| 1. |
- Siebenmann, C, et al.
(författare)
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Hemoglobin mass and intravascular volume kinetics during and after exposure to 3,454-m altitude
- 2015
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Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 119:10, s. 1194-1201
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Tidskriftsartikel (refereegranskat)abstract
- Siebenmann C, Cathomen A, Hug M, Keiser S, Lundby AK, Hilty MP, Goetze JP, Rasmussen P, Lundby C. Hemoglobin mass and intravascular volume kinetics during and after exposure to 3,454 m altitude. J Appl Physiol 119: 1194-1201, 2015. First published March 6, 2015; doi:10.1152/japplphysiol.01121.2014.-High altitude (HA) exposure facilitates a rapid contraction of plasma volume (PV) and a slower occurring expansion of hemoglobin mass (Hbmass). The kinetics of the Hbmass expansion has never been examined by multiple repeated measurements, and this was our primary study aim. The second aim was to investigate the mechanisms mediating the PV contraction. Nine healthy, normally trained sea-level (SL) residents (8 males, 1 female) sojourned for 28 days at 3,454 m. Hbmass was measured and PV was estimated by carbon monoxide rebreathing at SL, on every 4th day at HA, and 1 and 2 wk upon return to SL. Four weeks at HA increased Hbmass by 5.26% (range 2.5-11.1%; P < 0.001). The individual Hbmass increases commenced with up to 12 days of delay and reached a maximal rate of 4.04±1.02 g/day after 14.9±5.2 days. The probability for Hbmass to plateau increased steeply after 20-24 days. Upon return to SL Hbmass decayed by-2.46 ± 2.3 g/day, reaching values similar to baseline after 2 wk. PV, aldosterone concentration, and renin activity were reduced at HA (P < 0.001) while the total circulating protein mass remained unaffected. In summary, the Hbmass response to HA exposure followed a sigmoidal pattern with a delayed onset and a plateau after ∼3 wk. The decay rate of Hbmass upon descent to SL did not indicate major changes in the rate of erythrolysis. Moreover, our data support that PV contraction at HA is regulated by the renin-angiotensin-aldosterone axis and not by changes in oncotic pressure. © 2015 The American Physiological Society.
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| 2. |
- Calbet, José A L, et al.
(författare)
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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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Ingår i: Journal of Physiology. - 0022-3751 .- 1469-7793. ; 593:20, s. 4649-4664
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Tidskriftsartikel (refereegranskat)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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| 3. |
- Jacobs, Robert A., et al.
(författare)
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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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Ingår i: Journal of Physiology. - : Blackwell Publishing. - 0022-3751 .- 1469-7793. ; 594:5, s. 1151-1166
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Tidskriftsartikel (refereegranskat)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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| 4. |
- Fluck, D., et al.
(författare)
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Cerebrovascular reactivity is increased with acclimatization to 3,454m altitude
- 2015
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Ingår i: Journal of Cerebral Blood Flow and Metabolism. - : SAGE Publications. - 0271-678X .- 1559-7016. ; 35:8, s. 1323-1330
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Tidskriftsartikel (refereegranskat)abstract
- Controversy exists regarding the effect of high-altitude exposure on cerebrovascular CO2 reactivity (CVR). Confounding factors in previous studies include the use of different experimental approaches, ascent profiles, duration and severity of exposure and plausibly environmental factors associated with altitude exposure. One aim of the present study was to determine CVR throughout acclimatization to high altitude when controlling for these. Middle cerebral artery mean velocity (MCAv(mean)) CVR was assessed during hyperventilation (hypocapnia) and CO2 administration (hypercapnia) with background normoxia (sea level (SL)) and hypoxia (3,454 m) in nine healthy volunteers (26 +/- 4 years (mean +/- s.d.)) at SL, and after 30 minutes (HA0), 3 (HA3) and 22 (HA22) days of high-altitude (3,454 m) exposure. At altitude, ventilation was increased whereas MCAv(mean) was not altered. Hypercapnic CVR was decreased at HA0 (1.16% +/- 0.16%/mm Hg, mean +/- s.e.m.), whereas both hyper- and hypocapnic CVR were increased at HA3 (3.13% +/- 0.18% and 2.96% +/- 0.10%/mm Hg) and HA22 (3.32% +/- 0.12% and 3.24% +/- 0.14%/mm Hg) compared with SL (1.98% +/- 0.22% and 2.38% +/- 0.10%/mmHg; P<0.01) regardless of background oxygenation. Cerebrovascular conductance (MCAv(mean)/mean arterial pressure) CVR was determined to account for blood pressure changes and revealed an attenuated response. Collectively our results show that hypocapnic and hypercapnic CVR are both elevated with acclimatization to high altitude.
