in _ VO 2peak is characterized by large interindividual variations (Young et al. 1985;Fulco et al. 1998;Chapman et al. 1999Chapman et al. , 2011Ogawa et al. 2007;Chapman 2013), with individuals showing greater reductions in _ VO 2peak exhibiting smaller increases in ventilation in response to hypoxia (Lawler et al. 1988;Gavin et al. 1998;Ogawa et al. 2007;Chapman 2013). ...
We tested whether expiratory flow limitation (EFL) occurs in endurance athletes in a moderately hypobaric hypoxic environment equivalent to 2500 m above sea level and, if so, whether EFL inhibits peak ventilation (Epeak), thereby exacerbating the hypoxia‐induced reduction in peak oxygen uptake (O2peak). Seventeen young male endurance runners performed incremental exhaustive running on separate days under hypobaric hypoxic (560 mmHg) and normobaric normoxic (760 mmHg) conditions. Oxygen uptake (O2), minute ventilation (E), arterial O2 saturation (SpO2), and operating lung volume were measured throughout the incremental exercise. Among the runners tested, 35% exhibited EFL (EFL group, n = 6) in the hypobaric hypoxic condition, whereas the rest did not (Non‐EFL group, n = 11). There were no differences between the EFL and Non‐EFL groups for Epeak and O2peak under either condition. Percent changes in Epeak (4 ± 4 vs. 2 ± 4%) and O2peak (−18 ± 6 vs. −16 ± 6%) from normobaric normoxia to hypobaric hypoxia also did not differ between the EFL and Non‐EFL groups (all P > 0.05). No differences in maximal running velocity, SpO2, or operating lung volume were detected between the two groups under either condition. These results suggest that under the moderate hypobaric hypoxia (2500 m above sea level) frequently used for high‐attitude training, ~35% of endurance athletes may exhibit EFL, but their ventilatory and metabolic responses during maximal exercise are similar to those who do not exhibit EFL. This is the first study demonstrating that expiratory flow limitation occurs in some competitive endurance runners under moderate hypobaric hypoxia. However, expiratory flow limitation does not appear to affect ventilatory or metabolic responses during maximal exercise under moderate hypobaric hypoxia. Our results provide new information pertaining to the regulation of breathing during exercise at high altitude.
... Since the peak power output achieved is also reduced in hypoxia, an alternative hypothesis could be that HR max is lowered due to a decrease in exercise effort. However, maximal plasma lactate and catecholamine concentrations (Stenberg et al., 1966;Bouissou et al., 1986;Lundby et al., 2000Lundby et al., , 2001a as well as perceptual responses (Horstman et al., 1979) at the termination of exercise are often similar at altitude and sea level. Maximal skeletal muscle VO 2 could also dictate maximal cardiac output in hypoxia (Wagner, 2000). ...
The use of exercise intervention in hypoxia has grown in popularity amongst patients, with encouraging results compared to similar intervention in normoxia. The prescription of exercise for patients largely rely on heart rate recordings (percentage of maximal heart rate (HRmax) or heart rate reserve). It is known that HRmax decreases with high altitude and the duration of the stay (acclimatization). At an altitude typically chosen for training (2,000-3,500 m) conflicting results have been found. Whether or not this decrease exists or not is of importance since the results of previous studies assessing hypoxic training based on HR may be biased due to improper intensity. By pooling the results of 86 studies, this literature review emphasizes that HRmax decreases progressively with increasing hypoxia. The dose–response is roughly linear and starts at a low altitude, but with large inter-study variabilities. Sex or age does not seem to be a major contributor in the HRmax decline with altitude. Rather, it seems that the greater the reduction in arterial oxygen saturation, the greater the reduction in HRmax, due to an over activity of the parasympathetic nervous system. Only a few studies reported HRmax at sea/low level and altitude with patients. Altogether, due to very different experimental design, it is difficult to draw firm conclusions in these different clinical categories of people. Hence, forthcoming studies in specific groups of patients are required to properly evaluate (1) the HRmax change during acute hypoxia and the contributing factors, and (2) the physiological and clinical effects of exercise training in hypoxia with adequate prescription of exercise training intensity if based on heart rate.
... The CaO 2 may be reduced by reducing hemoglobin concentration isovolemically and by carbon monoxide administration. These two interventions show a reduction in V O 2 max that is proportional to the magnitude of the reduction achieved in CaO 2 (6,15,23,30). ...
