title: Verapamil acutely reduces ventricular-vascular stiffening and improves aerobic exercise performance in elderly individuals.
abstract: OBJECTIVE
  We tested the hypothesis that acute intravenous verapamil acutely enhances aerobic exercise performance in healthy older individuals in association with a combined reduction of ventricular systolic and arterial vascular stiffnesses.
  
  
  BACKGROUND
  Age-related vascular stiffening coupled with systolic ventricular stiffening may limit cardiovascular reserve and, thus, exercise performance in aged individuals.
  
  
  METHODS
  Nineteen healthy volunteers with mean age 70 +/- 10 years underwent maximal-effort upright ergometry tests on two separate days after receiving either 0.15 mg/kg i.v. verapamil or 0.5 N saline in a double-blind, randomized, crossover study.
  
  
  RESULTS
  Baseline vascular stiffness, indexed by arterial pulse-wave velocity (Doppler) and augmentation index (carotid tonometry) declined with verapamil (-5.9 +/- 2.1% and -31.7 +/- 12.8%, respectively, both p < 0.05). Preload-adjusted maximal ventricular power, a surrogate for ventricular end-systolic stiffness, also declined by -9.5 +/- 3.6%. Peripheral resistance and peak filling rate were unchanged. With verapamil, exercise duration prior to the anaerobic threshold (AT) increased by nearly 50% (260 +/- 129 to 387 +/- 176 s) with a corresponding 13.4 +/- 4.7% rise in oxygen consumption (VO2) at that time (both p < 0.01). Total exercise duration prolonged by +6 +/- 2.7% (p < 0.05) with no change in maximal VO2. Baseline cardiodepression from verapamil reversed by peak exercise with net increases in stroke volume and cardiac output (p < 0.05).
  
  
  CONCLUSIONS
  Acute intravenous verapamil reduces ventriculovascular stiffening and improves aerobic exercise performance in healthy aged individuals. This highlights a role for heart-arterial coupling in modulating exertional capacity in the elderly, suggesting a potentially therapeutic target for aged individuals with exertional limitations.
authors.affiliation: Department of Medicine, Johns Hopkins University Medical Institutions, Baltimore, Maryland 21287, USA.
authors.forename: C H
authors.initials: CH
authors.lastname: Chen
authors.forename: M
authors.initials: M
authors.lastname: Nakayama
authors.forename: M
authors.initials: M
authors.lastname: Talbot
authors.forename: E
authors.initials: E
authors.lastname: Nevo
authors.forename: B
authors.initials: B
authors.lastname: Fetics
authors.forename: G
authors.initials: G
authors.lastname: Gerstenblith
authors.forename: L C
authors.initials: LC
authors.lastname: Becker
authors.forename: D A
authors.initials: DA
authors.lastname: Kass
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D018592:Cross-Over Studies; D004311:Double-Blind Method; D005080:Exercise Test / Q000187:drug effects*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects*; D013318:Stroke Volume / Q000187:drug effects; D016896:Treatment Outcome; D014655:Vascular Resistance / Q000187:drug effects*; D016277:Ventricular Function, Left / Q000187:drug effects; D014700:Verapamil / Q000494:pharmacology*
chemical_list: D002121:Calcium Channel Blockers; D014700:Verapamil