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Somatosensory feedback has little influence on endurance exercise performance
Response to Marcora's Letter to the Editor
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Samuele M. Marcora, Senior Lecturer in Exercise Physiology School of Sport, Health and Exercise Sciences, Bangor University, Wales, UK
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s.m.marcora{at}bangor.ac.uk Samuele M. Marcora
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Amann and Dempsey (1) have proposed that inhibitory afferent feedback from fatigued locomotor muscles is a major determinant of central neural drive, and thus performance, during high-intensity endurance exercise in normoxia. However, in our opinion, the results presented here by Amann et al. (2) argue against such hypothesis. First of all, the higher central motor command required to produce a similar submaximal pedal force may simply be a compensatory adjustment to the reduced neuromuscular responsiveness (i.e., muscle force production in response to a given level of voluntary effort) caused by epidural anaesthesia, as demonstrated by the significant reduction in maximal voluntary quadriceps strength. Even if Amann and colleagues were right, and somatosensory feedback from the limbs does indeed exert inhibitory influences on central neural drive during whole body endurance exercise, its effect would be surprisingly small. In fact, pharmacologic blockade of sensory pathways ascending from locomotor muscles increased average EMG activity during the time trial only slightly, from 40.1 to 43.7% of maximal voluntary effort. Obviously, there must be other more important mechanisms (e.g., perception of effort and motivation, refs. 3-4) preventing subjects to voluntarily increase central motor command to much higher levels. Finally, it is clear that reduced neuromuscular responsiveness is more important than afferent feedback from metabolically stressed locomotor muscles in determining endurance exercise performance. In fact, time to complete the 5K trial was 4.2% longer in the epidural condition compared to control (P < 0.05). This finding is in agreement with our recent study demonstrating that an exercise-induced reduction in maximal voluntary quadriceps strength significantly reduces time to exhaustion during intense cycling exercise independently from metabolic stress (5). References 1. Amann M, Dempsey JA. Locomotor muscle fatigue modifies central motor drive in healthy humans and imposes a limitation to exercise performance. J Physiol. 2008; 586(1): 161-73. 2. Amann M, Proctor LT, Sebranek JJ, Eldridge MW, Pegelow DF, Dempsey JA. Somatosensory feedback from the limbs exerts inhibitory influences on central neural drive during whole body endurance exercise. J Appl Physiol (September 11, 2008). doi:10.1152/japplphysiol.90456.2008 3. Marcora S. Is peripheral locomotor muscle fatigue during endurance exercise a variable carefully regulated by a negative feedback system? J Physiol. 2008; 586(7): 2027-8. 4. Marcora SM. Do we really need a central governor to explain brain regulation of exercise performance? Eur J Appl Physiol (July 10, 2008). 10.1007/s00421-008-0818-3 5. Marcora SM, Bosio A, de Morree HM. Locomotor muscle fatigue increases cardiorespiratory responses and reduces performance during intense cycling exercise independently from metabolic stress. Am J Physiol Regul Integr Comp Physiol. 2008; 294(3): R874-83. |
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Markus Amann, PhD, Institute of Physiology, and ETH Zürich, Exercise Physiology University of Zurich, Switzerland
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markus.amann{at}physiol.biol.ethz.ch Markus Amann, PhD
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We firstly need to clarify the misleading first sentence in Marcora’s letter. He took different sentences from some of our previous papers (1, 2), as well as personal communications, to build his critique of our most recent paper (3). Indeed, we previously proposed that the central projection of muscle afferents exerts inhibitory influences on the determination of central motor drive (CMD) during exercise and we further hypothesized that this might limit endurance exercise performance (1, 2). However, in the current study we used epidural lidocaine (L3-L4) to block locomotor muscle afferents during 5 km cycling time-trial (3). We were fully aware of the well known detrimental (local) effects of local anesthetics on motor nerve activity and associated consequences for the force- and power-generating capacity of the locomotor muscles. Therefore, we clearly state, throughout the paper, that our findings are solely restricted to address potential changes only in CMD, but the findings are not suitable to address the effects of muscle afferents on exercise performance. We repeatedly and explicitly emphasize in our writing that, due to the effects of lidocaine on motor nerves, we do not expect improvements in exercise performance – even in the case of a potentially increased CMD. In other words, we clearly emphasize the absolute necessity to dissociate increases in CMD from changes in exercise performance if muscle afferents are blocked via a local anesthetic – a crucial detail not to be overlooked. Having this clarified, we now respond in detail to the letter to the editor. First, the argument presented for a “compensatory adjustment to the reduced neuromuscular responsiveness”, as proposed by the author, remains unclear to us. Second, in contrast to Marcora, we deliberately refrain from evaluating the absolute magnitude of the effect of muscle afferents on CMD as indirectly estimated via surface EMG. Although the difference in relative vastus lateralis surface EMG between the epidural vs control trial was significant, various limitations to this technique –as clearly outlined in the manuscript– prohibit us from judging the absolute effect. Third, we emphasize, throughout the manuscript, that locomotor muscle afferents depict only one of various determinants of the magnitude of CMD during exercise. It needs to be stressed that our data is not suited to allow a comparison of the relative influence of muscle afferents vs other determinants of central motor drive during the time trial exercise. The relative contributions of the various factors remain untested. Finally, “metabolic stress” might not have been very high in Marcora’s study where they observed reduced time to exhaustion in athletes with substantial muscle damage (micro trauma) (4). However, the associated increased level of prostaglandins and leukotrienes in the trial with injured legs depict additional agents (in addition to the exercise-induced increases in metabolic stimuli) stimulating type III/IV muscle afferents during exercise. Thus, the inhibitory effect on the determination of the magnitude of CMD exerted by these fibers cannot be excluded. 1. Amann M, and Dempsey JA. Locomotor muscle fatigue modifies central motor drive in healthy humans and imposes a limitation to exercise performance. J Physiol 586.1: 161-173, 2008. 2. Amann M, Eldridge MW, Lovering AT, Stickland MK, Pegelow DF, and Dempsey JA. Arterial oxygenation influences central motor output and exercise performance via effects on peripheral locomotor muscle fatigue. J Physiol (Lond) 575.3: 937-952, 2006. 3. Amann M, Proctor LT, Sebranek JJ, Eldridge MW, Pegelow DF, and Dempsey JA. Somatosensory feedback from the limbs exerts inhibitory influences on central neural drive during whole body endurance exercise. J Appl Physiol doi:10.1152/japplphysiol.90456.2008: 2008. 4. Marcora SM, Bosio A, and de Morree HM. Locomotor muscle fatigue increases cardiorespiratory responses and reduces performance during intense cycling exercise independently from metabolic stress. Am J Physiol Regul Integr Comp Physiol 294: R874-883, 2008. Markus Amann (1,2), Lester T. Proctor (1), Joshua J. Sebranek (1), Marlowe W. Eldridge (1), David F. Pegelow (1), Jerome A. Dempsey (1) 1 University of Wisconsin-Madison Medical School 2 University of Zürich, Institute of Physiology, and ETH Zürich, Exercise Physiology |
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