The Experts below are selected from a list of 291 Experts worldwide ranked by ideXlab platform
Jes Olesen - One of the best experts on this subject based on the ideXlab platform.
-
in vivo evidence of altered skeletal muscle blood flow in chronic tension type headache
Headache, 2003Co-Authors: Messoud Ashina, Bente Stallknecht, Lars Bendtsen, Jan Fog Pedersen, H Galbo, Peter Dalgaard, Jes OlesenAbstract:Brain. 2002 Feb;125(Pt 2):320-326 Painful impulses from tender pericranial muscles may play a major role in the pathophysiology of chronic tension-type headache. Firm evidence for peripheral muscle pathology as a cause of muscle pain and chronic headache is still lacking. Using a microdialysis technique, we aimed to estimate in vivo blood flow and interstitial lactate concentrations in the trapezius muscle at rest and during Static Exercise in patients with chronic tension-type headache and in healthy subjects. We recruited 16 patients with chronic tension-type headache and 17 healthy control subjects. Two microdialysis catheters were inserted into the trapezius muscle (on the non-dominant side) of subjects, and dialysates were collected at rest, 15 and 30 min after the start of Static Exercise (10% of maximal force) and 15 and 30 min after the Exercise was completed. All samples were coded and analysed blind. The primary endpoints were to detect a difference between patients and controls in changes of muscle blood flow and the interstitial lactate concentration from baseline to Exercise and post-Exercise periods. The increase in muscle blood flow from baseline to Exercise and post-Exercise periods was significantly lower in patients than controls (P = 0.03). There was no difference in resting blood flow between patients and controls (P = 0.43). Resting interstitial concentration of lactate did not differ between patients (2.51 ± *T0.18 mM; mean ± standard error of the mean) and controls (2.35 ± 0.23 mM, P = 0.57). There was no difference in change in interstitial lactate from baseline to Exercise and post-Exercise periods between patients and controls (P = 0.38). The present study provides in vivo evidence of decreased blood flow in response to Static Exercise in a tender muscle in patients with chronic tension-type headache. We suggest that, because of increased excitability of neurones in the CNS, the central interpretation and response to normal sensory input are altered in patients with chronic tension-type headache. This may lead to enhanced sympathetically mediated vasoconstriction and thereby a decreased blood flow in response to Static Exercise. Comment: An important study which links decreased blood flow in Statically Exercised trapezius muscle in patients with chronic tension-type headache (CTTH) with muscle tenderness. A better understanding of the pathophysiology of CTTH may provide a clue to novel therapeutic maneuvers. DSM
-
tender points are not sites of ongoing inflammation in vivo evidence in patients with chronic tension type headache
Cephalalgia, 2003Co-Authors: Messoud Ashina, Bente Stallknecht, Lars Bendtsen, Jan Fog Pedersen, H Galbo, S Schifter, Jes OlesenAbstract:Increased muscle tenderness is the most prominent finding in patients with tension-type headache, and it has recently been shown that muscle blood flow is diminished in response to Static Exercise in tender points in these patients. Although tenderness has been ascribed to local inflammation and release of inflammatory mediators, the interstitial concentration of inflammatory mediators has not previously been studied in tender muscles of patients with tension-type headache. The aim of the present study was to investigate in vivo concentrations of prostaglandin E2 (PGE2), adenosine 5'-triphosphate (ATP), glutamate, bradykinin and other metabolites in a tender point of patients with chronic tension-type headache, in the resting state as well as in response to Static Exercise, and to compare findings with measurements in a matched non-tender point of healthy controls. We recruited 16 patients with chronic tension-type headache and 17 healthy control subjects. Two microdialysis catheters were inserted into th...
