Exertional Desaturation in Idiopathic Pulmonary Fibrosis: The Role of Oxygen Supplementation in Modifying Cerebral-Skeletal Muscle Oxygenation and Systemic Hemodynamics

Respiration ◽  
2021 ◽  
pp. 1-13
Author(s):  
Konstantina Dipla ◽  
Afroditi K. Boutou ◽  
Aikaterini Markopoulou ◽  
Georgia Pitsiou ◽  
Stavros Papadopoulos ◽  
...  

<b><i>Background:</i></b> In patients with idiopathic pulmonary fibrosis (IPF) with isolated exertional desaturation, there are limited data regarding the effectiveness of oxygen supplementation during exercise training; the underlying mechanisms that contribute to these responses are unknown. <b><i>Objectives:</i></b> To examine in these IPF patients the effects of oxygen supplementation during submaximal exercise (vs. medical air) on cerebral/skeletal muscle oxygenation and systemic hemodynamics. <b><i>Methods:</i></b> In this randomized, cross-over, placebo-controlled trial, IPF patients (<i>n</i> = 13; 63.4 ± 9.6 years) without resting hypoxemia but a significant desaturation during maximal cardiopulmonary exercise testing underwent 2 steady-state exercise trials (65% peak-work-load), breathing either oxygen-enriched or medical air. Cerebral/skeletal muscle oxygenation (near-infrared spectroscopy) and beat-by-beat hemodynamics (photoplethysmography) were monitored. <b><i>Results:</i></b> In the air protocol, from the initial minutes of submaximal exercise, patients exhibited a marked decline in cerebral oxygenated hemoglobin (O<sub>2</sub>Hb) and an abrupt rise in deoxygenated hemoglobin (HHb). Oxygen supplementation alleviated desaturation, lessened dyspnea, and prolonged exercise duration (<i>p</i> &#x3c; 0.01). Oxygen supplementation during exercise (i) attenuated cerebral deoxygenation (cerebral-HHb: 0.7 ± 1.9 vs. 2.5 ± 1.5 μmol/L, O<sub>2</sub> and air protocol; <i>p</i> = 0.009) and prevented cerebral-Hb<sub>difference</sub> decline (2.1 ± 2.7 vs. −1.7 ± 2.0 μmol/L; <i>p</i> = 0.001), (ii) lessened the decline in muscle O<sub>2</sub>-saturation index, and (iii) at isotime exercise, it resulted in lower muscle-HHb (<i>p</i> = 0.05) and less leg fatigue (<i>p</i> &#x3c; 0.05). No differences between protocols were observed in exercise cardiac output and vascular resistance. <b><i>Conclusions:</i></b> IPF patients with isolated exertional hypoxemia exhibit an inability to increase/maintain cerebral oxygenation during submaximal exercise. Correcting desaturation with O<sub>2</sub> supplementation prevented the decline in brain oxygenation, improved muscle oxygenation, and lessened dyspnea, suggesting an efficacy of acute oxygen supplementation during exercise training in protecting brain hypoxia in these IPF patients.

2014 ◽  
Vol 307 (4) ◽  
pp. R396-R404 ◽  
Author(s):  
Bruno T. Roseguini ◽  
Daniel M. Hirai ◽  
Maria C. Alencar ◽  
Roberta P. Ramos ◽  
Bruno M. Silva ◽  
...  

Endothelial dysfunction caused by defective nitric oxide (NO) signaling plays a pivotal role in the pathogenesis of intermittent claudication (IC). In the present study, we evaluated the acute effects of sildenafil, a phosphodiesterase type 5 inhibitor that acts by prolonging NO-mediated cGMP signaling in vascular smooth muscle, on blood pressure (BP), skeletal muscle oxygenation, and walking tolerance in patients with IC. A randomized, double-blind, crossover study was conducted in which 12 men with stable IC received two consecutive doses of 50 mg of sildenafil or matching placebo and underwent a symptom-limited exercise test on the treadmill. Changes in gastrocnemius deoxy-hemoglobin by near-infrared spectroscopy estimated peripheral muscle O2delivery-to-utilization matching. Systolic BP was significantly lower during the sildenafil trial relative to placebo during supine rest (∼15 mmHg), submaximal exercise (∼14 mmHg), and throughout recovery (∼18 mmHg) ( P < 0.05). Diastolic BP was also lower after sildenafil during upright rest (∼6 mmHg) and during recovery from exercise (∼7 mmHg) ( P < 0.05). Gastrocnemius deoxygenation was consistently reduced during submaximal exercise (∼41%) and at peak exercise (∼34%) following sildenafil compared with placebo ( P < 0.05). However, pain-free walking time (placebo: 335 ± 42 s vs. sildenafil: 294 ± 35 s) and maximal walking time (placebo: 701 ± 58 s vs. sildenafil: 716 ± 62 s) did not differ between trials. Acute administration of sildenafil lowers BP and improves skeletal muscle oxygenation during exercise but does not enhance walking tolerance in patients with IC. Whether the beneficial effects of sildenafil on muscle oxygenation can be sustained over time and translated into positive clinical outcomes deserve further consideration in this patient population.


