The Experts below are selected from a list of 246 Experts worldwide ranked by ideXlab platform
Lothar A. Blatter - One of the best experts on this subject based on the ideXlab platform.
-
Beta-Adrenergic Stimulation Increases the Intra-SR Ca Termination Threshold for Spontaneous Ca Release in Cardiac Myocytes
Biophysical Journal, 2013Co-Authors: Joshua T. Maxwell, Timothy L. Domeier, Lothar A. BlatterAbstract:In the heart, beta-Adrenergic Stimulation is associated with pro-arrhythmic Ca waves that occur as the result of the sarcoplasmic reticulum (SR) Ca content reaching a critical threshold level. Recently, we have shown that beta-Adrenergic Stimulation increases the intra-SR Ca threshold for Ca wave initiation, potentially serving as a protective mechanism against pro-arrhythmic Ca release during beta-Adrenergic Stimulation (Domeier et al., 2012). However, data regarding the termination of such release and details on the regulation of this process have yet to be elucidated. In this study we directly and dynamically measured the intra-SR Ca level ([Ca]SR) at which spontaneous Ca waves terminate (termination threshold) under control conditions and during beta-Adrenergic Stimulation. Application of the beta-Adrenergic receptor agonist isoproterenol (ISO; 1 μM) resulted in an increase in basal [Ca]SR. Importantly, in the presence of ISO the [Ca]SR at which spontaneous Ca waves terminated was also increased compared to control conditions. In addition, the depletion amplitude of spontaneous Ca waves was decreased in the presence of ISO compared to control conditions. When [Ca]SR was subsequently lowered in the presence of ISO to that observed under control conditions (by reducing extracellular Ca and partially inhibiting SERCA with cyclopiazonic acid or thapsigargin), the [Ca]SR at which spontaneous release terminated was still increased compared to control conditions. Likewise, the depletion amplitude remained decreased compared to control conditions. These data indicate that during beta-Adrenergic Stimulation in the heart, both the intra-SR Ca threshold at which spontaneous Ca waves initiate and terminate is increased, while the amount of Ca released during Ca waves is decreased. The Ca wave termination level may represent an important mode of altering diastolic Ca wave amplitude, and thus, the arrhythmogenic potential of the cell during acute beta-Adrenergic Stimulation.
-
β-Adrenergic Stimulation increases the intra-sarcoplasmic reticulum Ca2+ threshold for Ca2+ wave generation.
The Journal of physiology, 2012Co-Authors: Timothy L. Domeier, Joshua T. Maxwell, Lothar A. BlatterAbstract:Key points • In the heart, Ca2+ waves are arrhythmogenic spontaneous sarcoplasmic reticulum (SR) Ca2+ release events that arise when the Ca2+ content in the SR reaches a critical threshold level. • β-Adrenergic signalling induces Ca2+ waves in cardiac myocytes, but it remains unclear if this is due to a decrease in the Ca2+ wave threshold or more simply due to an increase in SR Ca2+ content. • We used direct, dynamic measurement of SR Ca2+ levels to show that the Ca2+ wave threshold is unexpectedly increased during β-Adrenergic Stimulation. • Our data show that the primary cause of Ca2+ waves following acute β-Adrenergic Stimulation is the increase in SR Ca2+ content and not a decrease in the Ca2+ wave threshold. • We propose that the elevation of the Ca2+ wave threshold represents a protective mechanism against arrhythmogenic events during periods of β-Adrenergic Stimulation. Abstract β-Adrenergic signalling induces positive inotropic effects on the heart that associate with pro-arrhythmic spontaneous Ca2+ waves. A threshold level of sarcoplasmic reticulum (SR) Ca2+ ([Ca2+]SR) is necessary to trigger Ca2+ waves, and whether the increased incidence of Ca2+ waves during β-Adrenergic Stimulation is due to an alteration in this threshold remains controversial. Using the low-affinity Ca2+ indicator fluo-5N entrapped within the SR of rabbit ventricular myocytes, we addressed this controversy by directly monitoring [Ca2+]SR and Ca2+ waves during β-Adrenergic Stimulation. Electrical pacing in elevated extracellular Ca2+ ([Ca2+]o= 7 mm) was used to increase [Ca2+]SR to the threshold where Ca2+ waves were consistently observed. The β-Adrenergic agonist isoproterenol (ISO; 1 μm) increased [Ca2+]SR well above the control threshold and consistently triggered Ca2+ waves. However, when [Ca2+]SR was subsequently lowered in the presence of ISO (by lowering [Ca2+]o to 1 mm and partially inhibiting sarcoplasmic/endoplasmic reticulum calcium ATPase with cyclopiazonic acid or thapsigargin), Ca2+ waves ceased to occur at a [Ca2+]SR that was higher than the control threshold. Furthermore, for a set [Ca2+]SR level the refractoriness of wave occurrence (Ca2+ wave latency) was prolonged during β-Adrenergic Stimulation, and was highly dependent on the extent that [Ca]SR exceeded the wave threshold. These data show that acute β-Adrenergic Stimulation increases the [Ca2+]SR threshold for Ca2+ waves, and therefore the primary cause of Ca2+ waves is the robust increase in [Ca2+]SR above this higher threshold level. Elevation of the [Ca2+]SR wave threshold and prolongation of wave latency represent potentially protective mechanisms against pro-arrhythmogenic Ca2+ release during β-Adrenergic Stimulation.