-
in vivo evidence of altered skeletal muscle blood flow in chronic tension type headache
Brain, 2002Co-Authors: Messoud Ashina, Bente Stallknecht, Lars Bendtsen, Jan Fog Pedersen, H Galbo, Peter Dalgaard, Jes OlesenAbstract:Painful impulses from tender pericranial muscles may play a major role in the pathophysiology of chronic tension‐type headache. Firm evidence for peripheral muscle pathology as a cause of muscle pain and chronic headache is still lacking. Using a microdialysis technique, we aimed to estimate in vivo blood flow and interstitial lactate concentrations in the trapezius muscle at rest and during Static Exercise in patients with chronic tension‐type headache and in healthy subjects. We recruited 16 patients with chronic tension‐type headache and 17 healthy control subjects. Two microdialysis catheters were inserted into the trapezius muscle (on the non‐dominant side) of subjects, and dialysates were collected at rest, 15 and 30 min after the start of Static Exercise (10% of maximal force) and 15 and 30 min after the Exercise was completed. All samples were coded and analysed blind. The primary endpoints were to detect a difference between patients and controls in changes of muscle blood flow and the interstitial lactate concentration from baseline to Exercise and post‐Exercise periods. The increase in muscle blood flow from baseline to Exercise and post‐Exercise periods was significantly lower in patients than controls ( P = 0.03). There was no difference in resting blood flow between patients and controls ( P = 0.43). Resting interstitial concentration of lactate did not differ between patients (2.51 ± 0.18 mM; mean ± standard error of the mean) and controls (2.35 ± 0.23 mM, P = 0.57). There was no difference in change in interstitial lactate from baseline to Exercise and post‐Exercise periods between patients and controls ( P = 0.38). The present study provides in vivo evidence of decreased blood flow in response to Static Exercise in a tender muscle in patients with chronic tension‐type headache. We suggest that, because of increased excitability of neurones in the CNS, the central interpretation and response to normal sensory input are altered in patients with chronic tension‐type headache. This may lead to enhanced sympathetically mediated vasoconstriction and thereby a decreased blood flow in response to Static Exercise.
Narihiko Kondo - One of the best experts on this subject based on the ideXlab platform.
-
β adrenergic receptor blockade does not modify non thermal sweating during Static Exercise and following muscle ischemia in habitually trained individuals
European Journal of Applied Physiology, 2018Co-Authors: Tatsuro Amano, Yoshimitsu Inoue, Anna Igarashi, Naoto Fujii, Daichi Hiramatsu, Narihiko KondoAbstract:This study investigated the influence of β-adrenergic receptor blockade on sweating during bilateral Static knee extension (KE) and lateral isometric handgrip (IH) Exercises followed by post-Exercise muscle ischemia (PEMI) in habitually trained individuals. Ten habitually trained men (maximum oxygen uptake, 57.1 ± 3.4 ml kg−1 min−1) were mildly heated by increasing their skin temperature, and bilateral KE or lateral IH Exercises at an intensity of 60% maximum voluntary contraction were subsequently performed for 1 min, followed by PEMI to stimulate muscle metaboreceptors for 2 min. Sweat rates were measured on the bilateral forearms (KE) or thighs (IH) transdermally administered with 1% propranolol (propranolol, a non-selective β-adrenergic receptor inhibitor) or saline (control) via iontophoresis. Relative to the pre-Exercise baseline values, IH Exercise (P = 0.038) followed by PEMI (P = 0.041) similarly increased sweat rates on the thighs at both control and propranolol sites (baseline, 0.05 ± 0.04 vs. 0.05 ± 0.04; IH, 0.14 ± 0.12 vs. 0.15 ± 0.14; PEMI, 0.14 ± 0.16 vs. 0.14 ± 0.16 mg cm−2 min−1). KE increased sweat rates on the forearms (P = 0.001) at both control and propranolol sites similarly (baseline, 0.02 ± 0.03 vs. 0.02 ± 0.03; KE, 0.21 ± 0.19 vs. 0.20 ± 0.18), whereas PEMI did not significantly induce sweating at these sites (P = 0.260) (0.09 ± 0.12 and 0.10 ± 0.12 mg cm−2 min−1, respectively). These results suggest that non-thermal drives induced by Static Exercise and PEMI do not elicit β-adrenergic sweating in habitually trained individuals even when the non-thermal drives are originated from leg(s) under the conditions in the present study.
