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.

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.

Suppressing lipolysis increases interleukin-6 at rest and during prolonged moderate-intensity exercise in humans

2004 ◽  
Vol 97 (2) ◽  
pp. 689-696 ◽  
Author(s):  
Anna G. Holmes ◽  
Matthew J. Watt ◽  
Mark A. Febbraio
Keyword(s):  
Adipose Tissue ◽  
Body Mass ◽  
Maximal Oxygen Consumption ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Cycling Exercise ◽  
Blood Samples ◽  
Plasma Ffa ◽  
Exercise Induced ◽  
Exercise In Humans

IL-6 induces lipolysis when administered to humans. Consequently, it has been hypothesized that IL-6 is released from skeletal muscle during exercise to act in a “hormonelike” manner and increase lipolysis from adipose tissue to supply the muscle with substrate. In the present study, we hypothesized that suppressing lipolysis, and subsequent free fatty acid (FFA) availability, would result in a compensatory elevation in IL-6 at rest and during exercise. First, we had five healthy men ingest nicotinic acid (NA) at 30-min intervals for 120 min at rest [10 mg/kg body mass (initial dose), 5 mg/kg body mass (subsequent doses)]. Plasma was collected and analyzed for FFA and IL-6. After 120 min, plasma FFA concentration was attenuated (0 min: 0.26 ± 0.05 mmol/l; 120 min: 0.09 ± 0.02 mmol/l; P < 0.01), whereas plasma IL-6 was concomitantly increased approximately eightfold (0 min: 0.75 ± 0.18 pg/ml; 120 min: 6.05 ± 0.89 pg/ml; P < 0.001). To assess the effect of lipolytic suppression on the exercise-induced IL-6 response, seven active, but not specifically trained, men performed two experimental exercise trials with (NA) or without [control (Con)] NA ingestion 60 min before (10 mg/kg body mass) and throughout (5 mg/kg body mass every 30 min) exercise. Blood samples were obtained before ingestion, 60 min after ingestion, and throughout 180 min of cycling exercise at 62 ± 5% of maximal oxygen consumption. IL-6 gene expression, in muscle and adipose tissue sampled at 0, 90, and 180 min, was determined by using semiquantitative real-time PCR. IL-6 mRNA increased in Con (rest vs. 180 min; P < 0.01) ∼13-fold in muscle and ∼42-fold in fat with exercise. NA increased (rest vs. 180 min; P < 0.01) IL-6 mRNA 34-fold in muscle, but the treatment effect was not statistically significant (Con vs. NA, P = 0.1), and 235-fold in fat (Con vs. NA, P < 0.01). Consistent with the study at rest, NA completely suppressed plasma FFA (180 min: Con, 1.42 ± 0.07 mmol/l; NA, 0.10 ± 0.01 mmol/l; P < 0.001) and increased plasma IL-6 (180 min: Con, 9.81 ± 0.98 pg/ml; NA, 19.23 ± 2.50 pg/ml; P < 0.05) during exercise. In conclusion, these data demonstrate that circulating IL-6 is markedly elevated at rest and during prolonged moderate-intensity exercise when lipolysis is suppressed.

scholarly journals Cardiac output during exercise by the open circuit acetylene washin method: comparison with direct Fick

2000 ◽  
Vol 88 (5) ◽  
pp. 1650-1658 ◽  
Author(s):  
B. D. Johnson ◽  
K. C. Beck ◽  
D. N. Proctor ◽  
J. Miller ◽  
N. M. Dietz ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Method Comparison ◽  
Arterial Oxygen Tension ◽  
Open Circuit ◽  
Peak Oxygen Consumption ◽  
Moderate Intensity ◽  
Arterial Oxygen ◽  
Computational Techniques ◽  
Moderate Intensity Exercise ◽  
End Tidal

