Publications by authors named "Daniela Flück"

23 Publications

  • Page 1 of 1

Carotid chemoreceptor control of muscle sympathetic nerve activity in hypobaric hypoxia.

Exp Physiol 2018 01 12;103(1):77-89. Epub 2017 Nov 12.

Zurich Center for Integrative Human Physiology (ZIHP), Institute of Physiology, University of Zurich, Switzerland.

New Findings: What is the central question of this study? High-altitude hypoxia increases muscle sympathetic nerve activity (MSNA), but whether intravenous infusion of dopamine, to blunt the responsiveness of the carotid chemoreceptors, reduces MSNA at high altitude is not known. What is the main finding and its importance? Muscle sympathetic nerve activity was elevated after 15-17 days of high-altitude hypoxia (3454 m) compared with values at 'sea level' (432 m). However, intravenous dopamine infusion to blunt the responsiveness of the carotid chemoreceptors did not significantly decrease MSNA either at sea level or at high altitude, suggesting that high-altitude sympathoexcitation arises via a different mechanism. High-altitude hypoxia causes pronounced sympathoexcitation, but the underlying mechanisms remain unclear. We tested the hypothesis that i.v. infusion of dopamine to attenuate carotid chemoreceptor responsiveness would reduce muscle sympathetic nerve activity (MSNA) at high altitude. Nine healthy individuals [mean (SD); 26 (4) years of age] were studied at 'sea level' (SL; Zurich) and at high altitude (ALT; 3454 m; 15-17 days after arrival), both while breathing the ambient air and during an acute incremental hypoxia test (eight 3 min stages; partial pressure of end-tidal O 90-45 mmHg). Intravenous infusions of dopamine (3 μg kg  min ) and placebo (saline) were administered on both study days, according to a single-blind randomized cross-over design. Sojourn to high altitude decreased the partial pressure of end-tidal O (to ∼60 mmHg) and increased minute ventilation [V̇E; mean ± SEM, SL versus ALT: saline, 8.6 ± 0.5 versus 11.3 ± 0.6 l min ; dopamine, 8.2 ± 0.5 versus 10.6 ± 0.8 l min ; P < 0.05] and MSNA burst frequency by ∼80% [SL versus ALT: saline, 16 ± 3 versus 28 ± 4 bursts min ; dopamine, 16 ± 4 versus 31 ± 4 bursts min ; P < 0.05) when breathing the ambient air, but were not different with dopamine. Increases in MSNA burst frequency and V̇E during the acute incremental hypoxia test were greater at ALT than SL (P < 0.05). Dopamine did not affect the magnitude of the MSNA burst frequency response to acute incremental hypoxia at either SL or ALT. However, V̇E was lower with dopamine than saline administration throughout the acute incremental hypoxia test at ALT. These data indicate that i.v. infusion of low-dose dopamine to blunt the responsiveness of the carotid chemoreceptors does not significantly decrease MSNA at high altitude.
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http://dx.doi.org/10.1113/EP086493DOI Listing
January 2018

Stability in neurovascular function at 3800m.

Physiol Behav 2017 Dec 28;182:62-68. Epub 2017 Sep 28.

Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia, Okanagan, Kelowna, Canada. Electronic address:

Hypoxia-induced neurocognitive impairments have been of clinical interest for centuries. The mechanisms responsible for these neurocognitive impairments at altitude are unclear, but may relate to the uncoupling of local neural activity with appropriate changes in cerebral blood flow (CBF; i.e., functional hyperemia). At both sea level and following 3 and 7days at 3800m (Barcroft Research Lab, White Mountain, CA, USA), transcranial Doppler was used to index CBF during three separate tasks designed to evoke cerebral functional hyperemia in 11 healthy individuals (26.6±5.5yrs, 2 females). The tasks were: 1) Visual stimulation (VS), with measurement of anterior and posterior CBF; 2) Verbal fluency (VF), with measurement of bilateral CBF; and 3) Visuospatial task (VST), with measurement of bilateral CBF. The VS evoked an increase from baseline to percent peak response in both the posterior (15.2±7.7%, P<0.01) and anterior (7.6±3.5%, P<0.01) cerebral hemispheres; however, the percent peak response was higher in the posterior brain, where visual regions are localized (P=0.01). The left-sided task, VF, resulted in an increase in both the left (12.2±4.0%, P<0.01) and right (9.0±4.4%, P<0.01) cerebral hemispheres; however, the percent peak response was higher in the left brain, where language centers are located (P<0.01). The right-sided task, VST, evoked an increase in both the left (13.9±7.1%, P<0.01) and right (16.8±6.7%, P<0.01) cerebral hemispheres; however, the percent peak response was higher in the right brain, where visuospatial regions are located (P<0.01). Each cerebral functional hyperemia response for all three tasks was unaffected by high altitude exposure (P>0.05). Overall, at least at 3800m, neurovascular function is intact with exposure to 3 and 7days of high altitude and likely does not explain the previous reports of neurocognitive impairment.
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http://dx.doi.org/10.1016/j.physbeh.2017.09.023DOI Listing
December 2017

Cerebrovascular and ventilatory responses to acute normobaric hypoxia in girls and women.

Physiol Rep 2017 Aug;5(15)

Centre for Heart Lung and Vascular Health School of Health and Exercise Sciences University of British Columbia, Kelowna, Canada.