-
changes in eccrine sweating on the glabrous skin of the palm and finger during isometric Exercise
Acta Physiologica, 2011Co-Authors: Tatsuro Amano, Yoshimitsu Inoue, Christiano A Machadomoreira, Nigel A. S. Taylor, Takeshi Nishiyasu, Y Kato, Narihiko KondoAbstract:AIM: The goals of this study were to investigate changes in the sweating and cutaneous vascular responses on the palm and the volar aspect of the index finger during sustained Static Exercise of increasing intensity and to determine whether the former can be attributed to altered sweat gland activity. METHODS: Five male and five female subjects performed maximal voluntary handgrip contractions (MVC: right hand) for 60 s at 20, 35 and 50% MVC (ambient temperature 25 °C, relative humidity 50%). RESULTS: The sweat rate and the number of activated sweat glands on the non-Exercised hand showed intensity-dependent increases (P < 0.05). At 35 and 50% MVC, finger sweat secretion was significantly higher than on the palm, which was primarily associated with the number of activated sweat glands (P < 0.05). In addition, there was a marked simultaneous decrease in the cutaneous vascular conductance for the finger at 35 and 50% MVC (P < 0.05), but not for the palm. CONCLUSION: Our results suggest that a difference exists between intensity-dependent increases of sudomotor responses within more than one glabrous skin site. Specifically, markedly greater sweating occurs on the volar finger than on the palmar surface during sustained Static Exercise. These differences in sweat rate mainly resulted from changes in the number of activated sweat glands. In addition, intra-segment variations in cutaneous blood flow on the glabrous hand are shown.
-
sweating responses to a sustained Static Exercise is dependent on thermal load in humans
Acta Physiologica Scandinavica, 2002Co-Authors: Narihiko Kondo, Manabu Shibasaki, Yoshimitsu Inoue, Ken Aoki, Takeshi Nishiyasu, N Horikawa, Craig G CrandallAbstract:The purpose of this project was to test the hypothesis that internal temperature modulates the sweating response to sustained handgrip Exercise. Ten healthy male subjects immersed their legs in 43 degrees C water for 30-40 min at an ambient temperatures of 30 degrees C and a relative humidity of 50%. Sweating responses to 50% maximal voluntary contraction isometric handgrip Exercise (IH) were measured following the onset of sweating (i.e. following slight increases in internal temperature), and after more pronounced increases in internal temperature. Oesophageal temperature (Tes) was significantly lower during the first bout of Exercise (37.54 +/- 0.07 degrees C) relative to the second bout (37.84 +/- 0.12 degrees C; P < 0.05). However, the increase in mean sweating rate (SR) from both the chest and forearm (non-glabrous skin) was significantly greater during the first IH bout relative to the second bout (P < 0.05). Increases in mean arterial blood pressure and palm SR (glabrous skin) did not differ significantly between Exercise bouts, while heart rate and rating of perceived effort were significantly greater during the second bout of IH. As Tes and mean skin temperature did not change during either bout of Exercise, the changes in SR from non-glabrous skin between the bouts of IH were likely because of non-thermal factors. These data suggest that sweating responses from non-glabrous skin during IH vary depending on the magnitude of thermal input as indicated by differing internal temperatures between bouts of IH. Moreover, these data suggest that the contribution of non-thermal factors in governing sweating from non-glabrous skin may be greatest when internal temperature is moderate (37.54 degrees C), but has less of an effect after greater elevations in internal temperature (i.e. 37.84 degrees C).
-
Effects of Exercise intensity on the sweating response to a sustained Static Exercise
Journal of Applied Physiology, 2000Co-Authors: Narihiko Kondo, Manabu Shibasaki, Hirotaka Tominaga, Shuichi Okada, Ken Aoki, Takeshi NishiyasuAbstract:To investigate how the sweating response to a sustained handgrip Exercise depends on changes in the Exercise intensity, the sweating response to Exercise was measured in eight healthy male subjects...