-
mechanisms of spontaneous calcium wave generation during beta Adrenergic Stimulation in rabbit ventricular myocytes
Biophysical Journal, 2010Co-Authors: Timothy L. Domeier, Lothar A. BlatterAbstract:The beta-Adrenergic signaling pathway represents the principal positive inotropic mechanism of the heart. While the effects of beta-Adrenergic Stimulation on L-type Ca channel Ca influx and SERCA-mediated sarcoplasmic reticulum (SR) Ca uptake are well established, the effects on SR Ca release through ryanodine receptor (RyR) release clusters remains highly controversial. Here, we examine SR Ca release in rabbit ventricular myocytes in the form of spontaneous Ca waves during beta-Adrenergic Stimulation with isoproterenol under controlled cytosolic and SR [Ca]. Cytosolic Ca was monitored using high-affinity Ca indicators indo-1 or rhod-2, while SR Ca was measured directly using the low-affinity Ca indicator fluo-5N or indirectly using the amplitude of the cytosolic Ca transient in response to 10 mM caffeine. Under control conditions, Ca waves were not observed following rest from 0.75 Hz pacing. In the presence of isoproterenol (500 nM), SR Ca content increased by 34% and spontaneous Ca waves were observed in 67% of cells during rest after pacing. However, when post-rest cytosolic Ca and SR Ca content were experimentally matched to control conditions using low extracellular Ca (100 uM versus 2 mM) and SERCA inhibition (7.5 uM cyclopiazonic acid), spontaneous Ca waves were never observed in the presence of isoproterenol. In contrast, pharmacological sensitization of the RyR with 250 uM caffeine induced Ca waves under control conditions (8/12 cells) and in the presence of isoproterenol at matched cytosolic Ca and SR Ca content (7/12). Together, these data suggest that spontaneous Ca release during beta-Adrenergic Stimulation is a result of increased RyR sensitivity in response to increased SR Ca content, and is not due to direct alterations in RyR function by the beta-Adrenergic signaling cascade.
Marleen A Van Baak - One of the best experts on this subject based on the ideXlab platform.
-
endocrine role of the renin angiotensin system in human adipose tissue and muscle effect of beta Adrenergic Stimulation
Hypertension, 2007Co-Authors: Gijs H Goossens, Ellen E. Blaak, Wilhelmus Hermanus Maria Saris, Johan W E Jocken, Paul M H Schiffers, Marleen A Van BaakAbstract:The renin-angiotensin system has been implicated in obesity-related hypertension and insulin resistance. We examined whether locally produced components of the renin-angiotensin system in adipose tissue and skeletal muscle play an endocrine role in vivo in humans. Furthermore, the effects of beta-Adrenergic Stimulation on plasma concentrations and tissue release of renin-angiotensin system components were investigated. Systemic renin-angiotensin system components and arteriovenous differences of angiotensin II (Ang II) and angiotensinogen (AGT) across abdominal subcutaneous adipose tissue and skeletal muscle were assessed in combination with measurements of tissue blood flow before and during systemic beta-Adrenergic Stimulation in 13 lean and 10 obese subjects. Basal plasma Ang II and AGT concentrations were not significantly different between lean and obese subjects. Ang II concentrations were increased in obese compared with lean subjects during beta-Adrenergic Stimulation (12.6+/-1.5 versus 8.1+/-1.0 pmol/L; P=0.04), whereas AGT concentrations remained unchanged. Plasma renin activity increased to a similar extent in lean and obese subjects during beta-Adrenergic Stimulation (both P<0.01). No net Ang II release across adipose tissue and skeletal muscle could be detected in both groups of subjects. However, AGT was released from adipose tissue and muscle during beta-Adrenergic Stimulation in obese subjects (both P<0.05). In conclusion, locally produced Ang II in adipose tissue and skeletal muscle exerts no endocrine role in lean and obese subjects. In contrast, AGT is released from adipose tissue and muscle in obese subjects during beta-Adrenergic Stimulation, which may contribute to the increased plasma Ang II concentrations during beta-Adrenergic Stimulation in obese subjects.