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| 5. |
- Keiser, S., et al.
(författare)
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Heat training increases exercise capacity in hot but not in temperate conditions: a mechanistic counter-balanced cross-over study
- 2015
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Ingår i: American Journal of Physiology-Heart and Circulatory Physiology. - : American Physiological Society. - 0363-6135 .- 1522-1539. ; 309:5
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Tidskriftsartikel (refereegranskat)abstract
- The aim was to determine the mechanisms facilitating exercise performance in hot conditions following heat training. In a counter-balanced order, seven males ((V) over dotO(2max) 61.2 +/- 4.4 ml.min(-1).kg(-1)) were assigned to either 10 days of 90-min exercise training in 18 or 38 degrees C ambient temperature (30% relative humidity) applying a cross-over design. Participants were tested for (V) over dotO(2max) and 30-min time trial performance in 18 (T18) and 38 degrees C (T38) before and after training. Blood volume parameters, sweat output, cardiac output ((Q) over dot), cerebral perfusion (i.e., middle cerebral artery velocity [MCAv(mean)]), and other variables were determined. Before one set of exercise tests in T38, blood volume was acutely expanded by 538 +/- 16 ml with an albumin solution (T38A) to determine the role of acclimatization induced hypervolemia on exercise performance. We furthermore hypothesized that heat training would restore MCAv(mean) and thereby limit centrally mediated fatigue. (V) over dotO(2max) and time trial performance were equally reduced in T38 and T38A (7.2 +/- 1.6 and 9.3 +/- 2.5% for (V) over dotO(2max); 12.8 +/- 2.8 and 12.9 +/- 2.8% for time trial). Following heat training both were increased in T38 (9.6 +/- 2.1 and 10.4 +/- 3.1%, respectively), whereas both (V) over dotO(2max) and time trial performance remained unchanged in T18. As expected, heat training augmented plasma volume (6 +/- 2%) and mean sweat output (26 +/- 6%), whereas sweat [Na+] became reduced by 19 +/- 7%. In T38 (Q) over dot(max) remained unchanged before (21.3 +/- 0.6 l/min) to after (21.7 +/- 0.5 l/min) training, whereas MCAv(mean) was increased by 13 +/- 10%. However, none of the observed adaptations correlated with the concomitant observed changes in exercise performance.
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| 6. |
- Keiser, S., et al.
(författare)
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Restoring heat stress-associated reduction in middle cerebral artery velocity does not reduce fatigue in the heat
- 2015
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Ingår i: Scandinavian Journal of Medicine & Science in Sports. - : Wiley. - 0905-7188. ; 25:S1, s. 145-153
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Tidskriftsartikel (refereegranskat)abstract
- Heat-induced hyperventilation may reduce PaCO2 and thereby cerebral perfusion and oxygenation and in turn exercise performance. To test this hypothesis, eight volunteers completed three incremental exercise tests to exhaustion: (a) 18 degrees C ambient temperature (CON); (b) 38 degrees C (HEAT); and (c) 38 degrees C with addition of CO2 to inspiration to prevent the hyperventilation-induced reduction in PaCO2 (HEAT+CO2). In HEAT and HEAT+CO2, rectal temperature was elevated prior to the exercise tests by means of hot water submersion and was higher (P<0.05) than in CON. Compared with CON, ventilation was elevated (P<0.01), and hence, PaCO2 reduced in HEAT. This caused a reduction (P<0.05) in mean cerebral artery velocity (MCAv(mean)) from 68.6 +/- 15.5 to 53.9 +/- 10.0cm/s, which was completely restored in HEAT+CO2 (68.8 +/- 5.8cm/s). Cerebral oxygenation followed a similar pattern. was 4.6 +/- 0.1L/min in CON and decreased (P<0.05) to 4.1 +/- 0.2L/min in HEAT and remained reduced in HEAT+CO2 (4.1 +/- 0.2L/min). Despite normalization of MCAv(mean) and cerebral oxygenation in HEAT+CO2, this did not improve exercise performance, and thus, the reduced MCAv(mean) in HEAT does not seem to limit exercise performance.
