| 1. |
- Calbet, José A L, et al.
(author)
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Limitations to oxygen transport and utilisation during sprint exercise in humans : evidence for a functional reserve in muscle O2 diffusing capacity.
- 2015
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In: Journal of Physiology. - 0022-3751 .- 1469-7793. ; 593:20, s. 4649-4664
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Journal article (peer-reviewed)abstract
- KEY POINTS SUMMARY: Severe acute hypoxia reduces sprint performance. Muscle VO2 during sprint exercise in normoxia is not limited by O2 delivery, O2 off-loading from haemoglobin or structure-dependent diffusion constraints in the skeletal muscle of young healthy men. A large functional reserve in muscle O2 diffusing capacity exists and remains available at exhaustion during exercise in normoxia, which is recruited during exercise in hypoxia. During whole-body incremental exercise to exhaustion in severe hypoxia leg VO2 is primarily dependent on convective O2 delivery and less limited by diffusion constraints than previously thought. The kinetics of O2 off-loading from haemoglobin does not limit VO2 peak in hypoxia. Our results indicate that the limitation to VO2 during short sprints resides in mechanisms regulating mitochondrial respiration.ABSTRACT: To determine the contribution of convective and diffusive limitations to VO2 peak during exercise in humans oxygen transport and haemodynamics were measured in eleven men (22 ± 2 years) during incremental (IE) and 30-s all-out sprints (Wingate test, WgT), in normoxia (Nx, PI O2 :143 mmHg) and hypoxia (Hyp, PI O2 :73 mmHg). Carboxyhaemoglobin (COHb) was increased to 6-7% before both WgTs to left-shift the oxyhaemoglobin dissociation curve. Leg VO2 was measured by the Fick method, and leg blood flow (BF) with thermodilution and muscle O2 diffusing capacity (DMO2 ) was calculated. In the WgT mean power output, leg BF, leg O2 delivery and leg VO2 were 7, 5, 28 and 23% lower in Hyp than Nx (P < 0.05), however, peak WgT DMO2 was higher in hypoxia (51.5 ± 9.7) than Nx (20.5 ± 3.0 ml min(-1) mmHg(-1) , P < 0.05). Despite a similar PaO2 (33.3 ± 2.4 and 34.1 ± 3.3 mmHg), mean capillary PO2 (16.7 ± 1.2 and 17.1 ± 1.6 mmHg), and peak perfusion during IE and WgT in Hyp, DMO2 and leg VO2 were 12 and 14% higher during WgT than IE in Hyp (both, P < 0.05). DMO2 was apparently insensitive to COHb (COHb: 0.7 vs 7%, in IE Hyp and WgT Hyp). At exhaustion, the Y equilibration index was well above 1.0 in both conditions, reflecting greater convective than diffusive limitation to the O2 transfer both in Nx and Hyp. In conclusion, muscle VO2 during sprint exercise is not limited by O2 delivery, the O2 off-loading from haemoglobin or structure-dependent diffusion constraints in the skeletal muscle. These findings reveal a remarkable functional reserve in muscle O2 diffusing capacity. This article is protected by copyright. All rights reserved.
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| 2. |
- Jacobs, Robert A., et al.
