Cerebral oxygenation decreases during exercise in humans with beta‐adrenergic blockade

Seifert, Thomas; Rasmussen, Peter; Secher, Niels H.; Nielsen, Henning Bay

doi:10.1111/j.1748-1716.2008.01946.x

Cited by 68 publications

(80 citation statements)

References 48 publications

(62 reference statements)

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“…Conscious deceptions that improve performance include using the Ramachandran mirror to observe the non-fatigued arm when working with the opposite arm (Tanaka et al, 2011), listening to music (Barwood et al, 2009; Lim et al, 2009; Schneider et al, 2010), the provision of inaccurate information provided by a clock that runs slowly (Morton, 2009) or of the actual distance to be covered (Paterson and Marino, 2004), or of the pace of a prior performance that had been deceptively increased by 2% (Stone et al, 2012), or of the true environmental conditions in which the exercise is being performed and the athlete’s real core body temperature response (Castle et al, 2012). Factors that influence performance and which are likely sensed subconsciously include the degree of arterial (Noakes and Marino, 2007) or cerebral oxygenation (Nybo and Rasmussen, 2007; Rupp and Perrey, 2008, 2009; Johnson et al, 2009; Seifert et al, 2009; Billaut et al, 2010; Rasmussen et al, 2010a,b), the size of the muscle glycogen stores (Rauch et al, 2005; Lima-Silva et al, 2010), the extent of fluid loss or thirst (Edwards et al, 2007; Edwards and Noakes, 2009), and variables relating to the rate of heat accumulation (Marino et al, 2000; Tucker et al, 2004, 2006c; Morante and Brotherhood, 2008; Altareki et al, 2009; Flouris and Cheung, 2009; Schlader et al, 2011). A variety of cooling techniques including to the lower body (Castle et al, 2006; Duffield et al, 2010), the upper body (Arngrimsson et al, 2004), the neck (Tyler et al, 2010; Tyler and Sunderland, 2011a,b), or palms (Kwon et al, 2010) all improve performance presumably by altering the nature of the sensory feedback to the control regions in the brain.…”

Section: The Central Governor Model Of Exercise Regulationmentioning

confidence: 99%

Fatigue is a Brain-Derived Emotion that Regulates the Exercise Behavior to Ensure the Protection of Whole Body Homeostasis

Noakes¹

2012

Front. Physio.

368

313

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An influential book written by A. Mosso in the late nineteenth century proposed that fatigue that “at first sight might appear an imperfection of our body, is on the contrary one of its most marvelous perfections. The fatigue increasing more rapidly than the amount of work done saves us from the injury which lesser sensibility would involve for the organism” so that “muscular fatigue also is at bottom an exhaustion of the nervous system.” It has taken more than a century to confirm Mosso’s idea that both the brain and the muscles alter their function during exercise and that fatigue is predominantly an emotion, part of a complex regulation, the goal of which is to protect the body from harm. Mosso’s ideas were supplanted in the English literature by those of A. V. Hill who believed that fatigue was the result of biochemical changes in the exercising limb muscles – “peripheral fatigue” – to which the central nervous system makes no contribution. The past decade has witnessed the growing realization that this brainless model cannot explain exercise performance. This article traces the evolution of our modern understanding of how the CNS regulates exercise specifically to insure that each exercise bout terminates whilst homeostasis is retained in all bodily systems. The brain uses the symptoms of fatigue as key regulators to insure that the exercise is completed before harm develops. These sensations of fatigue are unique to each individual and are illusionary since their generation is largely independent of the real biological state of the athlete at the time they develop. The model predicts that attempts to understand fatigue and to explain superior human athletic performance purely on the basis of the body’s known physiological and metabolic responses to exercise must fail since subconscious and conscious mental decisions made by winners and losers, in both training and competition, are the ultimate determinants of both fatigue and athletic performance.

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Section: The Central Governor Model Of Exercise Regulationmentioning

confidence: 99%

Fatigue is a Brain-Derived Emotion that Regulates the Exercise Behavior to Ensure the Protection of Whole Body Homeostasis

Noakes¹

2012

Front. Physio.