Physiological responses to hypoxia in children are incompletely understood. We aimed to characterize cerebrovascular and ventilatory responses to normobaric hypoxia in girls and women. Ten healthy girls (9.9 ± 1.7 years; mean ± SD; Tanner stage 1 and 2) and their mothers (43.9 ± 3.5 years) participated. Internal carotid (ICA) and vertebral artery (VA) velocity, diameter and flow (Duplex ultrasound) was recorded pre- and post-1 h of hypoxic exposure (FIO= 0.126;~4000 m) in a normobaric chamber. Ventilation (V˙E) and respiratory drive (/) expressed as delta change from baseline (∆%), and end-tidal carbon-dioxide (PCO) were collected at baseline (BL) and 5, 30 and 60 min of hypoxia (5/30/60 HYP). Heart rate (HR) and oxygen saturation (SpO) were also collected at these time-points. SpO declined similarly in girls (BL-97%; 60HYP-80%, <0.05) and women (BL-97%; 60HYP-83%, <0.05). Global cerebral blood flow (gCBF) increased in both girls (BL-687; 60HYP-912 mL·min, <0.05) and women (BL-472; 60HYP-651 mL·min, <0.01), though the ratio of ICA:VA (%) contribution to gCBF differed significantly (girls, 75:25%; women, 61:39%). The relative increase in V˙E peaked at 30HYP in both girls (27%, <0.05) and women (19%, <0.05), as did ∆%/ (girls, 41%; women, 27%, 's < 0.05). Tidal volume () increased in both girls and women at 5HYP, remaining elevated above baseline in girls at 30 and 60 HYP, but declined back toward baseline in women. Girls elicit similar increases in gCBF and ventilatory parameters in response to acute hypoxia as women, though the pattern and contributions mediating these responses appear developmentally divergent.
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http://dx.doi.org/10.14814/phy2.13372DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5555897PMC
August 2017

One session of remote ischemic preconditioning does not improve vascular function in acute normobaric and chronic hypobaric hypoxia.

Exp Physiol 2017 09 8;102(9):1143-1157. Epub 2017 Aug 8.

Centre for Heart, Lung and Vascular Health, School of Health and Exercise Science, University of British Columbia, Kelowna, BC, Canada.

New Findings: What is the central question of this study? It is suggested that remote ischemic preconditioning (RIPC) might offer protection against ischaemia-reperfusion injuries, but the utility of RIPC in high-altitude settings remains unclear. What is the main finding and its importance? We found that RIPC offers no vascular protection relative to pulmonary artery pressure or peripheral endothelial function during acute, normobaric hypoxia and at high altitude in young, healthy adults. However, peripheral chemosensitivity was heightened 24 h after RIPC at high altitude. Application of repeated short-duration bouts of ischaemia to the limbs, termed remote ischemic preconditioning (RIPC), is a novel technique that might have protective effects on vascular function during hypoxic exposures. In separate parallel-design studies, at sea level (SL; n = 16) and after 8-12 days at high altitude (HA; n = 12; White Mountain, 3800 m), participants underwent either a sham protocol or one session of four bouts of 5 min of dual-thigh-cuff occlusion with 5 min recovery. Brachial artery flow-mediated dilatation (FMD; ultrasound), pulmonary artery systolic pressure (PASP; echocardiography) and internal carotid artery (ICA) flow (ultrasound) were measured at SL in normoxia and isocapnic hypoxia (end-tidal PO2 maintained at 50 mmHg) and during normal breathing at HA. The hypoxic ventilatory response (HVR) was measured at each location. All measures at SL and HA were obtained at baseline (BL) and at 1, 24 and 48 h post-RIPC or sham. At SL, RIPC produced no changes in FMD, PASP, ICA flow, end-tidal gases or HVR in normoxia or hypoxia. At HA, although HVR increased 24 h post-RIPC compared with BL [2.05 ± 1.4 versus 3.21 ± 1.2 l min  (% arterial O saturation) , P < 0.01], there were no significant differences in FMD, PASP, ICA flow and resting end-tidal gases. Accordingly, a single session of RIPC is insufficient to evoke changes in peripheral, pulmonary and cerebral vascular function in healthy adults. Although chemosensitivity might increase after RIPC at HA, this did not confer any vascular changes. The utility of a single RIPC session seems unremarkable during acute and chronic hypoxia.
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http://dx.doi.org/10.1113/EP086441DOI Listing
September 2017

Extra- and intracranial blood flow regulation during the cold pressor test: influence of age.

J Appl Physiol (1985) 2017 Nov 29;123(5):1071-1080. Epub 2017 Jun 29.

School of Sport, Exercise, and Rehabilitation Sciences, College of Life and Environmental Sciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom.

We determined how the extra- and intracranial circulations respond to generalized sympathetic activation evoked by a cold pressor test (CPT) and whether this is affected by healthy aging. Ten young [23 ± 2 yr (means ± SD)] and nine older (66 ± 3 yr) individuals performed a 3-min CPT by immersing the left foot into 0.8 ± 0.3°C water. Common carotid artery (CCA) and internal carotid artery (ICA) diameter, velocity, and flow were simultaneously measured (duplex ultrasound) along with middle cerebral artery and posterior cerebral artery mean blood velocity (MCAv and PCAv) and cardiorespiratory variables. The increases in heart rate (~6 beats/min) and mean arterial blood pressure (~14 mmHg) were similar in young and older groups during the CPT ( < 0.01 vs. baseline). In the young group, the CPT elicited an ~5% increase in CCA diameter ( < 0.01 vs. baseline) and a tendency for an increase in CCA flow (~12%, = 0.08); in contrast, both diameter and flow remained unchanged in the older group. Although ICA diameter was not changed during the CPT in either group, ICA flow increased (~8%, = 0.02) during the first minute of the CPT in both groups. Whereas the CPT elicited an increase in MCAv and PCAv in the young group (by ~20 and ~10%, respectively, < 0.01 vs. baseline), these intracranial velocities were unchanged in the older group. Collectively, during the CPT, these findings suggest a differential mechanism(s) of regulation between the ICA compared with the CCA in young individuals and a blunting of the CCA and intracranial responses in older individuals. Sympathetic activation evoked by a cold pressor test elicits heterogeneous extra- and intracranial blood vessel responses in young individuals that may serve an important protective role. The extra- and intracranial responses to the cold pressor test are blunted in older individuals.
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http://dx.doi.org/10.1152/japplphysiol.00224.2017DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5792099PMC
November 2017

UBC-Nepal expedition: markedly lower cerebral blood flow in high-altitude Sherpa children compared with children residing at sea level.

J Appl Physiol (1985) 2017 Oct 1;123(4):1003-1010. Epub 2017 Jun 1.