(author)
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Twenty-eight days of exposure to 3,454 m increases mitochondrial volume density in human skeletal muscle
- 2015
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In: Journal of Physiology. - : Blackwell Publishing. - 0022-3751 .- 1469-7793. ; 594:5, s. 1151-1166
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Journal article (peer-reviewed)abstract
- The role of hypoxia on skeletal muscle mitochondria is controversial. Studies superimposing exercise training with hypoxic exposure demonstrate an increase in skeletal muscle mitochondrial volume density (MitoVD ) over equivalent normoxic training. In contrast, a reduction in both skeletal muscle mass and MitoVD have been reported following mountaineering expeditions. These observations may however be confounded by negative energy balance, which may obscure the results. Accordingly we sought to examine the effects of high altitude hypoxic exposure on mitochondrial characteristics, with emphasis on MitoVD , while minimizing changes in energy balance. For this purpose, skeletal muscle biopsies were obtained from 9 lowlanders at sea level (Pre) and following 7 (7 Days) and 28 (28 Days) days of exposure to 3454 m. Maximal ergometer power output, whole-body weight and composition, leg lean mass, and skeletal muscle fibre area all remained unchanged following the altitude exposure. Transmission electron microscopy determined intermyofibrillar (IMF) MitoVD was augmented (P = 0.028) by 11.5 ± 9.2% from Pre (5.05 ± 0.9%) to Day 28 (5.61 ± 0.04%). On the contrary, there was no change in subsarcolemmal (SS) MitoVD . As a result total MitoVD (IMF + SS) was increased (P = 0.031) from 6.20 ± 1.5% at Pre to 6.62 ± 1.4% on Day 28 (7.8 ± 9.3%). At the same time no changes in mass-specific respiratory capacities, mitochondrial protein or antioxidant content were found. This study demonstrates that skeletal muscle MitoVD may increase with 28 days acclimation to 3454 m.
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| 3. |
- Keiser, Stefanie, et al.
(author)
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Detection of blood volumes and haemoglobin mass by means of CO re-breathing and indocyanine green and sodium fluorescein injections
- 2017
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In: Scandinavian Journal of Clinical and Laboratory Investigation. - : Taylor & Francis. - 0036-5513 .- 1502-7686. ; 77:3, s. 164-174
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Journal article (peer-reviewed)abstract
- The main aim of the present study was to quantify the magnitude of differences introduced when estimating a given blood volume compartment (e.g. plasma volume) through the direct determination of another compartment (e.g. red cell volume) by multiplication of venous haematocrit and/or haemoglobin concentration. However, since whole body haematocrit is higher than venous haematocrit such an approach might comprise certain errors. To test this experimentally, four different methods for detecting blood volumes and haemoglobin mass (Hb(mass)) were compared, namely the carbon monoxide (CO) re-breathing (for Hb(mass)), the indocyanine green (ICG; for plasma volume [PV]) and the sodium fluorescein (SoF; for red blood cell volume [RBCV]) methods. No difference between ICG and CO re-breathing derived PV could be established when a whole body/venous haematocrit correction factor of 0.91 was applied (p=0.11, r=0.43, mean difference -340 +/- 612mL). In contrast, when comparing RBCV derived by the CO re-breathing and the SoF method, the SoF method revealed lower RBCV values as compared to the CO re-breathing method (p<0.05, r=0.95, mean difference -728 +/- 184mL). However, compared to the ICG and the SoF methods, the typical error (%TE) and hence reliability of the CO re-breathing method was lower for all measured parameters. Therefore, estimating blood volume compartments by the direct assessment of another compartment can be considered a suitable approach. The CO re-breathing method proved accurate in determining the induced phlebotomy and is at the same time judged easier to perform than any of the other methods.
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| 4. |
- Keramidas, Michail E., et al.
(author)
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A brief pre-exercise nap may alleviate physical performance impairments induced by short-term sustained operations with partial sleep deprivation - A field-based study
- 2018
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In: Chronobiology International. - : TAYLOR & FRANCIS INC. - 0742-0528 .- 1525-6073. ; 35:10, s. 1464-1470
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Journal article (peer-reviewed)abstract
- The purpose of the study was to evaluate the recuperative efficacy of pre-exercise napping on physical capacity after military sustained operations (SUSOPS) with partial sleep deprivation. Before and after a 2-day SUSOPS, 61 cadets completed a battery of questionnaires, and performed a 2-min lunges trial and a 3,000-m running time-trial. After the completion of SUSOPS, subjects were randomized to either a control [without pre-exercise nap (CON); n = 32] or a nap [with a 30-min pre-exercise nap (NAP); n = 29] group. SUSOPS enhanced perceived sleepiness and degraded mood in both groups. Following SUSOPS, the repetitions of lunges, in the CON group, were reduced by similar to 2.3%, albeit the difference was not statistically significant (p = 0.62). In the NAP group, however, the repetitions of lunges were increased by similar to 7.1% (p = 0.01). SUSOPS impaired the 3,000-m running performance in the CON group (similar to 2.3%; p = 0.02), but not in the NAP group (0.3%; p = 0.71). Present results indicate, therefore, that a relatively brief pre-exercise nap may mitigate physical performance impairments ensued by short-term SUSOPS.
