Central Governor Model Research Articles

Sustained Muscle EMG Activity to Contractile Failure During Incremental Exercise and Intense Constant Load Cycling: No Evidence of a Central Governor

Since 1997, debate has continued over the presence of a central governor that constrains neuromuscular activity during severe, intense exercise. This study aimed to challenge the central governor model (CGM) through acquiring surface electromyography (sEMG) data from the vastus lateralis (VL) and gluteus maximus (Gmax) muscles of 14 healthy participants during 4 different bouts of constant load, non-steady state cycling exercise (110, 125, 140, 160 %watts at the ventilation threshold), and 1 incremental bout to volitional exhaustion. sEMG activity was processed to isolate and capture each contraction of the VL and Gmax during all bouts of exercise. sEMG data was then graphed to profile sEMG root mean square (rms) activity over time with linear curve fitting used to quantify this relationship for data preceding (segment 1) and during the final 30s of each test (segment 2). Two-way repeated measures ANOVA was used to test for differences between the slopes of the two linear segments of the sEMG rms response of the VL for each bout. Results during the VO2max trial revealed a significant main effect for SEGMENT where segment 2 was significantly greater than segment 1 (F=6.741, p=0.023). During the critical power trails there were significant differences in sEMG rms for each of INTENSITY (F=9.349, p<0.001), SEGMENT (F=5.443, p=0.036), and the interaction effect (F=2.837, p=0.005). Muscle sEMG rms data revealed sustained increases in muscle activity in all bouts of intense exercise to volitional exhaustion in both the VL and Gmax, which is inconsistent with the predictions made from the CGM.

Competition Between Desired Competitive Result, Tolerable Homeostatic Disturbance, and Psychophysiological Interpretation Determines Pacing Strategy.

Scientific interest in pacing goes back >100years. Contemporary interest, both as a feature of athletic competition and as a window into understanding fatigue, goes back >30years. Pacing represents the pattern of energy use designed to produce a competitive result while managing fatigue of different origins. Pacing has been studied both against the clock and during head-to-head competition. Several models have been used to explain pacing, including the teleoanticipation model, the central governor model, the anticipatory-feedback-rating of perceived exertion model, the concept of a learned template, the affordance concept, the integrative governor theory, and as an explanation for "falling behind." Early studies, mostly using time-trial exercise, focused on the need to manage homeostatic disturbance. More recent studies, based on head-to-head competition, have focused on an improved understanding of how psychophysiology, beyond the gestalt concept of rating of perceived exertion, can be understood as a mediator of pacing and as an explanation for falling behind. More recent approaches to pacing have focused on the elements of decision making during sport and have expanded the role of psychophysiological responses including sensory-discriminatory, affective-motivational, and cognitive-evaluative dimensions. These approaches have expanded the understanding of variations in pacing, particularly during head-to-head competition.

How to be a better scientist: Lessons from scientific philosophy, the historical development of science, and past errors within exercise physiology

What is science? While a simple question, the answer is complex. Science is a process involving human behaviour, and due to the human influence, science is often not pursued correctly. In fact, one can argue that we still do not know what the “correct” pursuit of science should entail. This is because science remains a work in progress, differs for different questions, and we often are not aware of the mistakes made until years, or decades, later. Such mistakes are common, regardless of the discipline. Within exercise physiology, mistakes have been frequent and led to eventual corrections; the replacement of the post-exercise rate of oxygen consumption (V̇O2) debt concept with that of excess post-exercise V̇O2; the invalidation of the cellular production of lactic acid; improvements to maximal heart rate estimation; and on-going debate over the Central Governor Model. Improved training and education in the historical development of science and the contributions from scientific philosophy are important in providing an understanding of science, and more importantly, how to pursue “better” vs. “inferior” forms of science. The writings of Popper and Kuhn are core to enhanced understanding of how to improve the quality of science pursued. Unfortunately, quality education and training in the historical and philosophical development of science remain poor in most countries. Until inadequate educational training is overcome, there is sustained risk for the pursuit of science to remain inadequate, which in turn has a potential widespread detriment to humanity and the planet we live on.

