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Cardiac mechanics are impaired during fatiguing exercise and cold pressor test in healthy older adults
Author(s) -
Matthew D. Muller,
Jessica Mast,
Hardikkumar Patel,
Lawrence I. Sinoway
Publication year - 2012
Publication title -
journal of applied physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.253
H-Index - 229
eISSN - 8750-7587
pISSN - 1522-1601
DOI - 10.1152/japplphysiol.01165.2012
Subject(s) - cold pressor test , isometric exercise , medicine , heart rate , cardiology , ventricle , blood pressure , diastole , rate pressure product , hypoxia (environmental) , hemodynamics , oxygen , chemistry , organic chemistry
We sought to determine how the aging left ventricle (LV) responds to sympathetic nervous system (SNS) activation. Three separate echocardiographic experiments were conducted in 11 healthy young (26 ± 1 yr) and 11 healthy older (64 ± 1 yr) adults. Tissue Doppler imaging was used to measure systolic myocardial velocity (S(m)), early diastolic myocardial velocity (E(m)), and late diastolic myocardial velocity (A(m)) during isometric fatiguing handgrip (IFHG), a 2-min cold pressor test (CPT), and 5 min of normobaric hypoxia. Heart rate (HR) and mean arterial pressure (MAP) were also monitored on a beat-by-beat basis; rate pressure product (RPP) was used as an index of myocardial oxygen demand. At peak IFHG, the groups had similar increases in RPP, but the ΔS(m) was significantly greater (i.e., larger impairment) in the older subjects (-0.82 ± 0.13 cm/s) compared with the young subjects (0.37 ± 0.30 cm/s). At peak IFHG, the ΔE(m) was similar between older (-1.59 ± 0.68 cm/s) and young subjects (-1.06 ± 0.76 cm/s). In response to the CPT, both S(m) and E(m) were reduced in the older adults but did not change relative to baseline in the young subjects. Normobaric hypoxia elevated HR and RPP in both groups but did not alter Tissue Doppler parameters. These data indicate that S(m) and E(m) are reduced in healthy older adults during IFHG and CPT. We speculate that suboptimal LV adaptations to SNS stress may partly explain why acute heavy exertion can trigger myocardial ischemia.

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