-
Endocrine role of the renin-angiotensin system in human adipose tissue and muscle: effect of beta-Adrenergic Stimulation.
Hypertension (Dallas Tex. : 1979), 2007Co-Authors: Gijs H Goossens, Ellen E. Blaak, Wilhelmus Hermanus Maria Saris, Johan W E Jocken, Paul M H Schiffers, Marleen A Van BaakAbstract:The renin-angiotensin system has been implicated in obesity-related hypertension and insulin resistance. We examined whether locally produced components of the renin-angiotensin system in adipose tissue and skeletal muscle play an endocrine role in vivo in humans. Furthermore, the effects of beta-Adrenergic Stimulation on plasma concentrations and tissue release of renin-angiotensin system components were investigated. Systemic renin-angiotensin system components and arteriovenous differences of angiotensin II (Ang II) and angiotensinogen (AGT) across abdominal subcutaneous adipose tissue and skeletal muscle were assessed in combination with measurements of tissue blood flow before and during systemic beta-Adrenergic Stimulation in 13 lean and 10 obese subjects. Basal plasma Ang II and AGT concentrations were not significantly different between lean and obese subjects. Ang II concentrations were increased in obese compared with lean subjects during beta-Adrenergic Stimulation (12.6+/-1.5 versus 8.1+/-1.0 pmol/L; P=0.04), whereas AGT concentrations remained unchanged. Plasma renin activity increased to a similar extent in lean and obese subjects during beta-Adrenergic Stimulation (both P
-
Effect of beta1- and beta2-Adrenergic Stimulation on energy expenditure, substrate oxidation, and UCP3 expression in humans.
American journal of physiology. Endocrinology and metabolism, 2003Co-Authors: Joris Hoeks, Marleen A Van Baak, Matthijs K. C. Hesselink, Gabby B. Hul, Hubert Vidal, Wim H. M. Saris, Patrick SchrauwenAbstract:In humans, β-Adrenergic Stimulation increases energy and fat metabolism. In the case of β1-Adrenergic Stimulation, it is fueled by an increased lipolysis. We examined the effect of β2-Adrenergic st...
Helmut Drexler - One of the best experts on this subject based on the ideXlab platform.
-
Effects of α-Adrenergic Stimulation on the sarcolemmal Na+/Ca2+-exchanger in adult rat ventricular cardiocytes
Cardiovascular research, 1997Co-Authors: Hans Reinecke, Roland Vetter, Helmut DrexlerAbstract:The cardiac sarcolemmal Na+/Ca(2+)-exchanger (NCX) plays an important role in the maintenance of the myocardial Ca2+ homeostasis which is altered in cardiac hypertrophy and failure. The aim of the present study was to investigate whether alpha-Adrenergic Stimulation known to induce cardiac hypertrophy might be involved in the regulation of the sarcolemmal NCX. Adult rat ventricular cardiocytes (ARC) were isolated from male Sprague-Dawley rats. Phenylephrine, an alpha-Adrenergic agonist, was used as hypertrophic agent. NCX expression was measured by competitive RT-PCR and Western blot analysis. alpha-Adrenergic Stimulation of ARC with 10 microM phenylephrine for 24 h resulted in a significant increase of the NCX mRNA (2.5-fold) and the NCX protein level (1.8-fold). The changes on the expression level were blocked by the alpha 1-adrenoceptor antagonist prazosin. The data demonstrate that the NCX expression level is up-regulated by the activation of the alpha-Adrenergic signal transduction pathway. The increased NCX mRNA level induced by alpha-Adrenergic Stimulation appeared to be translated into increased NCX protein level.