Effects of combat sports on cerebellar function in adolescents: a resting-state fMRI study.

To evaluate the effects of combat sports on cerebellar function in adolescents based on resting-state functional MRI (rs-fMRI). Rs-fMRI data were acquired from the combat sports (CS) group (n = 32, aged 14.2 ± 1.1 years) and non-athlete healthy control (HC) group (n = 29, aged 14.8 ± 0.9 years). The amplitude of low-frequency fluctuation (ALFF), regional homogeneity (ReHo), and functional connectivity (FC) within the cerebellum was calculated and then compared between the two groups. None of these participants displayed intracranial lesions on conventional MRI and microhemorrhages on SWI. Compared with the HC group, the CS group showed decreased ALFF and ReHo in the bilateral cerebellum, mainly located in the inferior regions of the cerebellum (Cerebellum_8, Cerebellum_9, Cerebellum_7b, and Cerebellum_Crus2). While increased FC was found within the cerebellar network, mainly located in the superior regions near the midline (bilateral Cerebellum_6, Cerebellum_Crus1_R, and Vermis_6). There is no internetwork FC change between the CEN and other networks. This study confirmed extensive effects of combat sports on cerebellar rs-fMRI in adolescents, which could enhance the understanding of cerebellar regulatory mechanism under combat conditions, and provide additional information about cerebellar protective inhibition and compensatory adaptation. Adolescent combat participants are an ideal model to study training-induced brain plasticity and vulnerability. Relative to task-related fMRI, rs-fMRI can bring more information about cerebellar regulation and explain the Central Governor Model more comprehensively.

Brain function during central fatigue induced by intermittent high-intensity cycling.

The central governor model putatively explains the mechanism of endurance exercise-induced central fatigue, however high-intensity exercise-induced central fatigue strategies have not been investigated yet. This study aimed to examine how central fatigue affects neural response alterations, as measured by electroencephalographic (EEG) recordings, in intermittent high-intensity cycling. Neural responses were assessed by measuring the alteration of brainwaves based on spectral energy band estimates during an intermittent, high-intensity, 60-min exercise bout on a cycle ergometer. The cycle ergometer incline was changed every 10min in an intermittent pattern (10-20-5-20-5-10°). EEG was used to analyze altering brain function. Heart rate (HR), blood lactate (BL), and rating of perceived exertion (RPE) were measured after the participants completed each change in incline. The results showed that HR, BL, and RPE increased at an incline of 20° in comparison to a 5° incline. The spectral power of EEG was significantly increased (P˂0.01) in the alpha and beta frequency ranges with a change in inclines between 5 and 20°. The spectral power of the EEG was significantly increased (P˂0.01) over the whole frequency range from rest (theta + 251%, alpha + 165%, beta + 145%). Higher, relative intensities (10 and 20°) increased brain function, regardless of fatigue occurrence. HIIT (high-intensity interval training) led to an alteration in the neural response. Further work investigating the usefulness of HIIT to improve brain function is warranted.

Perceived Impact as the Underpinning Mechanism of the End-Spurt and U-Shape Pacing Patterns.

The end-spurt and U-shape reflect common pacing patterns across a variety of fields (e.g., running, swimming, cycling). To date, however, the literature lacks a clear, parsimonious account for these effects. Here, I propose these pacing patterns can be accounted for by a psychological mechanism termed perceived impact. As athletes perceive their actions to better affect task-progress, they become more motivated and perform better accordingly. To illustrate, if an athlete has five more laps to go during a race, completing the current lap closes 20% of the remaining distance. Alternatively, when she has two more laps to go, the current lap closes 50% of the remaining distance. In the latter case, the impact of completing a single lap on task-progress is perceived to be higher. Her motivation will increase accordingly near the end of the track – giving rise to an end-spurt. I demonstrate the mechanism’s predictive power by reproducing previous findings through simulations. I then move to discuss how this framework is theoretically insightful in view of previous accounts such as the Central Governor Model and the Psyco-Biological Model. I conclude this work with applied strategies for practitioners in their daily routines.

