Brian E. Hunt

Use of acetylene breathing to determine cardiac output in young and older adults.

PURPOSE The aims of this investigation were: 1). to establish the day-to-day reproducibility of open-circuit acetylene breathing for measuring exercise cardiac output (Q(c)) in young and older adults; and 2). to compare estimates of Q(c) from open-circuit acetylene breathing with estimates of Q(c) from previously established closed-circuit acetylene rebreathing. METHODS Twenty men (10 young: 28 +/- 1 yr; 10 older: 61 +/- 1 yr (mean +/- SE)) performed cycle ergometry exercise on 3 separate days. Q(c) was estimated using open-circuit acetylene breathing on 2 d, and closed-circuit acetylene rebreathing on 1 d. RESULTS Open-circuit acetylene breathing was highly reproducible (young: standard error of measurement (SEM) = 1.52 L.min (-1) limits of agreement (LOA) = 0.2 +/- 4.2 L.min (-1), coefficient of variation 6% < CV < 8%, day 2 = (0.9 x day 1) + 2.4, r = 0.90, P< 0.001, r (2)= 0.82; older: SEM = 0.94 L.min (-1), LOA = 0.1 +/- 2.8 L.min (-1), 4% < CV < 10%, day 2 = (1.0 x day 1) + 0, r = 0.91, < 0.001, r(2) = 0.82). Estimates of Q(c) from open-circuit acetylene breathing demonstrated good agreement with closed-circuit acetylene rebreathing (young: SEM = 1.52 L.min (-1), LOA = 0.9 +/- 4.4 L.min (-1), 5% < CV < 10%, open-circuit = (1.0 x closed-circuit) + 1.5, r = 0.89, < 0.001, r (2) = 0.79; older: SEM = 1.13 L.min (-1), LOA = 0.1 +/- 3.2 L.min (-1), 5% < CV < 9%, open-circuit = (0.9 x closed-circuit) + 1.6, r = 0.88, < 0.001, r(2) = 0.78). CONCLUSION These results demonstrate that open-circuit acetylene breathing provides reproducible measurements of Q(c) during exercise that demonstrate good agreement with values obtained from the acetylene rebreathing procedure in young and older healthy men.

Role of central circulatory factors in the fat-free mass-maximal aerobic capacity relation across age

Fat-free mass (FFM) (primarily skeletal muscle mass) is related to maximal aerobic capacity among healthy humans across the adult age range. The basis for this physiological association is assumed to be a direct relation between skeletal muscle mass and its capacity to consume oxygen. We tested the alternative hypothesis that FFM exerts its influence on maximal aerobic capacity in part via an association with central circulatory function. To do so, we analyzed data from 103 healthy sedentary adults aged 18-75 yr. FFM was strongly and positively related to maximal oxygen consumption ( r = 0.80, P < 0.001). FFM was also strongly and positively related to supine resting levels of blood volume ( r = 0.79, P < 0.001) and stroke volume ( r = 0.75, P < 0.001). Statistically controlling for the collective influences of blood volume and stroke volume abolished the tight relation between FFM and maximal oxygen consumption ( r = 0.12, not significant). These results indicate that 1) FFM may be an important physiological determinant of blood volume and stroke volume among healthy sedentary adult humans of varying age; and 2) this relation between FFM and central circulatory function appears to represent the primary physiological basis for the strong association between FFM and maximal aerobic capacity in this population. Our findings suggest that sarcopenia (loss of skeletal muscle mass with aging) may contribute to the age-related decline in maximal aerobic capacity primarily via reductions in blood volume and stroke volume rather than a direct effect on the oxygen-consuming potential of muscle per se.Fat-free mass (FFM) (primarily skeletal muscle mass) is related to maximal aerobic capacity among healthy humans across the adult age range. The basis for this physiological association is assumed to be a direct relation between skeletal muscle mass and its capacity to consume oxygen. We tested the alternative hypothesis that FFM exerts its influence on maximal aerobic capacity in part via an association with central circulatory function. To do so, we analyzed data from 103 healthy sedentary adults aged 18-75 yr. FFM was strongly and positively related to maximal oxygen consumption (r = 0.80, P < 0. 001). FFM was also strongly and positively related to supine resting levels of blood volume (r = 0.79, P < 0.001) and stroke volume (r = 0.75, P < 0.001). Statistically controlling for the collective influences of blood volume and stroke volume abolished the tight relation between FFM and maximal oxygen consumption (r = 0.12, not significant). These results indicate that 1) FFM may be an important physiological determinant of blood volume and stroke volume among healthy sedentary adult humans of varying age; and 2) this relation between FFM and central circulatory function appears to represent the primary physiological basis for the strong association between FFM and maximal aerobic capacity in this population. Our findings suggest that sarcopenia (loss of skeletal muscle mass with aging) may contribute to the age-related decline in maximal aerobic capacity primarily via reductions in blood volume and stroke volume rather than a direct effect on the oxygen-consuming potential of muscle per se.

Hemodynamic sequelae of age-related increases in arterial stiffness in healthy women

Stiffening of central arteries is believed to contribute to the increase in the incidence of cardiovascular disease with age, presumably through its adverse influence on arterial blood pressure. We found that (1) the physiologic link between age-related increases in arterial stiffness and blood pressure appears to be elevated systemic vascular resistance, and (2) increased arterial stiffness and systemic vascular resistance with age were inversely related to blood volume, stroke volume, and cardiac output.

Baroreflex responsiveness during ventilatory acclimatization in humans

We tested the hypothesis that the decline in muscle sympathetic activity during and after 8 h of poikilocapnic hypoxia (Hx) was associated with a greater sympathetic baroreflex-mediated responsiveness. In 10 healthy men and women (n=2), we measured beat-to-beat blood pressure (Portapres), carotid artery distension (ultrasonography), heart period, and muscle sympathetic nerve activity (SNA; microneurography) during two baroreflex perturbations using the modified Oxford technique before, during, and after 8 h of hypoxia (84% arterial oxygen saturation). The integrated baroreflex response [change of SNA (DeltaSNA)/change of diastolic blood pressure (DeltaDBP)], mechanical (Deltadiastolic diameter/DeltaDBP), and neural (DeltaSNA/Deltadiastolic diameter) components were estimated at each time point. Sympathetic baroreflex responsiveness declined throughout the hypoxic exposure and further declined upon return to normoxia [pre-Hx, -8.3+/-1.2; 1-h Hx, -7.2+/-1.0; 7-h Hx, -4.9+/-1.0; and post-Hx: -4.1+/-0.9 arbitrary integrated units (AIU) x min(-1) x mmHg(-1); P<0.05 vs. previous time point for 1-h, 7-h, and post-Hx values]. This blunting of baroreflex-mediated efferent outflow was not due to a change in the mechanical transduction of arterial pressure into barosensory stretch. Rather, the neural component declined in a similar pattern to that of the integrated reflex response (pre-Hx, -2.70+/-0.53; 1-h Hx, -2.59+/-0.53; 7-h Hx, -1.60+/-0.34; and post-Hx, -1.34+/-0.27 AIU x min(-1) x microm(-1); P < 0.05 vs. pre-Hx for 7-h and post-Hx values). Thus it does not appear as if enhanced baroreflex function is primarily responsible for the reduced muscle SNA observed during intermediate duration hypoxia. However, the central transduction of baroreceptor afferent neural activity into efferent neural activity appears to be reduced during the initial stages of peripheral chemoreceptor acclimatization.