An open-circuit (OpCirc) acetylene uptake cardiac output (Q˙t) method was modified for use during exercise. Two computational techniques were used. OpCirc1 was based on the integrated uptake vs. end-tidal change in acetylene, and OpCirc2 was based on an iterative finite difference modeling method. Six subjects [28–44 yr, peak oxygen consumption (V˙o 2) = 120% predicted] performed cycle ergometry exercise to compareQ˙t using OpCirc and direct Fick methods. An incremental protocol was repeated twice, separated by a 10-min rest, and subsequently subjects exercised at 85–90% of their peak work rate. Coefficient of variation of the OpCirc methods and Fick were highest at rest (OpCirc1, 7%, OpCirc2, 12%, Fick, 10%) but were lower at moderate to high exercise intensities (OpCirc1, 3%, OpCirc2, 3%, Fick, 5%). OpCirc1 and OpCirc2 Q˙t correlated highly with Fick Q˙t( R 2 = 0.90 and 0.89, respectively). There were minimal differences between OpCirc1 and OpCirc2 compared with Fick up to moderate-intensity exercise (<70% peakV˙o 2); however, both techniques tended to underestimate Fick at >70% peakV˙o 2. These differences became significant for OpCirc1 only. Part of the differences between Fick and OpCirc methods at the higher exercise intensities are likely related to inhomogeneities in ventilation and perfusion matching ( R 2 = 0.36 for Fick − OpCirc1 vs. alveolar-to-arterial oxygen tension difference). In conclusion, both OpCirc methods provided reproducible, reliable measurements ofQ˙t during mild to moderate exercise. However, only OpCirc2 appeared to approximate FickQ˙t at the higher work intensities.

scholarly journals Hippocampal Blood Flow Is Increased After 20 min of Moderate-Intensity Exercise

2019 ◽  
Vol 30 (2) ◽  
pp. 525-533 ◽  
Author(s):  
J J Steventon ◽  
C Foster ◽  
H Furby ◽  
D Helme ◽  
R G Wise ◽  
...  
Keyword(s):  
Blood Flow ◽  
Temporal Dynamics ◽  
Therapeutic Potential ◽  
Cerebrovascular Reactivity ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Exercise Interventions ◽  
Before And After ◽  
Exercise Induced

Abstract Long-term exercise interventions have been shown to be a potent trigger for both neurogenesis and vascular plasticity. However, little is known about the underlying temporal dynamics and specifically when exercise-induced vascular adaptations first occur, which is vital for therapeutic applications. In this study, we investigated whether a single session of moderate-intensity exercise was sufficient to induce changes in the cerebral vasculature. We employed arterial spin labeling magnetic resonance imaging to measure global and regional cerebral blood flow (CBF) before and after 20 min of cycling. The blood vessels’ ability to dilate, measured by cerebrovascular reactivity (CVR) to CO2 inhalation, was measured at baseline and 25-min postexercise. Our data showed that CBF was selectively increased by 10–12% in the hippocampus 15, 40, and 60 min after exercise cessation, whereas CVR to CO2 was unchanged in all regions. The absence of a corresponding change in hippocampal CVR suggests that the immediate and transient hippocampal adaptations observed after exercise are not driven by a mechanical vascular change and more likely represents an adaptive metabolic change, providing a framework for exploring the therapeutic potential of exercise-induced plasticity (neural, vascular, or both) in clinical and aged populations.

scholarly journals Physiological Changes at Altitude in Nonasthmatic and Asthmatic Subjects

2004 ◽  
Vol 11 (3) ◽  
pp. 197-199 ◽  
Author(s):  
Dianna Louie ◽  
Peter D Paré
Keyword(s):  
Peak Expiratory Flow ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Physiological Changes ◽  
High Altitudes ◽  
Exercise Challenge ◽  
Per Se ◽  
Expiratory Flow ◽  
Exercise Induced ◽  
Very High