A little bit more about Popper’s philosophy

Professor Robergs recently raised issues based on Popper’s philosophy about the Central Governor Model (CGM), whereby he concluded that the CGM is not a true scientific theory. Thus, he started...

Lessons from a broad view of science: a response to Dr Robergs’ article

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...

The Global Model of Pacing Process for Long and Ultra-Long Distance

Pacing process can be thought as a complex process in which the subject controls the intensity of exercise at any time. It is a key factor determining performance, notably in ultra-endurance events. We agree with the fact that perceived exertion is central in the process of pacing as proposed in the central governor model and the psycho-motivational model, notably. But we claim that using effort, as a unique parameter, is not sufficient and that motivation should be integrated in a more complete manner. The aim of this paper was to explore the role of effort but also other perceptive parameters and motivation in fatigue regulation and pacing process. The impact of motivation and feelings were also envisaged in order to propose a novel model of pacing adapted to ultra-endurance. We explore the manner in which objective and subjective characteristics of the task but also the factors of motivation, emotional state, the level of acceptation of emotional state and physiological state interact which each other in order that the athlete self-selects his intensity during fatiguing exercise. Finally, we propose a new “global model of pacing process” (GMPP) based on the self-determination theory, the theory of goal setting and task motivation, and the theory of energy conservation, in order to have a more holistic view of this complex process.

The Central Governor Model of Exercise Regulation Teaches Us Precious Little about the Nature of Mental Fatigue and Self-Control Failure.

Self-control is considered broadly important for many domains of life. One of its unfortunate features, however, is that it tends to wane over time, with little agreement about why this is the case. Recently, there has been a push to address this problem by looking to the literature in exercise physiology, specifically the work on the central governor model of physical fatigue. Trying to explain how and why mental performance wanes over time, the central governor model suggests that exertion is throttled by some central nervous system mechanism that receives information about energetic bodily needs and motivational drives to regulate exertion and, ultimately, to prevent homeostatic breakdown, chiefly energy depletion. While we admire the spirit of integration and the attempt to shed light on an important topic in psychology, our concern is that the central governor model is very controversial in exercise physiology, with increasing calls to abandon it altogether, making it a poor fit for psychology. Our concerns are threefold. First, while we agree that preservation of bodily homeostasis makes for an elegant ultimate account, the fact that such important homeostatic concerns can be regularly overturned with even slight incentives (e.g., a smile) renders the ultimate account impotent and points to other ultimate functions for fatigue. Second, despite the central governor being thought to take as input information about the metabolic needs of the body, there is no credible evidence that mental effort actually consumes inordinate amounts of energy that are not already circulating in the brain. Third, recent modifications of the model make the central governor appear like an all-knowing homunculus and unfalsifiable in principle, thus contributing very little to our understanding of why people tend to disengage from effortful tasks over time. We note that the latest models in exercise physiology have actually borrowed concepts and models from psychology to understand physical performance.

Using the Placebo Effect to Isolate Control Mechanisms of Athletic Performance: A Research Protocol

Placebo effects are common in all areas of medicine and beyond and thus, are also present when ergogenic aids are used to enhance performance in athletes. While they usually are regarded as secondary and a nuisance in relation to performance-improving nutritional supplements, we here propose to utilize them to investigate central control mechanisms of athletic performance. Following a brief review of the current literature on placebo effects in sports, we outline a research protocol designed to understand the neurobiological basis of endurance performance, limiting factors and the integration of central and peripheral fatigue mechanisms. A placebo response to ergogenic aids will be elicited to isolate and study both central and peripheral components of performance regulation. This protocol employs endurance performance measurements, electroencephalography, functional near-infrared spectroscopy and ratings of perceived exertion in order to quantify the performance altering placebo response elicited by a nutritional ergogenic aid. A model is proposed integrating the placebo response with current theories of performance determining and limiting factors such as the central governor model and the central fatigue hypothesis. The first experiment is concerned with the influence of the mode of administration of an ergogenic aid on endurance performance. In the second experiment, the cortical processes underlying increased motor performance will be investigated using electroencephalography. The third experiment will employ functional near-infrared spectroscopy to look at the integration of cortico-muscular feed forward and feedback signaling pathways mediating fatigue. This protocol provides an integrative approach for neuroscience and sports science research, investigating cortical processes involved in the placebo induced exploitation of residual central and peripheral resources causing better athletic performance. It also will affect prevention and treatment of diseases which may be caused by a lack of physical activity or which may cause a decrease in the ability to be physically active.