Lawrence I Sinoway - One of the best experts on this subject based on the ideXlab platform.
-
Changes of elastic properties of central arteries during acute Static Exercise and lower body negative pressure
European Journal of Applied Physiology, 2008Co-Authors: Charalampos Lydakis, Afsana Momen, Urs A Leuenberger, Cheryl Blaha, Michael Herr, Lawrence I SinowayAbstract:The aim of this investigation was to determine the acute effects of isometric fatiguing handgrip (IFHG) and lower body negative pressure (LBNP) on indices of central arterial stiffness. Thirteen subjects were studied. Renal blood velocity (Duplex Ultrasound) and blood pressure (Finapres) were monitored during IFHG and LBNP at −30 and −50 mmHg. Radial pulse-wave forms were recorded by applanation tonometry. Central aortic waveforms and other hemodynamic parameters were assessed using the Sphygmocor software. Renal vascular resistance index (RVRI; mean BP/renal blood velocity) was used as index of sympathetic nervous system (SNS) engagement. RVRI increased during both IFHG and LBNP indicating that SNS was engaged; however, BP increased only during the IFHG. Pulse-wave analysis showed that during the IFHG protocol the transit time of the pulse wave decreased and the peripheral pulse pressure/nonaugmented central pulse pressure ratio increased from baseline. Both of these measurements suggest an increase in central large artery stiffness. During LBNP no changes in the indices of central stiffness were noted, in spite of a similar level of sympathetic system engagement. Heart rate increased during both protocols, whereas augmentation index increased during the IFHG protocol and decreased during the LBNP. Our major conclusion was that blood pressure rather than sympathetic activity seems to play the major role in modulating the elastic properties of the central arteries. The decrease in augmentation index during the LBNP protocol can be attributed to the increased heart rate, given that there is a negative correlation between these two parameters.
-
changes of central haemodynamic parameters during mental stress and acute bouts of Static and dynamic Exercise
Journal of Human Hypertension, 2008Co-Authors: C Lydakis, Kristen S Gray, Afsana Momen, Urs A Leuenberger, Cheryl Blaha, S Gugoff, Michael D Herr, Lawrence I SinowayAbstract:Chronic dynamic (aerobic) Exercise decreases central arterial stiffness, whereas chronic resistance Exercise evokes the opposite effect. Nevertheless, there is little information available on the effects of acute bouts of Exercise. Also, there is limited data showing an increase of central arterial stiffness during acute mental stress. This study aimed to determine the effect of acute mental and physical (Static and dynamic Exercise) stress on indices of central arterial stiffness. Fifteen young healthy volunteers were studied. The following paradigms were performed: (1) 2 min of mental arithmetic, (2) short bouts (20 s) of Static handgrip at 20 and 70% of maximal voluntary contraction (MVC), (3) fatiguing handgrip at 40% MVC and (4) incremental dynamic knee extensor Exercise. Central aortic waveforms were assessed using SphygmoCor software. As compared to baseline, pulse wave transit time decreased significantly for all four interventions indicating that central arterial stiffness increased. During fatiguing handgrip there was a fall in the ratio of peripheral to central pulse pressure from 1.69+/-0.02 at baseline to 1.56+/-0.05 (P<0.05). In the knee extensor protocol a non-significant trend for the opposite effect was noted. The augmentation index increased significantly during the arithmetic, short Static and fatiguing handgrip protocols, whereas there was no change in the knee extensor protocol. We conclude that (1) during all types of acute stress tested in this study (including dynamic Exercise) estimated central stiffness increased, (2) during Static Exercise the workload posed on the left ventricle (expressed as change in central pulse pressure) is relatively higher than that posed during dynamic Exercise (given the same pulse pressure change in the periphery).
-
influence of sex and active muscle mass on renal vascular responses during Static Exercise
American Journal of Physiology-heart and Circulatory Physiology, 2006Co-Authors: Afsana Momen, Urs A Leuenberger, Brian Handly, Allen R Kunselman, Lawrence I SinowayAbstract:During Exercise, reflex renal vasoconstriction helps maintain blood pressure and redistributes blood flow to the contracting muscle. Sex and muscle mass have been shown to influence certain cardiov...
