The Experts below are selected from a list of 327 Experts worldwide ranked by ideXlab platform
Marcos A. Sanchez-gonzalez - One of the best experts on this subject based on the ideXlab platform.
-
Whole-body vibration attenuates the increase in leg arterial stiffness and aortic systolic blood pressure during post-exercise Muscle Ischemia
European Journal of Applied Physiology, 2011Co-Authors: Arturo Figueroa, Ryan Gil, Marcos A. Sanchez-gonzalezAbstract:Exercise with whole-body vibration (WBV) decreases brachial-ankle pulse wave velocity (baPWV), a marker of systemic arterial stiffness. To examine the effect of WBV on arterial responses, 12 young men underwent three experimental trials: (1) no-exercise control (CON), (2) static squat with WBV, and (3) static squat without WBV (no-WBV). Bilateral baPWV and femoral-ankle PWV (faPWV), carotid-femoral PWV (cfPWV), augmentation index (AIx), first (P1) and second (P2) systolic peaks, aortic systolic blood pressure (aSBP), and heart rate (HR) were assessed at rest, during 4-min post-exercise Muscle Ischemia (PEMI) on the left thigh, and 4-min recovery. During PEMI, right faPWV increased ( P
-
Whole-body vibration attenuates the increase in leg arterial stiffness and aortic systolic blood pressure during post-exercise Muscle Ischemia.
European journal of applied physiology, 2010Co-Authors: Arturo Figueroa, Ryan Gil, Marcos A. Sanchez-gonzalezAbstract:Exercise with whole-body vibration (WBV) decreases brachial-ankle pulse wave velocity (baPWV), a marker of systemic arterial stiffness. To examine the effect of WBV on arterial responses, 12 young men underwent three experimental trials: (1) no-exercise control (CON), (2) static squat with WBV, and (3) static squat without WBV (no-WBV). Bilateral baPWV and femoral-ankle PWV (faPWV), carotid-femoral PWV (cfPWV), augmentation index (AIx), first (P1) and second (P2) systolic peaks, aortic systolic blood pressure (aSBP), and heart rate (HR) were assessed at rest, during 4-min post-exercise Muscle Ischemia (PEMI) on the left thigh, and 4-min recovery. During PEMI, right faPWV increased (P < 0.05) after no-WBV and did not change after CON and WBV. Right baPWV, P2, and aSBP increased (P < 0.05) after both exercise trials, but the increase was lower (P < 0.05) after WBV than no-WBV. The increases in cfPWV (P < 0.05), AIx (P < 0.05), P1 (P < 0.01), and HR (P < 0.05) were similar in both trials during PEMI. During recovery, right faPWV and baPWV remained similar than rest after WBV and CON, but remained elevated (P < 0.05) after no-WBV. Aortic SBP, P1, and P2 remained elevated (P < 0.05) in both exercise trials during recovery, but the levels were lower (P < 0.05) than PEMI. Left faPWV and baPWV were reduced (P < 0.05) from rest in the three trials. CfPWV, AIx, and HR returned to resting levels in both exercises. WBV prevents the increases in faPWV and attenuates the increase in baPWV and aSBP induced by post-static squat Muscle Ischemia due to an attenuated P2 response.
Arturo Figueroa - One of the best experts on this subject based on the ideXlab platform.
-
Whole-body vibration attenuates the increase in leg arterial stiffness and aortic systolic blood pressure during post-exercise Muscle Ischemia
European Journal of Applied Physiology, 2011Co-Authors: Arturo Figueroa, Ryan Gil, Marcos A. Sanchez-gonzalezAbstract:Exercise with whole-body vibration (WBV) decreases brachial-ankle pulse wave velocity (baPWV), a marker of systemic arterial stiffness. To examine the effect of WBV on arterial responses, 12 young men underwent three experimental trials: (1) no-exercise control (CON), (2) static squat with WBV, and (3) static squat without WBV (no-WBV). Bilateral baPWV and femoral-ankle PWV (faPWV), carotid-femoral PWV (cfPWV), augmentation index (AIx), first (P1) and second (P2) systolic peaks, aortic systolic blood pressure (aSBP), and heart rate (HR) were assessed at rest, during 4-min post-exercise Muscle Ischemia (PEMI) on the left thigh, and 4-min recovery. During PEMI, right faPWV increased ( P
-
Whole-body vibration attenuates the increase in leg arterial stiffness and aortic systolic blood pressure during post-exercise Muscle Ischemia.
