Influence of Respiratory Muscle Blood Flow and Hypoxemia on Exercise Induced Diaphragmatic Fatigue in Humans

2009 ◽  
Vol 41 ◽  
pp. 8-9
Author(s):  
Jordan A. Guenette ◽  
Ioannis Vogiatzis ◽  
Spyros Zakynthinos ◽  
Robert Boushel ◽  
Peter D. Wagner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Respiratory Muscle ◽  
Muscle Blood Flow ◽  
Diaphragmatic Fatigue ◽  
Exercise Induced

scholarly journals Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists

2008 ◽  
Vol 586 (22) ◽  
pp. 5575-5587 ◽  
Author(s):  
Ioannis Vogiatzis ◽  
Dimitris Athanasopoulos ◽  
Robert Boushel ◽  
Jordan A. Guenette ◽  
Maria Koskolou ◽  
...  
Keyword(s):  
Blood Flow ◽  
Respiratory Muscle ◽  
Muscle Blood Flow ◽  
Diaphragmatic Fatigue ◽  
Exercise Induced

Human respiratory muscle blood flow measured by near-infrared spectroscopy and indocyanine green

2008 ◽  
Vol 104 (4) ◽  
pp. 1202-1210 ◽  
Author(s):  
Jordan A. Guenette ◽  
Ioannis Vogiatzis ◽  
Spyros Zakynthinos ◽  
Dimitrios Athanasopoulos ◽  
Maria Koskolou ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Infrared Spectroscopy ◽  
Respiratory Muscle ◽  
Near Infrared ◽  
Vastus Lateralis ◽  
Muscle Blood Flow ◽  
Work Of Breathing ◽  
Dilution Method ◽  
Transdiaphragmatic Pressure

Measurement of respiratory muscle blood flow (RMBF) in humans has important implications for understanding patterns of blood flow distribution during exercise in healthy individuals and those with chronic disease. Previous studies examining RMBF in humans have required invasive methods on anesthetized subjects. To assess RMBF in awake subjects, we applied an indicator-dilution method using near-infrared spectroscopy (NIRS) and the light-absorbing tracer indocyanine green dye (ICG). NIRS optodes were placed on the left seventh intercostal space at the apposition of the costal diaphragm and on an inactive control muscle (vastus lateralis). The primary respiratory muscles within view of the NIRS optodes include the internal and external intercostals. Intravenous bolus injection of ICG allowed for cardiac output (by the conventional dye-dilution method with arterial sampling), RMBF, and vastus lateralis blood flow to be quantified simultaneously. Esophageal and gastric pressures were also measured to calculate the work of breathing and transdiaphragmatic pressure. Measurements were obtained in five conscious humans during both resting breathing and three separate 5-min bouts of constant isocapnic hyperpnea at 27.1 ± 3.2, 56.0 ± 6.1, and 75.9 ± 5.7% of maximum minute ventilation as determined on a previous maximal exercise test. RMBF progressively increased (9.9 ± 0.6, 14.8 ± 2.7, 29.9 ± 5.8, and 50.1 ± 12.5 ml·100 ml−1·min−1, respectively) with increasing levels of ventilation while blood flow to the inactive control muscle remained constant (10.4 ± 1.4, 8.7 ± 0.7, 12.9 ± 1.7, and 12.2 ± 1.8 ml·100 ml−1·min−1, respectively). As ventilation rose, RMBF was closely and significantly correlated with 1) cardiac output ( r = 0.994, P = 0.006), 2) the work of breathing ( r = 0.995, P = 0.005), and 3) transdiaphragmatic pressure ( r = 0.998, P = 0.002). These data suggest that the NIRS-ICG technique provides a feasible and sensitive index of RMBF at different levels of ventilation in humans.

scholarly journals Exercise-induced hyperemia is associated with knee extensor fatigability in adults with type 2 diabetes

2019 ◽  
Vol 126 (3) ◽  
pp. 658-667 ◽  
Author(s):  
Jonathon W. Senefeld ◽  
Jacqueline K. Limberg ◽  
Kathleen M. Lukaszewicz ◽  
Sandra K. Hunter
Keyword(s):  
Type 2 Diabetes ◽  
Blood Flow ◽  
Lower Limb ◽  
Contractile Function ◽  
Muscle Blood Flow ◽  
Knee Extensor ◽  
Dynamic Exercise ◽  
Extensor Muscles ◽  
Exercise Induced