-
renal vasoconstrictor responses to Static Exercise during orthoStatic stress in humans effects of the muscle mechano and the baroreflexes
The Journal of Physiology, 2006Co-Authors: Afsana Momen, Urs A Leuenberger, Cheryl Blaha, Karen Thomas, Amir Gahremanpour, Ather Mansoor, Lawrence I SinowayAbstract:Renal circulatory adjustments to stress contribute to blood pressure and volume regulation. Both handgrip (HG) and disengagement of baroreflexes with lower body negative pressure (LBNP) can engage the sympathetic nervous system (SNS). However, the effect of simultaneous HG and LBNP on the renal circulation in humans is not known. Eighteen young healthy volunteers were studied. Beat-to-beat changes in renal blood flow velocity (RBV; Duplex Ultrasound), mean arterial pressure (MAP; Finapres) and heart rate (ECG) were monitored during (a) 15 s HG at 30% maximum voluntary contraction (MVC); (b) LBNP at -10 and -30 mmHg (each level for 5 min); and (c) 15 s HG (at 30% MVC) during LBNP at both levels. Renal vascular resistance index (RVR units) was calculated by dividing MAP by RBV. The increases in RVR during HG alone (12 +/- 6%) were not different from the responses noted during combined HG and LBNP (17 +/- 6% at -10 mmHg and 25 +/- 8% at -30 mmHg). These results suggest occlusion occurs between a neural circuit engaged during 15 s of HG (central command and/or the muscle mechanoreflex) and a circuit activated by LBNP. In additional experiments (n = 6), similar non-algebraic summation of RVR was seen during 15 s involuntary biceps contractions (engages only muscle reflexes) and LBNP. With respect to RVR, neural occlusion occurs between baroreflexes and the muscle mechanoreflex. Muscle mechanoreflex mediated renal vasoconstriction during short bouts of HG is not influenced by baroreflex disengagement.
-
renal vascular response to Static handgrip Exercise sympathetic vs autoregulatory control
American Journal of Physiology-heart and Circulatory Physiology, 2005Co-Authors: Afsana Momen, Urs A Leuenberger, Brian Handly, Douglas Bower, John P Boehmer, Susan M Lerner, Edward J Alfrey, Lawrence I SinowayAbstract:Static Exercise causes activation of the sympathetic nervous system, which results in increased blood pressure (BP) and renal vascular resistance (RVR). The question arises as to whether renal vasoconstriction that occurs during Static Exercise is due to sympathetic activation and/or related to a pressure-dependent renal autoregulatory mechanism. To address this issue, we monitored renal blood flow velocity (RBV) responses to two different handgrip (HG) Exercise paradigms in 7 kidney transplant recipients (RTX) and 11 age-matched healthy control subjects. Transplanted kidneys are functionally denervated. Beat-by-beat analyses of changes in RBV (observed via duplex ultrasound), BP, and heart rate were performed during HG Exercise in all subjects. An index of RVR was calculated as BP/RBV. In protocol 1, fatiguing HG Exercise (40% of maximum voluntary contraction) led to significant increases in RVR in both groups. However, at the end of Exercise, RVR was more than fourfold higher in control subjects than in the RTX group (88 vs. 20% increase over baseline; interaction, P < 0.001). In protocol 2, short bouts of HG Exercise (15 s) led to significant increases in RVR at higher workloads (50 and 70% of maximum voluntary contraction) in the control subjects (P < 0.001). RVR did not increase in the RTX group. In conclusion, we observed grossly attenuated renal vasoconstrictor responses to Exercise in RTX subjects, in whom transplanted kidneys were considered functionally denervated. Our results suggest that renal vasoconstrictor responses to Exercise in conscious humans are mainly dependent on activation of a neural mechanism.
Kanji Matsukawa - One of the best experts on this subject based on the ideXlab platform.
