Muscle oxygenation during incremental arm-cranking exercise in healthy and hypertensive elderly humans

POURPOSE: We evaluated the factors limiting aerobic arm exercise performance in compensated hypertensive vs healthy elderly males. We hypothesized that, due to cardiovascular modifications associated with high blood pressure, central factors play a larger role, in the age-related decline in arm exercise capacity, in hypertensive rather than in normotensive subjects. METHODS: Non-smoking elderly (14 normotensive, mean age ¡Ó SD 69 ¡Ó 5 yrs and 13 hypertensive, 68 ¡Ó 5) were compared to 10 young males (29 ¡Ó 6 yrs). The subjects performed an incremental arm-cranking test to exhaustion. Ventilation, gas exchange and heart rate (HR) were measured breath by breath (Quark b2, Cosmed, Italy). Changes in concentration of deoxygenated hemoglobin ([deoxyHb], an index of the ratio between O2 consumption and O2 delivery, similar to O2 extraction) were monitored non-invasively by near infrared spectroscopy (HEO-200, Omron, Japan) at the biceps brachii. O2 extraction was expressed as % of the value obtained during arm ischemia (physiological calibration). Peak data were compared for significant differences by one-way analysis of variance. As expected, peak exercise variables were significantly higher in the young compared to the elderly subjects. Yet, no differences in peak values of power output (83„b11; 89„b14 W), VO2 (1.62„b0.29; 1.64„b0.41 l*min-1), HR (147„b14; 152„b11 b*min-1), respiratory quotient (1.18„b0.06; 1.18„b0.08) and oxygen pulse (11„b1.8; 11„b2.4 ml*b-1) were detected in the healthy compared to the hypertensive elderly subjects. £G[deoxyHb] increased as a function of absolute and relative exercise intensity, reaching upon exhaustion 77„b17 and 68„b13 % of ischemia in healthy and hypertensive subjects, respectively (difference not significant). In both elderly populations, peak O2 extraction, was not significantly different from that of young healthy sedentaries (75„b12% of ischemia). CONCLUSIONS: Our data show that arm maximal exercise capacity is reduced to a similar extent in normotensive and hypertensive older compared to young subjects. Since O2 utilization by the working muscles appears unaffected, we suggest that an impairment of O2 delivery is the main responsible for the reduction of arm exercise capacity observed in elderly hypertensive subjects and age-matched healthy sedentaries, compared to young subjects. Furthermore, the relative role of central and peripheral factors in causing the age-related loss of arm exercise capacity is apparently not altered by pathophysiological factors related to compensated hypertension.