scholarly journals Pulmonary oedema following exercise in humans

2006 ◽  
Vol 31 (6) ◽  
pp. 759-760
Author(s):  
Alastair N.H. Hodges
Keyword(s):  
Pulmonary Oedema ◽  
Hypoxic Condition ◽  
Capillary Leakage ◽  
Lung Density ◽  
Subsequent Work ◽  
Cycling Exercise ◽  
Capillary Stress ◽  
Pulmonary Capillary ◽  
Oxygen Condition ◽  
Exercise Induced

Sub-clinical transient pulmonary oedema has been observed following exercise in both animals and, to some degree, humans. It has been proposed that transient pulmonary oedema, resulting from either pulmonary capillary leakage or capillary stress failure, may limit diffusion in the lung during and after exercise. Initially, to determine the minimal tolerable FIO2 for subsequent work in hypoxia, 10 aerobically trained males (VO2 max, 57.2 ± 7.95 mL·kg–1·min–1; age, 29.6 ± 5.8 y; height, 181.1 ± 8.3 cm; mass, 79.4 ± 5.6 kg) performed graded cycling work to maximal effort under 4 conditions of varying FIO2 (21%, 18%, 15%, and 12%) in a randomized blinded fashion. VO2 max and minimal SaO2 were significantly reduced while breathing 15% and 12% oxygen (VO2 max, 48.2 ± 7.9 and 31.5 ± 7.4 mL·kg–1·min–1, respectively). In the 12% oxygen condition, the majority of the subjects were not able to complete maximal exercise without SaO2 falling below 70%. Subsequently, to determine if transient pulmonary oedema occurs after sustained exercise, 10 highly trained male athletes (VO2 max, 65.0 ± 7.5 mL·kg–1·min–1; age, 25.9 ± 4.7 y; height, 184.1 ± 8.2 cm; mass, 79.4 ± 9.5 kg) underwent assessment of lung density by quantified magnetic resonance imaging before and 54.0 ± 17.2 and 100.7 ± 15.1 min after 60 min of cycling exercise (61.6% ± 9.5% VO2 max). The same 10 subjects underwent an identical measure before and 55.6 ± 9.8 and 104.3 ± 9.1 min after 60 min of cycling exercise (65.4% ± 7.1% hypoxic VO2 max) in hypoxia (FIO2 = 15.0%). Two subjects demonstrated mild exercise-induced arterial hypoxaemia (EIAH) (minSaO2 = 94.5% and 93.8%), and 7 demonstrated moderate EIAH (minSaO2 = 91.4% ± 1.1%) during a preliminary VO2 max test in normoxia. No significant differences (p < 0.05) were found in lung density after exercise in either condition. Mean lung densities, measured once pre- and twice post-exercise, were 0.177 ± 0.019, 0.181 ± 0.019, and 0.173 ± 0.019 g·mL–1 in the normoxic condition, and 0.178 ± 0.021, 0.174 ± 0.022, and 0.176 ± 0.019 g·mL–1 in the hypoxic condition. These results indicate that transient interstitial pulmonary oedema does not occur following sustained steady-state cycling exercise in normoxia or hypoxia. This diminishes the likelihood of pulmonary capillary leakage as a mechanism of transient pulmonary oedema, and, in turn, as a mechanism for changes in SaO2 during sustained exercise.

Human lung density is not altered following normoxic and hypoxic moderate-intensity exercise: implications for transient edema

2007 ◽  
Vol 103 (1) ◽  
pp. 111-118 ◽  
Author(s):  
Alastair N. H. Hodges ◽  
A. William Sheel ◽  
John R. Mayo ◽  
Donald C. McKenzie
Keyword(s):  
Arterial Oxygen Saturation ◽  
Moderate Intensity ◽  
Arterial Oxygen ◽  
Moderate Intensity Exercise ◽  
Lung Water ◽  
Lung Density ◽  
Cycling Exercise ◽  
Pulmonary Capillary ◽  
Interstitial Pulmonary Edema ◽  
Exercise Induced

The purpose of this study was to examine the effects of exercise on extravascular lung water as it may relate to pulmonary gas exchange. Ten male humans underwent measures of maximal oxygen uptake (V̇o2 max) in two conditions: normoxia (N) and normobaric hypoxia of 15% O2 (H). Lung density was measured by quantified MRI before and 48.0 ± 7.4 and 100.7 ± 15.1 min following 60 min of cycling exercise in N (intensity = 61.6 ± 9.5% V̇o2 max) and 55.5 ± 9.8 and 104.3 ± 9.1 min following 60 min cycling exercise in H (intensity = 65.4 ± 7.1% hypoxic V̇o2 max), where V̇o2 max = 65.0 ± 7.5 ml·kg−1·min−1 (N) and 54.1 ± 7.0 ml·kg−1·min−1 (H). Two subjects demonstrated mild exercise-induced arterial hypoxemia (EIAH) [minimum arterial oxygen saturation (SaO2 min) = 94.5% and 93.8%], and seven subjects demonstrated moderate EIAH (SaO2 min = 91.4 ± 1.1%) as measured noninvasively during the V̇o2 max test in N. Mean lung densities, measured once preexercise and twice postexercise, were 0.177 ± 0.019, 0.181 ± 0.019, and 0.173 ± 0.019 g/ml (N) and 0.178 ± 0.021, 0.174 ± 0.022, and 0.176 ± 0.019 g/ml (H), respectively. No significant differences ( P > 0.05) were found in lung density following exercise in either condition or between conditions. Transient interstitial pulmonary edema did not occur following sustained steady-state cycling exercise in N or H, indicating that transient edema does not result from pulmonary capillary leakage during sustained submaximal exercise.