... The CaO 2 may be reduced by reducing hemoglobin concentration isovolemically and by carbon monoxide administration. These two interventions show a reduction in V O 2 max that is proportional to the magnitude of the reduction achieved in CaO 2 (6,15,23,30). ...
... At a moderate latitude, this corresponds to an altitude of about 2,500 m. From this altitude and above, hypoxemia triggers a series of pulmonary and cardiovascular adjustments intended to maintain the organism's adequate oxygenation (1); such adjustments include increased pulmonary ventilation and cardiac output, with the latter almost exclusively due to increased heart rate (2)(3)(4). ...
... The maximal oxygen consumption (VO 2 max) decreases by about 1% per 100 m over 1,500 m (6). A great variation is found during maximal work at high altitude (4,000 m) with a 72% decline observed in VO 2 max along with the inability of maximum ventilation and maximum CaO to provide the organism with the required amount of oxygen (7). Night work brings changes in the cardiovascular system (8) while a prolonged upright posture may result into professional phlebopathies (9). ...
Any work activity performed at elevations over 3,000 m above sea level is considered as work at high altitude. The changing environmental conditions result in an adaptation of the human organism, mainly due to a reduced partial pressure of oxygen in the air and a proportional decrease in barometric pressure. We carried out a systematic review of the scientific literature in this field so as to develop a health and risk protocol as well as a procedure of ascent for researchers and staff expected to work in a science research lab at an altitude of 5,100 m asl. We wish to highlight the crucial role that occupational medicine plays in the formulation of a medical protocol used to assess the suitability of staff to work in environments posing high risks to human health, as in this case, and of a protocol of ascent minimizing the risk associated with changes in altitude.
... Notwithstanding, there are a few conditions in which the Q versus V˙O 2 relationship is altered. In fact it is shifted upward in acute hypoxia (Hartley et al., 1973;Hughes et al., 1968;Roca et al., 1989;Stenberg et al., 1966) and after moderate CO poisoning (González-Alonso et al., 2001;Vogel and Gleser, 1972). Both these conditions lead to a reduction of C a O 2 . ...
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.
... Maximal heart rate during exercise follows the decline in maximal oxygen uptake with increasing altitude [19]. The maximal heart rate response to sudden altitude exposure is variable, with some studies reporting no change [20] and a recent study, at higher altitude, reporting decreased peak heart rate with sudden ascent [21]. Whether the sinoatrial node is susceptible to brief, severe hypoxemia is unknown. ...
... The marathon and half marathons included in this study are held near sea level. Performance and cardiac function are undoubtedly impacted by the hypoxia encountered throughout the PP race: acute altitude exposure at simulated 4000 m (13 123 feet) increases heart rate and cardiac output during submaximal exercise to compensate for reduced arterial partial pressure of oxygen (PaO 2 ), but maximal HR is reduced slightly, possibly due to reduced oxygen delivery to cardiac tissue (Stenberg et al. 1966) or increased production of epinephrine, which may have additional performance effects as it speeds uptake of glucose into muscle cells (Richardson et al. 1998). Wehrlin and Hallen (2006) found a 1.9 bpm decrease in maximal HR per 1000 m–in keeping with Stenberg et al.'s (1966) result at 4000 m– beginning at least as low as 1000 m, encompassing most of the altitudes encountered at MWRR. ...
Online, accessible performance and heart rate data from running competitions are posted publicly or semi-publicly to social media. We tested the efficacy of one such data resource- Strava- as a tool in exercise physiology investigations by exploring heart rate differences in mountain racing and road racing running events. Heart rate and GPS pace data were gathered from Strava activities posted by 111 males aged 21-49, from two mountain races (Mt. Washington Road Race and Pike's Peak Ascent) and two road race distances (half marathon and marathon). Variables of interest included race finish time, average heart rate, time to complete the first half (by distance) of the race, time to complete the second half, average heart rate for both the first and second half, estimated maximal heart rate, and competitiveness (finish time as percentage of winning time). Mountain runners on average showed no change in heart rate in the second versus first half of the event, while road racers at the half marathon and marathon distances showed increased second-half heart rate. Mountain runners slowed considerably more in the second half than road runners. Heart rate increases in road races were likely reflective of cardiac drift. Altitude and other demands specific to mountain racing may explain why this was not observed in mountain races. Strava presents enormous untapped opportunity for exercise physiology research, enabling initial inquiry into physiological questions that may then be followed by targeted laboratory studies.