What Can Exercise Physiology Teach Us About the Nature of Mental Fatigue and Self-Control Failure: Commentary on Evans, Boggero, & Segerstrom, 2015

Self-control is considered broadly important for many domains of life. One of its unfortunate features, however, is that it tends to wane over time, with little agreement about why this is the case. Recently, there has been a push to address this problem by looking to the literature in exercise physiology, specifically the work on the central governor model of physical fatigue. Trying to explain how and why mental performance wanes over time, the central governor model suggests that exertion is throttled by some central nervous system mechanism that receives information about energetic bodily needs and motivational drives to regulate exertion and, ultimately, to prevent homeostatic breakdown, chiefly energy depletion. While we admire the spirit of integration and the attempt to shed light on an important topic in psychology, our concern is that the central governor model is very controversial in exercise physiologists, with increasing calls to abandon it altogether, making it a poor fit for psychology. Our concerns are threefold. First, while we agree that preservation of bodily homeostasis makes for an elegant ultimate account, the fact that such important homeostatic concerns can be regularly overturned with even slight incentives (e.g., a smile) renders the ultimate account impotent and points to other ultimate functions for fatigue. Second, despite the central governor being thought to take as input information about the metabolic needs of the body, there is no credible evidence that mental effort actually consumes inordinate amounts of energy that are not already circulating in the brain. Third, recent modifications of the model make the central governor appear like an all-knowing homunculus and unfalsifiable in principle, thus contributing very little to our understanding of why people tend to disengage from effortful tasks over time. We note that the latest models in exercise physiology have actually borrowed concepts and models from psychology to understand physical performance.

The evolutionary significance of fatigue

The evolutionary significance of fatigue

Muscle fatigue and muscle weakness: what we know and what we wish we did

Muscle fatigue and muscle weakness: what we know and what we wish we did

Thomas Kuhn's ‘Structure of Scientific Revolutions’ applied to exercise science paradigm shifts: example including the Central Governor Model

According to Thomas Kuhn, the scientific progress of any discipline could be distinguished by a pre-paradigm phase, a normal science phase and a revolution phase. The science advances when a...

Viewpoint: Are there valid concerns for completing a marathon at 39 weeks of pregnancy?

recently, widespread media attention has been given to Amber Danielle Miller, a 27-yr-old woman (163 cm tall), who, at 39 wk of pregnancy, gave birth following her completion of the Chicago Marathon on October 9, 2011 ([17][1], [19][2], [21][3]). She completed the Marathon in 6 h, 25 min, and 50 s

UCT taught me how to challenge beliefs

The world's first successful human heart transplantation on 2 December 1967 inspired me to study medicine at the University of Cape Town Faculty of Health Sciences. There I learned 5 key elements for a successful career in either medicine or science or both - perfectionism, passion, compassion, the dispassionate investigation of all the available evidence, and the need to challenge established beliefs for which the scientific evidence appears imperfect. Challenging such beliefs enabled us to prove that hyponatraemic encephalopathy was caused by persistent and heroic over-drinking during prolonged exercise, usually lasting more than 4 hours, and was unrelated to salt losses in sweat and urine; to understand that the brain not the muscles must regulate the exercise performance, and thus develop the Central Governor Model of Exercise; and to reconsider the dietary causes of the obesity and diabetic epidemic.

Is it Time to Retire the A.V. Hill Model?

