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Voluntary exercise training attenuates the enhanced sympathetic responses to muscle mechanoreflex activation in spontaneously hypertensive rats
Author(s) -
Mizuno Masaki,
Iwamoto Gary,
Vongpatanasin Wanpen,
Mitchell Jere,
Smith Scott
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.1055.8
Subject(s) - medicine , endocrinology , stimulation , sympathetic activity , skeletal muscle , sympathetic nervous system , spontaneously hypertensive rat , blood pressure , sympathetic nerve , mean arterial pressure , physical exercise , heart rate
Exercise training has beneficial effects on cardiovascular diseases such as hypertension. However, the underlying mechanisms remain to be elucidated. The purpose of this study was to examine whether regular exercise reduces abnormally exaggerated skeletal muscle mechanoreflex function in hypertension. Changes in renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) to stimulation of the muscle mechanoreflex were assessed in untrained normotensive Wistar‐Kyoto rats (WKY UT ; n = 6), exercise trained WKY (WKY ET ; n = 7; housed in cage with running wheel for 3 months), untrained spontaneously hypertensive rats (SHR UT ; n = 3) and exercise trained SHR (SHR ET ; n = 7). There was no difference between WKY UT and WKY ET in RSNA (40±11 vs. 47±11 %, respectively) and MAP (7.5±4.0 vs. 8.0±4.2 mmHg, respectively) responses to stimulating the mechanoreflex by passively stretching hindlimb muscles. Voluntary wheel running (3 months) significantly attenuated sympathetic responses to mechanoreflex stimulation in SHR ET compared with SHR UT (35±12 vs. 113±22 %, respectively, P<0.01 ). A similar MAP response profile was likewise produced (14±3 vs. 33±22 mmHg, respectively). In conclusion, our data provide the first direct evidence that voluntary exercise ameliorates abnormal mechanoreflex overactivity in hypertension. Supported by NIH HL‐088422 and HL‐113738