Centre for Heart, Lung, and Vascular Health, School of Health and Exercise Science, University of British Columbia, Kelowna, British Columbia, Canada.

Developmental cerebral hemodynamic adaptations to chronic high-altitude exposure, such as in the Sherpa population, are largely unknown. To examine hemodynamic adaptations in the developing human brain, we assessed common carotid (CCA), internal carotid (ICA), and vertebral artery (VA) flow and middle cerebral artery (MCA) velocity in 25 (9.6 ± 1.0 yr old, 129 ± 9 cm, 27 ± 8 kg, 14 girls) Sherpa children (3,800 m, Nepal) and 25 (9.9 ± 0.7 yr old, 143 ± 7 cm, 34 ± 6 kg, 14 girls) age-matched sea level children (344 m, Canada) during supine rest. Resting gas exchange, blood pressure, oxygen saturation and heart rate were assessed. Despite comparable age, height and weight were lower (both < 0.01) in Sherpa compared with sea level children. Mean arterial pressure, heart rate, and ventilation were similar, whereas oxygen saturation (95 ± 2 vs. 99 ± 1%, < 0.01) and end-tidal Pco (24 ± 3 vs. 36 ± 3 Torr, < 0.01) were lower in Sherpa children. Global cerebral blood flow was ∼30% lower in Sherpa compared with sea level children. This was reflected in a lower ICA flow (283 ± 108 vs. 333 ± 56 ml/min, = 0.05), VA flow (78 ± 26 vs. 118 ± 35 ml/min, < 0.05), and MCA velocity (72 ± 14 vs. 88 ± 14 cm/s, < 0.01). CCA flow was similar between Sherpa and sea level children (425 ± 92 vs. 441 ± 81 ml/min, = 0.52). Scaling flow and oxygen uptake for differences in vessel diameter and body size, respectively, led to the same findings. A lower cerebral blood flow in Sherpa children may reflect specific cerebral hemodynamic adaptations to chronic hypoxia. Cerebral blood flow is lower in Sherpa children compared with children residing at sea level; this may reflect a cerebral hemodynamic pattern, potentially due to adaptation to a hypoxic environment.
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http://dx.doi.org/10.1152/japplphysiol.00292.2017DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5668443PMC
October 2017

Passive heat stress reduces circulating endothelial and platelet microparticles.

Exp Physiol 2017 06;102(6):663-669

Department of Integrative Physiology, Integrative Vascular Biology Laboratory, University of Colorado, Boulder, CO, USA.

New Findings: What is the central question of this study? Does passive heat stress of +2°C oesophageal temperature change concentrations of circulating arterial endothelial- and platelet-derived microparticles in healthy adults? What is the main finding and its importance? Concentrations of circulating endothelial- and platelet-derived microparticles were markedly decreased in heat stress. Reductions in circulating microparticles might indicate favourable vascular changes associated with non-pathological hyperthermia. Interest in circulating endothelial- and platelet-derived microparticles (EMPs and PMPs, respectively) has increased because of their potential pathogenic role in vascular disease and as biomarkers for vascular health. Hyperthermia is commonly associated with a pro-inflammatory stress but might also provide vascular protection when the temperature elevation is non-pathological. Circulating microparticles might contribute to the cellular adjustments and resultant vascular impacts of hyperthermia. Here, we determined whether circulating concentrations of arterial EMPs and PMPs are altered by passive heat stress (+2°C oesophageal temperature). Ten healthy young men (age 23 ± 3 years) completed the study. Hyperthermia was achieved by circulating ∼49°C water through a water-perfused suit that covered the entire body except the hands, feet and head. Arterial (radial) blood samples were obtained immediately before heating (normothermia) and in hyperthermia. The mean ± SD oesophageal temperature in normothermia was 37.2 ± 0.1°C and in hyperthermia 39.1 ± 0.1°C. Concentrations of circulating EMPs and PMPs were markedly decreased in hyperthermia. Activation-derived EMPs were reduced by ∼30% (mean ± SD; from 61 ± 8 to 43 ± 7 microparticles μl ; P < 0.05) and apoptosis-derived EMPs by ∼45% (from 46 ± 7 to 23 ± 3 microparticles μl ; P < 0.05). Likewise, circulating PMPs were reduced by ∼75% in response to hyperthermia (from 256 ± 43 to 62 ± 14 microparticles μl ). These beneficial reductions in circulating EMPs and PMPs in response to a 2°C increase in core temperature might partly underlie the reported vascular improvements following therapeutic bouts of physiological hyperthermia.
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http://dx.doi.org/10.1113/EP086336DOI Listing
June 2017

Adenosine receptor-dependent signaling is not obligatory for normobaric and hypobaric hypoxia-induced cerebral vasodilation in humans.

J Appl Physiol (1985) 2017 Apr 12;122(4):795-808. Epub 2017 Jan 12.

Centre for Heart, Lung and Vascular Health, University of British Columbia, Okanagan Campus, School of Health and Exercise Sciences, Kelowna, British Columbia, Canada.