Recent publications by Emeritus Professor Roy Shephard propose that a "small group of investigators who have argued repeatedly (over the past 13 years) for a 'Central Governor'," should now either "Put up or shut up." Failing this, their 'hypothesis' should be 'consigned to the bottom draw for future reference'; but Professor Shephard's arguments are contradictory. Thus, in different sections of his article, Professor Shephard explains: why there is no need for a brain to regulate exercise performance; why there is no proof that the brain regulates exercise performance; and why the brain's proven role in the regulation of exercise performance is already so well established that additional comment and research is unnecessary. Hence, "The higher centres of an endurance athlete … call forth an initial effort … at a level where a minimal accumulation of lactate in the peripheral muscles is sensed." Furthermore, "a variety of standard texts have illustrated the many mutually redundant feedback loops (to the nervous system) that limit exercise." Yet, the figure from Professor Shephard's 1982 textbook does not contain any links between the nervous system, "many mutually redundant feedback loops" and skeletal muscle. This disproves his contradictory claims that although there is neither any need for, nor any proof of, any role of the brain in the regulation of exercise performance, the physiological mechanisms for this (non-existent) control were already well established in 1982. In contrast, the Central Governor Model (CGM) developed by our "small group … in a single laboratory" after 1998, provides a simple and unique explanation of how 'redundant feedback loops' can assist in the regulation of exercise behaviour. In this rebuttal to his article, I identify (i) the numerous contradictions included in Professor Shephard's argument; (ii) the real meaning of the facts that he presents; (iii) the importance of the evidence that he ignores; and (iv) the different philosophies of how science should be conducted according to either the Kuhnian or the Popperian philosophies of scientific discovery. My conclusion is that the dominance of an authoritarian Kuhnian philosophy, which refuses to admit genuine error or "the need to alter one's course of belief or action," explains why there is little appetite in the exercise sciences for the acceptance of genuinely novel ideas such as the CGM. Furthermore, to advance the case for the CGM, I now include evidence from more than 30 studies, which, in my opinion, can only be interpreted according to a model of exercise regulation where the CNS, acting in an anticipatory manner, regulates the exercise behaviour by altering skeletal muscle recruitment, specifically to ensure that homeostasis is maintained during exercise. Since few, if any, of those studies can be explained by the 'brainless' A.V. Hill Cardiovascular Model on which Professor Shephard bases his arguments, I argue that it is now the appropriate time to retire that model. Perhaps this will bring to an end the charade that holds either (i) that the brain plays no part in the regulation of exercise performance; or, conversely, (ii) that the role of the brain is already so well defined that further research by other scientists is unnecessary. However, this cannot occur in a discipline that is dominated by an authoritarian Kuhnian philosophy.

RESPONSE

Dear Editor-in-Chief: Thank you for the opportunity to respond. Although we welcome a critical analysis of our work, it appears that Lamberts and Noakes have misinterpreted what we wrote. We actually concluded, "Among well-trained subjects heterogeneous in V˙O2max and running performance, velocity at V˙O2max (vV˙O2max) is the best predictor of running performance because it integrates both maximal aerobic power and economy of running" (6). This is different than concluding that "the cardiovascular model (CVM) explains endurance performance better than the central governor model (CGM)," as they have claimed we did. Lamberts and Noakes label the classic model of physiological factors that determine endurance running performance "the cardiovascular model." We do not agree with this terminology because a number of factors (V˙O2max, running economy, and fractional utilization of V˙O2max) are involved (1,4,5). Lamberts and Noakes contend that "by recruiting the largest possible number of skeletal muscle fibers with the greatest contractile capacity, superior athletes will have the shortest foot contact times and the longest flight time, resulting in superior performance." However, sprinters should be able to recruit a larger number of muscle fibers with the greatest contractile ability because they possess the highest percentage type II muscle fibers. Sprinters also have shorter foot contact times and longer flight times than distance runners (2,3). If Lambert and Noakes were correct, then sprinters would be able to achieve higher peak treadmill velocities and would have faster 16-km run times than distance runners. Because this is not the case, it appears that something is wrong with their theory. We agree that cross-sectional studies cannot prove causation. However, alterations in O2 delivery (through blood doping, erythropoietin, beta blockade, induced anemia, and breathing hypoxic gas mixtures) will impact V˙O2max and endurance performance in predictable ways (1). These findings lend credibility to the claim that V˙O2max is a determinant of distance running performance. In addition, there are logical reasons why V˙O2max, running economy, and fractional utilization of V˙O2max are causally linked to distance running performance. Regarding the claim that we have not proven or disproven the central governor model (CGM), this is true. But the burden of proof for providing evidence to back up the CGM falls on Noakes et al. because they are the leading proponents of this model. Our study was not designed to test Dr. Noakes' CGM, which proposes that a central governor in the brain limits exercise performance to protect the heart and other organ systems from damage. Our study demonstrates that the same variables (V˙O2max and running economy) that are highly correlated with the 16-km run performance are also highly correlated with peak treadmill velocity. Lamberts and Noakes state, "Nor does [our] model predict that exercise performance is limited by oxygen delivery to the muscle…." This highlights the primary difference between the classic model for explaining distance running performance and the CGM. In our view, any model that does not acknowledge O2 delivery as a determinant of endurance exercise performance is severely flawed. James E. McLaughlin Exercise Physiology Department Lynchburg College Lynchburg, VA Edward T. Howley David R. Bassett, Jr. Department of Exercise, Sport, and Leisure Studies University of Tennessee Knoxville, TN

