Studies on the perfused rabbit ear artery preparation showed that withdrawal of Mg 2+ from extracellular fluid potentiated the responses to histamine and ATP but not to catecholamines. Similar results were obtained in [2xCa2+] Krebs solution. Increases in [Mg 2+] decreased responses to the three agonists to a similar extent. In subsequent experiments attempts were made to alter the availability of calcium for contraction induced by these agonists either by changing the [Ca 2+] of the Krebs solution or by using Ca 2+ influx inhibitors, ouabain and ryanodine. The effects of these agonists were compared to those observed when Mg2+ was altered. In general, the results obtained in perfused rabbit ear artery supported the hypothesis that changes in extracellular [Mg2+] affect the availability of calcium for contraction but were not consistent with the suggestion that Mg2+ alters Ca2+ influx. In a second type of preparation tension responses of superfused rings of ear artery were studied. Responses to changes in extracellular [Ca2+] and[ Mg2+] were found to differ slightly from those obtained in the perfused artery. A simultaneously perfused and superfused arterial preparation showed that responses to changes in [ Mg2+] and[Ca2+] were different if the agonist was administered to the adventitial surface of the vessel rather than via the intimal surface. The effects of alterations in extracellular [Mg 2+] were studied in mesenteric arteries from weight matched normotensive and spontaneously hypertensive rats (SHR). No differences in response to NA or ATP when extracellular [Mg 2+ ] was either increased or reduced were observed in the SHR compared to the normotensive animal. However, a difference in calcium dependence was demonstrated between the two types of vessels to NA. In contrast to mesenteric arteries, experiments on aortae from normotensive rats and SHR showed no differences in the calcium dependence of NA responses between normotensive and SHR vessels, whereas, [4xMg2+ ] Krebs solution reduced the responses of normotensive aorta to NA more than SHR. These results in the rat were not consistent with the hypothesis that alteration in [Mg 2+] can be explained in terms of altered calcium availability. Attempts to increase intracellular cyclic AMP with theophylline showed that the response to ED50 NA in both mesenteric arteries and aortae from normotensive were reduced more than SHR. It is concluded that the effect of changes in extracellular [Mg2+] on the reactivity of vascular muscle varies depending on the type of vessel and species of animal from which the vessel is taken. In addition when all the experimental results are considered, it is not possible to explain all the actions of altered [ Mg2+ ] simply in terms of changed calcium availability.

Studies on the perfused rabbit ear artery preparation showed that withdrawal of Mg 2+ from extracellular fluid potentiated the responses to histamine and ATP but not to catecholamines. Similar results were obtained in [2xCa2+] Krebs solution. Increases in [Mg 2+] decreased responses to the three agonists to a similar extent. In subsequent experiments attempts were made to alter the availability of calcium for contraction induced by these agonists either by changing the [Ca 2+] of the Krebs solution or by using Ca 2+ influx inhibitors, ouabain and ryanodine. The effects of these agonists were compared to those observed when Mg2+ was altered. In general, the results obtained in perfused rabbit ear artery supported the hypothesis that changes in extracellular [Mg2+] affect the availability of calcium for contraction but were not consistent with the suggestion that Mg2+ alters Ca2+ influx. In a second type of preparation tension responses of superfused rings of ear artery were studied. Responses to changes in extracellular [Ca2+] and[ Mg2+] were found to differ slightly from those obtained in the perfused artery. A simultaneously perfused and superfused arterial preparation showed that responses to changes in [ Mg2+] and[Ca2+] were different if the agonist was administered to the adventitial surface of the vessel rather than via the intimal surface. The effects of alterations in extracellular [Mg 2+] were studied in mesenteric arteries from weight matched normotensive and spontaneously hypertensive rats (SHR). No differences in response to NA or ATP when extracellular [Mg 2+ ] was either increased or reduced were observed in the SHR compared to the normotensive animal. However, a difference in calcium dependence was demonstrated between the two types of vessels to NA. In contrast to mesenteric arteries, experiments on aortae from normotensive rats and SHR showed no differences in the calcium dependence of NA responses between normotensive and SHR vessels, whereas, [4xMg2+ ] Krebs solution reduced the responses of normotensive aorta to NA more than SHR. These results in the rat were not consistent with the hypothesis that alteration in [Mg 2+] can be explained in terms of altered calcium availability. Attempts to increase intracellular cyclic AMP with theophylline showed that the response to ED50 NA in both mesenteric arteries and aortae from normotensive were reduced more than SHR. It is concluded that the effect of changes in extracellular [Mg2+] on the reactivity of vascular muscle varies depending on the type of vessel and species of animal from which the vessel is taken. In addition when all the experimental results are considered, it is not possible to explain all the actions of altered [ Mg2+ ] simply in terms of changed calcium availability.

Low-load blood flow restriction (LLBFR) training has been shown to elicit greater increases in muscle hypertrophy and strength compared to traditional low-load training, yet few studies have compared the effectiveness of different LLBFR protocols. To our knowledge, no previous study has compared the acute neuromuscular changes induced by two common LLBFR protocols: 30-15-15-15 repetitions (BFR-75) and four sets of repetitions performed to volitional failure (BFR-F). Therefore, the purpose of this study was to use surface electromyography (sEMG) to compare changes in muscle excitation and fatigue during BFR-75 and BFR-F protocols. Ten women (mean ± SD age = 22 ± 3.5 years) volunteered to participate in this investigation. Participants performed isokinetic, unilateral, concentric-eccentric, leg extension muscle actions at 30% maximal voluntary isometric contraction torque with BFR applied at 60% arterial occlusion pressure using a 12-centimeter-wide cuff. The sEMG amplitude and frequency values were measured from the rectus femoris muscle during the beginning and end of each set of exercise and analyzed using separate 2 [condition (BFR-75 and BFR-F)] x 8 [time (B1, E1, B2, E2, B3, E3, B4, E4)] repeated measures ANOVAs. For sEMG amplitude, there was no significant 2-way interaction (p = 0.486; ηₚ² = 0.118) or significant main effect for condition (p = 0.617; ηₚ² = 0.038), but there was a significant main effect for time (p < 0.001; ηₚ² = 0.520). SEMG amplitude increased across time during both protocols (B1 < E1, E2, B3, E3, B4, E4, p ≤ 0.001–0.049). For sEMG frequency, there was no significant 2-way interaction (p = 0.847; ηₚ² = 0.064) or significant main effect for condition (p = 0.825; ηₚ² = 0.007), but there was a significant main effect for time (p = 0.006; ηₚ² = 0.478). SEMG frequency decreased across time during both protocols (B1 > E1, B2, E2, B3, E3, B4, E4, p = 0.002–0.035). Thus, the implementation of the BFR-75 and BFR-F protocols elicited comparable neuromuscular responses that were consistent with fatiguing exercise, but investigators and clinicians may consider other factors such as participant/patient comfort, time, and rating of perceived exertion when determining which protocol to use.