Hypoxia increases cerebral blood flow (CBF) with the underlying signaling processes potentially including adenosine. A randomized, double-blinded, and placebo-controlled design, was implemented to determine if adenosine receptor antagonism (theophylline, 3.75 mg/Kg) would reduce the CBF response to normobaric and hypobaric hypoxia. In 12 participants the partial pressures of end-tidal oxygen ([Formula: see text]) and carbon dioxide ([Formula: see text]), ventilation (pneumotachography), blood pressure (finger photoplethysmography), heart rate (electrocardiogram), CBF (duplex ultrasound), and intracranial blood velocities (transcranial Doppler ultrasound) were measured during 5-min stages of isocapnic hypoxia at sea level (98, 90, 80, and 70% [Formula: see text]). Ventilation, [Formula: see text] and [Formula: see text], blood pressure, heart rate, and CBF were also measured upon exposure (128 ± 31 min following arrival) to high altitude (3,800 m) and 6 h following theophylline administration. At sea level, although the CBF response to hypoxia was unaltered pre- and postplacebo, it was reduced following theophylline ( < 0.01), a finding explained by a lower [Formula: see text] ( < 0.01). Upon mathematical correction for [Formula: see text], the CBF response to hypoxia was unaltered following theophylline. Cerebrovascular reactivity to hypoxia (i.e., response slope) was not different between trials, irrespective of [Formula: see text] At high altitude, theophylline ( = 6) had no effect on CBF compared with placebo ( = 6) when end-tidal gases were comparable ( > 0.05). We conclude that adenosine receptor-dependent signaling is not obligatory for cerebral hypoxic vasodilation in humans. The signaling pathways that regulate human cerebral blood flow in hypoxia remain poorly understood. Using a randomized, double-blinded, and placebo-controlled study design, we determined that adenosine receptor-dependent signaling is not obligatory for the regulation of human cerebral blood flow at sea level; these findings also extend to high altitude.
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http://dx.doi.org/10.1152/japplphysiol.00840.2016DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5407198PMC
April 2017

Parasympathetic withdrawal increases heart rate after 2 weeks at 3454 m altitude.

J Physiol 2017 03 24;595(5):1619-1626. Epub 2017 Jan 24.

Centre for Integrative Human Physiology, Institute of Physiology, University of Zürich, Zürich, Switzerland.

Key Points: Heart rate is increased in chronic hypoxia and we tested whether this is the result of increased sympathetic nervous activity, reduced parasympathetic nervous activity, or a non-autonomic mechanism. In seven lowlanders, heart rate was measured at sea level and after 2 weeks at high altitude after individual and combined pharmacological inhibition of sympathetic and/or parasympathetic control of the heart. Inhibition of parasympathetic control of the heart alone or in combination with inhibition of sympathetic control abolished the high altitude-induced increase in heart rate. Inhibition of sympathetic control of the heart alone did not prevent the high altitude-induced increase in heart rate. These results indicate that a reduced parasympathetic nervous activity is the main mechanism underlying the elevated heart rate in chronic hypoxia.

Abstract: Chronic hypoxia increases resting heart rate (HR), but the underlying mechanism remains incompletely understood. We investigated the relative contributions of the sympathetic and parasympathetic nervous systems, along with potential non-autonomic mechanisms, by individual and combined pharmacological inhibition of muscarinic and/or β-adrenergic receptors. In seven healthy lowlanders, resting HR was determined at sea level (SL) and after 15-18 days of exposure to 3454 m high altitude (HA) without drug intervention (control, CONT) as well as after intravenous administration of either propranolol (PROP), or glycopyrrolate (GLYC), or PROP and GLYC in combination (PROP+GLYC). Circulating noradrenaline concentration increased from 0.9 ± 0.4 nmol l at SL to 2.7 ± 1.5 nmol l at HA (P = 0.03). The effect of HA on HR depended on the type of autonomic inhibition (P = 0.006). Specifically, HR was increased at HA from 64 ± 10 to 74 ± 12 beats min during the CONT treatment (P = 0.007) and from 52 ± 4 to 59 ± 5 beats min during the PROP treatment (P < 0.001). In contrast, HR was similar between SL and HA during the GLYC treatment (110 ± 7 and 112 ± 5 beats min , P = 0.28) and PROP+GLYC treatment (83 ± 5 and 85 ± 5 beats min , P = 0.25). Our results identify a reduction in cardiac parasympathetic activity as the primary mechanism underlying the elevated HR associated with 2 weeks of exposure to hypoxia. Unexpectedly, the sympathoactivation at HA that was evidenced by increased circulating noradrenaline concentration had little effect on HR, potentially reflecting down-regulation of cardiac β-adrenergic receptor function in chronic hypoxia. These effects of chronic hypoxia on autonomic control of the heart may concern not only HA dwellers, but also patients with disorders that are associated with hypoxaemia.
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http://dx.doi.org/10.1113/JP273726DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5330924PMC
March 2017

Effect of Increased Blood Flow on Pulmonary Circulation Before and During High Altitude Acclimatization.

High Alt Med Biol 2016 Dec 18;17(4):305-314. Epub 2016 Oct 18.

1 Medical Intensive Care Unit, University Hospital of Zurich , Switzerland .

Matthias Peter Hilty, Andrea Mueller, Daniela Flück, Christoph Siebenmann, Peter Rasmussen, Stefanie Keiser, Katja Auinger, Carsten Lundby, and Marco Maggiorini. Effect of increased blood flow on the pulmonary circulation before and during high altitude acclimatization. High Alt Med Biol. 17:305-314, 2016.-Introduction and Methods: Acute exposure to high altitude increases pulmonary artery pressure (Ppa) and pulmonary vascular resistance (PVR). The evolution of Ppa and PVR with continuous hypoxic exposure remains, however, elusive. To test the hypothesis that altitude exposure leads to a persistent elevation in Ppa and PVR throughout acclimatization in seven healthy male subjects, echocardiography was performed at sea level (SL; 488 m) weekly during a 4-week sojourn at 3454 m (HA1-HA4) and upon return (SL2). Pulmonary artery catheterization and bilateral thigh cuff release maneuver were performed at SL and HA3 to study the properties of pulmonary circulation after 3 weeks of acclimatization.

Results: Pulmonary artery catheter determined that systolic Ppa (mean ± SEM) was increased from 20 ± 1 at SL to 27 ± 2 mmHg at HA3 (p < 0.01). Echocardiography assessed that systolic Ppa remained equally increased throughout acclimatization (26 ± 2, 25 ± 2, 25 ± 2, and 24 ± 2 mmHg at HA1-HA4; p = 0.93) and returned to baseline upon return (17 ± 2, 18 ± 1 mmHg at SL, SL2; p = 0.3). The same was shown for PVR. Right heart function remained unaffected. Thigh cuff release maneuvers at SL and HA3 resulted in similar increase in cardiac output (2.5 ± 0.5 and 2.2 ± 0.4 L/min; p = 0.61) without affecting mean Ppa.

