Pub Date : 1987-04-01DOI: 10.1152/PHYSREV.1987.67.2.325
H. E. Morgan
{"title":"The American Physiological Society in its centenary year.","authors":"H. E. Morgan","doi":"10.1152/PHYSREV.1987.67.2.325","DOIUrl":"https://doi.org/10.1152/PHYSREV.1987.67.2.325","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1987-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128375402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-11-01DOI: 10.1007/978-3-642-72735-1_39
D. Neisius, J. Wood, K. Hofbauer
{"title":"Renal vasodilatation after inhibition of renin or converting enzyme in marmoset.","authors":"D. Neisius, J. Wood, K. Hofbauer","doi":"10.1007/978-3-642-72735-1_39","DOIUrl":"https://doi.org/10.1007/978-3-642-72735-1_39","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"16 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1986-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133312135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1986-09-01DOI: 10.1097/00132586-198708000-00003
L. Saccá, R. Hendler, A. Picardi, R. Sherwin
To evaluate the role of splanchnic and renal tissues in epinephrine disposal, we infused epinephrine (60 ng X kg-1 X min-1) into nine human volunteers during hepatic (n = 6) and/or renal (n = 4) vein catheterization. During the infusion plasma epinephrine rose higher in the artery (1,345 +/- 126 pg/ml) than in the hepatic (218 +/- 42 pg/ml) or renal vein (528 +/- 95 pg/ml). Splanchnic plasma flow increased by 43% (P less than 0.001), whereas renal plasma flow was unchanged. Net epinephrine uptake increased to a greater extent (3-fold) in the splanchnic area as compared with the kidney, amounting to 32 +/- 3% and 10 +/- 2% of the infused epinephrine load, respectively. The splanchnic epinephrine clearance also increased by 50-60%, while fractional extraction remained stable at 80-85%. Renal epinephrine clearance and extraction was not significantly altered, however. Epinephrine infusion caused splanchnic norepinephrine uptake to increase as well, partially because of the increased plasma flow. In contrast, the kidney showed net norepinephrine production throughout. We conclude that the splanchnic area plays a much more important role than the kidney in the disposal of circulating epinephrine. The great efficiency of splanchnic epinephrine removal is further enhanced by epinephrine-induced hemodynamic changes that also promote the splanchnic uptake of norepinephrine.
为了评估内脏和肾脏组织在肾上腺素处理中的作用，我们在肝脏(n = 6)和/或肾脏(n = 4)静脉置管期间向9名志愿者注入肾上腺素(60 ng X kg-1 X min-1)。在输注过程中，血浆中动脉肾上腺素(1345 +/- 126 pg/ml)高于肝(218 +/- 42 pg/ml)或肾静脉肾上腺素(528 +/- 95 pg/ml)。内脏血浆流量增加了43% (P < 0.001)，而肾脏血浆流量没有变化。与肾脏相比，内脏的肾上腺素净摄取增加了更大程度(3倍)，分别占输注肾上腺素负荷的32 +/- 3%和10 +/- 2%。内脏肾上腺素清除率也增加了50-60%，而分离提取保持稳定在80-85%。然而，肾肾上腺素清除和提取没有明显改变。肾上腺素输注引起内脏去甲肾上腺素摄取增加，部分原因是血浆流量增加。相反，肾脏显示全身净去甲肾上腺素产生。我们得出结论，在循环肾上腺素的处理中，内脏比肾脏起着更重要的作用。肾上腺素引起的血流动力学改变也促进了去甲肾上腺素的内脏摄取，从而进一步提高了移植肾上腺素去除的效率。
{"title":"Splanchnic and renal contribution to disposal of infused epinephrine in humans.","authors":"L. Saccá, R. Hendler, A. Picardi, R. Sherwin","doi":"10.1097/00132586-198708000-00003","DOIUrl":"https://doi.org/10.1097/00132586-198708000-00003","url":null,"abstract":"To evaluate the role of splanchnic and renal tissues in epinephrine disposal, we infused epinephrine (60 ng X kg-1 X min-1) into nine human volunteers during hepatic (n = 6) and/or renal (n = 4) vein catheterization. During the infusion plasma epinephrine rose higher in the artery (1,345 +/- 126 pg/ml) than in the hepatic (218 +/- 42 pg/ml) or renal vein (528 +/- 95 pg/ml). Splanchnic plasma flow increased by 43% (P less than 0.001), whereas renal plasma flow was unchanged. Net epinephrine uptake increased to a greater extent (3-fold) in the splanchnic area as compared with the kidney, amounting to 32 +/- 3% and 10 +/- 2% of the infused epinephrine load, respectively. The splanchnic epinephrine clearance also increased by 50-60%, while fractional extraction remained stable at 80-85%. Renal epinephrine clearance and extraction was not significantly altered, however. Epinephrine infusion caused splanchnic norepinephrine uptake to increase as well, partially because of the increased plasma flow. In contrast, the kidney showed net norepinephrine production throughout. We conclude that the splanchnic area plays a much more important role than the kidney in the disposal of circulating epinephrine. The great efficiency of splanchnic epinephrine removal is further enhanced by epinephrine-induced hemodynamic changes that also promote the splanchnic uptake of norepinephrine.