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Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Blvd, Fort Worth, TX 76107-2699, USA

	Introduction

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In concert with Experimental Physiology's commitment to focus on Translation and Integration, we are pleased to publish a series of articles on the theme of Neural Control of the Circulation during Exercise. These articles summarize recent information regarding the vertical integration of a myriad of neural signals emanating from active skeletal muscle and the brain. The use of exercise is the sine qua non in experimental investigations of integrated neural control mechanisms and clinical diagnostic testing of cardiovascular function. The invited articles of this thematic issue provide a review of current thinking regarding the roles of the two major concepts of neural control of the circulation during exercise, i.e. central command and the exercise pressor reflex, their actions and their interactions in influencing arterial baroreflex control of arterial blood pressure in health and disease. The articles cover a spectrum of investigative approaches using: (i) clinical and integrative physiological measurements in animals and humans; (ii) studies identifying central neural mechanisms using electrophysiological and molecular biologic techniques in in vivo rat and mouse models; and (iii) state-of-the-art brain imaging techniques in humans. A major unresolved question of circulatory control seeks the answer to whether the arterial baroreflexes are ‘reset’ to regulate the prevailing arterial blood pressure induced by the exercise or whether they are ‘switched off’ or ‘ignored’. The bulk of the evidence indicates that the arterial baroreflex is ‘reset’. Subsequently, the mechanisms underlying the ‘resetting’ at the organ system level in healthy human subjects and how the baroreflex modifies the mechanisms of the exercise pressor reflex in the normal state and in the cardiac failure dog model are reviewed. The neurophysiological mechanisms involved are addressed using current molecular biological techniques as well as state-of-the-art imaging and complex monitoring of haemodynamic responses. In the past few years the scope of the investigations has broadened to address specific disease states, such as hypertension and congestive heart failure, using cellular and molecular biological techniques.

About the articles

The article by Joyner (2006) (Mayo Clinic) provides a historical background of the animal and human experiments that formed the foundation from which the questions addressed in the accompanying review articles were spawned. The historical importance of the work of John T. Shephard and David Donald, along with a description of the 1960s development of a revolutionary clinical technique of electrically stimulating the carotid sinus nerve to reduce symptoms of angina pectoris, provides support for the underlying philosophy of the journal. As noted by Coote & Paterson (2004), the philosophy of translation and integration was best described in a quote from Pascal:

I hold it equally impossible to know the parts without knowing the whole and to know the whole without knowing the parts in detail.

In those investigations designed to address the historical questions raised (Joyner, 2006) there is clear evidence that the arterial baroreflexes are reset at the onset of exercise and continue to be reset with increasing exercise intensity (Raven et al. 2006). Addressing the questions as to what neural mechanisms were involved in this resetting required a hypothetical model to integrate the established roles of both central command and the exercise pressor reflex in increasing arterial blood pressure. In human subjects these questions required innovative experimental protocols and the use of non-invasive and invasive techniques to selectively activate central command or the exercise pressor reflex (Raven et al. 2006). One set of human experiments that sought to selectively manipulate central command involved hypnotic suggestion and imagination, while identifying areas of brain activity via state-of-the-art brain imaging techniques (Williamson et al. 2006). Not surprisingly, the identification of specific central nuclei and central neural mechanisms requires in vivo animal preparations, which enable cellular, molecular and electrophysiological techniques to be used. During the past decade, ‘resetting’ was shown to be accomplished by central neural mechanisms that integrate neural signals from the cortex, the skeletal muscle and the baroreflexes. This integration appears to occur within the nucleus tractus solitarii (NTS) and rostral ventolateral medulla (Potts, 2006). Animal models of cardiac failure provide evidence that when the exercise pressor reflex is chronically activated the integration within the NTS results in an exacerbation of the sympathetic efferent outflow to the heart and peripheral vasculature, probably due to impaired ability of the baroreflex to buffer the exercise pressor reflex during exercise (O'Leary, 2006).

The invited and accepted original research submissions presented in this themed issue of Experimental Physiology (Raven et al. 2006; Joyner, 2006; Williamson et al. 2006; O'Leary, 2006; Potts, 2006; Gallagher et al. 2006; Smith et al. 2006; Koba et al. 2006; Nishiyasu et al. 2006) provide a roadmap by which the clinician, the integrative physiologist and the cellular and molecular biologist can address questions of physiology and pathophysiology concerning the neural control of the circulation during exercise. To develop these interactions, it is essential to establish a model of a working hypothesis which is based upon historical precedents to address the fundamental questions. Answering the questions raised by this model requires a multidisciplinary experimental approach that marries molecular and cellular mechanisms with the physiological mechanisms of organ system function.

	References

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Coote & Paterson (2005). Exp Physiol 90, 1–2.[Free Full Text]

Gallagher KM, Fadel PJ, Smith SA, Strømstad M, Ide K, Secher NH & Raven PB (2006). The interaction of central command and the exercise pressor reflex in mediating baroreflex resetting during exercise in men. Exp Physiol 91, 79–87.[Abstract/Free Full Text]

Joyner MJ (2006). Baroreceptor function during exercise: resetting the record. Exp Physiol 91, 27–36.[Abstract/Free Full Text]

Koba S, Yoshida T & Hayashi N (2006). Renal sympathetic and circulatory responses to activation of the exercise pressor reflex in rats. Exp Physiol 91, 111–119.[Abstract/Free Full Text]

Nishiyasu T, Maekawa T, Sone R, Tan N & Kondo N (2006). Effects of rhythmic muscle compression on cardiovascular responses and muscle oxygenation at rest and during dynamic exercise in humans. Exp Physiol 91, 103–109.[Abstract/Free Full Text]

O'Leary (2006). Exp Physiol 91, 73–77.[Abstract/Free Full Text]

Potts JT (2006). Inhibitory neurotransmission in the nucleus tractus solitarii: implications for baroreflex resetting during exercise. Exp Physiol 91, 59–72.[Abstract/Free Full Text]

Raven PB, Fadel PJ & Ogoh S (2006). Arterial baroreflex resetting during exercise: a current perspective. Exp Physiol 91, 37–49.[Abstract/Free Full Text]

Smith SA, Mitchell JH & Garry MG (2006). The exercise pressor reflex in health and disease. Exp Physiol 91, 89–102.[Abstract/Free Full Text]

Williamson JW, Fadel PJ & Mitchell JH (2006). New insights into central cardiovascular control during exercise in humans: a central command update. Exp Physiol 91, 51–58.[Abstract/Free Full Text]

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