Exercised-induced asthma is not due to exercise itself per se, but rather is due to cooling and/or drying of the airway because of the increased ventilation that accompanies exercise. Travel to high altitudes is accompanied by increased ventilation of cool, often dry, air, irrespective of the level of exertion, and by itself, this could represent an 'exercise' challenge for asthmatic subjects. Exercise-induced bronchoconstriction was measured at sea level and at various altitudes during a two-week trek through the Himalayas in a group of nonasthmatic and asthmatic subjects. The results of this study showed that in mild asthmatics, there was a significant reduction in peak expiratory flow at very high altitudes. Contrary to the authors' hypothesis, there was not a significant additional decrease in peak expiratory flow after exercise in the asthmatic subjects at high altitude. However, there was a significant fall in arterial oxygen saturation postexercise in the asthmatic subjects, a change that was not seen in the nonasthmatic subjects. These data suggest that asthmatic subjects develop bronchoconstriction when they go to very high altitudes, possibly via the same mechanism that causes exercise-induced asthma.

scholarly journals Impact of cocoa flavanol consumption on blood pressure responsiveness to exercise

2010 ◽  
Vol 103 (10) ◽  
pp. 1480-1484 ◽  
Author(s):  
Narelle M. Berry ◽  
Kade Davison ◽  
Alison M. Coates ◽  
Jonathan D. Buckley ◽  
Peter R. C. Howe
Keyword(s):  
Blood Pressure ◽  
Analysis Of Covariance ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Double Blind ◽  
Flow Mediated Dilatation ◽  
Dependent Flow ◽  
Exercise Induced ◽  
Response To Exercise ◽  
Cocoa Flavanols

Impaired endothelial vasodilatation may contribute to the exaggerated blood pressure (BP) responses to exercise in individuals who are overweight/obese. The present study investigated whether consumption of cocoa flavanols, which improve endothelium-dependent flow-mediated dilatation (FMD), can modify BP responsiveness to exercise. Twenty-one volunteers (eight females and thirteen males, 54·9 (se2·2) years, BMI 31·6 (se0·8) kg/m2, systolic BP 134 (se2) mmHg, diastolic BP (DBP) 87 (se2) mmHg) were randomised to consume single servings of either a high-flavanol (HF, 701 mg) or a low-flavanol (LF, 22 mg) cocoa beverage in a double-blind, cross-over design with 3–7-d washout between treatments. Two hours after cocoa consumption, FMD was measured, followed by continuous beat-to-beat assessment (Finapres™) of BP before and during 10 min of cycling at 75 % of age-predicted maximum heart rate. Averaged data from two assessments on each type of beverage were compared by analysis of covariance using pre-exercise BP as the covariate. Pre-exercise BP was similar after taking LF and HF (153 (se3)/88 (se3)v. 153 (se4)/87 (se2) mmHg, respectively,P>0·05). However, the BP response to exercise (area under BP curve) was attenuated by HF compared with LF. BP increases were 68 % lower for DBP (P = 0·03) and 14 % lower for mean BP (P = 0·05). FMD measurements were higher after taking HF than after taking LF (6·1 (se0·6) %v. 3·4 (se0·5) %,P < 0·001). By facilitating vasodilation and attenuating exercise-induced increases in BP, cocoa flavanols may decrease cardiovascular risk and enhance the cardiovascular benefits of moderate intensity exercise in at-risk individuals.

Physical Activity, Exercise, and the Immune System: Three Lines of Research That Have Driven the Field

2015 ◽  
Vol 4 (1) ◽  
pp. 118-125
Author(s):  
Jeffrey A. Woods ◽  
Brandt D. Pence
Keyword(s):  
Immune System ◽  
Immune Function ◽  
Acute Exercise ◽  
Prolonged Exercise ◽  
Moderate Intensity ◽  
Upper Respiratory Tract ◽  
Moderate Intensity Exercise ◽  
Exercise Immunology ◽  
Upper Respiratory ◽  
Exercise Induced

Exercise immunology is a relatively new discipline in the exercise sciences that seeks to understand how exercise affects the immune system and susceptibility to infectious and chronic diseases. This brief review will focus on three major observations that have driven the field to date including: (1) acute exercise-induced leukocytosis, (2) the observation that intense, prolonged exercise results in upper respiratory tract symptoms, and (3) the paradoxical effect of acute and chronic exercise on inflammation. This framework will be used to examine the mechanisms and implications behind these seminal observations. Data generally support the conclusion that moderate intensity exercise enhances immune function, whereas prolonged, intense exercise diminishes immune function.