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| 5. |
- Kölegård, Roger, et al.
(author)
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Cardiac performance is influenced by rotational changes of position in the transversal plane, both in the horizontal and 60° head-up postures
- 2018
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In: Clinical Physiology and Functional Imaging. - : John Wiley & Sons. - 1475-0961 .- 1475-097X. ; 38:6, s. 1021-1028
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Journal article (peer-reviewed)abstract
- Background: Echocardiography is usually performed with the subject/patient lying in the left lateral position (LLP), because the acoustic window is better in this than in the supine position (SP). The aim was to investigate cardiac responses to rotational changes of position in the transversal plane, from SP to LLP while horizontal, and from leaning on the back (HUT-LB) to leaning on the left side (HUT-LL) while tilted 60° head-up from the horizontal. Methods: Healthy men (n = 12) underwent 10-min HUT provocations. Cardiac variables were measured using two-dimensional echocardiography, Doppler, tissue Doppler imaging and arterial pressures using a volume-clamp method. Results: In horizontal posture, cardiac volumes were smaller in SP than in LLP: end-diastolic volume (EDV) by 14%, end-systolic volume (ESV) by 13%, stroke volume (SV) by 14%, and cardiac output (CO) by 16% (P<0·03). In addition, the mitral annular plane systolic excursion (MAPSE) was 11% smaller (P = 0·001) and the left ventricle isovolumic relaxation time (IVRT) 27% longer in SP than in LLP. The ejection fraction, heart rate, arterial pressure and pulmonary ventilation were similar in SP and LLP. During HUT, EDV, SV, CO and MAPSE were smaller, and IVRT was longer, in HUT-LB than in HUT-LL, by −19%, −20%, −17%, −18% and +35%, respectively (P<0·04). Conclusions: Cardiac performance is enhanced in LLP versus SP and in HUT-LL versus HUT-LB, which can be attributed to improved venous return, conceivably, wholly or in part, due to increased hydrostatic pressure gradients between the caval veins and the heart in the LLP and HUT-LL positions.
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| 6. |
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| 7. |
- Siebenmann, Christoph, et al.
(author)
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Cutaneous exposure to hypoxia does not affect skin perfusion in humans
- 2017
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In: Acta Physiologica. - : Wiley-Blackwell. - 1748-1708 .- 1748-1716. ; 220:3, s. 361-369
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Journal article (peer-reviewed)abstract
- Aim: Experiments have indicated that skin perfusion in mice is sensitive to reductions in environmental O-2 availability. Specifically, a reduction in skin-surface PO2 attenuates transcutaneous O-2 diffusion, and hence epidermal O-2 supply. In response, epidermal HIF-1 alpha expression increases and facilitates initial cutaneous vasoconstriction and subsequent nitric oxide-dependent vasodilation. Here, we investigated whether the same mechanism exists in humans. Methods: In a first experiment, eight males rested twice for 8 h in a hypobaric chamber. Once, barometric pressure was reduced by 50%, while systemic oxygenation was preserved by O-2-enriched (42%) breathing gas (Hypoxia(Skin)), and once barometric pressure and inspired O-2 fraction were normal (Control(1)). In a second experiment, nine males rested for 8 h with both forearms wrapped in plastic bags. O-2 was expelled from one bag by nitrogen flushing (Anoxia(Skin)), whereas the other bag was flushed with air (Control(2)). In both experiments, skin blood flux was assessed by laser Doppler on the dorsal forearm, and HIF-1 alpha expression was determined by immunohistochemical staining in forearm skin biopsies. Results: Skin blood flux during Hypoxia(Skin) and Anoxia(Skin) remained similar to the corresponding Control trial (P = 0.67 and P = 0.81). Immunohistochemically stained epidermal HIF-1 alpha was detected on 8.2 +/- 6.1 and 5.3 +/- 5.7% of the analysed area during Hypoxia(Skin) and Control(1) (P = 0.30) and on 2.3 +/- 1.8 and 2.4 +/- 1.8% during Anoxia(Skin) and Control(2) (P = 0.90) respectively. Conclusion: Reductions in skin-surface PO2 do not affect skin perfusion in humans. The unchanged epidermal HIF-1 alpha expression suggests that epidermal O-2 homoeostasis was not disturbed by Hypoxia(Skin)/Anoxia(Skin), potentially due to compensatory increases in arterial O-2 extraction.