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"118 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1986-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127989992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cineangiographic examination of reindeer exposed to local (hypothalamic) or general heating and cooling revealed that the angular oculi veins are constricted during cold stress but dilated during heat stress. Moreover, during heat stress a segment of the facial vein appeared to be occluded, causing the cold venous return from the nasal mucosa to be routed directly to the cavernous sinus for selective cooling of the brain. Histological examination of the vasoactive segment of the facial vein showed unusually thick longitudinal and circular layers of smooth muscle cells. Obstruction of angular oculi blood flow by clamping of the veins in the heat-stressed animal resulted in an immediate rise in brain temperature. When reindeer under heat stress shift from closed- to open-mouth panting, only the expiratory phase of the respiratory cycle takes place through the mouth, whereas inspiration through the nose is continued. In this way, cooling of the nasal mucosa and, hence, cooling of the brain, is maintained.
{"title":"Selective cooling of the brain in reindeer.","authors":"H. K. Johnsen, A. Blix, J. Mercer, K. Bolz","doi":"10.7557/2.6.1-APP.627","DOIUrl":"https://doi.org/10.7557/2.6.1-APP.627","url":null,"abstract":"Cineangiographic examination of reindeer exposed to local (hypothalamic) or general heating and cooling revealed that the angular oculi veins are constricted during cold stress but dilated during heat stress. Moreover, during heat stress a segment of the facial vein appeared to be occluded, causing the cold venous return from the nasal mucosa to be routed directly to the cavernous sinus for selective cooling of the brain. Histological examination of the vasoactive segment of the facial vein showed unusually thick longitudinal and circular layers of smooth muscle cells. Obstruction of angular oculi blood flow by clamping of the veins in the heat-stressed animal resulted in an immediate rise in brain temperature. When reindeer under heat stress shift from closed- to open-mouth panting, only the expiratory phase of the respiratory cycle takes place through the mouth, whereas inspiration through the nose is continued. In this way, cooling of the nasal mucosa and, hence, cooling of the brain, is maintained.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"57 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1986-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116080859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1985-04-01DOI: 10.1249/00005768-198504000-00113
G. Brooks, W. Stanley, E. Gertz, J. Wisneski, D. Morris, R. Neese
To investigate the relationships between oxygen consumption (VO2) and the rates of systemic lactate appearance (Ra) and disappearance (Rd), six healthy males were studied at rest and during continuous graded exercise using a primed continuous infusion of lactate tracer. Subjects exercised for 6 min at 300, 600, 900, and 1,200 kg . m . min-1. L-(+)-[1-14C]lactate was infused intravenously, and arterial samples were drawn at rest and every 2 min throughout the exercise period. Ra and Rd were calculated using nonsteady-state equations. At rest Ra and Rd were 14.4 +/- 1.8 and 15.1 +/- 2.2 mumol . kg-1 . min-1, respectively. Near steady-state values were observed toward the end of the first two work loads. Ra and Rd values were 32.8 +/- 2.3 and 37.4 +/- 1.3 mumol . kg-1 . min-1 during min 5 and 6 at 300 kg . m . min-1 and were 59.1 +/- 2.6 and 55.4 +/- 2.3 mumol . kg-1 . min-1 during min 5 and 6 at 600 kg . m . min-1. Ra was significantly greater than Rd at both 900 and 1,200 kg . m . min-1. Ra and Rd averaged 145.4 +/- 10.5 and 110.2 +/- 5.6 mumol . kg-1 . min-1, respectively, during the last 2 min at 900 kg . m . min-1, and 309.4 +/- 20.8 and 169.7 +/- 10.6 mumol . kg-1 . min-1, respectively, at 1,200 kg . m . min-1.