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peer-reviewed, Background and purpose: The development of public policies must be guided by full knowledge of the health–disease process of the population. Aerobic exercises are recommended for rehabilitation in stroke patients, and have been shown to improve heart rate variability (HRV). Our aim was to compare the cardiac autonomic modulation of elderly stroke patients with that of healthy elderly people during and after an acute bout of aerobic exercise. Methods: A total of 60 elderly people participated in the study (30 in the control group, mean age of 67 ± 4 years; 30 in the stroke group, mean age of 69 ± 3 years). HRV was analyzed in rest—10 min of rest in supine position; exercise—the 30 min of peak exercise; and recovery—30 min in supine position post-exercise. Results: Taking rest and exercises together, for SDNN, RMSSD, pNN50, RRTri, and TINN, there was no difference between the stroke and control groups (p = 0.062; p = 0.601; p = 0.166; p = 0.224, and p = 0.059, respectively). The HF (ms2 ) was higher and the LF/HF ratio was lower for the stroke group than the control group (p < 0.001 and p = 0.007, respectively). The SD2 was lower for the stroke group than for the control group (p = 0.041). Conclusion: Stroke patients present reduced variability at rest, sympathetic predominance during exercise, and do not return to baseline after the 30 min of recovery, with similar responses found in the healthy elderly group. Keywords: autonomic nervous system; aging; heart rate variability.

Purpose: This study compared blood pressure, heart rate variability (HRV) and forearm blood flow, at rest and in response to sympathoexcitatory stressors between normotensive and mildly hypertensive participants. Methods: Participants aged 30-79 years with normal blood pressure (n = 49) or mild hypertension (n = 17), with no history of taking antihypertensive medication, were recruited. Participants completed a cold pressor test (CPT) followed by an ischaemic handgrip test (IHGT). Blood pressure, HRV, forearm blood flow and vascular resistance were measured at rest and in response to each test. Results: The CPT and IHGT evoked greater increases in mean arterial blood pressure in hypertensive participants (CPT: 10 ± 2 mmHg, IHGT: 9 ± 1 mmHg) compared with normotensive participants (CPT: 5 ± 1 mmHg, IHGT: 3 ± 1 mmHg; P < 0.05). Resting high frequency power, which is a parameter of HRV associated with parasympathetic cardiac modulation, was lower in hypertensive participants (hypertensive: 31.73 ± 4.07 nu; normotensive: 42.08 ± 2.22 nu; P = 0.026) and was negatively correlated with systolic blood pressure (r = -0.272, P = 0.03) and mean arterial pressure across all participants (r = -0.258, P < 0.05). There were no differences in HRV or forearm blood flow responses to the CPT or IHGT between groups. Conclusion: This study demonstrated that sympathoexcitatory stress evoked by the CPT and IHGT induces an augmented blood pressure response in individuals with mild hypertension, which supports the notion that autonomic dysfunction is likely to contribute to the pathogenesis of hypertension. It remains to be determined whether the hypertensive response is mediated through alterations in cardiac activity, peripheral vascular resistance or both.

Purpose: This study compared blood pressure, heart rate variability (HRV) and forearm blood flow, at rest and in response to sympathoexcitatory stressors between normotensive and mildly hypertensive participants. Methods: Participants aged 30-79 years with normal blood pressure (n = 49) or mild hypertension (n = 17), with no history of taking antihypertensive medication, were recruited. Participants completed a cold pressor test (CPT) followed by an ischaemic handgrip test (IHGT). Blood pressure, HRV, forearm blood flow and vascular resistance were measured at rest and in response to each test. Results: The CPT and IHGT evoked greater increases in mean arterial blood pressure in hypertensive participants (CPT: 10 ± 2 mmHg, IHGT: 9 ± 1 mmHg) compared with normotensive participants (CPT: 5 ± 1 mmHg, IHGT: 3 ± 1 mmHg; P < 0.05). Resting high frequency power, which is a parameter of HRV associated with parasympathetic cardiac modulation, was lower in hypertensive participants (hypertensive: 31.73 ± 4.07 nu; normotensive: 42.08 ± 2.22 nu; P = 0.026) and was negatively correlated with systolic blood pressure (r = -0.272, P = 0.03) and mean arterial pressure across all participants (r = -0.258, P < 0.05). There were no differences in HRV or forearm blood flow responses to the CPT or IHGT between groups. Conclusion: This study demonstrated that sympathoexcitatory stress evoked by the CPT and IHGT induces an augmented blood pressure response in individuals with mild hypertension, which supports the notion that autonomic dysfunction is likely to contribute to the pathogenesis of hypertension. It remains to be determined whether the hypertensive response is mediated through alterations in cardiac activity, peripheral vascular resistance or both.

Purpose: This study compared blood pressure, heart rate variability (HRV) and forearm blood flow, at rest and in response to sympathoexcitatory stressors between normotensive and mildly hypertensive participants. Methods: Participants aged 30-79 years with normal blood pressure (n = 49) or mild hypertension (n = 17), with no history of taking antihypertensive medication, were recruited. Participants completed a cold pressor test (CPT) followed by an ischaemic handgrip test (IHGT). Blood pressure, HRV, forearm blood flow and vascular resistance were measured at rest and in response to each test. Results: The CPT and IHGT evoked greater increases in mean arterial blood pressure in hypertensive participants (CPT: 10 ± 2 mmHg, IHGT: 9 ± 1 mmHg) compared with normotensive participants (CPT: 5 ± 1 mmHg, IHGT: 3 ± 1 mmHg; P < 0.05). Resting high frequency power, which is a parameter of HRV associated with parasympathetic cardiac modulation, was lower in hypertensive participants (hypertensive: 31.73 ± 4.07 nu; normotensive: 42.08 ± 2.22 nu; P = 0.026) and was negatively correlated with systolic blood pressure (r = -0.272, P = 0.03) and mean arterial pressure across all participants (r = -0.258, P < 0.05). There were no differences in HRV or forearm blood flow responses to the CPT or IHGT between groups. Conclusion: This study demonstrated that sympathoexcitatory stress evoked by the CPT and IHGT induces an augmented blood pressure response in individuals with mild hypertension, which supports the notion that autonomic dysfunction is likely to contribute to the pathogenesis of hypertension. It remains to be determined whether the hypertensive response is mediated through alterations in cardiac activity, peripheral vascular resistance or both.