Intercostal muscle blood flow is elevated in old rats during submaximal exercise

2019 ◽  
Vol 263 ◽  
pp. 26-30 ◽  
Author(s):  
Joshua R. Smith ◽  
K. Sue Hageman ◽  
Craig A. Harms ◽  
David C. Poole ◽  
Timothy I. Musch
1988 ◽  
Vol 65 (4) ◽  
pp. 1514-1519 ◽  
Author(s):  
M. Manohar

The present study was carried out 1) to compare blood flow in the costal and crural regions of the equine diaphragm during quiet breathing at rest and during graded exercise and 2) to determine the fraction of cardiac output needed to perfuse the diaphragm during near-maximal exercise. By the use of radionuclide-labeled 15-micron-diam microspheres injected into the left atrium, diaphragmatic and intercostal muscle blood flow was studied in 10 healthy ponies at rest and during three levels of exercise (moderate: 12 mph, heavy: 15 mph, and near-maximal: 19-20 mph) performed on a treadmill. At rest, in eucapnic ponies, costal (13 +/- 3 ml.min-1.100 g-1) and crural (13 +/- 2 ml.min-1.100 g-1) phrenic blood flows were similar, but the costal diaphragm received a much larger percentage of cardiac output (0.51 +/- 0.12% vs. 0.15 +/- 0.03% for crural diaphragm). Intercostal muscle perfusion at rest was significantly less than in either phrenic region. Graded exercise resulted in significant progressive increments in perfusion to these tissues. Although during exercise, crural diaphragmatic blood flow was not different from intercostal muscle blood flow, these values remained significantly less (P less than 0.01) than in the costal diaphragm. At moderate, heavy, and near-maximal exercise, costal diaphragmatic blood flow (123 +/- 12, 190 +/- 12, and 245 +/- 18 ml.min-1.100 g-1) was 143%, 162%, and 162%, respectively, of that for the crural diaphragm (86 +/- 10, 117 +/- 8, and 151 +/- 14 ml.min-1.100 g-1).(ABSTRACT TRUNCATED AT 250 WORDS)


2009 ◽  
Vol 587 (14) ◽  
pp. 3665-3677 ◽  
Author(s):  
Ioannis Vogiatzis ◽  
Dimitris Athanasopoulos ◽  
Helmut Habazettl ◽  
Wolfgang M. Kuebler ◽  
Harrieth Wagner ◽  
...  

1995 ◽  
Vol 268 (1) ◽  
pp. H330-H335 ◽  
Author(s):  
R. M. McAllister ◽  
J. C. Sansone ◽  
M. H. Laughlin

Hyperthyroidism is associated with exercise intolerance. Previous research, however, has shown that cardiac output is either normal or enhanced during exercise in the hyperthyroid state. We therefore hypothesized that blood flow to working skeletal muscle is augmented in hyperthyroid animals during in vivo submaximal exercise and, consequently, that noncardiovascular factors are responsible for intolerance to exercise. To test this hypothesis, rats were made hyperthyroid (Hyper) over 6–12 wk with injections of triiodothyronine (300 micrograms/kg). Hyperthyroidism was evidenced by left ventricular hypertrophy [euthyroid (Eut), 2.12 +/- 0.05 mg/g body wt; Hyper, 2.78 +/- 0.06; P < 0.005], 25–60% increases in citrate synthase activities in Hyper hindlimb muscles over those of Eut rats, and higher preexercise heart rates (Eut, 415 +/- 18 beats/min; Hyper, 479 +/- 19; P < 0.025). Regional blood flows were determined by the radiolabeled microsphere method, preexercise, and at 1–2 min of treadmill running at 15 m/min (0% grade). Total hindlimb muscle blood flow preexercise was unaffected (Eut, 31 +/- 4 ml.min-1.(100) g-1, n = 11; Hyper, 40 +/- 6, n = 9; not significant) but was higher (P < 0.025) in Hyper (127 +/- 17, n = 9) compared with Eut (72 +/- 11, n = 9) during treadmill running. During exercise, flows to individual muscles and muscle sections were approximately 50–150% higher in Hyper compared with Eut rats. Visceral blood flows were largely similar between groups. These findings indicate that hyperthyroidism is associated with augmented blood flow to skeletal muscle during submaximal exercise. Thus hypoperfusion of skeletal muscle does not account for the poor exercise tolerance characteristic of hyperthyroidism.