Critical Care ◽  
2009 ◽  
Vol 13 (Suppl 5) ◽  
pp. S8 ◽  
Author(s):  
Laurent Heyer ◽  
Alexandre Mebazaa ◽  
Etienne Gayat ◽  
Matthieu Resche-Rigon ◽  
Christophe Rabuel ◽  
...  

2015 ◽  
Vol 308 (2) ◽  
pp. R105-R111 ◽  
Author(s):  
Wladimir M. Medeiros ◽  
Mari C. T. Fernandes ◽  
Diogo P. Azevedo ◽  
Flavia F. M. de Freitas ◽  
Beatriz C. Amorim ◽  
...  

Central cardiorespiratory and gas exchange limitations imposed by chronic obstructive pulmonary disease (COPD) impair ambulatory skeletal muscle oxygenation during whole body exercise. This investigation tested the hypothesis that peripheral factors per se contribute to impaired contracting lower limb muscle oxygenation in COPD patients. Submaximal neuromuscular electrical stimulation (NMES; 30, 40, and 50 mA at 50 Hz) of the quadriceps femoris was employed to evaluate contracting skeletal muscle oxygenation while minimizing the influence of COPD-related central cardiorespiratory constraints. Fractional O2 extraction was estimated by near-infrared spectroscopy (deoxyhemoglobin/myoglobin concentration; deoxy-[Hb/Mb]), and torque output was measured by isokinetic dynamometry in 15 nonhypoxemic patients with moderate-to-severe COPD (SpO2 = 94 ± 2%; FEV1 = 46.4 ± 10.1%; GOLD II and III) and in 10 age- and gender-matched sedentary controls. COPD patients had lower leg muscle mass than controls (LMM = 8.0 ± 0.7 kg vs. 8.9 ± 1.0 kg, respectively; P < 0.05) and produced relatively lower absolute and LMM-normalized torque across the range of NMES intensities ( P < 0.05 for all). Despite producing less torque, COPD patients had similar deoxy-[Hb/Mb] amplitudes at 30 and 40 mA ( P > 0.05 for both) and higher deoxy-[Hb/Mb] amplitude at 50 mA ( P < 0.05). Further analysis indicated that COPD patients required greater fractional O2 extraction to produce torque (i.e., ↑Δdeoxy-[Hb/Mb]/torque) relative to controls ( P < 0.05 for 40 and 50 mA) and as a function of NMES intensity ( P < 0.05 for all). The present data obtained during submaximal NMES of small muscle mass indicate that peripheral abnormalities contribute mechanistically to impaired contracting skeletal muscle oxygenation in nonhypoxemic, moderate-to-severe COPD patients.


Respirology ◽  
2017 ◽  
Vol 22 (5) ◽  
pp. 957-964 ◽  
Author(s):  
Leona M. Dowman ◽  
Christine F. McDonald ◽  
Steven Bozinovski ◽  
Ross Vlahos ◽  
Rebecca Gillies ◽  
...  

Critical Care ◽  
2009 ◽  
Vol 13 (Suppl 5) ◽  
pp. S7 ◽  
Author(s):  
Daniel S Martin ◽  
Denny ZH Levett ◽  
Michael Mythen ◽  
Mike PW Grocott ◽  

2017 ◽  
Vol 14 (127) ◽  
pp. 20160992 ◽  
Author(s):  
B. Zeller-Plumhoff ◽  
T. Roose ◽  
G. F. Clough ◽  
P. Schneider

The supply of oxygen in sufficient quantity is vital for the correct functioning of all organs in the human body, in particular for skeletal muscle during exercise. Disease is often associated with both an inhibition of the microvascular supply capability and is thought to relate to changes in the structure of blood vessel networks. Different methods exist to investigate the influence of the microvascular structure on tissue oxygenation, varying over a range of application areas, i.e. biological in vivo and in vitro experiments, imaging and mathematical modelling. Ideally, all of these methods should be combined within the same framework in order to fully understand the processes involved. This review discusses the mathematical models of skeletal muscle oxygenation currently available that are based upon images taken of the muscle microvasculature in vivo and ex vivo . Imaging systems suitable for capturing the blood vessel networks are discussed and respective contrasting methods presented. The review further informs the association between anatomical characteristics in health and disease. With this review we give the reader a tool to understand and establish the workflow of developing an image-based model of skeletal muscle oxygenation. Finally, we give an outlook for improvements needed for measurements and imaging techniques to adequately investigate the microvascular capability for oxygen exchange.


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