(ABSTRACT TRUNCATED AT 250 WORDS)
{"title":"Systemic lactate kinetics during graded exercise in man.","authors":"G. Brooks, W. Stanley, E. Gertz, J. Wisneski, D. Morris, R. Neese","doi":"10.1249/00005768-198504000-00113","DOIUrl":"https://doi.org/10.1249/00005768-198504000-00113","url":null,"abstract":"To investigate the relationships between oxygen consumption (VO2) and the rates of systemic lactate appearance (Ra) and disappearance (Rd), six healthy males were studied at rest and during continuous graded exercise using a primed continuous infusion of lactate tracer. Subjects exercised for 6 min at 300, 600, 900, and 1,200 kg . m . min-1. L-(+)-[1-14C]lactate was infused intravenously, and arterial samples were drawn at rest and every 2 min throughout the exercise period. Ra and Rd were calculated using nonsteady-state equations. At rest Ra and Rd were 14.4 +/- 1.8 and 15.1 +/- 2.2 mumol . kg-1 . min-1, respectively. Near steady-state values were observed toward the end of the first two work loads. Ra and Rd values were 32.8 +/- 2.3 and 37.4 +/- 1.3 mumol . kg-1 . min-1 during min 5 and 6 at 300 kg . m . min-1 and were 59.1 +/- 2.6 and 55.4 +/- 2.3 mumol . kg-1 . min-1 during min 5 and 6 at 600 kg . m . min-1. Ra was significantly greater than Rd at both 900 and 1,200 kg . m . min-1. Ra and Rd averaged 145.4 +/- 10.5 and 110.2 +/- 5.6 mumol . kg-1 . min-1, respectively, during the last 2 min at 900 kg . m . min-1, and 309.4 +/- 20.8 and 169.7 +/- 10.6 mumol . kg-1 . min-1, respectively, at 1,200 kg . m . min-1.(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"72 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1985-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122607708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1985-04-01DOI: 10.1249/00005768-198504000-00230
D. Hood, R. Terjung
An isolated single rat hindlimb muscle preparation was used to examine leucine metabolism during steady-state conditions as a function of metabolic rate (VO2) and leucine concentration. The rates of muscle leucine uptake and leucine oxidation (measured as alpha-decarboxylation) were dependent on leucine delivery. At a physiological leucine concentration (0.1 mM), leucine uptake and alpha-ketoisocaproic acid (KIC) release during rest was 12.8 +/- 0.4 and 1.86 +/- 0.06 nmol.min-1.g-1 g, respectively. Leucine oxidation was 2.35 +/- 0.11 nmol.min-1.g-1 (n = 24) and if fully oxidized could account for only 3-4% of the resting VO2. This fraction was reduced to approximately 1% during contractions. The rate of leucine oxidation progressively increased, up to two to three times above rest (6-7 nmol.min-1.g-1), during contractions of graded frequency (7.5, 15, 30, 45, and 60 tetani/min) in a manner related to the eightfold increase in VO2 of the mixed fiber muscle. The fraction of muscle leucine uptake that was transaminated (i.e., leucine decarboxylation + KIC release) increased from 33% at rest to approximately 60% during contractions. The increase in leucine oxidation during contractions was probably primarily due to the high oxidative fast-twitch, red muscle mass, whose VO2 was estimated to increase up to 24-fold above rest. On the basis of our observed rates of muscle leucine alpha-decarboxylation, it is reasonable to attribute the rates of whole-body leucine oxidation of nontrained individuals during exercise to leucine oxidation by the working muscle.