Conclusions: Prolonged altitude exposure leads to a persistent increase in Ppa and PVR without affecting right heart function and is fully reversible within 1 week after return to SL. The thigh cuff release maneuver-induced increase in cardiac output suggests a preserved ability of pulmonary circulation to cope with sudden remarkable increase in pulmonary blood flow throughout acclimatization.
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http://dx.doi.org/10.1089/ham.2016.0004DOI Listing
December 2016

Cerebrovascular reactivity in the developing brain: influence of sex and maturation.

J Physiol 2016 09;594(17):4709-10

Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia, Okanagan, Kelowna, Canada.

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http://dx.doi.org/10.1113/JP272366DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5009775PMC
September 2016

Barcoding lichen-forming fungi using 454 pyrosequencing is challenged by artifactual and biological sequence variation.

Genome 2016 Sep 26;59(9):685-704. Epub 2016 May 26.

a Biodiversity and Conservation Biology, Swiss Federal Research Institute WSL, Switzerland.

Although lichens (lichen-forming fungi) play an important role in the ecological integrity of many vulnerable landscapes, only a minority of lichen-forming fungi have been barcoded out of the currently accepted ∼18 000 species. Regular Sanger sequencing can be problematic when analyzing lichens since saprophytic, endophytic, and parasitic fungi live intimately admixed, resulting in low-quality sequencing reads. Here, high-throughput, long-read 454 pyrosequencing in a GS FLX+ System was tested to barcode the fungal partner of 100 epiphytic lichen species from Switzerland using fungal-specific primers when amplifying the full internal transcribed spacer region (ITS). The present study shows the potential of DNA barcoding using pyrosequencing, in that the expected lichen fungus was successfully sequenced for all samples except one. Alignment solutions such as BLAST were found to be largely adequate for the generated long reads. In addition, the NCBI nucleotide database-currently the most complete database for lichen-forming fungi-can be used as a reference database when identifying common species, since the majority of analyzed lichens were identified correctly to the species or at least to the genus level. However, several issues were encountered, including a high sequencing error rate, multiple ITS versions in a genome (incomplete concerted evolution), and in some samples the presence of mixed lichen-forming fungi (possible lichen chimeras).
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http://dx.doi.org/10.1139/gen-2015-0189DOI Listing
September 2016

A short period of high-intensity interval training improves skeletal muscle mitochondrial function and pulmonary oxygen uptake kinetics.

J Appl Physiol (1985) 2016 Jun 4;120(11):1319-27. Epub 2016 Feb 4.

Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich, Switzerland

The aim of the present study was to examine whether improvements in pulmonary oxygen uptake (V̇o2) kinetics following a short period of high-intensity training (HIT) would be associated with improved skeletal muscle mitochondrial function. Ten untrained male volunteers (age 26 ± 2 yr; mean ± SD) performed six HIT sessions (8-12 × 60 s at incremental test peak power; 271 ± 52 W) over a 2-wk period. Before and after the HIT period, V̇o2 kinetics was modeled during moderate-intensity cycling (110 ± 19 W). Mitochondrial function was assessed with high-resolution respirometry (HRR), and maximal activities of oxidative enzymes citrate synthase (CS) and cytochrome c oxidase (COX) were accordingly determined. In response to HIT, V̇o2 kinetics became faster (τ: 20.4 ± 4.4 vs. 28.9 ± 6.1 s; P < 0.01) and fatty acid oxidation (ETFP) and leak respiration (LN) both became elevated (P < 0.05). Activity of CS and COX did not increase in response to training. Both before and after the HIT period, fast V̇o2 kinetics (low τ values) was associated with large values for ETFP, electron transport system capacity (ETS), and electron flow specific to complex II (CIIP) (P < 0.05). Collectively, these findings support that selected measures of mitochondrial function obtained with HRR are important for fast V̇o2 kinetics and better markers than maximal oxidative enzyme activity in describing the speed of the V̇o2 response during moderate-intensity exercise.
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http://dx.doi.org/10.1152/japplphysiol.00115.2015DOI Listing
June 2016

Twenty-eight days of exposure to 3454 m increases mitochondrial volume density in human skeletal muscle.

J Physiol 2016 Mar 28;594(5):1151-66. Epub 2015 Oct 28.

Zürich Centre for Integrative Human Physiology, Institute of Physiology, University of Zürich, Switzerland.

The role of hypoxia on skeletal muscle mitochondria is controversial. Studies superimposing exercise training on hypoxic exposure demonstrate an increase in skeletal muscle mitochondrial volume density (Mito(VD)) over equivalent normoxic training. In contrast, reductions in both skeletal muscle mass and Mito(VD) 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 Mito(VD), while minimizing changes in energy balance. For this purpose, skeletal muscle biopsies were obtained from nine lowlanders at sea level (Pre) and following 7 and 28 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 that intermyofibrillar (IMF) Mito(VD) was augmented (P = 0.028) by 11.5 ± 9.2% from Pre (5.05 ± 0.9%) to 28 Days (5.61 ± 0.04%). In contrast, there was no change in subsarcolemmal (SS) Mito(VD). As a result, total Mito(VD) (IMF + SS) was increased (P = 0.031) from 6.20 ± 1.5% at Pre to 6.62 ± 1.4% at 28 Days (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 Mito(VD) may increase with 28 days acclimation to 3454 m.
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http://dx.doi.org/10.1113/JP271118DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4771777PMC
March 2016

Haematological rather than skeletal muscle adaptations contribute to the increase in peak oxygen uptake induced by moderate endurance training.

J Physiol 2015 Oct 14;593(20):4677-88. Epub 2015 Sep 14.

Zurich Centre for Integrative Human Physiology (ZIHP), University of Zurich, Institute of Physiology, Switzerland.