-
Effects of α-Adrenergic Stimulation on the sarcolemmal Na+/Ca2+-exchanger in adult rat ventricular cardiocytes
Cardiovascular research, 1997Co-Authors: Hans Reinecke, Roland Vetter, Helmut DrexlerAbstract:¨ b () Max-Delbruck-Centrum fur Molekulare Medizin MDC , Berlin-Buch, Germany ¨¨ Abstract q 2q . 2q Objective: The cardiac sarcolemmal Na rCa -exchanger NCX plays an important role in the maintenance of the myocardial Ca homeostasis which is altered in cardiac hypertrophy and failure. The aim of the present study was to investigate whether a-Adrenergic Stimulation known to induce cardiac hypertrophy might be involved in the regulation of the sarcolemmal NCX. Methods: Adult rat . ventricular cardiocytes ARC were isolated from male Sprague-Dawley rats. Phenylephrine, an a-Adrenergic agonist, was used as hypertrophic agent. NCX expression was measured by competitive RT-PCR and Western blot analysis. Results: a-Adrenergic Stimulation . of ARC with 10 mM phenylephrine for 24 h resulted in a significant increase of the NCX mRNA 2.5-fold and the NCX protein level .1.8-fold . The changes on the expression level were blocked by the a -adrenoceptor antagonist prazosin. Conclusions: The data 1 demonstrate that the NCX expression level is up-regulated by the activation of the a-Adrenergic signal transduction pathway. The increased NCX mRNA level induced by a-Adrenergic Stimulation appeared to be translated into an increased NCX protein level. q 1997 Elsevier Science B.V.
Timothy L. Domeier - One of the best experts on this subject based on the ideXlab platform.
-
Beta-Adrenergic Stimulation Increases the Intra-SR Ca Termination Threshold for Spontaneous Ca Release in Cardiac Myocytes
Biophysical Journal, 2013Co-Authors: Joshua T. Maxwell, Timothy L. Domeier, Lothar A. BlatterAbstract:In the heart, beta-Adrenergic Stimulation is associated with pro-arrhythmic Ca waves that occur as the result of the sarcoplasmic reticulum (SR) Ca content reaching a critical threshold level. Recently, we have shown that beta-Adrenergic Stimulation increases the intra-SR Ca threshold for Ca wave initiation, potentially serving as a protective mechanism against pro-arrhythmic Ca release during beta-Adrenergic Stimulation (Domeier et al., 2012). However, data regarding the termination of such release and details on the regulation of this process have yet to be elucidated. In this study we directly and dynamically measured the intra-SR Ca level ([Ca]SR) at which spontaneous Ca waves terminate (termination threshold) under control conditions and during beta-Adrenergic Stimulation. Application of the beta-Adrenergic receptor agonist isoproterenol (ISO; 1 μM) resulted in an increase in basal [Ca]SR. Importantly, in the presence of ISO the [Ca]SR at which spontaneous Ca waves terminated was also increased compared to control conditions. In addition, the depletion amplitude of spontaneous Ca waves was decreased in the presence of ISO compared to control conditions. When [Ca]SR was subsequently lowered in the presence of ISO to that observed under control conditions (by reducing extracellular Ca and partially inhibiting SERCA with cyclopiazonic acid or thapsigargin), the [Ca]SR at which spontaneous release terminated was still increased compared to control conditions. Likewise, the depletion amplitude remained decreased compared to control conditions. These data indicate that during beta-Adrenergic Stimulation in the heart, both the intra-SR Ca threshold at which spontaneous Ca waves initiate and terminate is increased, while the amount of Ca released during Ca waves is decreased. The Ca wave termination level may represent an important mode of altering diastolic Ca wave amplitude, and thus, the arrhythmogenic potential of the cell during acute beta-Adrenergic Stimulation.
-
β-Adrenergic Stimulation increases the intra-sarcoplasmic reticulum Ca2+ threshold for Ca2+ wave generation.
