. Exercise training changes autonomic cardiovascular balance in mice. J Appl Physiol 96: 2174-2178, 2004. First published January 16, 2004 10.1152/ japplphysiol.00870.2003.-Experiments were performed to investigate the influence of exercise training on cardiovascular function in mice. Heart rate, arterial pressure, baroreflex sensitivity, and autonomic control of heart rate were measured in conscious, unrestrained male C57/6J sedentary ( n ϭ 8) and trained mice (n ϭ 8). The exercise training protocol used a treadmill (1 h/day; 5 days/wk for 4 wk). Baroreflex sensitivity was evaluated by the tachycardic and bradycardic responses induced by sodium nitroprusside and phenylephrine, respectively. Autonomic control of heart rate and intrinsic heart rate were determined by use of methylatropine and propranolol. Resting bradycardia was observed in trained mice compared with sedentary animals [485 Ϯ 9 vs. 612 Ϯ 5 beats/min (bpm)], whereas mean arterial pressure was not different between the groups (106 Ϯ 2 vs. 108 Ϯ 3 mmHg). Baroreflex-mediated tachycardia was significantly enhanced in the trained group (6.97 Ϯ 0.97 vs. 1.6 Ϯ 0.21 bpm/ mmHg, trained vs. sedentary), whereas baroreflex-mediated bradycardia was not altered by training. The tachycardia induced by methylatropine was significantly increased in trained animals (139 Ϯ 12 vs. 40 Ϯ 9 bpm, trained vs. sedentary), whereas the propranolol effect was significantly reduced in the trained group (49 Ϯ 11 vs. 97 Ϯ 11 bpm, trained vs. sedentary). Intrinsic heart rate was similar between groups. In conclusion, dynamic exercise training in mice induced a resting bradycardia and an improvement in baroreflex-mediated tachycardia. These changes are likely related to an increased vagal and decreased sympathetic tone, similar to the exercise response observed in humans. bradycardia; autonomic nervous system; baroreflex; blood pressure RESTING BRADYCARDIA, INDUCED by exercise training, has been well documented in humans and animals; however, the mechanisms underlying the effect are not well understood. Studies in humans suggest that increased vagal activity is responsible for the decrease in heart rate (HR) (31, 32). In contrast, in young trained rats the resting bradycardia was more likely due to alterations in cardiac pacemaker function, a regulator of intrinsic heart rate (IHR), rather than to increased vagal activity (24). Moreover, the improvement in baroreflex control of HR observed in trained animals (3, 10, 11) and humans (1, 26) may also play a role in the basal HR changes.Exercise training induces cardiovascular and metabolic changes that are dependent on exercise intensity and duration as well as physiological condition (1, 8-10, 26, 30). Studies in mice demonstrate that treadmill exercise resulted in linear increases in HR, maximum oxygen consumption (V O 2 max ), and respiratory exchange ratio, similar to that seen in larger species (11). A test of ␤-adrenergic stimulation suggested that sympathetic tone was not altered, whereas vagal input was reduced. Swimming (4-w...

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