It remains unclear whether improvements in peak oxygen uptake (V̇(O2peak)) following endurance training (ET) are primarily determined by central and/or peripheral adaptations. Herein, we tested the hypothesis that the improvement in V̇(O2peak) following 6 weeks of ET is mainly determined by haematological rather than skeletal muscle adaptations. Sixteen untrained healthy male volunteers (age = 25 ± 4 years, V̇(O2peak) = 3.5 ± 0.5 l min(-1)) underwent supervised ET (6 weeks, 3-4 sessions per week). V̇(O2peak), peak cardiac output (Q̇(peak)), haemoglobin mass (Hb(mass)) and blood volumes were assessed prior to and following ET. Skeletal muscle biopsies were analysed for mitochondrial volume density (Mito(VD)), capillarity, fibre types and respiratory capacity (OXPHOS). After the post-ET assessment, red blood cell volume (RBCV) was re-established at the pre-ET level by phlebotomy and V̇(O2peak) and Q̇(peak) were measured again. We speculated that the contribution of skeletal muscle adaptations to the ET-induced increase in V̇(O2peak) would be revealed when controlling for haematological adaptations. V̇(O2peak) and Q̇(peak) were increased (P < 0.05) following ET (9 ± 8 and 7 ± 6%, respectively) and decreased (P < 0.05) after phlebotomy (-7 ± 7 and -10 ± 7%). RBCV, plasma volume and Hb(mass) all increased (P < 0.05) after ET (8 ± 4, 4 ± 6 and 6 ± 5%). As for skeletal muscle adaptations, capillary-to-fibre ratio and total Mito(VD) increased (P < 0.05) following ET (18 ± 16 and 43 ± 30%), but OXPHOS remained unaltered. Through stepwise multiple regression analysis, Q̇(peak), RBCV and Hb(mass) were found to be independent predictors of V̇(O2peak). In conclusion, the improvement in V̇(O2peak) following 6 weeks of ET is primarily attributed to increases in Q̇(peak) and oxygen-carrying capacity of blood in untrained healthy young subjects.
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http://dx.doi.org/10.1113/JP270250DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4606528PMC
October 2015

Heat training increases exercise capacity in hot but not in temperate conditions: a mechanistic counter-balanced cross-over study.

Am J Physiol Heart Circ Physiol 2015 Sep 6;309(5):H750-61. Epub 2015 Jul 6.

Zürich Center for Integrative Human Physiology, Institute of Physiology, University of Zürich, Zürich, Switzerland; Food and Nutrition and Sport Science, Gothenburg University, Gothenburg, Sweden

The aim was to determine the mechanisms facilitating exercise performance in hot conditions following heat training. In a counter-balanced order, seven males (V̇o2max 61.2 ± 4.4 ml·min(-1)·kg(-1)) were assigned to either 10 days of 90-min exercise training in 18 or 38°C ambient temperature (30% relative humidity) applying a cross-over design. Participants were tested for V̇o2max and 30-min time trial performance in 18 (T18) and 38°C (T38) before and after training. Blood volume parameters, sweat output, cardiac output (Q̇), cerebral perfusion (i.e., middle cerebral artery velocity [MCAvmean]), 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 MCAvmean and thereby limit centrally mediated fatigue. V̇o2max and time trial performance were equally reduced in T38 and T38A (7.2 ± 1.6 and 9.3 ± 2.5% for V̇o2max; 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 V̇o2max 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 Q̇max remained unchanged before (21.3 ± 0.6 l/min) to after (21.7 ± 0.5 l/min) training, whereas MCAvmean was increased by 13 ± 10%. However, none of the observed adaptations correlated with the concomitant observed changes in exercise performance.
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http://dx.doi.org/10.1152/ajpheart.00138.2015DOI Listing
September 2015

Cerebrovascular reactivity is increased with acclimatization to 3,454 m altitude.

J Cereb Blood Flow Metab 2015 Aug 25;35(8):1323-30. Epub 2015 Mar 25.

1] Zurich Center for Integrative Human Physiology (ZIHP), Zurich, Switzerland [2] Institute of Physiology, ZIHP, University of Zurich, Zurich, Switzerland [3] Department of Food and Nutrition and Sport Science, Gothenburg University, Gothenburg, Sweden.

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%/mm Hg; 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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http://dx.doi.org/10.1038/jcbfm.2015.51DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4528007PMC
August 2015

Age, aerobic fitness, and cerebral perfusion during exercise: role of carbon dioxide.

Am J Physiol Heart Circ Physiol 2014 Aug;307(4):H515-23

Middle cerebral artery mean velocity (MCAvmean) is attenuated with increasing age both at rest and during exercise. The aim of this study was to determine the influence of the age-dependent reduction in arterial Pco2 (PaCO2) and physical fitness herein. We administered supplemental CO2 (CO2 trial) or no additional gas (control trial) to the inspired air in a blinded and randomized manner, and assessed middle cerebral artery mean flow velocity during graded exercise in 1) 21 young [Y; age 24 ± 3 yr (±SD)] volunteers of whom 11 were trained (YT) and 10 considered untrained (YUT), and 2) 17 old (O; 66 ± 4 yr) volunteers of whom 8 and 9 were considered trained (OT) and untrained (OUT), respectively. A resting hypercapnic reactivity test was also performed. MCAvmean and PaCO2 were lower in O [44.9 ± 3.1 cm/s and 30 ± 1 mmHg (±SE)] compared with Y (59.3 ± 2.3 cm/s and 34 ± 1 mmHg, P < 0.01) at rest, independent of aerobic fitness level. The age-related decreases in MCAvmean and PaCO2 persisted during exercise. Supplemental CO2 reduced the age-associated decline in MCAvmean by 50%, suggesting that PaCO2 is a major component in the decline. On the other hand, relative hypercapnic reactivity was neither influenced by age (P = 0.46) nor aerobic fitness (P = 0.36). Although supplemental CO2 attenuated exercise-induced reduction in cerebral oxygenation (near-infrared spectroscopy), this did not influence exercise performance. In conclusion, PaCO2 contributes to the age-associated decline in MCAvmean at rest and during exercise; however exercise capacity did not diminish this age effect.
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http://dx.doi.org/10.1152/ajpheart.00177.2014DOI Listing
August 2014

Hypoxic training: effect on mitochondrial function and aerobic performance in hypoxia.