The Journal of physiology, 2012Co-Authors: Timothy L. Domeier, Joshua T. Maxwell, Lothar A. BlatterAbstract:Key points • In the heart, Ca2+ waves are arrhythmogenic spontaneous sarcoplasmic reticulum (SR) Ca2+ release events that arise when the Ca2+ content in the SR reaches a critical threshold level. • β-Adrenergic signalling induces Ca2+ waves in cardiac myocytes, but it remains unclear if this is due to a decrease in the Ca2+ wave threshold or more simply due to an increase in SR Ca2+ content. • We used direct, dynamic measurement of SR Ca2+ levels to show that the Ca2+ wave threshold is unexpectedly increased during β-Adrenergic Stimulation. • Our data show that the primary cause of Ca2+ waves following acute β-Adrenergic Stimulation is the increase in SR Ca2+ content and not a decrease in the Ca2+ wave threshold. • We propose that the elevation of the Ca2+ wave threshold represents a protective mechanism against arrhythmogenic events during periods of β-Adrenergic Stimulation. Abstract β-Adrenergic signalling induces positive inotropic effects on the heart that associate with pro-arrhythmic spontaneous Ca2+ waves. A threshold level of sarcoplasmic reticulum (SR) Ca2+ ([Ca2+]SR) is necessary to trigger Ca2+ waves, and whether the increased incidence of Ca2+ waves during β-Adrenergic Stimulation is due to an alteration in this threshold remains controversial. Using the low-affinity Ca2+ indicator fluo-5N entrapped within the SR of rabbit ventricular myocytes, we addressed this controversy by directly monitoring [Ca2+]SR and Ca2+ waves during β-Adrenergic Stimulation. Electrical pacing in elevated extracellular Ca2+ ([Ca2+]o= 7 mm) was used to increase [Ca2+]SR to the threshold where Ca2+ waves were consistently observed. The β-Adrenergic agonist isoproterenol (ISO; 1 μm) increased [Ca2+]SR well above the control threshold and consistently triggered Ca2+ waves. However, when [Ca2+]SR was subsequently lowered in the presence of ISO (by lowering [Ca2+]o to 1 mm and partially inhibiting sarcoplasmic/endoplasmic reticulum calcium ATPase with cyclopiazonic acid or thapsigargin), Ca2+ waves ceased to occur at a [Ca2+]SR that was higher than the control threshold. Furthermore, for a set [Ca2+]SR level the refractoriness of wave occurrence (Ca2+ wave latency) was prolonged during β-Adrenergic Stimulation, and was highly dependent on the extent that [Ca]SR exceeded the wave threshold. These data show that acute β-Adrenergic Stimulation increases the [Ca2+]SR threshold for Ca2+ waves, and therefore the primary cause of Ca2+ waves is the robust increase in [Ca2+]SR above this higher threshold level. Elevation of the [Ca2+]SR wave threshold and prolongation of wave latency represent potentially protective mechanisms against pro-arrhythmogenic Ca2+ release during β-Adrenergic Stimulation.
-
mechanisms of spontaneous calcium wave generation during beta Adrenergic Stimulation in rabbit ventricular myocytes
Biophysical Journal, 2010Co-Authors: Timothy L. Domeier, Lothar A. BlatterAbstract:The beta-Adrenergic signaling pathway represents the principal positive inotropic mechanism of the heart. While the effects of beta-Adrenergic Stimulation on L-type Ca channel Ca influx and SERCA-mediated sarcoplasmic reticulum (SR) Ca uptake are well established, the effects on SR Ca release through ryanodine receptor (RyR) release clusters remains highly controversial. Here, we examine SR Ca release in rabbit ventricular myocytes in the form of spontaneous Ca waves during beta-Adrenergic Stimulation with isoproterenol under controlled cytosolic and SR [Ca]. Cytosolic Ca was monitored using high-affinity Ca indicators indo-1 or rhod-2, while SR Ca was measured directly using the low-affinity Ca indicator fluo-5N or indirectly using the amplitude of the cytosolic Ca transient in response to 10 mM caffeine. Under control conditions, Ca waves were not observed following rest from 0.75 Hz pacing. In the presence of isoproterenol (500 nM), SR Ca content increased by 34% and spontaneous Ca waves were observed in 67% of cells during rest after pacing. However, when post-rest cytosolic Ca and SR Ca content were experimentally matched to control conditions using low extracellular Ca (100 uM versus 2 mM) and SERCA inhibition (7.5 uM cyclopiazonic acid), spontaneous Ca waves were never observed in the presence of isoproterenol. In contrast, pharmacological sensitization of the RyR with 250 uM caffeine induced Ca waves under control conditions (8/12 cells) and in the presence of isoproterenol at matched cytosolic Ca and SR Ca content (7/12). Together, these data suggest that spontaneous Ca release during beta-Adrenergic Stimulation is a result of increased RyR sensitivity in response to increased SR Ca content, and is not due to direct alterations in RyR function by the beta-Adrenergic signaling cascade.