{"title":"Leucine metabolism in perfused rat skeletal muscle during contractions.","authors":"D. Hood, R. Terjung","doi":"10.1249/00005768-198504000-00230","DOIUrl":"https://doi.org/10.1249/00005768-198504000-00230","url":null,"abstract":"An isolated single rat hindlimb muscle preparation was used to examine leucine metabolism during steady-state conditions as a function of metabolic rate (VO2) and leucine concentration. The rates of muscle leucine uptake and leucine oxidation (measured as alpha-decarboxylation) were dependent on leucine delivery. At a physiological leucine concentration (0.1 mM), leucine uptake and alpha-ketoisocaproic acid (KIC) release during rest was 12.8 +/- 0.4 and 1.86 +/- 0.06 nmol.min-1.g-1 g, respectively. Leucine oxidation was 2.35 +/- 0.11 nmol.min-1.g-1 (n = 24) and if fully oxidized could account for only 3-4% of the resting VO2. This fraction was reduced to approximately 1% during contractions. The rate of leucine oxidation progressively increased, up to two to three times above rest (6-7 nmol.min-1.g-1), during contractions of graded frequency (7.5, 15, 30, 45, and 60 tetani/min) in a manner related to the eightfold increase in VO2 of the mixed fiber muscle. The fraction of muscle leucine uptake that was transaminated (i.e., leucine decarboxylation + KIC release) increased from 33% at rest to approximately 60% during contractions. The increase in leucine oxidation during contractions was probably primarily due to the high oxidative fast-twitch, red muscle mass, whose VO2 was estimated to increase up to 24-fold above rest. On the basis of our observed rates of muscle leucine alpha-decarboxylation, it is reasonable to attribute the rates of whole-body leucine oxidation of nontrained individuals during exercise to leucine oxidation by the working muscle.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"16 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1985-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114174803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1985-02-01DOI: 10.1152/JAPPL.1985.58.2.313
J. DiStefano
{"title":"The modeling methodology forum: an expanded department.","authors":"J. DiStefano","doi":"10.1152/JAPPL.1985.58.2.313","DOIUrl":"https://doi.org/10.1152/JAPPL.1985.58.2.313","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"7 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1985-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129433920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1984-04-01DOI: 10.1249/00005768-198404000-00313
E. Richter, T. Ploug, H. Galbo
We reinvestigated the prevailing concept that muscle contractions only elicit increased muscle glucose uptake in the presence of a so-called "permissive" concentration of insulin (Berger et al., Biochem. J. 146: 231-238, 1975; Vranic and Berger, Diabetes 28: 147-163, 1979). Hindquarters from rats in severe ketoacidosis were perfused with a perfusate containing insulin antiserum. After 60 min perfusion, electrical stimulation increased glucose uptake of the contracting muscles fivefold. Also, subsequent contractions increased glucose uptake in hindquarters from nondiabetic rats perfused for 1.5 h in the presence of antiserum. 3-O-methylglucose uptake was increased markedly by contractions in fast-twitch red and white fibers that were severely glycogen depleted but not in slow-twitch red fibers that were not glycogen depleted. In hindquarters from ketoacidotic rats perfused exactly as by Berger et al., 3-O-methylglucose uptake increased during contractions and glucose uptake was negative at rest and zero during contractions. An increase in muscle transport and uptake of glucose during contractions does not require the presence of insulin. Furthermore, glucose transport in contracting muscle may only increase if glycogen is depleted.
我们重新研究了流行的概念，即肌肉收缩只会在所谓的“允许”胰岛素浓度存在时引起肌肉葡萄糖摄取增加(Berger等人，Biochem)。[j] . 21 (2);Vranic和Berger，糖尿病28:147-163,1979)。用含胰岛素抗血清的灌注液灌注严重酮症酸中毒大鼠后腿。灌注60分钟后，电刺激使收缩肌肉的葡萄糖摄取增加了5倍。此外，随后的收缩增加了非糖尿病大鼠在抗血清存在下灌注1.5小时后后腿的葡萄糖摄取。3- o -甲基葡萄糖摄取在糖原严重耗尽的快速收缩红纤维和白纤维中显著增加，而在糖原未耗尽的慢收缩红纤维中则没有明显增加。在与Berger等人完全相同灌注的酮症酸中毒大鼠的后腿中，3- o -甲基葡萄糖摄取在收缩期间增加，葡萄糖摄取在静止时为负，在收缩期间为零。收缩时肌肉运输和葡萄糖摄取的增加不需要胰岛素的存在。此外，只有当糖原耗尽时，收缩肌肉中的葡萄糖转运才会增加。
{"title":"Increased muscle glucose uptake during contractions: no need for insulin.","authors":"E. Richter, T. Ploug, H. Galbo","doi":"10.1249/00005768-198404000-00313","DOIUrl":"https://doi.org/10.1249/00005768-198404000-00313","url":null,"abstract":"We reinvestigated the prevailing concept that muscle contractions only elicit increased muscle glucose uptake in the presence of a so-called \"permissive\" concentration of insulin (Berger et al., Biochem. J. 146: 231-238, 1975; Vranic and Berger, Diabetes 28: 147-163, 1979). Hindquarters from rats in severe ketoacidosis were perfused with a perfusate containing insulin antiserum. After 60 min perfusion, electrical stimulation increased glucose uptake of the contracting muscles fivefold. Also, subsequent contractions increased glucose uptake in hindquarters from nondiabetic rats perfused for 1.5 h in the presence of antiserum. 