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ARTICLES: Andrew W. Subudhi, Brittany R. Miramon, Matthew E. Granger, and Robert C. Roach Frontal and motor cortex oxygenation during maximal exercise in normoxia and hypoxia J Appl Physiol 2009; 106: 1153-1158 [Abstract] [Full text] [PDF]

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Brain oxygenation and regulation of exercise performance

Samuele M Marcora   (12 February 2009)

Cerebral oxygenation changes is not explained by the central governor model

Stephane PERREY   (20 March 2009)

Brain oxygenation and regulation of exercise performance 12 February 2009
Samuele M Marcora, Senior Lecturer in Exercise Physiology School of Sport, Health and Exercise Sciences, Bangor University, Wales, UK Send letter to journal: Re: Brain oxygenation and regulation of exercise performance s.m.marcora{at}bangor.ac.uk Samuele M Marcora	To the Editor: Subudhi and colleagues (3) suggest that prefrontal oxygenation would be one of the many afferent signals influencing complex regulation of motor drive during high intensity exercise. The authors support this statement by citing St Clair Gibson and Noakes’s paper descibing the central governor model (2). This theory claims that central neural drive to the locomotor muscles is directly regulated by an intelligent system (the central governor) which makes complex and subconscious decisions on the basis of many afferent signals reflecting the physiological conditions of the body. Before using the central governor model to explain exercise performance, its supporters should provide biological evidence that the neural machinery of this complex and intelligent system actually exists. Therefore, I pose the following questions to Subudhi and colleagues: 1) Is there any evidence that chemoreceptors sensitive to oxygen concentration are present at cortical level? 2) If the answer is yes, where and how do they send their afferent signals? In other words, where is the central governor located in the brain, and what are the afferent pathways connecting the oxygen receptors in the prefrontal cortex to the central governor? Personally, I think that the central governor is a classic example of what Chris Frith calls a “homunculus” (1). In other words, when we think about how our brain works, we often fall into the trap of creating another smaller brain (in this case the central governor) inside the brain we are trying to explain. Clearly, this is not a satisfactory way of understanding how the brain regulates exercise performance. References 1. Frith C. Making up the mind: how the brain creates our mental world. Blackwell Publishing, Malden (MA), 2007. 2. St Clair Gibson A, Noakes TD. Evidence for complex system integration and dynamic neural regulation of skeletal muscle recruitment during exercise in humans. Br J Sports Med 38: 797-806, 2004. 3. Subudhi AW, Miramon BR, Granger ME, Roach RC. Frontal and motor cortex oxygenation during maximal exercise in normoxia and hypoxia. J Appl Physiol (January 15, 2009). doi:10.1152/japplphysiol.91475.2008
Cerebral oxygenation changes is not explained by the central governor model 20 March 2009
Stephane PERREY, PhD Motor Efficiency and Deficiency, University of Montpellier I Send letter to journal: Re: Cerebral oxygenation changes is not explained by the central governor model stephane.perrey{at}univ-montp1.fr Stephane PERREY	To the editor: The eLetter by SM Marcora to the recent paper of Subudhi et al. (6) raised indirectly a key issue on human brain activity function during exercise that is remarkably sparse. While this elegant study proposed new findings on cortical oxygenation with promising multichannel NIRS method, some interpretation/discussion deserve comments. First decreased cerebral oxygenation might reflect reduced central motor command at volitional fatigue in response to whole-body (3, 5) and local (4) exercise with reduced skeletal muscle recruitment in cycling but not during a local fatiguing exercise (4). However, there is still no salient evidence showing that exercise is regulated “in anticipation” by an intelligent, complex system as the CGM. This hypothesis should be put aside here. Second, a new hypothesis may be proposed based on established concepts in cognitive psychology and the neurosciences as well as empirical work on the functional neuroanatomy of higher mental processes. Because of processing in the brain is competing and brain has finite metabolic resources, the transient hypofrontality hypothesis suggests that during exhausting exercise the neural activation required to run motor patterns, assimilate sensory inputs and coordinate regulation results in a decrease of neural activity in brain structures, such as the prefrontal cortex (2). The brain will downregulate neural structures performing functions that an exercising individual can afford to disengage (2). To sum up, decrease in cerebral oxygenation limits exercise capacity (5) but it is not clear how physiological data that support a state of transient hypofrontality correlate with psychological function during exercise, particularly mental processes that limit also exercise tolerance (1). References 1. Marcora SM, Staiano W, Manning V. Mental fatigue impairs physical performance in humans. J Appl Physiol 106: 857-864, 2009. 2. Perrey S. Non-invasive NIR spectroscopy of human brain function during exercise. Methods. 45: 289-299, 2008. 3. Rupp T, Perrey S. Prefrontal cortex oxygenation and neuromuscular responses to exhaustive exercise. Eur J Appl Physiol 102: 153-163, 2008. 4. Rupp T, Perrey S. Effect of severe hypoxia on prefrontal cortex and muscle oxygenation responses at rest and during exhaustive exercise. Adv Exp Med Biol, 645: 329-334, 2009. 5. Seifert T, Rasmussen P, Secher NH, Nielsen HB. Cerebral oxygenation decreases during exercise in humans with beta-adrenergic blockade. Acta Physiol (Oxf), in press. 6. Subudhi AW, Miramon BR, Granger ME, Roach RC. Frontal and motor cortex oxygenation during maximal exercise in normoxia and hypoxia. J Appl Physiol, in press.