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Neuroendocrine Factors
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Table 3.3 shows the primary hormones affecting substrate control and mobilization during resistance exercise, which includes catecholamines, cortisol, insulin, glucagon, GH, and thyroxin. Ratios of hormones having antagonistic effects are often better indicators of the control of metabolic actions than individual hormones. For example, the insulin-to-glucagon ratio (I:G) may be a better indicator of blood glucose control than either hormone alone (103, 141, 229). During resistance training exercise, substantial increases in serum concentrations of lactate and glucose can occur (141, 211). These metabolic exercise responses result from energy production (fast glycolysis) and the mobilization of glucose through glycogenolysis. There is little doubt that the neuroendocrine system is activated to aid in driving these responses (107). Hormonal responses involved in supporting the short-term metabolic alterations resulting from resistance exercise would include catecholamines, glucagon, thyroxin, and perhaps cortisol as it potentiates the release of EPI (Table 3.3).
Molecular sport nutrition
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Mark Hearris, Nathan Hodson, Javier Gonzalez, James P. Morton
Glycogen concentrations reflect the balance of glycogen breakdown (glycogenolysis) and glycogen production (glycogen synthesis). Glycogenolysis is mainly regulated by the enzymes glycogen phosphorylase and debranching enzyme, which act on the terminal α‐1,4‐glycosidic linked glucose residues, and the α‐1,6‐branchpoints in the glycogen molecule, respectively. Glycogen phosphorylase is activated by AMP or IMP and inhibited by ATP and glucose-6-phosphate. Finally, muscle glycogen is also subject to autoregulation, which means that a high glycogen concentration stimulates glycogen breakdown, which is likely to be by activating glycogen phosphorylase (17).
Biochemical Adaptations to Early Extrauterine Life
Published in Emilio Herrera, Robert H. Knopp, Perinatal Biochemistry, 2020
José M. Medina, Carlos Vicario, María C. Juanes, Emilio Fernández
It is well known that the newborn undergoes a profound hypoglycemia during the immediate postnatal period.1,2,64 Both human (Figures 5 and 6) and rat (Figures 2 and 4) newborns show very low blood glucose concentration throughout the first day of extrauterine life. However, immediately after delivery, normoglycemia is transiently reached (Figures 4 and 5).65,66 Since glycogenolysis and gluconeogenesis are not induced in these circumstances,2 the transient enhancement of glycemia may be due to the inhibition of glucose utilization caused by hypoxia.67 In the rat, after 2 h there is a tendency to regain normoglycemia (Figure 4), which is probably due to the stimulation of liver glycogenolysis and the progressive induction of gluconeogenesis.2,61 This hypoglycemic period is longer in man (Figure 6) probably because of the delay in the induction of gluconeogenesis observed in this species.68 It is surprising that the delay in the onset of glycogenolysis apparently enhances the vulnerability of the newborn. However, lactate availability (Figures 5 and 7) during this period may supply energy to neonatal tissues reserving glucose from glycogen for special metabolic purposes (see Section III.B).
Anti-diabetic and hypolipidemic effects of Cinnamon cassia bark extracts: an in vitro, in vivo, and in silico approach
Published in Archives of Physiology and Biochemistry, 2023
K. Vijayakumar, B. Prasanna, R. L. Rengarajan, A. Rathinam, S. Velayuthaprabhu, A. Vijaya Anand
Carbohydrate metabolising enzymes play an important role in the regulation of glucose level (O’Doherty et al.1999). In the present study, the glucokinase level is decreased in STZ-induced diabetic rats; this may be due to the decreasing concentration of insulin after the treatment of C. cassia, the level of glucokinase is increased. This increasing concentration of glucokinase initiates the glycolysis process, and this process reduces the glucose concentration in the blood. Glucose-6-phosphatase is another enzyme involved in the gluconeogenesis and glycogenolysis process (Maiti et al.2004). In the present study, the level of glucose-6-phosphatase is increased, and this may be due to the damage of the liver by the toxin. After the treatment of C. cassia, the level of this enzyme is decreased, this may be due to the liver cell regeneration effect or the increasing concentration of insulin.
Current and emerging gluconeogenesis inhibitors for the treatment of Type 2 diabetes
Published in Expert Opinion on Pharmacotherapy, 2021
When there is insufficient insulin effect, glucose levels rise abnormally leading to the condition of diabetes that has afflicted mankind since the beginning of time. The cause of diabetes is inability to secrete sufficient insulin to suppress glycogenolysis, lipolysis, and gluconeogenesis. Diabetes has been classified into two major types. Type 1 diabetes is caused by a primary deficiency of insulin production, due to an ongoing progressive immune attack on the β cell. Type 2 diabetes is also characterized by a loss of insulin secretory capacity, but there is coexisting resistance to insulin effects in various body tissues [41]. Insulin resistance is characterized by reduced glucose transport across the cell membrane and deficient activity of genomic insulin response units. There is a strong relationship between adipose tissue activity and insulin resistance. Gluconeogenesis and lipogenesis are inseparably intervowen [41,42]. Fatty acids generated by lipolysis play a dominant role in reducing insulin action in the liver and also in muscle. Fat buildup in the liver (nonalcoholic fatty liver disease) contributes to insulin resistance. There is increasing understanding of the primary interaction between white adipose tissue metabolism and gluconeogenesis. Over the past half century, there has been a steady progress in unraveling the biochemical pathways of insulin action and of insulin resistance [41].
Effects of Exercise With and Without Energy Replacement on Substrate Utilization in the Fasting State
Published in Journal of the American College of Nutrition, 2020
Jie Kang, Saif B. Hasan, Nicole A. Ellis, Ira T. Vought, Nicholas A. Ratamess, Jill A. Bush, Avery D. Faigenbaum
When assessed under the exercise condition, the enhanced fat oxidation due to prior exercise seems to diminish, especially at higher intensity. As shown in Table 2, both RER and FOX were trending lower in EO or ER than NE especially during low-intensity exercise. However, even with the effect size (i.e., η2) that are considered “large” (i.e., 0.14 or higher) (33), the differences were marginal, with p values for RER and FOX reaching only 0.10 and 0.08 at 50% VO2max and 0.11 and 0.18 at 70% VO2max, respectively. The lack of significant differences observed during exercise suggests that factors that govern substrate utilization may differ between rest (or post-exercise period) and exercise. As mentioned earlier, an increase in fat utilization at rest or post-exercise can be caused by an increased lipolysis that leads to increased free fatty acid availability. During exercise, especially at higher intensities, however, factors other than fatty acid availability may supersede such regulatory process. It has long been demonstrated that during intense exercise, there will be increased glycogenolysis and glycolysis due to an increased sympathetic drive coupled with an accumulation of signaling molecules, i.e., adenosine diphosphate, inorganic phosphate, and hydrogen ion (34). With more glycogen being degraded into glucose and used, fat utilization reduces (35). Indeed, we observed a much higher COX at 70% VO2max that was nearly identical across the three experimental conditions.