European journal of applied physiology, 2010Co-Authors: Arturo Figueroa, Ryan Gil, Marcos A. Sanchez-gonzalezAbstract:Exercise with whole-body vibration (WBV) decreases brachial-ankle pulse wave velocity (baPWV), a marker of systemic arterial stiffness. To examine the effect of WBV on arterial responses, 12 young men underwent three experimental trials: (1) no-exercise control (CON), (2) static squat with WBV, and (3) static squat without WBV (no-WBV). Bilateral baPWV and femoral-ankle PWV (faPWV), carotid-femoral PWV (cfPWV), augmentation index (AIx), first (P1) and second (P2) systolic peaks, aortic systolic blood pressure (aSBP), and heart rate (HR) were assessed at rest, during 4-min post-exercise Muscle Ischemia (PEMI) on the left thigh, and 4-min recovery. During PEMI, right faPWV increased (P < 0.05) after no-WBV and did not change after CON and WBV. Right baPWV, P2, and aSBP increased (P < 0.05) after both exercise trials, but the increase was lower (P < 0.05) after WBV than no-WBV. The increases in cfPWV (P < 0.05), AIx (P < 0.05), P1 (P < 0.01), and HR (P < 0.05) were similar in both trials during PEMI. During recovery, right faPWV and baPWV remained similar than rest after WBV and CON, but remained elevated (P < 0.05) after no-WBV. Aortic SBP, P1, and P2 remained elevated (P < 0.05) in both exercise trials during recovery, but the levels were lower (P < 0.05) than PEMI. Left faPWV and baPWV were reduced (P < 0.05) from rest in the three trials. CfPWV, AIx, and HR returned to resting levels in both exercises. WBV prevents the increases in faPWV and attenuates the increase in baPWV and aSBP induced by post-static squat Muscle Ischemia due to an attenuated P2 response.
-
Cardiovagal baroreflex and aortic hemodynamic responses to isometric exercise and post-exercise Muscle Ischemia in resistance trained men.
Scandinavian journal of medicine & science in sports, 2009Co-Authors: Arturo Figueroa, Shirin Hooshmand, M. Figueroa, A. M. BadaAbstract:Arterial stiffness is associated with reduced baroreflex sensitivity (BRS) and resistance training; thus a potentially increased cardiovascular risk in resistance-trained (RT) individuals. The effects of resistance training on arterial stiffness and BRS have been evaluated at rest, but cardiovascular abnormalities that are not shown at rest may be revealed during recovery after exercise. Aortic systolic (aSBP) and diastolic blood pressure (aDBP), stroke volume (SV), augmentation index (AIx), vagal activity, BRS responses to isometric handgrip (IHG), and post-exercise Muscle Ischemia (PEMI) were evaluated in 10 RT and 10 untrained (UT) men (21+/-1 years). Resting aDBP and AIx were lower in RT compared with UT. Heart rate recovery, BRS, and vagal reactivation during PEMI were similar in both groups. Increases in aSBP (13+/-11 mmHg), AIx (5+/-10%), and SV (12+/-12%) during IHG further increased during PEMI (8+/-14 mmHg, 12+/-6%, and 10+/-8%). Increases in aDBP from rest to PEMI were higher in RT (17+/-9 mmHg) compared with UT (7+/-8 mmHg). The lower resting aDBP and the enhanced response to PEMI suggest beneficial adaptations in RT men. Wave reflection, aortic SBP, and cardiovagal BRS responses to IHG and PEMI are not affected by resistance training in young healthy men.
Edith Tzeng - One of the best experts on this subject based on the ideXlab platform.
-
MyD88 and TRIF mediate divergent inflammatory and regenerative responses to skeletal Muscle Ischemia.
Physiological reports, 2014Co-Authors: Ulka Sachdev, Xiangdong Cui, Edith TzengAbstract:We have previously shown that MyD88 KO mice appear protected from ischemic Muscle injury while TRIF KO mice exhibit sustained necrosis after femoral artery ligation (FAL). However, our previous data did not differentiate whether the protective effect of absent MyD88 signaling was secondary to attenuated injury after FAL or quicker recovery from the insult. The purpose of this study was to delineate these different possibilities. On the basis of previous findings, we hypothesized that MyD88 signaling promotes enhanced inflammation while TRIF mediates regeneration after skeletal Muscle Ischemia. Our results show that after FAL, both MyD88 KO mice and TRIF KO mice have evidence of Ischemia, as do their control counterparts. However, MyD88 KO mice had lower levels of serum IL-6 24 h after FAL, while TRIF KO mice demonstrated sustained serum IL-6 up to 1 week after injury. Additionally, MyD88 KO mice had higher nuclear content and larger myofibers than control animals 1 week after injury. IL-6 is known to have differential effects in myoblast function, and can inhibit proliferation and differentiation. In tibialis anterior Muscle harvested from injured animals, IL-6 levels were higher and the proliferative marker MyoD was lower in TRIF KO mice by PCR. Furthermore, expression of MyD88 appeared to be higher in skeletal Muscle of TRIF KO mice. In vitro, we showed that myoblast differentiation and proliferation were attenuated in response to IL-6 treatment giving credence to the finding that low IL-6 in MyD88 KO mice may be responsible for larger myocyte sizes 1 week after FAL. We conclude that MyD88 and TRIF work in concert to mediate a balanced response to ischemic injury.