-
central command does not suppress baroreflex control of cardiac sympathetic nerve activity at the onset of spontaneous motor activity in the decerebrate cat
Journal of Applied Physiology, 2016Co-Authors: Kanji Matsukawa, Kei Ishii, Ryota Asahara, Mitsuhiro IdesakoAbstract:Our laboratory has reported that central command blunts the sensitivity of the aortic baroreceptor-heart rate (HR) reflex at the onset of voluntary Static Exercise in animals. We have examined whether baroreflex control of cardiac sympathetic nerve activity (CSNA) and/or cardiovagal baroreflex sensitivity are altered at the onset of spontaneously occurring motor behavior, which was monitored with tibial nerve activity in paralyzed, decerebrate cats. CSNA exhibited a peak increase (126 ± 17%) immediately after Exercise onset, followed by increases in HR and mean arterial pressure (MAP). With development of the pressor response, CSNA and HR decreased near baseline, although spontaneous motor activity was not terminated. Atropine methyl nitrate (0.1-0.2 mg/kg iv) with little central influence delayed the initial increase in HR but did not alter the response magnitudes of HR and CSNA, while atropine augmented the pressor response. The baroreflex-induced decreases in CSNA and HR elicited by brief occlusion of the abdominal aorta were challenged at the onset of spontaneous motor activity. Spontaneous motor activity blunted the baroreflex reduction in HR by aortic occlusion but did not alter the baroreflex inhibition of CSNA. Similarly, atropine abolished the baroreflex reduction in HR but did not influence the baroreflex inhibition of CSNA. Thus it is likely that central command increases CSNA and decreases cardiac vagal outflow at the onset of spontaneous motor activity while preserving baroreflex control of CSNA. Accordingly, central command must attenuate cardiovagal baroreflex sensitivity against an excess rise in MAP as estimated from the effect of muscarinic blockade.
-
differential contribution of central command to the cardiovascular responses during Static Exercise of ankle dorsal and plantar flexion in humans
Journal of Applied Physiology, 2011Co-Authors: Kanji Matsukawa, Nan Liang, Tomoko Nakamoto, Seina MochizukiAbstract:To examine whether central command contributes differently to the cardiovascular responses during voluntary Static Exercise engaged by different muscle groups, we encouraged healthy subjects to perform voluntary and electrically evoked involuntary Static Exercise of ankle dorsal and plantar flexion. Each Exercise was conducted with 25% of the maximum voluntary force of the right ankle dorsal and plantar flexion, respectively, for 2 min. Heart rate (HR) and mean arterial blood pressure (MAP) were recorded, and stroke volume, cardiac output (CO), and total peripheral resistance were calculated. With voluntary Exercise, HR, MAP, and CO significantly increased during dorsal flexion (the maximum increase, HR: 12 ± 2.3 beats/min; MAP: 14 ± 2.0 mmHg; CO: 1 ± 0.2 l/min), whereas only MAP increased during plantar flexion (the maximum increase, 6 ± 2.0 mmHg). Stroke volume and total peripheral resistance were unchanged throughout the two kinds of voluntary Static Exercise. With involuntary Exercise, there were no significant changes in all cardiovascular variables, irrespective of dorsal or plantar flexion. Furthermore, before the force onset of voluntary Static Exercise, HR and MAP started to increase without muscle contraction, whereas they had no significant changes with involuntary Exercise at the moment. The present findings indicate that differential contribution of central command is responsible for the different cardiovascular responses to Static Exercise, depending on the strength of central control of the contracting muscle.
