scholarly journals Looking into Central Governor Theory

2017 ◽  
Vol 3 (1) ◽  
pp. 8-9
Author(s):  
Fernando Pompeu ◽  
Keyword(s):  
2009 ◽  
Vol 34 (5) ◽  
pp. 858-865 ◽  
Author(s):  
Liesl de Milander ◽  
Dan J. Stein ◽  
Malcolm Collins

Previous studies have identified an association of genetic variants believed to alter physiological and biochemical processes locally within the skeletal muscle and therefore performance in the Ironman triathlon. There is growing evidence that the serotonergic system and circulating interleukin (IL)-6 levels are also involved in mediating endurance capacity. Investigators have demonstrated that recombinant human IL-6 administration and serotonergic neurotransmission manipulation, with 5-hydroxytryptamine transporter (5-HTT) and monoamine oxidase A (MAO-A) inhibitors, prior to exercise, can alter running performance, consistent with a central governor hypothesis. The aim of this study was to investigate possible associations of functional polymorphisms within the IL-6 , 5-HTT , and MAO-A genes with endurance performance of Ironman triathletes. Four hundred sixty-eight male Caucasian triathletes who completed the 2000 and (or) 2001 South African Ironman Triathlon and 200 healthy Caucasian male controls were genotyped for the –174 IL-6 G/C, 5-HTT 40 base pair (bp) insertion–deletion and 30 bp variable number of tandem repeats (VNTR) MAO-A gene polymorphisms. There were no significant differences in the relative genotype distributions within the IL-6 (p = 0.636), 5-HTT (p = 0.659), and MOA-A (p = 0.227) polymorphisms when the fastest-fnishing, middle-finishing, and slowest-finishing triathletes, as well as the control groups, were compared. There were no direct associations between the IL-6 –174 G/C, 5-HTT 44 bp insertion–deletion, and MAO-A 30 bp VNTR gene polymorphisms and endurance performance in the 2000 and (or) 2001 South African Ironman Triathlons. The neurogenetic basis of the central governor requires further investigation.


2019 ◽  
Vol 26 (1) ◽  
pp. 21-42 ◽  
Author(s):  
Sophie Laguesse ◽  
Dorit Ron

Although historically research has focused on transcription as the central governor of protein expression, protein translation is now increasingly being recognized as a major factor for determining protein levels within cells. The central nervous system relies on efficient updating of the protein landscape. Thus, coordinated regulation of mRNA localization, initiation, or termination of translation is essential for proper brain function. In particular, dendritic protein synthesis plays a key role in synaptic plasticity underlying learning and memory as well as cognitive processes. Increasing evidence suggests that impaired mRNA translation is a common feature found in numerous psychiatric disorders. In this review, we describe how malfunction of translation contributes to development of psychiatric diseases, including schizophrenia, major depression, bipolar disorder, and addiction.


2018 ◽  
Vol 4 (1) ◽  
pp. e000353
Author(s):  
Flavio Oliveira Pires

Dr Robergs suggested that the central governor model (CGM) is not a well-worded theory, as it deviated from the tenant of falsification criteria. According to his view of science, exercise researches with the intent to prove rather than disprove the theory contribute little to new knowledge and condemn the theory to the label of pseudoscience. However, exercise scientists should be aware of limitations of the falsification criteria. First, the number of potential falsifiers for a given hypothesis is always infinite so that there is no mean to ensure asymmetric comparison between theories. Thus, assuming a competition between CGM and dichotomised central versus peripheral fatigue theories, scientists guided by the falsification principle should know, a priori, all possible falsifiers between these two theories in order to choose the finest one, thereby leading to an oversimplification of the theories. Second, the failure to formulate refutable hypothesis may be a simple consequence of the lack of instruments to make crucial measurements. The use of refutation principles to test the CGM theory requires capable technology for online feedback and feedforward measures integrated in the central nervous system, in a real-time exercise. Consequently, falsification principle is currently impracticable to test CGM theory. The falsification principle must be applied with equilibrium, as we should do with positive induction process, otherwise Popperian philosophy will be incompatible with the actual practice in science. Rather than driving the scientific debate on a biased single view of science, researchers in the field of exercise sciences may benefit more from different views of science.


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