... The marathon and half marathons included in this study are held near sea level. Performance and cardiac function are undoubtedly impacted by the hypoxia encountered throughout the PP race: acute altitude exposure at simulated 4000 m (13 123 feet) increases heart rate and cardiac output during submaximal exercise to compensate for reduced arterial partial pressure of oxygen (PaO 2 ), but maximal HR is reduced slightly, possibly due to reduced oxygen delivery to cardiac tissue (Stenberg et al. 1966) or increased production of epinephrine, which may have additional performance effects as it speeds uptake of glucose into muscle cells (Richardson et al. 1998). Wehrlin and Hallen (2006) found a 1.9 bpm decrease in maximal HR per 1000 m-in keeping with Stenberg et al.'s (1966) result at 4000 m-beginning at least as low as 1000 m, encompassing most of the altitudes encountered at MWRR. ...
Online, accessible performance and heart rate data from running competitions are posted publicly or semi-publicly to social media. We tested the efficacy of one such data resource- Strava- as a tool in exercise physiology investigations by exploring heart rate differences in mountain racing and road racing running events. Heart rate and GPS pace data were gathered from Strava activities posted by 111 males aged 21–49, from two mountain races (Mt. Washington Road Race and Pike's Peak Ascent) and two road race distances (half marathon and marathon). Variables of interest included race finish time, average heart rate, time to complete the first half (by distance) of the race, time to complete the second half, average heart rate for both the first and second half, estimated maximal heart rate, and competitiveness (finish time as percentage of winning time). Mountain runners on average showed no change in heart rate in the second versus first half of the event, while road racers at the half marathon and marathon distances showed increased second-half heart rate. Mountain runners slowed considerably more in the second half than road runners. Heart rate increases in road races were likely reflective of cardiac drift. Altitude and other demands specific to mountain racing may explain why this was not observed in mountain races. Strava presents enormous untapped opportunity for exercise physiology research, enabling initial inquiry into physiological questions that may then be followed by targeted laboratory studies.
... Elliot et al. (10) reported a 14% reduction the first day after arrival at 406 mmHg at 84% VO 2 max in eight subjects. Stenberg et al. (31) showed a 14% reduction upon acute Fig. 6. V E STPD/VO 2 vs. percent of VO 2 max for this study and from the mean data from Operation Everest (OE) and Silver Hut (SH) studies as shown in Fig. 5C and D exposure to 462 mmHg in a protocol similar to ours in six subjects. ...
This study compared the ventilation response to an incremental ergometer exercise at two altitudes: 633 mmHg (resident altitude = 1,600 m) and following acute decompression to 455 mmHg (≈,350 m altitude) in eight male cyclists and runners. At 455 mmHg, the VESTPD at RER <1.0 was significantly lower and the VEBTPS was higher because of higher breathing frequency; at VO2max, both VESTPD and VEBTPS were not significantly different. As percent of VO2max, the VEBTPS was nearly identical and VESTPD was 30% lower throughout the exercise at 455 mmHg. The lower VESTPD at lower pressure differs from two classical studies of acclimatized subjects (Silver Hut and OEII), where VESTPD at submaximal workloads was maintained or increased above that at sea level. The lower VESTPD at 455 mmHg in unacclimatized subjects at submaximal workloads results from acute respiratory alkalosis due to the initial fall in HbO2 (≈0.17 pHa units), reduction in PACO2 (≈5 mmHg) and higher PAO2 throughout the exercise, which are partially pre-established during acclimatization. Regression equations from these studies predict VESTPD from VO2 and PB in unacclimatized and acclimatized subjects. The attainment of ventilatory acclimatization to altitude can be estimated from the measured vs. predicted difference in VESTPD at low workloads after arrival at altitude.
... Gli effetti dell'esposizione acuta all'altitudine sul sistema cardiovascolare sono stati ampiamente studiati negli anni passati [1][2]. Nei soggetti normali alcuni investigatori hanno riscontrato modesti aumenti dei valori pressori [3], altri una lieve riduzione [4], altri ancora nessuna modificazione [5]. Due articoli hanno riportato la risposta della pressione arteriosa all'altitudine in soggetti ipertesi, dimostrando un modesto aumento dei valori sistolici [3] in uno studio e nessun cambiamento nell'altro [5]. ...
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.