-
control of heart rate variability by cardiac parasympathetic nerve activity during voluntary Static Exercise in humans with tetraplegia
Journal of Applied Physiology, 2007Co-Authors: Makoto Takahashi, Akihiro Sakaguchi, Kanji Matsukawa, Kotaro Kawaguchi, Tomoko Nakamoto, Hirotsugu Tsuchimochi, Kiyoshi OnariAbstract:Heart rate (HR) is controlled solely by via cardiac parasympathetic outflow in tetraplegic individuals, who lack supraspinal control of sympathetic outflows and circulating catecholamines but have intact vagal pathways. A high-frequency component (HF; at 0.15-0.40 Hz) of the power spectrum of HR variability and its relative value against total power (HF/Total) were assessed using a wavelet transform to identify cardiac parasympathetic outflow. The relative contribution of cardiac parasympathetic and sympathetic outflows to controlling HR was estimated by comparing the HF/Total-HR relationship between age-matched tetraplegic and normal men. Six tetraplegic men with complete cervical spinal cord injury performed Static arm Exercise at 35% of the maximal voluntary contraction until exhaustion. Although resting cardiac output and arterial blood pressure were lower in tetraplegic than normal subjects, HR, HF, and HF/Total were not statistically different between the two groups. When tetraplegic subjects developed the same force during Exercise as normal subjects, HF and HF/Total decreased to 67-90% of the preExercise control and gradually recovered 1.5 min after Exercise. The amount and time course of the changes in HF/Total during and after Exercise coincided well between both groups. In contrast, the increase in HR at the start of Exercise was blunted in tetraplegic compared with normal subjects, and the HR recovery following Exercise was also delayed. It is likely that, although the withdrawal response of cardiac parasympathetic outflow is preserved in tetraplegic subjects, sympathetic decentralization impairs the rapid acceleration of HR at the onset of Exercise and the rapid deceleration following Exercise.
-
gadolinium does not blunt the cardiovascular responses at the onset of voluntary Static Exercise in cats a predominant role of central command
American Journal of Physiology-heart and Circulatory Physiology, 2007Co-Authors: Kanji Matsukawa, Tomoko Nakamoto, Atsushi InomotoAbstract:The cardiovascular adaptation at the onset of voluntary Static Exercise is controlled by the autonomic nervous system. Two neural mechanisms are responsible for the cardiovascular adaptation: one i...
-
central command blunts sensitivity of arterial baroreceptor heart rate reflex at onset of voluntary Static Exercise
American Journal of Physiology-heart and Circulatory Physiology, 2006Co-Authors: Kanji Matsukawa, Hidehiko Komine, Tomoko Nakamoto, Jun MurataAbstract:We have reported that baroreflex bradycardia by stimulation of the aortic depressor nerve is blunted at the onset of voluntary Static Exercise in conscious cats. Central command may contribute to t...
Messoud Ashina - One of the best experts on this subject based on the ideXlab platform.
-
in vivo evidence of altered skeletal muscle blood flow in chronic tension type headache
Headache, 2003Co-Authors: Messoud Ashina, Bente Stallknecht, Lars Bendtsen, Jan Fog Pedersen, H Galbo, Peter Dalgaard, Jes OlesenAbstract:Brain. 2002 Feb;125(Pt 2):320-326 Painful impulses from tender pericranial muscles may play a major role in the pathophysiology of chronic tension-type headache. Firm evidence for peripheral muscle pathology as a cause of muscle pain and chronic headache is still lacking. Using a microdialysis technique, we aimed to estimate in vivo blood flow and interstitial lactate concentrations in the trapezius muscle at rest and during Static Exercise in patients with chronic tension-type headache and in healthy subjects. We recruited 16 patients with chronic tension-type headache and 17 healthy control subjects. Two microdialysis catheters were inserted into the trapezius muscle (on the non-dominant side) of subjects, and dialysates were collected at rest, 15 and 30 min after the start of Static Exercise (10% of maximal force) and 15 and 30 min after the Exercise was completed. All samples were coded and analysed blind. The primary endpoints were to detect a difference between patients and controls in changes of muscle blood flow and the interstitial lactate concentration from baseline to Exercise and post-Exercise periods. The increase in muscle blood flow from baseline to Exercise and post-Exercise periods was significantly lower in patients than controls (P = 0.03). There was no difference in resting blood flow between patients and controls (P = 0.43). Resting interstitial concentration of