1997 ◽  
Vol 273 (4) ◽  
pp. H1787-H1793 ◽  
Author(s):  
Maria D. Koskolou ◽  
Robert C. Roach ◽  
José A. L. Calbet ◽  
Göran Rådegran ◽  
Bengt Saltin

We hypothesized that reducing arterial O2 content ([Formula: see text]) by lowering the hemoglobin concentration ([Hb]) would result in a higher blood flow, as observed with a low [Formula: see text], and maintenance of O2 delivery. Seven young healthy men were studied twice, at rest and during two-legged submaximal and peak dynamic knee extensor exercise in a control condition (mean control [Hb] 144 g/l) and after 1–1.5 liters of whole blood had been withdrawn and replaced with albumin {mean drop in [Hb] 29 g/l (range 19–38 g/l); low [Hb]}. Limb blood flow (LBF) was higher ( P < 0.01) with low [Hb] during submaximal exercise (i.e., at 30 W, LBF was 2.5 ± 0.1 and 3.0 ± 0.1 l/min for control [Hb] and low [Hb], respectively; P < 0.01), resulting in a maintained O2 delivery and O2 uptake for a given workload. However, at peak exercise, LBF was unaltered (6.5 ± 0.4 and 6.6 ± 0.6 l/min for control [Hb] and low [Hb], respectively), which resulted in an 18% reduction in O2 delivery ( P < 0.01). This occurred despite peak cardiac output in neither condition reaching >75% of maximal cardiac output (∼26 l/min). It is concluded that a low CaO2 induces an elevation in submaximal muscle blood flow and that O2 delivery to contracting muscles is tightly regulated.


2004 ◽  
Vol 96 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Timothy I. Musch ◽  
Kevin E. Eklund ◽  
K. Sue Hageman ◽  
David C. Poole

Maximal aerobic capacity and the ability to sustain submaximal exercise (Ex) declines with advancing age. Whether altered muscle blood flow (BF) plays a mechanistic role in these effects remains to be resolved. The present investigation determined the effects of aging on the hemodynamic and regional BF response to submaximal Ex in rats. Heart rate (HR), mean arterial pressure (MAP), and BF to different organs (kidneys, splanchnic organs, and 28 hindlimb muscles) were determined at rest and during submaximal treadmill Ex (20 m/min, 5% grade) with radiolabeled microspheres in young (Y; 6-8 mo old, 339 ± 8 g, n = 9) and old (O; 27-29 mo old, 504 ± 18 g, n = 7) Fischer 344 × Brown Norway rats. Results demonstrated that HR, MAP, and BF to the pancreas, small and large intestine, and total hindlimb musculature were similar between Y and O rats at rest. BF to the kidneys, spleen, and stomach were 33, 60, and 43% lower, respectively, in O compared with Y rats. BF to the total hindlimb musculature increased ( P < 0.05) during Ex and was similar for both Y and O rats (Y: 16 ± 3 to 124 ± 7 vs. O: 20 ± 3 to 137 ± 12 ml·min-1·100 g-1). However, in O vs. Y rats, BF was reduced in 6 (highly oxidative) and elevated in 8 (highly glycolytic) of the 28 individual hindquarter muscles or muscle parts examined ( P < 0.05). During Ex, BF to the spleen and stomach decreased ( P < 0.05) from rest in Y rats, whereas BF decreased in the kidneys, pancreas, spleen, stomach, as well as the small and large intestines of O rats. In conclusion, these data demonstrate that, despite similar increases in total hindlimb BF in Y and O rats during submaximal Ex, there is a profound BF redistribution from highly oxidative to highly glycolytic muscles.


2010 ◽  
Vol 109 (2) ◽  
pp. 388-395 ◽  
Author(s):  
Dimitris Athanasopoulos ◽  
Zafeiris Louvaris ◽  
Evgenia Cherouveim ◽  
Vasilis Andrianopoulos ◽  
Charis Roussos ◽  
...  

We investigated whether expiratory muscle loading induced by the application of expiratory flow limitation (EFL) during exercise in healthy subjects causes a reduction in quadriceps muscle blood flow in favor of the blood flow to the intercostal muscles. We hypothesized that, during exercise with EFL quadriceps muscle blood flow would be reduced, whereas intercostal muscle blood flow would be increased compared with exercise without EFL. We initially performed an incremental exercise test on eight healthy male subjects with a Starling resistor in the expiratory line limiting expiratory flow to ∼ 1 l/s to determine peak EFL exercise workload. On a different day, two constant-load exercise trials were performed in a balanced ordering sequence, during which subjects exercised with or without EFL at peak EFL exercise workload for 6 min. Intercostal (probe over the 7th intercostal space) and vastus lateralis muscle blood flow index (BFI) was calculated by near-infrared spectroscopy using indocyanine green, whereas cardiac output (CO) was measured by an impedance cardiography technique. At exercise termination, CO and stroke volume were not significantly different during exercise, with or without EFL (CO: 16.5 vs. 15.2 l/min, stroke volume: 104 vs. 107 ml/beat). Quadriceps muscle BFI during exercise with EFL (5.4 nM/s) was significantly ( P = 0.043) lower compared with exercise without EFL (7.6 nM/s), whereas intercostal muscle BFI during exercise with EFL (3.5 nM/s) was significantly ( P = 0.021) greater compared with that recorded during control exercise (0.4 nM/s). In conclusion, increased respiratory muscle loading during exercise in healthy humans causes an increase in blood flow to the intercostal muscles and a concomitant decrease in quadriceps muscle blood flow.