NORMAL PULMONARY-CAPILLARY PRESSURES IN THE LATE PHASE OF NEUROGENIC PULMONARY ŒDEMA

The Lancet ◽  
1976 ◽  
Vol 307 (7957) ◽  
pp. 494 ◽  
Author(s):  
A. Harari ◽  
M. Rapin ◽  
B. Regnier ◽  
J. Comoy ◽  
J.P. Caron
Keyword(s):  
Pulmonary Oedema ◽  
Late Phase ◽  
Neurogenic Pulmonary Oedema ◽  
Pulmonary Capillary ◽  
Capillary Pressures

Exercise-induced VA/Q inequality in subjects with prior high-altitude pulmonary edema

1996 ◽  
Vol 81 (2) ◽  
pp. 922-932 ◽  
Author(s):  
A. Podolsky ◽  
M. W. Eldridge ◽  
R. S. Richardson ◽  
D. R. Knight ◽  
E. C. Johnson ◽  
...  
Keyword(s):  
Standard Deviation ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Control Group ◽  
Pulmonary Capillary ◽  
High Altitude Pulmonary Edema ◽  
History Of ◽  
Capillary Pressures ◽  
Exercise Induced

Ventilation-perfusion (VA/Q) mismatch has been shown to increase during exercise, especially in hypoxia. A possible explanation is subclinical interstitial edema due to high pulmonary capillary pressures. We hypothesized that this may be pathogenetically similar to high-altitude pulmonary edema (HAPE) so that HAPE-susceptible people with higher vascular pressures would develop more exercise-induced VA/Q mismatch. To examine this, seven healthy people with a history of HAPE and nine with similar altitude exposure but no HAPE history (control) were studied at rest and during exercise at 35, 65, and 85% of maximum 1) at sea level and then 2) after 2 days at altitude (3,810 m) breathing both normoxic (inspired Po2 = 148 Torr) and hypoxic (inspired Po2 = 91 Torr) gas at both locations. We measured cardiac output and respiratory and inert gas exchange. In both groups, VA/Q mismatch (assessed by log standard deviation of the perfusion distribution) increased with exercise. At sea level, log standard deviation of the perfusion distribution was slightly higher in the HAPE-susceptible group than in the control group during heavy exercise. At altitude, these differences disappeared. Because a history of HAPE was associated with greater exercise-induced VA/Q mismatch and higher pulmonary capillary pressures, our findings are consistent with the hypothesis that exercise-induced mismatch is due to a temporary extravascular fluid accumulation.

scholarly journals Activated protein C protects against ventilator-induced pulmonary capillary leak

2009 ◽  
Vol 296 (6) ◽  
pp. L1002-L1011 ◽  
Author(s):  
James H. Finigan ◽  
Adel Boueiz ◽  
Emily Wilkinson ◽  
Rachel Damico ◽  
Jarrett Skirball ◽  
...  
Keyword(s):  
Lung Injury ◽  
Protein C ◽  
Activated Protein C ◽  
Coagulation System ◽  
Blue Dye ◽  
Specific Gene ◽  
Capillary Leakage ◽  
Endothelial Protein C Receptor ◽  
Pulmonary Endothelium ◽  
Pulmonary Capillary

The coagulation system is central to the pathophysiology of acute lung injury. We have previously demonstrated that the anticoagulant activated protein C (APC) prevents increased endothelial permeability in response to edemagenic agonists in endothelial cells and that this protection is dependent on the endothelial protein C receptor (EPCR). We currently investigate the effect of APC in a mouse model of ventilator-induced lung injury (VILI). C57BL/6J mice received spontaneous ventilation (control) or mechanical ventilation (MV) with high (HVT; 20 ml/kg) or low (LVT; 7 ml/kg) tidal volumes for 2 h and were pretreated with APC or vehicle via jugular vein 1 h before MV. In separate experiments, mice were ventilated for 4 h and received APC 30 and 150 min after starting MV. Indices of capillary leakage included bronchoalveolar lavage (BAL) total protein and Evans blue dye (EBD) assay. Changes in pulmonary EPCR protein and Rho-associated kinase (ROCK) were assessed using SDS-PAGE. Thrombin generation was measured via plasma thrombin-antithrombin complexes. HVT induced pulmonary capillary leakage, as evidenced by significant increases in BAL protein and EBD extravasation, without significantly increasing thrombin production. HVT also caused significant decreases in pulmonary, membrane-bound EPCR protein levels and increases in pulmonary ROCK-1. APC treatment significantly decreased pulmonary leakage induced by MV when given either before or after initiation of MV. Protection from capillary leakage was associated with restoration of EPCR protein expression and attenuation of ROCK-1 expression. In addition, mice overexpressing EPCR on the pulmonary endothelium were protected from HVT-mediated injury. Finally, gene microarray analysis demonstrated that APC significantly altered the expression of genes relevant to vascular permeability at the ontology (e.g., blood vessel development) and specific gene (e.g., MAPK-associated kinase 2 and integrin-β6) levels. These findings indicate that APC is barrier-protective in VILI and that EPCR is a critical participant in APC-mediated protection.