-
Abstract 234: MyD88 and TRIF Mediate Divergent Responses Following Skeletal Muscle Ischemia
Arteriosclerosis Thrombosis and Vascular Biology, 2012Co-Authors: Ulka Sachdev, Xiangdong Cui, Ryan M. Mcenaney, Edith TzengAbstract:Introduction: We have shown that TLR2 mediates Muscle regeneration and angiogenesis after Muscle Ischemia, independent of TLR4. Downstream signaling of TLR2 and TLR4 include MyD88 (TLR2 and 4) and TRIF (TLR4 and 3) pathways. We hypothesize that MyD88 is required for normal angiogenesis and Muscle regeneration following Ischemia while TRIF is not. Methods: MyD88 -/- (KO), TRIF KO and control C57B6 mice (WT) (N=4-7) underwent femoral artery ligation on the right hindlimb, and sham operation on the left. LDPI was performed at day 14 and anterior tibialis Muscle was collected to quantify Muscle necrosis and regeneration. Vascular structures were identified with CD31 staining. Results: MyD88 KO and WT mice demonstrated partial perfusion recovery by 14 days while TRIF KO had minimal recovery. Despite this, there were significantly fewer vascular structures in MyD88 KO mice while TRIF KO had the greatest (17.9±1.5 MyD88 KO; 55.3±6.8 WT; 69.1±5.2 TRIF KO; p Conclusions: Contrary to our hypothesis, TRIF appears to be required for normal Muscle regeneration and functional angiogenesis after Ischemia, while MyD88 is an important mediator of hypoxic injury. These results, along with our prior findings that Muscle regeneration is independent of TLR4, suggest that TLR3 may play a key role in ischemic Muscle recovery independent of angiogenesis.
William A. Zamboni - One of the best experts on this subject based on the ideXlab platform.
-
Acute microvascular action of vascular endothelial growth factor in skeletal Muscle Ischemia/reperfusion injury.
Plastic and reconstructive surgery, 2005Co-Authors: Wei Z. Wang, Xin-hua Fang, Linda L. Stepheson, Kayvan T. Khiabani, William A. ZamboniAbstract:Background: The purpose of this study was to investigate the acute action of vascular endothelial growth factor (VEGF) in the microcirculation of skeletal Muscle subject to Ischemia/reperfusion in vivo and to determine the role of nitric oxide synthase in VEGF-induced microvascular protection. Methods: A vascular pedicle isolated rat cremaster Muscle model coupled with local intraarterial infusion technique was used. Each Muscle underwent 4 hours of zero-flow warm Ischemia followed by 2 hours of reperfusion. Femoral artery cannulation was performed before reperfusion. The infusate was administered by continuous infusion into the arterial tree of the Muscle beginning at 1 minute before reperfusion and at the rate of 0.1 ml/hour throughout the entire reperfusion period. Three groups were designed: (1) the Ischemia/reperfusion group, with infusion normal saline; (2) the VEGF plus Ischemia/reperfusion group, with infusion of recombinant human VEGF 165 protein; and (3) the L-NA plus VEGF plus Ischemia/reperfusion group, with infusion of N w -nitro-L-arginine (L-NA; a nonselective nitric oxide synthase antagonist) mixed with VEGF 165 protein. After 2 hours of reperfusion, microcirculation measurements including arteriole diameter, capillary perfusion, and endothelium-dependent and endothelium-independent vasodilatation were performed. The Muscle was harvested and processed for reverse-transcriptase polymerase chain reaction for measuring eNOS and endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) gene expression. Results: Reperfusion caused significant microvascular alterations including vasocon-striction, poor capillary perfusion, and endothelial dysfunction in the skeletal Muscle. These alterations were significantly attenuated by intraarterial infusion of VEGF during reperfusion, but the beneficial effect of VEGF was reduced significantly by coadministration of L-NA. Reverse-transcriptase polymerase chain reaction study revealed that Ischemia/reperfusion depressed eNOS mRNA expression but enhanced iNOS mRNA expression. Intraarterial infusion of VEGF during reperfusion amplified mRNA expression of eNOS but not of iNOS. Conclusions: Local intraarterial infusion of VEGF produced significant microvascular protection from skeletal Muscle Ischemia/reperfusion injury. The VEGF-induced enhancement of eNOS may play an important mechanistic role.
Donal S. O'leary - One of the best experts on this subject based on the ideXlab platform.
