Observations Upon the Rate-Limiting Role of Blood Flow in the Regulation of Respiration of Skeletal Muscle During Intermittent Exercise

1975 ◽  
pp. 65-69 ◽  
Author(s):  
A. Corsi ◽  
A. L. Granata ◽  
M. Midrio ◽  
M. Turchetto
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Intermittent Exercise ◽  
Regulation Of Respiration ◽  
Rate Limiting

Vasodilation induced by endothelin: role of EDRF and prostanoids in rat hindquarters

1990 ◽  
Vol 259 (6) ◽  
pp. H1835-H1841 ◽  
Author(s):  
E. H. Ohlstein ◽  
L. Vickery ◽  
C. Sauermelch ◽  
R. N. Willette
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Perfusion Pressure ◽  
Microvascular Perfusion ◽  
Hemodynamic Effects ◽  
Hemodynamic Responses ◽  
Pithed Rats ◽  
Dose Dependent

Hemodynamic responses to endothelin (ET-1) were studied in hindquarters of anesthetized rats and also in isolated buffer-perfused hindquarters of pithed rats. ET-1 (10-100 pmol ia) produced brief dose-related increases in hindquarter blood flow. Acetylcholine (ACh. 0.3-1 micrograms ia) produced similar vasodilator responses. Hemodynamic responses elicited by either ET-1 or ACh were not significantly altered by pretreatment with indomethacin. ET-1 produced dose-dependent increases in skeletal muscle microvascular perfusion, whereas ET-1 had no effect on cutaneous microvascular perfusion, suggesting that vasodilation in the skeletal muscle of the hindlimb contributes to the increase in hindquarter blood flow induced by ET-1. Hemodynamic effects of ET-1 and ACh were studied in the isolated in situ buffer-perfused hindquarters of pithed rats. ET-1 (0.01-300 pmol ia) produced only dose-dependent increases in hindquarter perfusion pressure under basal conditions or when the vascular preparation was precontracted with methoxamine. ET-1 induced vasorelaxation was not observed. ACh (3 microgram ia) produced a 64% reduction in hindquarter perfusion pressure; indicative of endothelium-dependent relaxation. ET-3 (0.1-300 pmol) produced only dose-dependent increases in hindquarter perfusion pressure. When hemodynamic effects of ET-1 were studied under conditions of constant pressure, results were similar to those obtained under constant flow. This study demonstrates that in the rat hindquarters endothelium-derived relaxing factors and prostanoids do not appear to be mediators of endothelin-induced vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

High dietary salt reduces the contribution of 20-HETE to arteriolar oxygen responsiveness in skeletal muscle

2007 ◽  
Vol 292 (3) ◽  
pp. H1507-H1515 ◽  
Author(s):  
Paul J. Marvar ◽  
John R. Falck ◽  
Matthew A. Boegehold
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
High Salt ◽  
Tissue Blood Flow ◽  
Dietary Salt ◽  
Metabolic Demand ◽  
Long Term Effect ◽  
Arteriolar Tone

The coupling of tissue blood flow to cellular metabolic demand involves oxygen-dependent adjustments in arteriolar tone, and arteriolar responses to oxygen can be mediated, in part, by changes in local production of 20-HETE. In this study, we examined the long-term effect of dietary salt on arteriolar oxygen responsiveness in the exteriorized, superfused rat spinotrapezius muscle and the role of 20-HETE in this responsiveness. Rats were fed either a normal-salt (NS, 0.45%) or high-salt (HS, 4%) diet for 4–5 wk. There was no difference in steady-state tissue Po2 between NS and HS rats, and elevation of superfusate oxygen content from 0% to 10% caused tissue Po2 to increase by the same amount in both groups. However, the resulting reductions in arteriolar diameter and blood flow were less in HS rats than NS rats. Inhibition of 20-HETE formation with N-methylsulfonyl-12,12-dibromododec-11-enamide (DDMS) or 17-octadecynoic acid (17-ODYA) attenuated oxygen-induced constriction in NS rats but not HS rats. Exogenous 20-HETE elicited arteriolar constriction that was greatly reduced by the large-conductance Ca2+-activated potassium (KCa) channel inhibitors tetraethylammonium chloride (TEA) and iberiotoxin (IbTx) in NS rats and a smaller constriction that was less sensitive to TEA or IbTx in HS rats. Arteriolar responses to exogenous angiotensin II were similar in both groups but more sensitive to inhibition with DDMS in NS rats. Norepinephrine-induced arteriolar constriction was similar and insensitive to DDMS in both groups. We conclude that 20-HETE contributes to oxygen-induced constriction of skeletal muscle arterioles via inhibition of KCa channels and that a high-salt diet impairs arteriolar responses to increased oxygen availability due to a reduction in vascular smooth muscle responsiveness to 20-HETE.