Med Sci Sports Exerc 2014 Oct;46(10):1936-45

1Ecole Nationale des Sports de Montagne, site de l'Ecole Nationale de Ski et d'Alpinisme, Chamonix, FRANCE; 2Department of Exercise and Sport Sciences, University of Copenhagen, Copenhagen, DENMARK; 3Zürich Center for Integrative Human Physiology, University of Zürich, Zürich, SWITZERLAND; 4Institute of Physiology, University of Zürich, Zürich, SWITZERLAND; and 5Exercise Physiology, Institute of Human Movement Sciences, Eidgenössische Technische Hochschule Zürich, Zürich, SWITZERLAND.

Purpose: The effects of hypoxic training on exercise performance remain controversial. Here, we tested the hypotheses that i) hypoxic training possesses ergogenic effects at sea level and altitude and ii) the benefits are primarily mediated by improved mitochondrial function of the skeletal muscle.

Methods: We determined aerobic performance (incremental test to exhaustion and time trial for a set amount of work) in moderately trained subjects undergoing 6 wk of endurance training (3-4 times per week, 60 min per session) in normoxia (placebo, n = 8) or normobaric hypoxia (FIO2 = 0.15, n = 9) using a double-blind and randomized design. Exercise tests were performed in normoxia and acute hypoxia (FIO2 = 0.15). Skeletal muscle mitochondrial respiratory capacities and electron coupling efficiencies were measured via high-resolution respirometry. Total hemoglobin mass was assessed by carbon monoxide rebreathing.

Results: Skeletal muscle respiratory capacity was not altered by training or hypoxia; however, electron coupling control respective to fat oxidation slightly diminished with hypoxic training. Hypoxic training did increase total hemoglobin mass more than the placebo (8.4% vs 3.3%, P = 0.02). In normoxia, hypoxic training had no additive effect on maximal measures of oxygen uptake or time trial performance. In acute hypoxia, hypoxic training conferred no advantage on maximal oxygen uptake but tended to enhance time trial performance more than normoxic training (52% vs 32%, P = 0.09).

Conclusions: Our data suggest that, in moderately trained subjects, 6 wk of hypoxic training possesses no ergogenic effect at sea level. It is not excluded that hypoxic training might facilitate endurance capacity at moderate altitude; however, this issue is still open and needs to be further examined.
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http://dx.doi.org/10.1249/MSS.0000000000000321DOI Listing
October 2014

Phlebotomy eliminates the maximal cardiac output response to six weeks of exercise training.

Am J Physiol Regul Integr Comp Physiol 2014 May 12;306(10):R752-60. Epub 2014 Mar 12.

Zürich Center for Integrative Human Physiology (ZIHP), University of Zürich, Zürich, Switzerland; Food & Nutrition & Sport Science, Gothenburg University, Sweden

With this study we tested the hypothesis that 6 wk of endurance training increases maximal cardiac output (Qmax) relatively more by elevating blood volume (BV) than by inducing structural and functional changes within the heart. Nine healthy but untrained volunteers (Vo2max 47 ± 5 ml·min(-1)·kg(-1)) underwent supervised training (60 min; 4 times weekly at 65% Vo2max for 6 wk), and Qmax was determined by inert gas rebreathing during cycle ergometer exercise before and after the training period. After the training period, blood volume (determined in duplicates by CO rebreathing) was reestablished to pretraining values by phlebotomy and Qmax was quantified again. Resting echography revealed no structural heart adaptations as a consequence of the training intervention. After the training period, plasma volume (PV), red blood cell volume (RBCV), and BV increased (P < 0.05) by 147 ± 168 (5 ± 5%), 235 ± 64 (10 ± 3%), and 382 ± 204 ml (7 ± 4%), respectively. Vo2max was augmented (P < 0.05) by 10 ± 7% after the training period and decreased (P < 0.05) by 8 ± 7% with phlebotomy. Concomitantly, Qmax was increased (P < 0.05) from 18.9 ± 2.1 to 20.4 ± 2.3 l/min (9 ± 6%) as a consequence of the training intervention, and after normalization of BV by phlebotomy Qmax returned to pretraining values (18.1 ± 2.5 l/min; 12 ± 5% reversal). Thus the exercise training-induced increase in BV is the main mechanism increasing Qmax after 6 wk of endurance training in previously untrained subjects.
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http://dx.doi.org/10.1152/ajpregu.00028.2014DOI Listing
May 2014

Effects of aging on the association between cerebrovascular responses to visual stimulation, hypercapnia and arterial stiffness.

Front Physiol 2014 19;5:49. Epub 2014 Feb 19.

Department of Physiology and Pharmacology, Faculty of Medicine, University of Calgary Calgary, AB, Canada ; Department of Clinical Neurosciences, Faculty of Medicine, University of Calgary Calgary, AB, Canada ; Hotchkiss Brain Institute, Faculty of Medicine, University of Calgary Calgary, AB, Canada ; Faculty of Kinesiology, University of Calgary Calgary, AB, Canada ; The Libin Cardiovascular Institute of Alberta, Faculty of Medicine, University of Calgary Calgary, AB, Canada.

