Literature DB >> 11515804

Training reduces autonomic cardiovascular responses to both exercise-dependent and -independent stimuli in humans.

S E O'Sullivan1, C Bell.   

Abstract

Training attenuates the sympathetic pressor response to dynamic exercise. However, it is uncertain how training alters other patterns of cardiovascular autonomic activation. Therefore, we have quantified circulatory responses to a series of standard autonomic tests in highly fit and unfit subjects and examined the effects of a short-term training programme on these responses. Subjects were defined as either unfit (n = 8) or fit (n = 8) on the basis of training history and a maximal fitness test (VO2peak 54 +/- 2.3 cf. 68 +/- 2.8 (ml min(-1)) kg(-1), means + S.E.M., P < 0.05). On a separate day, the blood pressure, heart rate and forearm vascular conductance responses to a sustained handgrip to fatigue, 2 min mental arithmetic and 2 min of cold exposure were measured. All stimuli were associated with elevated blood pressures and heart rates, but these responses were significantly attenuated in the trained group. In the untrained subjects, forearm vascular conductance increased during exercise (from 0.032 +/- 0.004 to 0.05 +/- 0.007 (ml min(-1)) 100 ml(-1) mm Hg(-1), P < 0.05) and during mental arithmetic (from 0.028 +/- 0.003 to 0.04 +/- 0.006 (ml min(-1)) 100 ml(-1) mm Hg(-1) , p < 0.05), but trained subjects showed no rise in conductance during either test. All untrained subjects undertook a moderate intensity 5-week training programme, which significantly increased VO2peak (54 +/- 2.3 to 57 +/- 2 (ml min(-1)) kg(-1), p < 0.05). Qualitatively similar blunting of pressor, tachycardic and vasodilator responses were seen in this group post-training. These results demonstrate that the blunting of sympathetic vasomotor activation that follows training is not restricted to reflexes associated with exercise, and does not depend on training being prolonged or intense.

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Year:  2001        PMID: 11515804     DOI: 10.1016/S1566-0702(01)00288-0

Source DB:  PubMed          Journal:  Auton Neurosci        ISSN: 1566-0702            Impact factor:   3.145


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