1989 ◽  
Vol 141 (1) ◽  
pp. 87-95
Author(s):  
M. D. Delp ◽  
M. H. Laughlin ◽  
R. B. Armstrong

During prolonged submaximal exercise muscle blood flow has been shown to increase progressively in rats and miniature swine. This study was designed to test the hypothesis that the increases in muscle blood flow are associated with progressive elevations in body temperature in rats. Colonic temperature and muscle blood flow (determined using radioactive microspheres) were measured after 15, 30 and 45 min of exercise in rats exercising on a treadmill at 15 m min-1 on a 0 degree incline. Total hindlimb muscle blood flow increased from 79 +/− 8 ml min-1 100 g-1 at 15 min to 95 +/− 10 ml min-1 100 g-1 at 30 min (P less than 0.05). The greatest increases in blood flow occurred in the deep extensor muscles of the hindlimb. For example, in the red portion of the gastrocnemius muscle, blood flow increased from 197 +/− 15 ml min-1 100 g-1 at 15 min to 285 +/− 17 ml min-1 100 g-1 at 30 min (P less than 0.05). Colonic temperature, however, remained stable at 38.5 degrees C over this period. These data indicate that the progressive hyperaemia in muscle was unrelated to body temperature.


2012 ◽  
Vol 113 (12) ◽  
pp. 1846-1851 ◽  
Author(s):  
Zachary Barrett-O'Keefe ◽  
Jan Helgerud ◽  
Peter D. Wagner ◽  
Russell S. Richardson

Maximal strength training (MST) reduces pulmonary oxygen uptake (V̇o2) at a given submaximal exercise work rate (i.e., efficiency). However, whether the increase in efficiency originates in the trained skeletal muscle, and therefore the impact of this adaptation on muscle blood flow and arterial-venous oxygen difference (a-vO2diff), is unknown. Thus five trained subjects partook in an 8-wk MST intervention consisting of half-squats with an emphasis on the rate of force development during the concentric phase of the movement. Pre- and posttraining measurements of pulmonary V̇o2 (indirect calorimetry), single-leg blood flow (thermodilution), and single-leg a-vO2diff (blood gases) were performed, to allow the assessment of skeletal muscle V̇o2 during submaximal cycling [237 ± 23 W; ∼60% of their peak pulmonary V̇o2 (V̇o2peak)]. Pulmonary V̇o2peak (∼4.05 l/min) and peak work rate (∼355 W), assessed during a graded exercise test, were unaffected by MST. As expected, following MST there was a significant reduction in pulmonary V̇o2 during steady-state submaximal cycling (∼237 W: 3.2 ± 0.1 to 2.9 ± 0.1 l/min). This was accompanied by a significant reduction in single-leg V̇o2 (1,101 ± 105 to 935 ± 93 ml/min) and single-leg blood flow (6,670 ± 700 to 5,649 ± 641 ml/min), but no change in single-leg a-vO2diff (16.7 ± 0.8 to 16.8 ±0.4 ml/dl). These data confirm an MST-induced reduction in pulmonary V̇o2 during submaximal exercise and identify that this change in efficiency originates solely in skeletal muscle, reducing muscle blood flow, but not altering muscle a-vO2diff.


2012 ◽  
Vol 90 (11) ◽  
pp. 1498-1505 ◽  
Author(s):  
Steven W. Copp ◽  
Peter J. Schwagerl ◽  
Daniel M. Hirai ◽  
David C. Poole ◽  
Timothy I. Musch

Excess reactive oxygen species are implicated in the impaired peripheral vascular function evident during exercise in older individuals. We tested the hypothesis that an acute infusion of the antioxidant ascorbic acid (AA) in old rats would improve antioxidant capacity and reduce oxidative stress and, therefore, elevate hindlimb muscle blood flow at rest and during treadmill exercise in muscles containing principally type I and IIa muscle fibers. Total and individual hindlimb skeletal muscle blood flow was measured (radiolabeled microspheres) in old rats (26–28 months) at rest (n = 8) and during treadmill exercise (n = 8; 20 m·min–1, 5% grade) before and after AA treatment (76 mg·(kg body mass)–1 intra-arterial (i.a.) injection). AA elevated total antioxidant capacity (rest, ∼37%; and exercise, 31%) and reduced oxidative stress (∼26%, exercise only). AA reduced resting total hindlimb muscle blood flow (control, 25 ± 3; AA, 16 ± 2 mL·min–1·(100 g)–1; p < 0.05) and blood flow to 8 of 28 individual muscles with no fiber-type correlation (p > 0.05). During exercise there was no effect of AA on total hindlimb muscle blood flow (control, 154 ± 14; AA, 162 ± 13 mL·min–1·(100 g)–1; p > 0.05) or blood flow to any individual muscle. This disconnect between whole-body antioxidant status and skeletal muscle blood flow in old rats mandates consideration when pursuing antioxidant treatments experimentally or clinically in older populations.


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