In moderate hypoxia [partial pressure of inspired oxygen (PIO2) =85mmHg-111mmHg], the reduction in maximal oxygen consumption (V̇O2max) has been attributed to arterial desaturation, whereas in severe hypoxia (PIO2<85mmHg), elevated pulmonary artery pressure (PAP) is thought to impair peak cardiac output (Q̇) and therefore V̇O2max. The purpose of this study was to examine whether reducing PAP with inhaled nitric oxide (iNO, a selective pulmonary vasodilator) would increase V̇O2max in moderate and severe acute hypoxia. Twelve young, healthy participants (mean V̇O2max = 45.3 ± 12.2 mL/kg/min), with normal lung function completed the randomized double-blind crossover study over six sessions. Experimental cardiopulmonary exercise tests (CPET) were completed on separate days with participants under the following conditions: A) acute moderate hypoxia (PIO2=89 mmHg), B) acute severe hypoxia (PIO2=79 mmHg), C) acute moderate hypoxia with 40ppm iNO, and D) acute severe hypoxia with 40ppm iNO (order randomized). On separate days, rest, and exercise (60 watt) echocardiography were conducted to determine right ventricular systolic pressure (RVSP/PAP) under conditions A-D. Resting RVSP was reduced by 2.5±0.8 mmHg with iNO in moderate hypoxia (p=0.01) and 1.8±0.2 mmHg in severe hypoxia (p=0.05); however, iNO had no effect on peak Q̇ or V̇O2max in either hypoxic condition. Despite reducing RVSP with iNO in hypoxia, peak Q̇ and V̇O2max were unaffected, suggesting that iNO may not improve exercise tolerance in healthy participants during hypoxic exercise.
Sex differences in physiological responses to various stressors, including exercise, have been well documented. However, the specific impact of these differences on exposure to hypoxia, both at rest and during exercise, has remained underexplored. Many studies on the physiological responses to hypoxia have either excluded women or included only a limited number without analyzing sex-related differences. To address this gap, this comprehensive review conducted an extensive literature search to examine changes in physiological functions related to oxygen transport and consumption in hypoxic conditions. The review encompasses various aspects, including ventilatory responses, cardiovascular adjustments, hematological alterations, muscle metabolism shifts, and autonomic function modifications. Furthermore, it delves into the influence of sex hormones, which evolve throughout life, encompassing considerations related to the menstrual cycle and menopause. Among these physiological functions, the ventilatory response to exercise emerges as one of the most sex-sensitive factors that may modify reactions to hypoxia. While no significant sex-based differences were observed in cardiac hemodynamic changes during hypoxia, there is evidence of greater vascular reactivity in women, particularly at rest or when combined with exercise. Consequently, a diffusive mechanism appears to be implicated in sex-related variations in responses to hypoxia. Despite well-established sex disparities in hematological parameters, both acute and chronic hematological responses to hypoxia do not seem to differ significantly between sexes. However, it is important to note that these responses are sensitive to fluctuations in sex hormones, and further investigation is needed to elucidate the impact of the menstrual cycle and menopause on physiological responses to hypoxia.
When combining two conditions of reduced oxygen availability, anemia and hypoxia, human physiological responses are highly challenged to maintain arterial oxygen delivery, especially during whole-body exercise. The aim of this study was to compare the cardiorespiratory responses of mildly anemic women with those of healthy controls, while cycling in normobaric hypoxia. Two groups of young females were matched for age, weight, height, and involvement in physical activity, one with normal hemoglobin, hematocrit, and ferritin levels and another suffering from mild iron deficiency anemia (10 < (Hb) < 12 g/dL, 34 < Hct < 37%, ferritin < 15 μg/L). They cycled to exhaustion under normoxia and hypoxia (FIO2 0.21 and 0.14), and their physiological responses were compared at 40, 80, and 100% VO2max of the specific condition. The two groups differed (p < 0.05) mainly at the higher exercise intensities; the anemic participants exhibited similar heart rate but lower oxygen pulse than their control counterparts, as well as a larger drop in maximal oxygen uptake. However, they sustained maximal effort by employing the anaerobic metabolism to a larger extent, which stimulated a greater ventilatory response. It appears that iron deficiency anemia of mild severity, which is commonly observed in young athletic females, impacts physiological responses during whole-body exercise in the presence of moderate hypoxia.
