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Influence of menstrual cycle phase on muscle metaboreflex control of cardiac baroreflex sensitivity, heart rate and blood pressure in humans
Author(s) -
Hartwich Doreen,
Aldred Sarah,
Fisher James P.
Publication year - 2013
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2012.066498
Subject(s) - baroreflex , medicine , heart rate , blood pressure , cardiology , endocrinology , skeletal muscle
New Findings• What is the central question of this study? Oestrogen has been reported to modify exercise‐induced autonomic responses and to impact on exercising skeletal muscle blood flow. Together, these oestrogenic influences might attenuate metabolite accumulation and muscle metaboreflex activation during exercise. Moreover, in dogs and in humans, the muscle metaboreflex has been reported to decrease cardiac baroreflex sensitivity during dynamic exercise. • What is the main finding and its importance? Endogenous fluctuations in oestrogen between the early and late follicular phases of the menstrual cycle in healthy women, do not modify either the increase in heart rate and blood pressure or the reduction in spontaneous cardiac baroreflex sensitivity evoked by muscle metaboreflex activation.We sought to determine whether menstrual cycle phase influences muscle metaboreflex control of spontaneous cardiac baroreflex sensitivity (cBRS), blood pressure (BP) and heart rate (HR). Twenty‐three young women not taking oral contraceptives were studied during the early (EF; low oestrogen, low progesterone) and late follicular menstrual phases (LF; high oestrogen, low progesterone). Protocol 1 consisted of leg cycling at low (21 ± 2 W) and moderate workloads (71 ± 3 W) in free‐flow conditions and with partial flow restriction (bilateral thigh‐cuff inflation at 100 mmHg) to activate the muscle metaboreflex. Protocol 2 consisted of rhythmic hand‐grip exercise with incremental upper arm‐cuff inflation (0, 80, 100 and 120 mmHg) to elicit graded metaboreflex activation. Both protocols were followed by post‐exercise ischaemia. Leg cycling decreased cBRS (EF, 20 ± 5, 6 ± 1 and 1 ± 0.1 ms mmHg −1 ; and LF, 19 ± 3, 6 ± 0.4, 1 ± 0.1 ms mmHg −1 during rest, low‐ and moderate‐intensity leg cycling, respectively) and increased HR in an intensity‐dependent manner, while BP remained unchanged. Partial flow restriction during leg cycling decreased cBRS, and increased HR and BP. During post‐exercise ischaemia, HR and BP remained elevated, while cBRS remained suppressed (EF, 4.2 ± 0.6 ms mmHg −1 ; and LF, 4.7 ± 0.5 ms mmHg −1 ; P < 0.05 versus rest). Cardiac baroreflex sensitivity was unchanged during hand‐grip with and without partial flow restriction and post‐exercise ischaemia. No differences in cBRS, HR or BP responses were observed between EF and LF at any time during either protocol. These data indicate that endogenous fluctuations in oestrogen between the EF and LF phases of the menstrual cycle do not influence muscle metaboreflex control of cBRS, BP or HR in young women.