scholarly journals The role of acetic acid on glucose uptake and blood flow rates in the skeletal muscle in humans with impaired glucose tolerance

2015 ◽  
Vol 69 (6) ◽  
pp. 734-739 ◽  
Author(s):  
P Mitrou ◽  
E Petsiou ◽  
E Papakonstantinou ◽  
E Maratou ◽  
V Lambadiari ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Acetic Acid ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Glucose Uptake ◽  
Flow Rates

scholarly journals Increases in skeletal muscle ATGL and its inhibitor G0S2 following 8 weeks of endurance training in metabolically different rat skeletal muscles

2016 ◽  
Vol 310 (2) ◽  
pp. R125-R133 ◽  
Author(s):  
Patrick C. Turnbull ◽  
Amanda B. Longo ◽  
Sofhia V. Ramos ◽  
Brian D. Roy ◽  
Wendy E. Ward ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Skeletal Muscles ◽  
Gene Identification ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Hind Limb Muscle ◽  
Sciatic Nerve Stimulation ◽  
Rate Limiting

Adipose triglyceride lipase (ATGL) catalyzes the rate-limiting removal of the first fatty acid from a triglyceride. ATGL is activated by comparative gene identification-58 and inhibited by G(0)/G(1) switch gene-2 protein (G0S2). Research in other tissues and cell culture indicates that inhibition is dependent on relative G0S2-to-ATGL protein content. G0S2 may also have several roles within mitochondria; however, this has yet to be observed in skeletal muscle. The purpose of this study was to determine if muscle G0S2 relative to ATGL content would decrease to facilitate intramuscular lipolysis following endurance training. Male Sprague-Dawley rats ( n = 10; age 51–53 days old) were progressively treadmill trained at a 10% incline for 8 wk ending with 25 m/min for 1 h compared with control. Sciatic nerve stimulation for hind-limb muscle contraction (and lipolysis) was administered for 30 min to one leg, leaving the opposing leg as a resting control. Soleus (SOL), red gastrocnemius (RG), and white gastrocnemius were excised from both legs following stimulation or control. ATGL protein increased in all trained muscles. Unexpectedly, G0S2 protein was greater in the trained SOL and RG. In RG-isolated mitochondria, G0S2 also increased with training, yet mitochondrial G0S2 content was unaltered with acute contraction; therefore, any role of G0S2 in the mitochondria does not appear to be acutely mediated by content alone. In summary, G0S2 increased with training in oxidative muscles and mitochondria but not following acute contraction, suggesting that inhibition is not through relative G0S2-to-ATGL content but through more complicated intracellular mechanisms.

scholarly journals Erythrocytes and the regulation of human skeletal muscle blood flow and oxygen delivery: role of erythrocyte count and oxygenation state of haemoglobin

2006 ◽  
Vol 572 (1) ◽  
pp. 295-305 ◽  
Author(s):  
José González-Alonso ◽  
Stefan P. Mortensen ◽  
Ellen A. Dawson ◽  
Niels H. Secher ◽  
Rasmus Damsgaard
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Delivery ◽  
Human Skeletal Muscle ◽  
Muscle Blood Flow ◽  
Erythrocyte Count ◽  
Skeletal Muscle Blood Flow

Nitric oxide in the regulation of vasomotor tone in human skeletal muscle

1999 ◽  
Vol 276 (6) ◽  
pp. H1951-H1960 ◽  
Author(s):  
G. Rådegran ◽  
B. Saltin
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Human Skeletal Muscle ◽  
Initial Rate ◽  
Knee Extensor ◽  
Vasomotor Tone ◽  
Arterial Infusion ◽  
Femoral Artery Blood Flow