THE IMPORTANCE OF A CORRECT STUDY DESIGN TO DIFFERENTIATE BETWEEN TWO OPPOSING MODELS

Dear Editor-in-Chief: The study of McLaughlin et al. (2) used the outcomes of four different running tests (V˙O2max test, LT test, running economy (RE) test, and peak treadmill velocity (PTV) test) to predict performance in a 16-km time trial run. Linear regression analyses were used to determine which parameter best predicts 16-km running performance. Velocity at V˙O2max (r = −0.972) was found to be the strongest predictor of 16-km running performance followed by V˙O2max (r = −0.907) and PTV (r = −0.902). As velocity at V˙O2max is predicted from the V˙O2max and RE measurement, the authors concluded that the cardiovascular model (CVM) (1) explains endurance performance better than the central governor model (CGM) (4), which they argue requires that the PTV should be the premier performance predictor. Our original suggestion that PVT is linked to muscle power rather that to maximal oxygen transport (5) resulted in the development of the CGM (3,4). This model argues that exercise performance is regulated to maintain homeostasis in all bodily systems (3,4) and is not simply the result of superior muscle power as suggested by McLaughlin et al. (2), nor does this model predict that exercise performance is limited by oxygen delivery to the muscle, as suggested by the CVM. Instead the CGM argues that by recruiting the largest possible number of skeletal muscle fibers with the greatest contractile capacity, superior athletes will have the shortest foot contact times and the longest flight times (6), resulting in the highest maintainable running speeds and superior endurance performance. On the basis of their finding that "velocity at V˙O2max" had the strongest relationship with 16-km running performance, McLaughlin et al. (2) conclude that the capacity for oxygen delivery to the muscle together with RE determines endurance running performance. However, as their cross-sectional research design cannot prove causation, they cannot conclude that the CVM explains running performance better than the CGM. Furthermore, the overlap in 95% confidence intervals for velocity at V˙O2max (r = 0.92-0.99) and PTV (r = 0.74-0.96) suggests that it cannot even be reasonably concluded that velocity at V˙O2max is a better predictor of the 16-km running time than is the PTV. The main point of this letter is to point out that the study of McLaughlin et al. (2) was not designed to determine causality. To compare the predictions of the CGM and the CVM, measurements such as muscle recruitment, muscle contractility, muscle force production, foot contact, and flight times need to be measured in addition to traditional CVM variables such as V˙O2max and its derivates. In the absence of these measurements, McLaughlin et al. seem to have overinterpreted the significance of their findings to find support for the CVM. This example emphasizes the importance of designing the correct experiment to prove causality and the danger of the overinterpretation of findings from an inappropriate research design. Robert Patrick Lamberts Timothy David Noakes UCT/MRC Research Unit for Exercise Science and Sports Medicine Department of Human Biology University of Cape Town Cape Town, South Africa