3-O-methylglucose uptake was increased markedly by contractions in fast-twitch red and white fibers that were severely glycogen depleted but not in slow-twitch red fibers that were not glycogen depleted. In hindquarters from ketoacidotic rats perfused exactly as by Berger et al., 3-O-methylglucose uptake increased during contractions and glucose uptake was negative at rest and zero during contractions. An increase in muscle transport and uptake of glucose during contractions does not require the presence of insulin. Furthermore, glucose transport in contracting muscle may only increase if glycogen is depleted.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"96 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1984-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114953517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1984-04-01DOI: 10.1249/00005768-198404000-00270
G. Dohm, G. J. Kasperek, H. Barakat
Gluconeogenic enzymes were assayed after varying periods of exercise and recovery to determine how rapidly changes occur and whether they persist after the cessation of exercise. Untrained male rats (250 g) ran on a treadmill at 28 m/min and were killed after varying periods of exercise and recovery. Livers were quickly removed and analyzed for maximal enzyme activities (saturating levels of substrate) and submaximal activities (low-substrate concentrations). The most significant enzyme changes during exercise were increased maximal activity of phosphoenolpyruvate carboxykinase (PEPCK) and decreased submaximal activity of phosphofructokinase (PFK). Submaximal PFK activity was decreased by 30 min of exercise and remained at that low level up to exhaustion (172 +/- 16 min). Changes in submaximal PFK activity are in response to decreased concentrations of fructose-2,6-bisphosphate that were decreased to approximately one-tenth the control value after 30 min of exercise and remained low throughout exercise and 1 h of recovery. The PEPCK activity progressively increased during exercise and was highest at exhaustion. The cAMP level was significantly elevated in liver of rats exercised for 30 min and continued to rise with duration. Six hours after exercise PEPCK and submaximal PFK activities were the same in control and exercised-rested rats. The change in PEPCK activity is consistent with an increase in the rate of enzyme synthesis and/or a decrease in enzyme degradation during exercise, whereas the lowered activity of PFK likely reflects covalent modification of 6-phospho-fructo-2-kinase/fructose-2,6-bisphosphatase.
{"title":"Time course of changes in gluconeogenic enzyme activities during exercise and recovery.","authors":"G. Dohm, G. J. Kasperek, H. Barakat","doi":"10.1249/00005768-198404000-00270","DOIUrl":"https://doi.org/10.1249/00005768-198404000-00270","url":null,"abstract":"Gluconeogenic enzymes were assayed after varying periods of exercise and recovery to determine how rapidly changes occur and whether they persist after the cessation of exercise. Untrained male rats (250 g) ran on a treadmill at 28 m/min and were killed after varying periods of exercise and recovery. Livers were quickly removed and analyzed for maximal enzyme activities (saturating levels of substrate) and submaximal activities (low-substrate concentrations). The most significant enzyme changes during exercise were increased maximal activity of phosphoenolpyruvate carboxykinase (PEPCK) and decreased submaximal activity of phosphofructokinase (PFK). Submaximal PFK activity was decreased by 30 min of exercise and remained at that low level up to exhaustion (172 +/- 16 min). Changes in submaximal PFK activity are in response to decreased concentrations of fructose-2,6-bisphosphate that were decreased to approximately one-tenth the control value after 30 min of exercise and remained low throughout exercise and 1 h of recovery. The PEPCK activity progressively increased during exercise and was highest at exhaustion. The cAMP level was significantly elevated in liver of rats exercised for 30 min and continued to rise with duration. Six hours after exercise PEPCK and submaximal PFK activities were the same in control and exercised-rested rats. The change in PEPCK activity is consistent with an increase in the rate of enzyme synthesis and/or a decrease in enzyme degradation during exercise, whereas the lowered activity of PFK likely reflects covalent modification of 6-phospho-fructo-2-kinase/fructose-2,6-bisphosphatase.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1984-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115773490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1983-11-01DOI: 10.1152/ajpregu.1983.245.5.R619
J. Rall
{"title":"Mones Berman--the man and his legacy to quantitative biology.","authors":"J. Rall","doi":"10.1152/ajpregu.1983.245.5.R619","DOIUrl":"https://doi.org/10.1152/ajpregu.1983.245.5.R619","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"58 3","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1983-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132531082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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