The role of nitric oxide (NO) as a regulator of vasomotor tone has been investigated in resting and exercising human skeletal muscle. At rest, NO synthase (NOS) inhibition by intra-arterial infusion of N G-monomethyl-l-arginine decreased femoral artery blood flow (FABF, ultrasound Doppler) from 0.39 ± 0.08 to 0.18 ± 0.03 l/min ( P < 0.01), i.e., by ∼52%, and increased leg O2 extraction from 62.1 ± 9.8 to 100.9 ± 4.5 ml/l ( P < 0.004); thus leg O2 uptake (V˙o 2, 22 ± 4 ml/min, ∼0.75 ml ⋅ min−1 ⋅ 100 g−1) was unaltered [not significant ( P = NS)]. Mean arterial pressure (MAP) increased by 8 ± 2 mmHg ( P < 0.01). Heart rate (HR, 53 ± 3 beats/min) was unaltered ( P = NS). The NOS inhibition had, however, no effect on the initial rate of rise or the magnitude of FABF (4.8 ± 0.4 l/min, ∼163 ml ⋅ min−1 ⋅ 100 g−1), MAP (117 ± 3 mmHg), HR (98 ± 5 beats/min), or legV˙o 2 (704 ± 55 ml/min, ∼24 ml ⋅ min−1 ⋅ 100 g−1, P = NS) during submaximal, one-legged, dynamic knee-extensor exercise. Similarly, FABF (7.6 ± 1.0 l/min, ∼258 ml ⋅ min−1 ⋅ 100 g−1), MAP (140 ± 8 mmHg), and leg V˙o 2(1,173 ± 139 ml/min, ∼40 ml ⋅ min−1 ⋅ 100 g−1) were unaffected at termination of peak effort ( P = NS). Peak HR (137 ± 3 beats/min) was, however, lowered by 10% ( P < 0.01). During recovery, NOS inhibition reduced FABF by ∼34% ( P< 0.04), which was compensated for by an increase in the leg O2 extraction by ∼41% ( P < 0.04); thus legV˙o 2 was unaltered ( P = NS). In conclusion, these findings indicate that NO is not essential for the initiation or maintenance of active hyperemia in human skeletal muscle but support a role for NO during rest, including recovery from exercise. Moreover, changes in blood flow during rest and recovery caused by NOS inhibition are accompanied by reciprocal changes in O2 extraction, and thusV˙o 2 is maintained.

scholarly journals The role of perfusion in the oxygen extraction capability of skin and skeletal muscle

2016 ◽  
Vol 310 (10) ◽  
pp. H1277-H1284 ◽  
Author(s):  
Clare E. Thorn ◽  
Angela C. Shore
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Occlusion ◽  
Flow Regulation ◽  
Reflectance Spectroscopy ◽  
Oxygen Extraction ◽  
Forearm Skin ◽  
Obese Subjects ◽  
The Difference

Oxygen extraction (OE) by all cells is dependent on an adequate supply of oxygen in proximal blood vessels and the cell's need and ability to uptake that oxygen. Here the role of blood flow in regulating OE in skin and skeletal muscle was investigated in lean and obese men. OE was derived by two optical reflectance spectroscopy techniques: 1) from the rate of fall in mean blood saturation during a 4 min below knee arterial occlusion, and thus no blood flow, in calf skin and skeletal muscle and 2) in perfused, unperturbed skin, using the spontaneous falls in mean blood saturation induced by vasomotion in calf and forearm skin of 24 subjects, 12 lean and 12 obese. OE in perfused skin was significantly higher in lean compared with obese subjects in forearm (Mann-Whitney, P < 0.004) and calf ( P < 0.001) and did not correlate with OE in unperfused skin (ρ = −0.01, P = 0.48). With arterial occlusion and thus no blood flow, skin OE in lean and obese subjects no longer differed ( P = 0.23, not significant). In contrast in skeletal muscle with arterial occlusion and no blood flow, the difference in OE between lean and obese subjects occurred, with obese subjects exhibiting significantly higher OE ( P < 0.012). The classic model of metabolic blood flow regulation to support oxygen extraction is evident in perfused skin; OE is perturbed without blood flow and reduced in obesity. In resting skeletal muscle other mechanism(s), independent of blood flow, are implicated in oxygen extraction.

scholarly journals Abnormal skeletal muscle bioenergetics during exercise in patients with heart failure: role of reduced muscle blood flow.

Circulation ◽  
1986 ◽  
Vol 73 (6) ◽  
pp. 1127-1136 ◽  
Author(s):  
D H Wiener ◽  
L I Fink ◽  
J Maris ◽  
R A Jones ◽  
B Chance ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Patients With Heart Failure
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