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| 8. |
- Siebenmann, Christoph, et al.
(author)
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Does cerebral hypoxia facilitate central fatigue?
- 2016
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In: Experimental Physiology. - : IEEE Press. - 0958-0670 .- 1469-445X. ; 101:9, s. 1173-1177
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Journal article (peer-reviewed)abstract
- New Findings: What is the topic of this review? This review addresses whether a mismatch between cerebral O2 demand and delivery accelerates the development of central fatigue during endurance-type exercise. What advances does it highlight? The difficulty with studying the importance of cerebral O2 availability for exercise performance is to manipulate cerebral O2 availability independently of muscular O2 availability. The different approaches to overcome this limitation indicate that cerebral oxygenation is not a major limiting factor in normoxia, but may limit performance in submaximal exercise tasks in hypoxia. Central fatigue originates within the central nervous system and is characterized by a decrease in voluntary muscle activation. Reduced systemic O2 availability can facilitate central fatigue by enhancing the afferent input of the chemosensitive nerves that play a pivotal role in development of central fatigue. There is accumulating evidence that, in some situations, inadequate O2 availability to the brain itself promotes central fatigue. This short review presents some of the recent findings supporting a direct effect of inadequate cerebral O2 availability on central fatigue and addresses the persisting limitations.
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| 9. |
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| 10. |
- Siebenmann, Christoph, et al.
(author)
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Hypoxia increases exercise heart rate despite combined inhibition of beta-adrenergic and muscarinic receptors
- 2015
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In: American Journal of Physiology. Heart and Circulatory Physiology. - : American Physiological Society. - 0363-6135 .- 1522-1539. ; 308:12, s. H1540-H1546
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Journal article (peer-reviewed)abstract
- Hypoxia increases the heart rate response to exercise, but the mechanism(s) remains unclear. We tested the hypothesis that the tachycardic effect of hypoxia persists during separate, but not combined, inhibition of beta-adrenergic and muscarinic receptors. Nine subjects performed incremental exercise to exhaustion in normoxia and hypoxia (fraction of inspired O-2 = 12%) after intravenous administration of 1) no drugs (Cont), 2) propranolol (Prop), 3) glycopyrrolate (Glyc), or 4) Prop + Glyc. HR increased with exercise in all drug conditions (P < 0.001) but was always higher at a given workload in hypoxia than normoxia (P < 0.001). Averaged over all workloads, the difference between hypoxia and normoxia was 19.8 +/- 13.8 beats/min during Cont and similar (17.2 +/- 7.7 beats/min, P = 0.95) during Prop but smaller (P < 0.001) during Glyc and Prop + Glyc (9.8 +/- 9.6 and 8.1 +/- 7.6 beats/min, respectively). Cardiac output was enhanced by hypoxia (P < 0.002) to an extent that was similar between Cont, Glyc, and Prop + Glyc (2.3 +/- 1.9, 1.7 +/- 1.8, and 2.3 +/- 1.2 l/min, respectively, P > 0.4) but larger during Prop (3.4 +/- 1.6 l/min, P = 0.004). Our results demonstrate that the tachycardic effect of hypoxia during exercise partially relies on vagal withdrawal. Conversely, sympathoexcitation either does not contribute or increases heart rate through mechanisms other than beta-adrenergic transmission. A potential candidate is beta-adrenergic transmission, which could also explain why a tachycardic effect of hypoxia persists during combined beta-adrenergic and muscarinic receptor inhibition.
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