368

313

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“…Under severe hypoxic conditions, several studies reported a relationship between performance and cerebral deoxygenation during various exercise modes such as repeated sprints (Smith and Billaut, 2010), incremental exercise (Peltonen et al, 2009;Subudhi et al, 2009;Vogiatzis et al, 2011), and static maximal muscle contraction to exhaustion Rupp and Perrey, 2009;Goodall et al, 2010). Similarly, exacerbation of the exercise-induced cerebral deoxygenation with nonselective beta-blockade reduces maximal exercise performance under normoxic conditions (Seifert et al, 2009). From these findings, it was hypothesized that reduced cerebral DO 2 and associated cerebral tissue deoxygenation may be a limiting factor of performance during exercise in severe hypoxia ; Amann and Dempsey, 2008; Amann and Kayser, 2009).…”

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confidence: 96%

Fatigue and Exhaustion in Hypoxia: The Role of Cerebral Oxygenation

Fan

Kayser

2016

High Altitude Medicine & Biology

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Fan, Jui-Lin, and Bengt Kayser. Fatigue and exhaustion in hypoxia: the role of cerebral oxygenation. High Alt Med Biol. 17:72-84, 2016.-It is well established that ascent to high altitude is detrimental to one's aerobic capacity and exercise performance. However, despite more than a century of research on the effects of hypoxia on exercise performance, the underlying mechanisms remain incompletely understood. While the cessation of exercise, or the reduction of its intensity, at exhaustion, implies reduced motor recruitment by the central nervous system, the mechanisms leading up to this muscular derecruitment remain elusive. During exercise in normoxia and moderate hypoxia (∼1500-2500 m), peripheral fatigue and activation of muscle afferents probably play a major role in limiting exercise performance. Meanwhile, studies suggested that cerebral tissue deoxygenation may play a pivotal role in impairing aerobic capacity during exercise in more severe hypoxic conditions (∼4500-6000 m). However, recent studies using end-tidal CO2 clamping, to improve cerebral tissue oxygenation during exercise in hypoxia, failed to demonstrate an improvement in exercise performance. In light of these recent findings, which seem to contradict the hypothetical role of cerebral tissue deoxygenation as a performance limiting factor at high altitude, this short review aims to provide a critical reappraisal of the extant literature and ends exploring some potential avenues for further research in this field.

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“…Calculation of the cerebral mitochondrial O 2 tension (P Mito O 2 ) integrates a global measure of cerebral oxygenation in which a reduction in P Mito O 2 of more than 5-6 mmHg is associated with elevated cerebral lactate production, a low OCI, and development of fatigue (24,31). Also, the global cerebral metabolic rate of O 2 (CMRO 2 ) remains stable during moderate exercise, but CMRO 2 increases during strenuous exercise (28,31).…”

mentioning

confidence: 99%

Cerebral oxygenation and metabolism during exercise following three months of endurance training in healthy overweight males

Seifert¹,

Rasmussen²,

Brassard³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Endurance training improves muscular and cardiovascular fitness, but the effect on cerebral oxygenation and metabolism remains unknown. We hypothesized that 3 mo of endurance training would reduce cerebral carbohydrate uptake with maintained cerebral oxygenation during submaximal exercise. Healthy overweight males were included in a randomized, controlled study (training: n = 10; control: n = 7). Arterial and internal jugular venous catheterization was used to determine concentration differences for oxygen, glucose, and lactate across the brain and the oxygen-carbohydrate index [molar uptake of oxygen/(glucose + (1/2) lactate); OCI], changes in mitochondrial oxygen tension (DeltaP(Mito)O(2)) and the cerebral metabolic rate of oxygen (CMRO(2)) were calculated. For all subjects, resting OCI was higher at the 3-mo follow-up (6.3 +/- 1.3 compared with 4.7 +/- 0.9 at baseline, mean +/- SD; P < 0.05) and coincided with a lower plasma epinephrine concentration (P < 0.05). Cerebral adaptations to endurance training manifested when exercising at 70% of maximal oxygen uptake (approximately 211 W). Before training, both OCI (3.9 +/- 0.9) and DeltaP(Mito)O(2) (-22 mmHg) decreased (P < 0.05), whereas CMRO(2) increased by 79 +/- 53 micromol x 100 x g(-1) min(-1) (P < 0.05). At the 3-mo follow-up, OCI (4.9 +/- 1.0) and DeltaP(Mito)O(2) (-7 +/- 13 mmHg) did not decrease significantly from rest and when compared with values before training (P < 0.05), CMRO(2) did not increase. This study demonstrates that endurance training attenuates the cerebral metabolic response to submaximal exercise, as reflected in a lower carbohydrate uptake and maintained cerebral oxygenation.

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Cerebral oxygenation decreases during exercise in humans with beta‐adrenergic blockade

Abstract: Propranolol attenuated the increase in cardiac output of consequence for cerebral perfusion and oxygenation. We suggest that a decrease in cerebral oxygenation limits exercise capacity.

Cited by 68 publications

References 48 publications

Fatigue is a Brain-Derived Emotion that Regulates the Exercise Behavior to Ensure the Protection of Whole Body Homeostasis

Fatigue is a Brain-Derived Emotion that Regulates the Exercise Behavior to Ensure the Protection of Whole Body Homeostasis

Fatigue and Exhaustion in Hypoxia: The Role of Cerebral Oxygenation

Cerebral oxygenation and metabolism during exercise following three months of endurance training in healthy overweight males

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