Acclima(tiza)tion to heat or hypoxia enhances work capacity in hot and hypoxic environmental conditions, respectively; an acclimation response considered to be mediated by stimuli-specific molecular/systemic adaptations and potentially facilitated by the addition of exercise sessions. Promising findings at the cellular level provided the impetus for recent studies investigating whether acclimation to one stressor will ultimately facilitate whole body performance when exercise is undertaken in a different environmental condition. The present critical mini-review examines the theory of cross-adaptation between heat and hypoxia with particular reference to the determinants of aerobic performance. Indeed, early functional adaptations (improved exercise economy, enhanced oxyhemoglobin saturation) succeeded by later morphological adaptations (increased hemoglobin mass) might aid acclimatized humans perform aerobic work in an alternative environmental setting. Longer-term acclimation protocols that focus on the specific adaptation kinetics (and further allow for the adaptation reversal) will elucidate the exact physiological mechanisms that might mediate gains in aerobic performance or explain the lack thereof.
New findings:
What is the central question of this study? Does a 35-day horizontal bedrest impair thermoeffector responses during whole-body submaximal exercise performed in temperate conditions? What is the main finding and its importance? Cardiovascular and muscular deconditioning ensued from prolonged recumbency, seems to augment, at least to a degree, the exercise-induced increase in body core temperature, most likely due to an impairment in non-evaporative heat loss. The response is a function of the absolute exercise intensity imposed.
Abstract:
We examined the effects of a 35-day horizontal bedrest on thermoregulation during whole-body exercise. Fifteen healthy men were randomly assigned to either a bedrest (BR; n = 10), or a control (CON; n = 5) group. Prior to bedrest, both groups performed a 40-min constant-load upright cycling at 30% of their peak workload (Wpeak ; PRE). One and two days after bedrest, the BR group performed, in a randomised counterbalanced order, two 40-min trials at 30% of: (i) the pre-bedrest Wpeak (i.e., at a fixed absolute intensity; POST-A), and (ii) the post-bedrest Wpeak (i.e., at a fixed relative intensity; POST-R). The CON group conducted only the POST-A trial, at the same time intervals. During the trials, rectal (Trec ) and skin temperatures, and the forehead sweating rate (SwR) were monitored. In the CON group, no differences were observed between the trials. Bedrest potentiated moderately the Trec elevation during the latter part of POST-A (∼0.10°C; P≤0.05), but not of POST-R (∼0.04°C; P = 0.11). In both post-bedrest trials, was attenuated by ∼1.5-2.0° C throughout (P<0.01), whereas the forehead SwR was not modulated. Trec and were similar in POST-A and POST-R; yet the forehead SwR was more dependent on the relative workload imposed (P = 0.04). Present findings therefore suggest that the cardiovascular and muscular deconditioning ensued from a 35-day bedrest may aggravate the exercise-induced increase in body core temperature when working at a given absolute intensity, most likely due to an impairment in non-evaporative heat loss. This article is protected by copyright. All rights reserved.
Blood pressure is a function of cardiac output and peripheral vascular resistance. During graded exercise testing (GXT), systolic blood pressure (SBP) is expected to increase gradually along with work rate, oxygen consumption, heart rate, and cardiac output. Individuals exposed to chronic endurance training attain a greater exercise SBP than in their untrained state and sedentary counterparts, but it is currently unknown what is considered a safe upper limit. This review discusses key studies examining blood pressure response in sedentary individuals and athletes. We highlight the physiological characteristics of highly fit individuals in terms of cardiovascular physiology and exercise blood pressure and review the state of the current literature regarding the safety of high SBP during exercise in this particular subgroup. Findings from this review indicate that a consensus on what is a normal SBP response to exercise in highly fit subjects and direct causation linking high GXT SBP to pathology is lacking. Consequently, applying GXT SBP guidelines developed for a “normal” population to endurance trained individuals appears unsupported at this time. Lack of evidence for poor outcomes leads us to infer that elevated peak SBP in this subgroup could more likely reflect an adaptive response to training, rather than a pathological outcome. Future studies should track clinical outcomes of those achieving elevated SBP and develop athlete specific guidelines.