Aging is associated with decreased vascular compliance and diminished neurovascular- and hypercapnia-evoked cerebral blood flow (CBF) responses. However, the interplay between arterial stiffness and reduced CBF responses is poorly understood. It was hypothesized that increased cerebral arterial stiffness is associated with reduced evoked responses to both, a flashing checkerboard visual stimulation (i.e., neurovascular coupling), and hypercapnia. To test this hypothesis, 20 older (64 ± 8 year; mean ± SD) and 10 young (30 ± 5 year) subjects underwent a visual stimulation (VS) and a hypercapnic test. Blood velocity through the posterior (PCA) and middle cerebral (MCA) arteries was measured concurrently using transcranial Doppler ultrasound (TCD). Cerebral and systemic vascular stiffness were calculated from the cerebral blood velocity and systemic blood pressure waveforms, respectively. Cerebrovascular (MCA: young = 76 ± 15%, older = 98 ± 19%, p = 0.004; PCA: young = 80 ± 16%, older = 106 ± 17%, p < 0.001) and systemic (young = 59 ± 9% and older = 80 ± 9%, p < 0.001) augmentation indices (AI) were higher in the older group. CBF responses to VS (PCA: p < 0.026) and hypercapnia (PCA: p = 0.018; MCA: p = 0.042) were lower in the older group. A curvilinear model fitted to cerebral AI and age showed AI increases until ~60 years of age, after which the increase levels off (PCA: R (2) = 0.45, p < 0.001; MCA: R (2) = 0.31, p < 0.001). Finally, MCA, but not PCA, hypercapnic reactivity was inversely related to cerebral AI (MCA: R (2) = 0.28, p = 0.002; PCA: R (2) = 0.10, p = 0.104). A similar inverse relationship was not observed with the PCA blood flow response to VS (R (2) = 0.06, p = 0.174). In conclusion, older subjects had reduced neurovascular- and hypercapnia-mediated CBF responses. Furthermore, lower hypercapnia-mediated blood flow responses through the MCA were associated with increased vascular stiffness. These findings suggest the reduced hypercapnia-evoked CBF responses through the MCA, in older individuals may be secondary to vascular stiffening.
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http://dx.doi.org/10.3389/fphys.2014.00049DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3928624PMC
March 2014

Neurovascular decoupling is associated with severity of cerebral amyloid angiopathy.

Neurology 2013 Nov 4;81(19):1659-65. Epub 2013 Oct 4.

From the Department of Radiology, Seaman Family MR Centre (S.P., C.R.M., R.F., B.G.G., E.E.S.), Departments of Clinical Neurosciences (E.D., G.K., N.S., K.S., A.C., N.P., M.J.P., R.F., B.G.G., E.E.S.), Physiology and Pharmacology (C.D.S., A.B., D.F., M.J.P.), and Community Health Sciences (G.H.F., E.E.S.), University of Calgary, Canada; Institute of Human Movement Sciences and Sport (D.F.), ETH Zurich, Switzerland; Hotchkiss Brain Institute (M.J.P., R.F., B.G.G., E.E.S.), and Faculty of Kinesiology (M.J.P.), University of Calgary; Foothills Medical Centre, Alberta Health Services, Canada.

Objectives: We used functional MRI (fMRI), transcranial Doppler ultrasound, and visual evoked potentials (VEPs) to determine the nature of blood flow responses to functional brain activity and carbon dioxide (CO2) inhalation in patients with cerebral amyloid angiopathy (CAA), and their association with markers of CAA severity.

Methods: In a cross-sectional prospective cohort study, fMRI, transcranial Doppler ultrasound CO2 reactivity, and VEP data were compared between 18 patients with probable CAA (by Boston criteria) and 18 healthy controls, matched by sex and age. Functional MRI consisted of a visual task (viewing an alternating checkerboard pattern) and a motor task (tapping the fingers of the dominant hand).

Results: Patients with CAA had lower amplitude of the fMRI response in visual cortex compared with controls (p = 0.01), but not in motor cortex (p = 0.22). In patients with CAA, lower visual cortex fMRI amplitude correlated with higher white matter lesion volume (r = -0.66, p = 0.003) and more microbleeds (r = -0.78, p < 0.001). VEP P100 amplitudes, however, did not differ between CAA and controls (p = 0.45). There were trends toward reduced CO2 reactivity in the middle cerebral artery (p = 0.10) and posterior cerebral artery (p = 0.08).

Conclusions: Impaired blood flow responses in CAA are more evident using a task to activate the occipital lobe than the frontal lobe, consistent with the gradient of increasing vascular amyloid severity from frontal to occipital lobe seen in pathologic studies. Reduced fMRI responses in CAA are caused, at least partly, by impaired vascular reactivity, and are strongly correlated with other neuroimaging markers of CAA severity.
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http://dx.doi.org/10.1212/01.wnl.0000435291.49598.54DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3812103PMC
November 2013

Improvements in exercise performance with high-intensity interval training coincide with an increase in skeletal muscle mitochondrial content and function.

J Appl Physiol (1985) 2013 Sep 20;115(6):785-93. Epub 2013 Jun 20.

Zurich Center for Integrative Human Physiology (ZIHP Zurich, Switzerland;

Six sessions of high-intensity interval training (HIT) are sufficient to improve exercise capacity. The mechanisms explaining such improvements are unclear. Accordingly, the aim of this study was to perform a comprehensive evaluation of physiologically relevant adaptations occurring after six sessions of HIT to determine the mechanisms explaining improvements in exercise performance. Sixteen untrained (43 ± 6 ml·kg(-1)·min(-1)) subjects completed six sessions of repeated (8-12) 60 s intervals of high-intensity cycling (100% peak power output elicited during incremental maximal exercise test) intermixed with 75 s of recovery cycling at a low intensity (30 W) over a 2-wk period. Potential training-induced alterations in skeletal muscle respiratory capacity, mitochondrial content, skeletal muscle oxygenation, cardiac capacity, blood volumes, and peripheral fatigue resistance were all assessed prior to and again following training. Maximal measures of oxygen uptake (Vo2peak; ∼8%; P = 0.026) and cycling time to complete a set amount of work (∼5%; P = 0.008) improved. Skeletal muscle respiratory capacities increased, most likely as a result of an expansion of skeletal muscle mitochondria (∼20%, P = 0.026), as assessed by cytochrome c oxidase activity. Skeletal muscle deoxygenation also increased while maximal cardiac output, total hemoglobin, plasma volume, total blood volume, and relative measures of peripheral fatigue resistance were all unaltered with training. These results suggest that increases in mitochondrial content following six HIT sessions may facilitate improvements in respiratory capacity and oxygen extraction, and ultimately are responsible for the improvements in maximal whole body exercise capacity and endurance performance in previously untrained individuals.
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http://dx.doi.org/10.1152/japplphysiol.00445.2013DOI Listing
September 2013