scholarly journals Red Blood Cell Aging as a Homeostatic Response to Exercise-Induced Stress

2019 ◽  
Vol 9 (22) ◽  
pp. 4827 ◽  
Author(s):  
Joames K. Freitas Leal ◽  
Dan Lazari ◽  
Coen C.W.G. Bongers ◽  
Maria T.E. Hopman ◽  
Roland Brock ◽  
...  
Keyword(s):  
Blood Cell ◽  
Red Blood Cells ◽  
Red Blood Cell ◽  
Blood Cells ◽  
Molecular Mechanisms ◽  
Moderate Intensity ◽  
Cell Aging ◽  
Moderate Intensity Exercise ◽  
Induced Stress ◽  
Exercise Induced

Our knowledge on the molecular mechanisms of red blood cell aging is mostly derived from in vitro studies. The Four Days Marches of Nijmegen in the Netherlands, the world’s largest yearly walking event, constitutes a unique possibility to study the effect of mechanical and biochemical stressors occurring during moderate-intensity exercise on red blood cell aging in vivo. Therefore, longitudinal measurements were performed of biophysical, immunological, and functional red blood cell characteristics that are known to change during aging. Our data show that moderate-intensity exercise induces the generation of a functionally improved red blood cell population with a higher deformability and a decreased tendency to aggregate. This is likely to be associated with an early removal of the oldest red blood cells from the circulation, as deduced from the (dis)appearance of removal signals. Thus, the physiological red blood cell aging process maintains homeostasis in times of moderate-intensity exercise-induced stress, probably by accelerated aging and subsequent removal of the oldest, most vulnerable red blood cells.

Low chemoresponsiveness and inadequate hyperventilation contribute to exercise-induced hypoxemia

1995 ◽  
Vol 79 (2) ◽  
pp. 575-580 ◽  
Author(s):  
C. A. Harms ◽  
J. M. Stager
Keyword(s):  
Oxygen Consumption ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Arterial Oxygen Saturation ◽  
Maximal Oxygen Consumption ◽  
Co2 Production ◽  
Arterial Oxygen ◽  
Ventilatory Parameters ◽  
Exercise Induced ◽  
End Tidal

Is inadequate hyperventilation a cause of the exercise-induced hypoxemia observed in some athletes during intense exercise? If so, is this related to low chemoresponsiveness? To test the hypothesis that exercise-induced hypoxemia, inadequate hyperventilation, and chemoresponsiveness are related, 36 nonsmoking healthy men were divided into hypoxemic (Hyp; n = 13) or normoxemic (Nor; n = 15) groups based on arterial oxygen saturation (SaO2; Hyp < or = 90%, Nor > 92%) observed during maximum O2 uptake (VO2max). Men with intermediate SaO2 values (n = 8) were only included in correlation analysis. Ventilatory parameters were collected at rest, during a treadmill maximal oxygen consumption (VO2max) test, and during a 5-min run at 90% VO2max. Chemoresponsiveness at rest was assessed via hypoxic ventilatory response (HVR) and hypercapnic ventilatory response (HCVR). VO2max was not significantly different between Nor and Hyp. SaO2 was 93.8 +/- 0.9% (Nor) and 87.7 +/- 2.0% (Hyp) at VO2max. End-tidal PO2 and the ratio of minute ventilation to oxygen consumption (VE/VO2) were lower while PETCO2 was higher for Hyp (P < or = 0.01). End-tidal PO2, end-tidal PCO2, and VE/VO2 correlated (P < or = 0.05) to SaO2 (r = 0.84, r = -0.70, r = 0.72, respectively), suggesting that differences in oxygenation were due to differences in ventilation. HVR and HCVR were significantly lower for Hyp. HVR was related to VE/VO2 (r = 0.43), and HCVR was related to the ratio of VE to CO2 production at VO2max (r = 0.61)

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