Int J Sports Med 2017; 38(04): 270-277
DOI: 10.1055/s-0042-123044
Physiology & Biochemistry
© Georg Thieme Verlag KG Stuttgart · New York

Captopril does not Potentiate Post-Exercise Hypotension: A Randomized Crossover Study

Andréia Cristiane Carrenho Queiroz
1   School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil
2   Federal University of Juiz de Fora, Minas Gerais, Brazil
,
Julio Cesar Silva Sousa Jr.
1   School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil
,
Natan Daniel Silva Jr.
1   School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil
,
Eleonora Tobaldini
3   Department of Biomedical and Clinical Sciences “L. Sacco”, Medicine and Physiopathology, L. Sacco Hospital, University of Milan, Milan, Italy
,
Katia Coelho Ortega
4   General Hospital, University of São Paulo, São Paulo, Brazil
,
Edilamar Menezes de Oliveira
1   School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil
,
Patricia Chakur Brum
1   School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil
,
Nicola Montano
3   Department of Biomedical and Clinical Sciences “L. Sacco”, Medicine and Physiopathology, L. Sacco Hospital, University of Milan, Milan, Italy
,
Decio Mion Jr.
4   General Hospital, University of São Paulo, São Paulo, Brazil
,
Taís Tinucci
1   School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil
,
Claudia Lucia de Moraes Forjaz
1   School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil
› Author Affiliations
Further Information

Publication History



accepted after revision 23 November 2016

Publication Date:
20 February 2017 (online)

Abstract

To evaluate whether captopril (3×50 mg/day) potentiates post-resistance exercise hypotension (PREH) in hypertensives (HT), 12 HT men received captopril and placebo for 4 weeks each in a double-blinded, randomized-crossover design. On each therapy, subjects underwent 2 sessions: Control (C – rest) and Resistance Exercise (RE – 7 exercises, 3 sets to moderate fatigue, 50% of 1 RM –repetition maximum). Measurements were taken before and after 30–60 min (Post1) and 7 h (Post2), and ambulatory blood pressure (BP) was monitored for 24 h. There were no differences in PREH characteristics and mechanisms between the placebo and captopril periods. At Post1, systolic/diastolic BP decreased significantly and similarly after RE with both therapies (Placebo=−13±2/−9±1 mmHg vs. Captopril=−12±2/−10±1 mmHg, P<0.05). RE reduced cardiac output in some subjects and systemic vascular resistance in others. Heart rate and cardiac sympathetic modulation increased, while stroke volume and baroreflex sensitivity decreased after RE (Placebo: +13±2 bpm, +21±5 nu, −11±5 ml, −4±2 ms/mmHg; Captopril: +13±2 bpm, +35±4 nu, 17±5 ml, −3±1 ms/mmHg, P<0.05). At Post2, all variables returned to pre-intervention values. Ambulatory BP was similar between the sessions. Thus, captopril did not potentiate the magnitude and duration of PREH in HT men, and it did not influence PREH mechanisms.

 
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