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| 7. |
- Nordsborg, N B, et al.
(författare)
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Erythropoietin does not reduce plasma lactate, H(+) , and K(+) during intense exercise.
- 2015
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Ingår i: Scandinavian Journal of Medicine and Science in Sports. - : Wiley. - 0905-7188 .- 1600-0838. ; 25:6, s. e566-e575
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Tidskriftsartikel (refereegranskat)abstract
- It is investigated if recombinant human erythropoietin (rHuEPO) treatment for 15 weeks (n = 8) reduces extracellular accumulation of metabolic stress markers such as lactate, H(+) , and K(+) during incremental exhaustive exercise. After rHuEPO treatment, normalization of blood volume and composition by hemodilution preceded an additional incremental test. Group averages were calculated for an exercise intensity ∼80% of pre-rHuEPO peak power output. After rHuEPO treatment, leg lactate release to the plasma compartment was similar to before (4.3 ± 1.6 vs 3.9 ± 2.5 mmol/min) and remained similar after hemodilution. Venous lactate concentration was higher (P < 0.05) after rHuEPO treatment (7.1 ± 1.6 vs 5.2 ± 2.1 mM). Leg H(+) release to the plasma compartment after rHuEPO was similar to before (19.6 ± 5.4 vs 17.6 ± 6.0 mmol/min) and remained similar after hemodilution. Nevertheless, venous pH was lower (P < 0.05) after rHuEPO treatment (7.18 ± 0.04 vs 7.22 ± 0.05). Leg K(+) release to the plasma compartment after rHuEPO treatment was similar to before (0.8 ± 0.5 vs 0.7 ± 0.7 mmol/min) and remained similar after hemodilution. Additionally, venous K(+) concentrations were similar after vs before rHuEPO (5.3 ± 0.3 vs 5.1 ± 0.4 mM). In conclusion, rHuEPO does not reduce plasma accumulation of lactate, H(+) , and K(+) at work rates corresponding to ∼80% of peak power output.
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| 8. |
- Siebenmann, C., et al.
(författare)
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Cardiac output during exercise: A comparison of four methods
- 2015
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Ingår i: Scandinavian Journal of Medicine & Science in Sports. - : Wiley. - 0905-7188. ; 25:1
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Tidskriftsartikel (refereegranskat)abstract
- Several techniques assessing cardiac output (Q) during exercise are available. The extent to which the measurements obtained from each respective technique compares to one another, however, is unclear. We quantified Q simultaneously using four methods: the Fick method with blood obtained from the right atrium (Q(Fick-M)), Innocor (inert gas rebreathing; Q(Inn)), Physioflow (impedance cardiography; Q(Phys)), and Nexfin (pulse contour analysis; Q(Pulse)) in 12 male subjects during incremental cycling exercise to exhaustion in normoxia and hypoxia (FiO2=12%). While all four methods reported a progressive increase in Q with exercise intensity, the slopes of the Q/oxygen uptake (VO2) relationship differed by up to 50% between methods in both normoxia [4.9 +/- 0.3, 3.9 +/- 0.2, 6.0 +/- 0.4, 4.8 +/- 0.2L/min per L/min (mean +/- SE) for Q(Fick-M), Q(Inn), Q(Phys) and Q(Pulse), respectively; P=0.001] and hypoxia (7.2 +/- 0.7, 4.9 +/- 0.5, 6.4 +/- 0.8 and 5.1 +/- 0.4L/min per L/min; P=0.04). In hypoxia, the increase in the Q/VO2 slope was not detected by Nexfin. In normoxia, Q increases by 5-6L/min per L/min increase in VO2, which is within the 95% confidence interval of the Q/VO2 slopes determined by the modified Fick method, Physioflow, and Nexfin apparatus while Innocor provided a lower value, potentially reflecting recirculation of the test gas into the pulmonary circulation. Thus, determination of Q during exercise depends significantly on the applied method.
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