scholarly journals Effect of hydration on exercise-induced growth hormone response

2001 ◽  
pp. 445-450 ◽  
Author(s):  
C Peyreigne ◽  
D Bouix ◽  
C Fedou ◽  
J Mercier
Keyword(s):  
Growth Hormone ◽  
Plasma Volume ◽  
Water Loss ◽  
Fluid Intake ◽  
Spring Water ◽  
Hormone Response ◽  
Healthy Male ◽  
Cycling Exercise ◽  
Exercise Induced ◽  
First Session

DESIGN: Growth hormone (GH) has demonstrated water-retaining effects in subjects at rest, whereas other research has indicated that GH may stimulate sweating. Thus, the aim of this study was to investigate the effect of fluid intake on the exercise-induced GH response. METHODS: Seven healthy male volunteers (age: 27.4+/-1.3 years, weight: 74.5+/-1.1 kg, height: 179.3+/-2.3 cm) performed a 40-min submaximal rectangular cycling exercise in two different sessions. The first session (Session 1) was performed without water intake, and the second (Session 2) involved the ingestion of spring water (four intakes) corresponding to the volume of water lost during the first session. RESULTS: In session 1, the water loss was 568+/-32 ml. In Session 2, the volume of water loss was not significantly different from the volume of fluid intake (524+/-16 versus 568+/-32 ml respectively). The decrease in plasma volume was significantly reduced in Session 2 (-6.69+/-1.59% versus -11.3+/-1.89%; P<0.05). In Session 1, the GH concentration was significantly lower than that during Session 2 after 25 min (3.04+/-1.05 versus 5.26+/-1.81; P<0.05) and after 40 min (13.7+/-3.55 versus 17.60+/-4.14 ng/ml; P<0.05) of exercise. The total GH response was significantly lower in Session 1 than in Session 2 (136.6+/-39.2 versus 202.4+/-58.9 ng/ml x min; P<0.05). CONCLUSIONS: We conclude that the exercise-induced GH response decreases when exercise is performed without fluid intake.

scholarly journals Insulin inhibits autophagy signaling independent of counterregulatory hormone levels but does not affect the effects of exercise

2018 ◽  
Vol 125 (4) ◽  
pp. 1204-1209 ◽  
Author(s):  
Andreas Buch Møller ◽  
Thomas Schmidt Voss ◽  
Mikkel Holm Vendelbo ◽  
Steen Bønløkke Pedersen ◽  
Niels Møller ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Acute Exercise ◽  
Kinase Activity ◽  
Counterregulatory Hormones ◽  
Cycling Exercise ◽  
Local Factors ◽  
Inhibitory Site ◽  
Series Of Experiments ◽  
Exercise Induced

Acute exercise increases autophagic signaling through Unc-51 like kinase-1 (ULK1) in human skeletal muscle during both anabolic and catabolic conditions. The aim of the present study was to investigate if changes in ULK1 Ser555 phosphorylation during exercise are reflected by changes in phosphorylation of a newly identified ULK1 substrate (ATG14 Ser29) and to elucidate the involvement of circulatory hormones in the regulation of autophagy in human skeletal muscle. We show that 1 h of cycling exercise increases ATG14 Ser29 phosphorylation during both hyperinsulinemic euglycemic and euinsulinemic euglycemic conditions. This could suggest that counterregulatory hormones stimulate autophagy in skeletal muscle, as circulating concentrations of these hormones are highly elevated during exercise. Furthermore, ATG14 Ser29 correlated positively with ULK1 phosphorylation, suggesting that ULK1 Ser555 (activating site) phosphorylation reflects ULK1 kinase activity. In a separate series of experiments, we show that insulin stimulates ULK1 phosphorylation at Ser757 (inhibitory site) in both hypoglycemic and euglycemic conditions, suggesting that counterregulatory hormones (such as epinephrine, norepinephrine, growth hormone, and glucagon) have limited effects on autophagy signaling in human skeletal muscle. In conclusion, 1 h of cycling exercise increases phosphorylation of ATG14 at Ser29 in a pattern that mirrors ULK1 phosphorylation at Ser555. Moreover, insulin effects on autophagy signaling in human skeletal muscle are independent of hypoglycemic and euglycemic conditions. NEW & NOTEWORTHY Autophagy signaling is regulated in a hierarchical order by exercise, insulin, and counterregulatory hormones. Exercise-induced autophagy signaling is stimulated by local factors in skeletal muscle rather than circulatory hormones. Unc-51 like kinase-1 (ULK1) phosphorylation at Ser555 reflects ULK1 kinase activity.

Sign in / Sign up

Export Citation Format

Share Document