-
Attenuated Muscle metaboreflex-induced pressor response during postexercise Muscle Ischemia in renovascular hypertension
American journal of physiology. Regulatory integrative and comparative physiology, 2015Co-Authors: Marty D. Spranger, Jasdeep Kaur, Javier A. Sala-mercado, Abhinav C. Krishnan, Alberto Alvarez, Tiago M. Machado, Donal S. O'learyAbstract:During dynamic exercise, Muscle metaboreflex activation (MMA; induced via partial hindlimb Ischemia) markedly increases mean arterial pressure (MAP), and MAP is sustained when the Ischemia is maintained following the cessation of exercise (postexercise Muscle Ischemia, PEMI). We previously reported that the sustained pressor response during PEMI in normal individuals is driven by a sustained increase in cardiac output (CO) with no peripheral vasoconstriction. However, we have recently shown that the rise in CO with MMA is significantly blunted in hypertension (HTN). The mechanisms sustaining the pressor response during PEMI in HTN are unknown. In six chronically instrumented canines, hemodynamic responses were observed during rest, mild exercise (3.2 km/h), MMA, and PEMI in the same animals before and after the induction of HTN [Goldblatt two kidney, one clip (2K1C)]. In controls, MAP, CO and HR increased with MMA (+52 ± 6 mmHg, +2.1 ± 0.3 l/min, and +37 ± 7 beats per minute). After induction of HTN, MAP at rest increased from 97 ± 3 to 130 ± 4 mmHg, and the metaboreflex responses were markedly attenuated (+32 ± 5 mmHg, +0.6 ± 0.2 l/min, and +11 ± 3 bpm). During PEMI in HTN, HR and CO were not sustained, and MAP fell to normal recovery levels. We conclude that the attenuated metaboreflex-induced HR, CO, and MAP responses are not sustained during PEMI in HTN.
-
Mechanisms mediating the Muscle metaboreflex pressor response during post-exercise Muscle Ischemia are altered in hypertension (1170.2)
The FASEB Journal, 2014Co-Authors: Marty D. Spranger, Jasdeep Kaur, Javier A. Sala-mercado, Abhinav C. Krishnan, Alberto Alvarez, Donal S. O'learyAbstract:During dynamic exercise, Muscle metaboreflex activation (MMA; induced via partial hindlimb Ischemia) markedly increases mean arterial pressure (MAP) and MAP is sustained when the Ischemia is maintained following the cessation of exercise (post-exercise Muscle Ischemia - PEMI). We previously reported that the sustained pressor response during PEMI in normal individuals is driven by a sustained increase in cardiac output (CO) with no peripheral vasoconstriction. However, we have recently shown that the rise in CO with MMA is significantly blunted in hypertension (HTN). The mechanisms sustaining the pressor response during PEMI in HTN are unknown. In six chronically instrumented canines, hemodynamic responses were observed during rest, mild exercise (3.2 kph), MMA and PEMI in the same animals before and after the induction of HTN (2K1C). In control, MAP, CO and HR increased with MMA (+52 ± 6 mmHg, +2.1 ± 0.3 l/min and +37 ± 7 bpm). After the induction of HTN (MAP at rest increased from 97 ± 3 to 130 ± 4 mmHg...
-
Role of cardiac output versus peripheral vasoconstriction in mediating Muscle metaboreflex pressor responses: dynamic exercise versus postexercise Muscle Ischemia
American journal of physiology. Regulatory integrative and comparative physiology, 2013Co-Authors: Marty D. Spranger, Jasdeep Kaur, Javier A. Sala-mercado, Matthew Coutsos, Doug Stayer, Robert A. Augustyniak, Donal S. O'learyAbstract:Muscle metaboreflex activation (MMA) during submaximal dynamic exercise in normal individuals increases mean arterial pressure (MAP) via increases in cardiac output (CO) with little peripheral vasoconstriction. The rise in CO occurs primarily via increases in heart rate (HR) with maintained or slightly increased stroke volume. When the reflex is sustained during recovery (postexercise Muscle Ischemia, PEMI), HR declines yet MAP remains elevated. The role of CO in mediating the pressor response during PEMI is controversial. In seven chronically instrumented canines, steady-state values with MMA during mild exercise (3.2 km/h) were observed by reducing hindlimb blood flow by ∼60% for 3–5 min. MMA during exercise was followed by 60 s of PEMI. Control experiments consisted of normal exercise and recovery. MMA during exercise increased MAP, HR, and CO by 55.3 ± 4.9 mmHg, 42.5 ± 6.9 beats/min, and 2.5 ± 0.4 l/min, respectively. During sustained MMA via PEMI, MAP remained elevated and CO remained well above the normal recovery levels. Neither MMA during dynamic exercise nor during PEMI significantly affected peripheral vascular conductance. We conclude that the sustained increase in MAP during PEMI is driven by a sustained increase in CO not peripheral vasoconstriction.