Reports of VO2 response differences between normoxia and hypoxia during incremental exercise do not agree. In this study VO2 and VE were obtained from 15-s averages at identical work rates during continuous incremental cycle exercise in 8 subjects under ambient pressure (633 mmHg ≈1,600 m) and during duplicate tests in acute hypobaric hypoxia (455 mmHg ≈4,350 m), ranging from 49 to 100% of VO2 peak in hypoxia and 42-87% of VO2 peak in normoxia. The average VO2 was 96 mL/min (619 mL) lower at 455 mmHg (n.s. P = 0.15) during ramp exercises. Individual response points were better described by polynomial than linear equations (mL/min/W). The VE was greater in hypoxia, with marked individual variation in the differences which correlated significantly and directly with the VO2 difference between 455 mmHg and 633 mmHg (P = 0.002), likely related to work of breathing (Wb). The greater VE at 455 mmHg resulted from a greater breathing frequency. When a subject's hypoxic ventilatory response is high, the extra work of breathing reduces mechanical efficiency (E). Mean ∆E calculated from individual linear slopes was 27.7 and 30.3% at 633 and 455 mmHg, respectively (n.s.). Gross efficiency (GE) calculated from mean VO2 and work rate and correcting for Wb from a VE-VO2 relationship reported previously, gave corresponding values of 20.6 and 21.8 (P = 0.05). Individual variation in VE among individuals overshadows average trends, as also apparent from other reports comparing hypoxia and normoxia during progressive exercise and must be considered in such studies.
Millions of people live, work, and play in regions of the world where weather is intemperate or at terrestrial elevations where ambient oxygen pressure is less than at sea level. Exposure to extremes of heat, cold, or hypobaric hypoxia can elicit a variety of physiological responses in humans, which assist the body to re-establish and/or maintain homeostasis under the influence of new environmental conditions. Those physiological responses can have nutritional implications.
La charge de travail peut être évaluée de différentes façons. Des méthodes objectives (pression artérielle et fréquence cardiaque) et/ou subjectives (échelle de Borg CR10) ont été utilisées tant en laboratoire que sur le terrain. L'étude en laboratoire quantifie les astreintes cardiovasculaires et subjectives développées par 30 sujets jeunes (15 femmes et 15 hommes) au cours de 7 tests d'endurance statique appliqués à différents groupes musculaires du membre supérieur dominant. Les paramètres objectifs et subjectifs augmentent linéairement au cours des tests jusqu'à leur maximum. Les coûts cardiaque et tensionnel maxima sont respectivement de 20 à 36 bpm et de 22 à 33 mm Hg. Le coût subjectif est de 10 sur l'échelle de Borg. L'étude de terrain s'est effectuée dans un abattoir de porcs. Les astreintes subjectives recueillies pendant 5 moments prédéfinis des 8 heures de travail sont associées à un enregistrement vidéo pour l'étude des postes de 11 désosseurs et de 10 pareurs (7 femmes et 14 hommes). Les résultats ont permis de préciser les plaintes des salariés, les postes ressentis comme les plus pénibles et l'effet "fatigue" au cours de la journée. Dans ces 2 études, la comparaison de données objectives et subjectives, permet d'appréhender les intérêts et les limites des échelles de Borg comme méthode d'évaluation ergonomique de la charge de travail.
Exercise intolerance is a condition where the patient is unable to undertake physical exercise at the level and/or for the duration that would be expected of someone in his or her age and general physical condition. When this inability is triggered by impaired function of one or more of the physiological systems (i.e. central haemodynamic, respiratory, peripheral muscles), the result is the intensification of the perceptions of dyspnoea, often in conjunction with peripheral muscle discomfort that is often triggered by peripheral muscle fatigue [1].
We developed a periodic hypobaric hypoxic environment (PHHE) system. Characteristics of this system varied between decreased pressure at an altitude of 1,500 m for 180 seconds and increased pressure at an altitude of 0 m for 180 seconds. The present study aimed to determine the effects of PHHE on physiological responses during endurance exercise and recovery after exercise. This study included 12 healthy men, and they provided written informed consent. All subjects performed a cycling exercise for 30 minutes and recovered after exercise for 10 minutes. The exercise protocol was performed with 20% maximum oxygen uptake for 6 minutes (warm-up), 40 % for 18 minutes (main exercise), and 20 % for 6 minutes (cool down). We established two experimental conditions: exercise with the PHHE and the control (C). The C condition involved exercise using the PHHE at an altitude of 0 m, and the atmospheric pressure was not changed. In the PHHE condition, the atmospheric pressure was changed periodically from 967 to 817 hPa (the external pressure was 1,008 hPa). Subjects’ heart rate (HR), blood pressure (BP), arterial oxygen saturation (SpO2), rating of perceived exertion, and respiratory responses were measured in both conditions. The SpO2, HR and systolic BP during exercise were significantly lower in the PHHE condition than in the C condition. The HR post-exercise was significantly lower. After exercise, the ln HF, an index of cardiac parasympathetic nervous system modulation, was significantly higher. In conclusion, during endurance exercise, cardiocirculatory responses in the PHHE condition were decreased.