The aim of this study was to compare fatigability, contractile function, and blood flow to the knee extensor muscles after dynamic exercise in patients with type 2 diabetes mellitus (T2DM) and controls. The hypotheses were that patients with T2DM would demonstrate greater fatigability than controls, and greater fatigability would be associated with a lower exercise-induced increase in blood flow and greater impairments in contractile function. Patients with T2DM ( n = 15; 8 men; 62.4 ± 9.0 yr; 30.4 ± 7.7 kg/m2; 7,144 ± 3,294 steps/day) and 15 healthy control subjects (8 men, 58.4 ± 6.9 yr; 28.4 ± 4.6 kg/m2; 7,893 ± 2,323 steps/day) were matched for age, sex, body mass index, and physical activity. Fatigability was quantified as the reduction in knee extensor power during a 6-min dynamic exercise. Before and after exercise, vascular ultrasonography and electrical stimulation were used to assess skeletal muscle blood flow and contractile properties, respectively. Patients with T2DM had greater fatigability (30.0 ± 20.1% vs. 14.6 ± 19.0%, P < 0.001) and lower exercise-induced hyperemia (177 ± 90% vs. 194 ± 79%, P = 0.04) than controls but similar reductions in the electrically evoked twitch amplitude (37.6 ± 24.8% vs. 31.6 ± 30.1%, P = 0.98). Greater fatigability of the knee extensor muscles was associated with postexercise reductions in twitch amplitude ( r = 0.64, P = 0.001) and lesser exercise-induced hyperemia ( r = −0.56, P = 0.009). Patients with T2DM had greater lower-limb fatigability during dynamic exercise, which was associated with reduced contractile function and lower skeletal muscle blood flow. Thus, treatments focused on enhancing perfusion and reversing impairments in contractile function in patients with T2DM may offset lower-limb fatigability and aid in increasing exercise capacity. NEW & NOTEWORTHY Although prior studies compare patients with type 2 diabetes mellitus (T2DM) with lean controls, our study includes controls matched for age, body mass, and physical activity to more closely assess the effects of T2DM. Patients with T2DM demonstrated no impairment in macrovascular endothelial function, evidenced by similar flow-mediated dilation to controls. However, patients with T2DM had greater fatigability and reduced exercise-induced increase in blood flow (hyperemia) after a lower-limb dynamic fatiguing exercise compared with controls.

Measurement of Respiratory Muscle Blood Flow in Humans Using Near Infrared Spectroscopy and Indocyanine Green

2008 ◽  
Vol 40 (Supplement) ◽  
pp. S304
Author(s):  
Jordan A. Guenette ◽  
Ioannis Vogiatzis ◽  
Spyros Zakythinos ◽  
Dimitrios Athanasopoulos ◽  
Spyretta Golemati ◽  
...  
Keyword(s):  
Blood Flow ◽  
Infrared Spectroscopy ◽  
Indocyanine Green ◽  
Near Infrared Spectroscopy ◽  
Respiratory Muscle ◽  
Near Infrared ◽  
Muscle Blood Flow

Blood Flow Index Using Near Infrared Spectroscopy and Indocyanine Green Dye as a Minimally Invasive Method for Assessing Respiratory Muscle Blood Flow in Humans

CHEST Journal ◽  
2010 ◽  
Vol 138 (4) ◽  
pp. 917A
Author(s):  
Jordan A. Guenette ◽  
William R. Henderson ◽  
Paolo B. Dominelli ◽  
Jordan S. Querido ◽  
Donald E. Griesdale ◽  
...  
Keyword(s):  
Blood Flow ◽  
Infrared Spectroscopy ◽  
Minimally Invasive ◽  
Respiratory Muscle ◽  
Near Infrared ◽  
Muscle Blood Flow ◽  
Flow Index ◽  
Indocyanine Green Dye ◽  
Blood Flow Index ◽  
Invasive Method

scholarly journals Respiratory muscle blood flow steal during exercise in heart failure

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Thomas Patrick Olson ◽  
Michael J Joyner ◽  
Niki M Dietz ◽  
John H Eisenach ◽  
Timothy B Curry ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Respiratory Muscle ◽  
Muscle Blood Flow

Respiratory muscle blood flow in oleic acid-induced pulmonary edema

1986 ◽  
Vol 60 (6) ◽  
pp. 1849-1856 ◽  
Author(s):  
S. Magder ◽  
R. Erian ◽  
C. Roussos
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oleic Acid ◽  
Pulmonary Edema ◽  
Respiratory Muscle ◽  
Supply And Demand ◽  
Muscle Blood Flow ◽  
Dynamic Compliance ◽  
Control Value ◽  
Pressure Time

If respiratory muscle blood flow (RMBF) demands in pulmonary edema are large enough, an imbalance between supply and demand could lead to respiratory muscle failure. Therefore, to determine the magnitude of RMBF in this condition we produced pulmonary edema by injecting oleic acid into the pulmonary circulation and measured RMBF with radiolabeled microspheres injected into the left atrium. We then related changes in muscle blood flow to changes in respiratory variables including frequency of breathing (fb, breaths/min), tidal volume (VT, ml), ventilation (VE, ml . kg-1 . min-1), pleural pressure-time index (PTI, cmH2O), and dynamic compliance (Cdyn, 1/cmH2O) at 0 (control), 30, 60, and 120 min. Cardiac output and blood pressure did not change throughout the experiment, but hypoxia became progressively more severe with a final PO2 of 37 +/- 10 Torr. With pulmonary edema, fb rose from a control value of 32 +/- 13 to 111 +/- 33 at peak, VE rose from 237 +/- 90 to 806 +/- 188, but VT did not change. PTI rose from 54 +/- 16 to 180 +/- 48, and Cdyn decreased from 0.06 +/- 0.02 to 2.02 +/- 0.01. Diaphragmatic blood flow (Qdi) rose from 16.0 +/- 6.26 to 120.1 +/- 54.5 ml . min-1 X 100 g-1 and accounted for 55% of the total RMBF of 217 +/- 100 ml/min. The RMBF accounted for 11.4 +/- 4.7% of the cardiac output at peak affect. The rise in Qdi was best predicted by PTI and to a smaller extent by PO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory muscle blood flows during physiological and chemical hyperpnea in the rat

