Physical Exercise Performance in Temperate and Warm Environments Is Decreased by an Impaired Arterial Baroreflex

et al. (2013) Physical Exercise Performance in Temperate and Warm Environments Is Decreased by an Impaired Arterial Baroreflex. PLoS ONE 8(8): e72005. doi:10.1371/journal.pone.0072005 Physical Exercise Performance in Temperate and Warm Environments Is Decreased by an Impaired Arterial Baroreflex Washington Pires 0 Samuel P. Wanner 0 Milene R. M. Lima 0 Ivana A. T. Fonseca 0 Ubirajara Fumega 0 Andrea S. Haibara 0 Cndido C. Coimbra 0 Nilo R. V. Lima 0 Andrej A. Romanovsky, St. Joseph's Hospital and Medical Center, United States of America 0 1 Exercise Physiology Laboratory, Department of Physical Education, School of Physical Education, Physiotherapy and Occupational Therapy, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil, 2 Department of Physiology and Biophysics, Institute of Biological Sciences, Universidade Federal de Minas Gerais , Belo Horizonte, Minas Gerais , Brazil The present study aimed to investigate whether running performance in different environments is dependent on intact arterial baroreceptor reflexes. We also assessed the exercise-induced cardiovascular and thermoregulatory responses in animals lacking arterial baroafferent signals. To accomplish these goals, male Wistar rats were subjected to sinoaortic denervation (SAD) or sham surgery (SHAM) and had a catheter implanted into the ascending aorta to record arterial pressure and a telemetry sensor implanted in the abdominal cavity to record core temperature. After recovering from these surgeries, the animals were subjected to constant- or incremental-speed exercises performed until the voluntary interruption of effort under temperate (25 C) and warm (35 C) conditions. During the constant-speed exercises, the running time until the rats were fatigued was shorter in SAD rats in both environments. Although the core temperature was not significantly different between the groups, tail skin temperature was higher in SAD rats under temperate conditions. The denervated rats also displayed exaggerated increases in blood pressure and double product compared with the SHAM rats; in particular, in the warm environment, these exaggerated cardiovascular responses in the SAD rats persisted until they were fatigued. These SAD-mediated changes occurred in parallel with increased variability in the very low and low components of the systolic arterial pressure power spectrum. The running performance was also affected by SAD during the incremental-speed exercises, with the maximal speed attained being decreased by approximately 20% in both environments. Furthermore, at the maximal power output tolerated during the incremental exercises, the mean arterial pressure, heart rate and double product were exaggerated in the SAD relative to SHAM rats. In conclusion, the chronic absence of the arterial baroafferents accelerates exercise fatigue in temperate and warm environments. Our findings also suggest that an augmented cardiovascular strain accounted for the early interruption of exercise in the SAD rats. - Funding: WP, MRML and IATF were recipients of fellowships from Coordenadoria de Apoio ao Pessoal de Nvel Superior (Brazil). The authors are indebted to the Conselho Nacional de Desenvolvimento Cientfico e Tecnolgico, Fundao de Amparo Pesquisa do Estado de Minas Gerais (PRI-00118-13), and Pr-Reitoria de Pesquisa da Universidade Federal de Minas Gerais for financial support. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing interests: The authors have declared that no competing interests exist. The physical exercise-induced increase in the demand of contracting muscles for oxygen and energetic substrates is a major challenge to body homeostasis and encompasses coordinated responses from the cardiovascular, ventilatory, hormonal, and thermoregulatory systems. To match the higher metabolic demands, landmark physiological responses, such as increases in heart rate (HR), mean arterial pressure (MAP), and the resetting of baroreflexes (which allows simultaneous increases in the HR and MAP), are usually observed immediately after exercise initiation [1,2,3]. The activation of the cardiovascular system occurs in parallel with the activation of the motor centers by a brain-mediated feed-forward mechanism (termed central command), which is integrated with the afferent stimuli from the muscle chemoreceptors (termed exercise pressor reflex) and from the arterial and cardiopulmonary baroreceptors. This integrated cardiovascular control provides physiological responses that match the requirements associated with a given exercise intensity [4]. The carotid and aortic baroreceptors buffer short-term fluctuations of blood pressure by modulating the brain stemmediated autonomic outflow to the heart and blood vessels. These baroreceptors are involved in the cardiac and hemodynamic responses to exercise [5]. Previous reports showed that the surgical removal of the arterial baroafferents of the rat (sinoaortic denervation procedure - SAD) produced exaggerated exercise-induced increases in blood pressure [6,7] and iliac vascular conductance [8], and an exaggerated reduction in mesenteric conductance [9]. These investigations regarding the consequences of an impaired baroreflex sensitivity on the physiological responses to exercise are clinically relevant considering that the loss of sensitivity is an outcome common to many diseases, such as diabetes, obesity, metabolic syndrome, and hypertension [10,11,12], and also considering that physical exercise is a nonpharmacological tool for the treatment of such diseases [13,14]. Although there is substantial evidence demonstrating the role of the arterial baroreceptors in generating adequate autonomiccardiovascular responses to exercise, no study has systematically investigated the effects of cardiovascular alterations induced by arterial barodenervation on prolonged physical performance. A theoretical model that has been recently used to explain exercise fatigue suggests that the interaction between an anticipatory feed-forward control and the afferent signals provided by peripheral receptors generates a conscious perception of effort, which regulates skeletal muscle recruitment and, consequently, exercise intensity [15,16,17]. However, the participation of afferent pathways in modulating physical performance is not universally accepted [18]. In response to exercises performed in a warm environment, the rates of heat dissipation must be greatly increased to avoid the occurrence of exertional hyperthermia, which may threaten survival. Therefore, aside from the high amounts of oxygenated blood and nutrients that are required in the working skeletal muscles, a higher percentage of the cardiac output is directed to the cutaneous vessels to dissipate the body heat [19]. It has been suggested that the higher and simultaneous requirement for blood in the muscles and cutaneous vessels in (...truncated)