Wilhelmus Hermanus Maria Saris - One of the best experts on this subject based on the ideXlab platform.
-
endocrine role of the renin angiotensin system in human adipose tissue and muscle effect of beta Adrenergic Stimulation
Hypertension, 2007Co-Authors: Gijs H Goossens, Ellen E. Blaak, Wilhelmus Hermanus Maria Saris, Johan W E Jocken, Paul M H Schiffers, Marleen A Van BaakAbstract:The renin-angiotensin system has been implicated in obesity-related hypertension and insulin resistance. We examined whether locally produced components of the renin-angiotensin system in adipose tissue and skeletal muscle play an endocrine role in vivo in humans. Furthermore, the effects of beta-Adrenergic Stimulation on plasma concentrations and tissue release of renin-angiotensin system components were investigated. Systemic renin-angiotensin system components and arteriovenous differences of angiotensin II (Ang II) and angiotensinogen (AGT) across abdominal subcutaneous adipose tissue and skeletal muscle were assessed in combination with measurements of tissue blood flow before and during systemic beta-Adrenergic Stimulation in 13 lean and 10 obese subjects. Basal plasma Ang II and AGT concentrations were not significantly different between lean and obese subjects. Ang II concentrations were increased in obese compared with lean subjects during beta-Adrenergic Stimulation (12.6+/-1.5 versus 8.1+/-1.0 pmol/L; P=0.04), whereas AGT concentrations remained unchanged. Plasma renin activity increased to a similar extent in lean and obese subjects during beta-Adrenergic Stimulation (both P<0.01). No net Ang II release across adipose tissue and skeletal muscle could be detected in both groups of subjects. However, AGT was released from adipose tissue and muscle during beta-Adrenergic Stimulation in obese subjects (both P<0.05). In conclusion, locally produced Ang II in adipose tissue and skeletal muscle exerts no endocrine role in lean and obese subjects. In contrast, AGT is released from adipose tissue and muscle in obese subjects during beta-Adrenergic Stimulation, which may contribute to the increased plasma Ang II concentrations during beta-Adrenergic Stimulation in obese subjects.
-
Endocrine role of the renin-angiotensin system in human adipose tissue and muscle: effect of beta-Adrenergic Stimulation.
Hypertension (Dallas Tex. : 1979), 2007Co-Authors: Gijs H Goossens, Ellen E. Blaak, Wilhelmus Hermanus Maria Saris, Johan W E Jocken, Paul M H Schiffers, Marleen A Van BaakAbstract:The renin-angiotensin system has been implicated in obesity-related hypertension and insulin resistance. We examined whether locally produced components of the renin-angiotensin system in adipose tissue and skeletal muscle play an endocrine role in vivo in humans. Furthermore, the effects of beta-Adrenergic Stimulation on plasma concentrations and tissue release of renin-angiotensin system components were investigated. Systemic renin-angiotensin system components and arteriovenous differences of angiotensin II (Ang II) and angiotensinogen (AGT) across abdominal subcutaneous adipose tissue and skeletal muscle were assessed in combination with measurements of tissue blood flow before and during systemic beta-Adrenergic Stimulation in 13 lean and 10 obese subjects. Basal plasma Ang II and AGT concentrations were not significantly different between lean and obese subjects. Ang II concentrations were increased in obese compared with lean subjects during beta-Adrenergic Stimulation (12.6+/-1.5 versus 8.1+/-1.0 pmol/L; P=0.04), whereas AGT concentrations remained unchanged. Plasma renin activity increased to a similar extent in lean and obese subjects during beta-Adrenergic Stimulation (both P
-
Beta-Adrenergic Stimulation of energy expenditure and forearm skeletal muscle metabolism in lean and obese men
American Journal of Physiology-endocrinology and Metabolism, 1994Co-Authors: Ellen E. Blaak, M. T. W. Pakbiers, Guido A. K. Heidendal, Gerrit J. Kemerink, Marleen A Van Baak, Wilhelmus Hermanus Maria SarisAbstract:The effect of beta-Adrenergic Stimulation on whole body energy expenditure and forearm skeletal muscle metabolism was investigated in lean and obese men. Whole body energy expenditure was determine...