2000 ◽  
Vol 88 (1) ◽  
pp. 186-194 ◽  
Author(s):  
David C. Poole ◽  
William L. Sexton ◽  
Bradley J. Behnke ◽  
Christine S. Ferguson ◽  
K. Sue Hageman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Respiratory Muscle ◽  
Maximal Exercise ◽  
Vastus Lateralis ◽  
Muscle Blood Flow ◽  
Oxidative Capacity ◽  
Blood Flows ◽  
Vasodilator Reserve ◽  
Exercise Muscle ◽  
Crural Diaphragm

Whether the diaphragm retains a vasodilator reserve at maximal exercise is controversial. To address this issue, we measured respiratory and hindlimb muscle blood flows and vascular conductances using radiolabeled microspheres in rats running at their maximal attainable treadmill speed (96 ± 5 m/min; range 71–116 m/min) and at rest while breathing either room air or 10% O2-8% CO2 (balance N2). All hindlimb and respiratory muscle blood flows measured increased during exercise ( P < 0.001), whereas increases in blood flow while breathing 10% O2-8% CO2 were restricted to the diaphragm only. During exercise, muscle blood flow increased up to 18-fold above rest values, with the greatest mass specific flows (in ml ⋅ min−1 ⋅ 100 g−1) found in the vastus intermedius (680 ± 44), red vastus lateralis (536 ± 18), red gastrocnemius (565 ± 47), and red tibialis anterior (602 ± 44). During exercise, blood flow was higher ( P < 0.05) in the costal diaphragm (395 ± 31 ml ⋅ min−1 ⋅ 100 g−1) than in the crural diaphragm (286 ± 17 ml ⋅ min−1 ⋅ 100 g−1). During hypoxia+hypercapnia, blood flows in both the costal and crural diaphragms (550 ± 70 and 423 ± 53 ml ⋅ min−1 ⋅ 100 g−1, respectively) were elevated ( P < 0.05) above those found during maximal exercise. These data demonstrate that there is a substantial functional vasodilator reserve in the rat diaphragm at maximal exercise and that hypoxia + hypercapnia-induced hyperpnea is necessary to elevate diaphragm blood flow to a level commensurate with its high oxidative capacity.

Respiratory muscle energetics during endotoxic shock in dogs

1986 ◽  
Vol 60 (2) ◽  
pp. 486-493 ◽  
Author(s):  
S. N. Hussain ◽  
R. Graham ◽  
F. Rutledge ◽  
C. Roussos
Keyword(s):  
Blood Flow ◽  
Respiratory Muscle ◽  
Muscle Blood Flow ◽  
Endotoxic Shock ◽  
Lactate Production ◽  
Respiratory Muscles ◽  
Experimental Period ◽  
Endotoxin Shock ◽  
Glycogen Depletion ◽  
Muscle Energetics

Respiratory muscle O2 consumption, lactate production, and endogenous substrate utilization during endotoxic shock were assessed in two groups of anesthetized spontaneously breathing dogs. In the endotoxin group (Escherichia coli endotoxin 10 mg/kg iv) and the sham group (saline iv), we sampled diaphragm, external intercostal, and gastrocnemius muscle tissue for glycogen and lactate concentrations before and after 3 h of the experimental period. Only in the endotoxin group did blood pressure and cardiac output decline significantly. Arterial O2 content did not change significantly during shock, whereas mixed venous, phrenic venous, and femoral venous O2 contents dropped to 8.0 +/- 1.1, 5.8 +/- 0.8, and 3.6 +/- 0.6 ml/dl at 60 min of shock, respectively, with little change thereafter. At 30 min of shock, femoral venous lactate rose higher than arterial values, whereas at 90 min of shock, onward, phrenic venous lactate was significantly higher than arterial concentrations. All muscle tissues showed significant lactate production and glycogen depletion after shock. In a second set of experiments we measured respiratory muscle blood flow during shock with radioactive microspheres. At 60 min of shock, diaphragmatic and intercostal blood flow rose by six- and twofold, respectively, whereas gastrocnemius blood flow declined significantly. We conclude that during endotoxin shock 1) the increased demands of the respiratory muscles are met by increasing blood flow and O2 extraction; 2) anaerobic metabolism and respiratory muscle substrate depletion, or both, may contribute to the observed fatigue.

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