lactate did not differ between patients (2.51 ± *T0.18 mM; mean ± standard error of the mean) and controls (2.35 ± 0.23 mM, P = 0.57). There was no difference in change in interstitial lactate from baseline to Exercise and post-Exercise periods between patients and controls (P = 0.38). The present study provides in vivo evidence of decreased blood flow in response to Static Exercise in a tender muscle in patients with chronic tension-type headache. We suggest that, because of increased excitability of neurones in the CNS, the central interpretation and response to normal sensory input are altered in patients with chronic tension-type headache. This may lead to enhanced sympathetically mediated vasoconstriction and thereby a decreased blood flow in response to Static Exercise. Comment: An important study which links decreased blood flow in Statically Exercised trapezius muscle in patients with chronic tension-type headache (CTTH) with muscle tenderness. A better understanding of the pathophysiology of CTTH may provide a clue to novel therapeutic maneuvers. DSM
-
tender points are not sites of ongoing inflammation in vivo evidence in patients with chronic tension type headache
Cephalalgia, 2003Co-Authors: Messoud Ashina, Bente Stallknecht, Lars Bendtsen, Jan Fog Pedersen, H Galbo, S Schifter, Jes OlesenAbstract:Increased muscle tenderness is the most prominent finding in patients with tension-type headache, and it has recently been shown that muscle blood flow is diminished in response to Static Exercise in tender points in these patients. Although tenderness has been ascribed to local inflammation and release of inflammatory mediators, the interstitial concentration of inflammatory mediators has not previously been studied in tender muscles of patients with tension-type headache. The aim of the present study was to investigate in vivo concentrations of prostaglandin E2 (PGE2), adenosine 5'-triphosphate (ATP), glutamate, bradykinin and other metabolites in a tender point of patients with chronic tension-type headache, in the resting state as well as in response to Static Exercise, and to compare findings with measurements in a matched non-tender point of healthy controls. We recruited 16 patients with chronic tension-type headache and 17 healthy control subjects. Two microdialysis catheters were inserted into th...
-
in vivo evidence of altered skeletal muscle blood flow in chronic tension type headache
Brain, 2002Co-Authors: Messoud Ashina, Bente Stallknecht, Lars Bendtsen, Jan Fog Pedersen, H Galbo, Peter Dalgaard, Jes OlesenAbstract:Painful impulses from tender pericranial muscles may play a major role in the pathophysiology of chronic tension‐type headache. Firm evidence for peripheral muscle pathology as a cause of muscle pain and chronic headache is still lacking. Using a microdialysis technique, we aimed to estimate in vivo blood flow and interstitial lactate concentrations in the trapezius muscle at rest and during Static Exercise in patients with chronic tension‐type headache and in healthy subjects. We recruited 16 patients with chronic tension‐type headache and 17 healthy control subjects. Two microdialysis catheters were inserted into the trapezius muscle (on the non‐dominant side) of subjects, and dialysates were collected at rest, 15 and 30 min after the start of Static Exercise (10% of maximal force) and 15 and 30 min after the Exercise was completed. All samples were coded and analysed blind. The primary endpoints were to detect a difference between patients and controls in changes of muscle blood flow and the interstitial lactate concentration from baseline to Exercise and post‐Exercise periods. The increase in muscle blood flow from baseline to Exercise and post‐Exercise periods was significantly lower in patients than controls ( P = 0.03). There was no difference in resting blood flow between patients and controls ( P = 0.43). Resting interstitial concentration of lactate did not differ between patients (2.51 ± 0.18 mM; mean ± standard error of the mean) and controls (2.35 ± 0.23 mM, P = 0.57). There was no difference in change in interstitial lactate from baseline to Exercise and post‐Exercise periods between patients and controls ( P = 0.38). The present study provides in vivo evidence of decreased blood flow in response to Static Exercise in a tender muscle in patients with chronic tension‐type headache. We suggest that, because of increased excitability of neurones in the CNS, the central interpretation and response to normal sensory input are altered in patients with chronic tension‐type headache. This may lead to enhanced sympathetically mediated vasoconstriction and thereby a decreased blood flow in response to Static Exercise.