Effects of electrically-stimulated exercise and passive motion on echocardiographically-derived wall motion and cardiodynamic function in tetraplegic persons.

The purposes of the study were (1) to characterize left ventricular wall motion, and the cardiodynamic and metabolic responses during electrical stimulation cycle ergometry (ESCE) exercise in tetraplegic people; (2) to test whether these responses linger into the post-exercise recovery period; and (3) to test whether they differ from those imposed by lower extremity continuous passive motion (CPM). Subjects were six tetraplegic males aged 25.8 +/- 3.1 (mean +/- SD) years with spinal cord injuries of 6.7 +/- 3.5 years' duration at the C5 and C6 levels (Frankel classifications A and B). On randomized non-consecutive days, subjects underwent either 30 min of steady-state exercise using transcutaneous electrically-stimulated contractions of bilateral quadriceps, hamstring, and gluteus muscle groups, or 30 min of continuous passive motion at 50 rpm. Data were taken at rest, min 15 and 30 of treatment, and min 5, 15, and 30 post-treatment. Stroke volume (SV) was measured echocardiographically as the product of the left ventricular outflow tract area and the integrated area under the left ventricular outflow tract flow-velocity curve acquired by doppler ultrasound. This value was multiplied by heart rate (HR) to determine the cardiac output (CO). Oxygen consumption (VO2) was monitored spirometrically, with arteriovenous oxygen difference (a-vO2DIFF) computed algebraically. Data were analyzed using repeated measures within-subjects design anaysis of variance, with significance accepted at the 0.05 level. Results showed five subjects had small hyperkinetic ventricles at rest that became more dynamic during ESCE than CPM. Though no systolic dysfunction was noted, all but one subject exhibited some degree of septal hypokinesis at rest and during exercise, possibly indicative of left ventricular noncompliance. Significant effects of condition (ESCE vs CPM), trial (measurement time point), and their interaction, were observed for CO (P < 0.05, 0.01, and 0.0001, respectively), HR (P < 0.0001, 0.05 and 0.005, respectively), and VO2 (P < 0.001, 0.05 and 0.005, respectively). A significant trial and condition by trial interaction was found for a-vO2DIFF (P < 0.05 and 0.0001, respectively). No effects for condition, trial or their interaction were found for SV or BPDIAS. Electrical stimulation cycle ergometry-treated subjects achieved peak VO2 of 712 +/- 300 ml min-1, 2.63 times baseline, with 56% elevation of a-vO2DIFF. Cardiac output increased from 3.5 +/- 1.51 min-1 to 6.0 +/- 2.11 min-1, an elevation solely attributable to a 57% increase in HR. Thus, both CO and a-vO2DIFF accounted for elevated VO2 during ESCE.(ABSTRACT TRUNCATED AT 400 WORDS)