In order to compare the work efficiency in hypoxia with that in normal environment, given work was loaded to five healthy male subjects in a decompression chamber. Hyoxia was induced by decompression to a simulated altitude of 4, 000 meter, where the subjects walked on a treadmill with a slope of 5% at a speed of 80 m/min for 10 minutes. Oxygen consumption, expiratory volume, R. Q., respiratory rate, heart rate, oxygen pulse, and oxygen removal were measured before, during and after the work. Blood samples were taken to determine lactate value before and after the work. The results obtained and the conclusion are as follows ;1) Vo2 at rest in the hypoxia was slightly less than that of the control, while the total oxygen consumed by the work was more in the hypoxia than the control value.2) Making correction for anaerobic mechanism, effect of respiratory and circulatory acceleration, and decreased air density on oxygen consumption revieled that the true work efficiency in hypoxia was completely same as in the controle.3) Respiratory quotient dropped in the early stage of the work, thereafter increased in the control, while it increased on work without initial drop in the hypoxia. Total extra CO2 eliminated by the work was significantly more than the control value.
This chapter presents a brief review of our knowledge of the effects of exposure of the resident of the plains to high altitude conditions on mountains. Although considerable attention has been paid to the study of the physiology of permanent residents of high altitude regions, the literature on the effects of high altitude on the sea-level residents and their reactions is even more extensive. The sea-level man at high altitude presents a number of unsolved problems of great fundamental importance in biology and medicine, often having close relation with military operations. Extremely valuable contributions to our knowledge of the reactions of man exposed to high altitude environment have been made in the course of numerous mountaineering expeditions to the Himalaya and Karakoram (118). Some recent work has also been undertaken by the Indian Army medical workers on the problems of troops operating at high altitude on the Himalaya. Quite contrary to the prevailing belief of those days, early experience of mountaineering on the Himalaya showed that the performance of the mountaineers, is fairly satisfactory up to an elevation of about 6900 m. Above this altitude was observed rapid and severe deterioration, marked progressive weakness, lethargy, failure to recover from fatigue, wasting of muscles and tissues, loss of appetite and a gradual decline of capacity for work. It is known, for example, that the strength of muscles in man at an altitude 2400 m is about one-third of that at sea level and at an altitude of 3400 m it is about one-fourth of the sea-level value. At altitudes between 2000 and 3400 m there is usually slight effect, but between 4000 and 5800 m the muscle fatigue is considerable and about 6100 m it becomes very pronounced.
High altitude (HA) is generally defined as land surface 10,000 feet (3,000 m) or more above sea level (SL). HA areas constitute about 5% of the total land mass. Numerous circulatory adaptations occur in normal SL residents exposed to HA and in permanent natives of HA. A brief description of normal and abnormal circulatory response to HA is presented in this review.
During muscular exercise the product of the cardiac output (Q̇) and the mixed-venous concentration of oxygen (\(C{\bar v_{{O_2}}}\)
) is constant and independent of the oxygen uptake (\({\dot V_{{O_2}}}\)
) (2).
In humans, oxygen flows from inspired air to the mitochondria against a resistance, which is overcome by an overall O2 pressure gradient. According to the O2 conductance equation, this resistance is provided by the sum of numerous in-series resistances, so that a progressive drop in O2 partial pressure from inspired air to the mitochondria takes place. This approach was applied to the study of the O2 transfer system at maximal exercise (22). In this case, at the steady-state, the flow of O2 is the same across each resistance and is equal to ̇Vo2max. Afterwards, a multifactorial model of ̇Vo2max limitation was developed, assuming that each of the resistances in-series (or their reciprocal, the conductances) provides a sizeable fraction of the overall limitation to ̇Vo2max. Three major groups of conductances were identified, namely 1) the pulmonary conductances, related to alveolar ventilation and to alveolar-capillary O2 transfer, 2) the cardiovascular conductance (Gq), due to cardiovascular oxygen transport, and 3) the muscular conductances, related to tissue O2 diffusion and utilisation. The second turned out to provide 60-to-70% of the overall ̇Vo2max limitation, at least during exercise with big muscle groups in normoxia (4, 5, 10).
