The rapid onset of vasodilatation within seconds of a single contraction suggests that the vasodilators involved may be products of skeletal muscle activation, such as potassium (K + ). To test the hypothesis that K + was in part responsible for the rapid dilatation produced by muscle contraction we stimulated four to five skeletal muscle fibres in the anaesthetized hamster cremaster preparation in situ and measured the change in diameter of arterioles at a site of overlap with the stimulated muscle fibres before and after a single contraction stimulated over a range of stimulus frequencies (4, 10, 20, 30, 40, 60 and 80 Hz; 250 ms train duration). Muscle fibres were stimulated in the absence and presence of an inhibitor of a source of K + , the voltage dependent K + channel inhibitor 3,4-diaminopyridine (DAP, 3 × 10 −4 M) and inhibitors of the K + dilatory signal transduction pathway, either a Na + K + -ATPase inhibitor (ouabain; 10 −4 M) or an inward rectifying K + channel inhibitor (barium chloride, BaCl 2 ; 5 × 10 −5 M). We observed significant inhibitions of the rapid dilatation at all stimulus frequencies with each inhibitor. The dilatory event at 4 s was significantly inhibited at all stimulus frequencies by an average of 65.7 ± 3.6%, 58.8 ± 6.1% and 64.4 ± 2.1% in the presence DAP, ouabain and BaCl 2 , respectively. These levels of inhibition did not correlate with non-specific changes in force generation by skeletal muscle measured in vitro. Therefore, our data support that K + is involved in the rapid dilatation in response to a single muscle contraction across a wide range of stimulus frequencies.
Armstrong ML, Dua AK, Murrant CL. Time course of vasodilation at the onset of repetitive skeletal muscle contractions. Am J Physiol Regul Integr Comp Physiol 292: R505-R515, 2007. First published August 24, 2006; doi:10.1152/ajpregu.00381.2006.-To characterize the vasodilatory response in the transition from a single skeletal contraction to a series of contractions, we measured the response of hamster cremaster muscle arterioles associated with four to five skeletal muscle fibers stimulated to contract for one, two, three, or four contractions (250-ms train duration) at 4-s intervals [15 contractions per minute (CPM)] for up to 12 s, at stimulus frequencies of 4, 10, 20, 30, 40, 60, and 80 Hz. To investigate the contribution of contraction frequency, we stimulated muscle fiber bundles at 30 or 60 CPM for 12 s at stimulus frequencies of 4, 20, and 60 Hz. Arteriolar diameters at the site of overlap with the stimulated muscle fibers were measured before and after each contraction. At 15 CPM at 4, 20, and 60 Hz, we observed a peak change in diameter following the first contraction of 1.1 Ϯ 0.1, 1.6 Ϯ 0.2, and 2.1 Ϯ 0.2 m that almost doubled in response to the second contraction (2.0 Ϯ 0.1, 3.0 Ϯ 0.1, and 3.8 Ϯ 0.1 m, respectively), but there was no further dilation following the third or fourth contraction. A similar response occurred at all stimulus and contraction frequencies tested. At 30 and 60 CPM at 60 Hz, the plateau after two contractions was followed by a further increase in diameter to a second plateau at 7-8 s. Therefore, the vasodilatory response in the transition from single to multiple contractions had components that were stimulation parameter dependent and independent and showed a plateauing behavior indicative of rapid changes in either the nature and/or concentration of vasodilators released or changes in vascular reactivity. stimulus frequency; arteriole; muscle contraction; contraction frequency THE PATTERN OF CHANGE IN BLOOD flow in response to skeletal muscle contractions is a multiphase process with an initial, rapid increase at the onset of contractions, followed by a slower change to a steady state over time (for example, Refs. 4,9,35,40,47,54,59). While vascular compression was thought to be the major process in developing the initial, rapid hyperemia (for review, see Ref. 55), rapid vasodilation has been conclusively identified as an important component of this response (21,30,33,41,57). The identity of the dilators responsible for the rapid dilation remain unclear. Since Gaskell (19), it has been hypothesized that the vasodilation responsible for the changes in blood flow in response to skeletal muscle contraction is due, in part, to dilatory products released from the active skeletal muscle cells themselves. Potential vasodilators released as a result of skeletal muscle activation and metabolism have been identified (for review, see Refs. 12, 27), but no single vasoactive substance has emerged as having a consistent, predominantly large contribution, especially at the onset of exercis...
To investigate the role of Adenosine (Ado) in response to a single contraction we stimulated 4–5 skeletal muscle fibres in a hamster cremaster preparation and measured the diameter of arterioles at the site of overlap with the stimulated muscle fibres before and after a single contraction (250ms train duration) at 4, 20 and 60Hz. Muscle fibres were stimulated prior to and following 30min incubation with Ado receptor antagonists 1,3‐dipropyl‐8‐sulphophenylxanthine (DPSPX, 10−5M) or xanthine amine congener (XAC,10−6M), or ecto‐5′‐nucleotidase inhibitor adenosine 5′‐[α,β‐methylene]diphosphate (AMPCP,10−5M). A dilation within 10s was observed at 4, 20 and 60Hz (1.0±0.2; 1.5±0.2; 2.0±0.2μm respectively) which was significantly attenuated by DPSPX (4Hz −0.1±0.2; 20Hz −0.2±0.3; 60Hz 0.04±0.2μm), XAC (4Hz 0.5±0.2; 20Hz 1.0±0.2; 60Hz 0.3±0.2μm), and AMPCP (4Hz 0.03±0.1; 20Hz −0.3±0.3; 60Hz −0.3±0.2μm). A secondary dilation at 20s at 20Hz (1.4±0.3μm) and 60Hz (1.1±0.1μm) was significantly attenuated by DPSPX (20Hz −0.1±0.1; 60Hz −0.1±0.3μm), XAC (20Hz 0.3±0.2; 60Hz 0.5±0.2) and AMPCP (20Hz 0.2±0.2; 60Hz 0.02±0.1μm). These findings implicate Ado in the vasodilations in response to a single muscle contraction.NSERC
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