Von jeher hat es den Menschen fasziniert, hohe Berggipfel zu bezwingen. Sein Drang nach Entdeckungen hat ihn heute bis in den Weltraum geführt. Permanente menschliche Wohnungen existieren bis in Höhen von über 4500 m. Es wird immer populärer, Sommer- und Winterferien in hohen Gebirgsgegenden zu verbringen unter Einbeziehung von schweren körperlichen Beanspruchungen wie Bergsteigen oder Skilaufen. Die Entscheidung, die Olympischen Spiele von 1968 nach Mexiko City in eine Höhe von 2300 m zu legen, hat ein spezielles Interessa an den Problemen der Leistungsfähigkeit und des Leistungsverhaltens in der Höhe geschaffen (Weihe, 1964; Dill, 1964; Luft, 1964 b; Hollmann u. Mitarb., 1965 b; Schweiz. Z. Sportmed. 14, 1, 1966; Margaria, 1967; Goddard, 1967; Jokl u. Jokl, 1968; Roskamm u. Mitarb., 1968).
Maximal oxygen consumption \( ({\dot V_{{O_2}}}\max ) \) undergoes a progressive reduction in hypoxia both acute and chronic as appears from Fig. 1 where data from various authors are summarized. Such decrease, for a pressure drop of half an atmosphere (corresponding to an altitude of about 5500 meters) ranges between 30% and 45%, independent of the degree of acclimatization and of the ethnic characteristics of the sub.iects. Common factors known to change \( {\dot V_{{O_2}}}\max \)
in opposite directions In hypoxia are:
1)
The decreased arterial O
2
saturation (%HbO2) due to decreased \( {P_{{I_{{O_2}}}}} \) and possibly to an impairment of the diffusion property of the lung. The arterial oxygen and carbon dioxide partial pressures \( P{a_{{O_2}}}{\kern 1pt} and{\kern 1pt} P{a_{C{O_2}}} \) of resident highlanders as well as of acclimatized lowlanders are plotted as a function of altitude in Fig. 2, along with the corresponding HbO2 saturation values (HbO2). At a barometric pressure of 380 torr (5500 m) %HbO2 drops to about 80%.
2)
The increased Blood hemoglobin (Hb) concentration. Hb concentration, after a prolonged exposure to 5500 m, may attain 130–140% of the sea level control value.
The present study is limited to lactate production in connection with exercise.
This paper deals with two different aspects of the cardiovascular adjustments that take place during true and simulated exercise. The first is concerned with the cardiovascular effects of electric shock compared with those arising during normal exercise. The second tends to give a biological meaning to the slope and the intercept of the linear relationships linking cardiac output and oxygen consumption during the steady state of submaximal exercise.
This chapter contains an analysis of the steady-state concept, as it is applied during light exercise. In this case, oxygen consumption increases upon exercise onset to attain a steady level, which can be maintained for a long period of time. The steady-state oxygen consumption is proportional to the exerted mechanical power. Under these circumstances, there is neither accumulation of lactate in blood nor changes in muscle phosphocreatine concentration: aerobic metabolism sustains the entire energy requirement of the exercising body. Once the steady state has been attained, the flow of oxygen is the same at all levels along the respiratory system. The quantitative relations determining the flow of oxygen across the alveoli and in blood are discussed. Special attention is given to the effects of ventilation—perfusion inequality and to the diffusion—perfusion interaction equations. The cardiovascular responses at exercise steady state are analysed in the context of the equilibrium between systemic oxygen delivery and systemic oxygen return. The relationship between oxygen consumption and power is discussed, along with the distinction between external and internal work during cycling. The concepts of mechanical efficiency of exercise and energy cost of locomotion are analysed. Concerning the latter, the distinction between aerodynamic work and frictional work is introduced. The roles of the cross-sectional surface area on the frontal plane and of air density in aerodynamic work are discussed. To end with, an equation linking ventilation, circulation and metabolism at exercise in a tight manner is developed, around the notion that the homeostasis of the respiratory system at exercise is maintained around given values of the constant oxygen return. This equation tells that, as long as we are during steady-state exercise in normoxia, any increase in the exercise metabolic rate requires an increase in ventilation that is proportional to that in oxygen consumption only if the pulmonary respiratory quotient stays invariant does not change, and an increase in cardiac output that is not proportional to the corresponding increase in oxygen consumption. At intense exercise, when lactate accumulation also occurs and hyperventilation superimposes, a new steady state would be attained only at \( P_{A}{\text{CO}}_{2} \) values lower than 40 mmHg: the homeostasis of the respiratory system would be modified. This new steady state, however, is never attained in fact, for reasons that are discussed in Chap. 3.
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