Rs. Richardson et al., Evidence of skeletal muscle metabolic reserve during whole body exercise in patients with chronic obstructive pulmonary disease, AM J R CRIT, 159(3), 1999, pp. 881-885
When freed from central cardiorespiratory limitations, healthy human skelet
al muscle has exhibited a significant metabolic reserve. We studied the exi
stence of this reserve in 10 severely compromised (FEV1 = 0.97 +/- SE 0.01)
patients with chronic obstructive pulmonary disease (COPD). To manipulate
O-2 supply and O-2 demand in locomotor and respiratory muscles, subjects pe
rformed both maximal conventional two-legged cycle ergometry (large muscle
mass) and single-leg knee extensor exercise (KE, small muscle mass) while b
reathing room air (RA), 100% O-2, and 79% helium + 21% O-2 (HeO2). With eac
h gas mixture, peak ventilation, peak heart rate, and perceived breathlessn
ess were lower in KE than cycle exercise (p < 0.05). Arterial O-2 saturatio
n and maximal work capacity increased in both exercise modalities while sub
jects breathed 100% O-2 (work: +10% bike, +25% KE, p < 0.05). HeO2 increase
d maximal work capacity on the cycle (+14%, p < 0.05) but had no effect on
KE. HeO2 resulted in the greatest maximum minute ventilation in both bike a
nd KE (p < 0.05) but had no effect on arterial O-2 saturation. Thus, a skel
etal muscle metabolic reserve in these patients with COPD is evidenced by:
(1) greater muscle mass specific work in KE; (2) greater work rates with hi
gher fraction of inspired oxygen (FIO2); (3) an even greater effect of FIO2
during KE (i.e., when the lungs are less challenged); and (4) the positive
effect of HeO2 on bicycle work rate. This skeletal muscle metabolic reserv
e suggests that reduced whole body exercise capacity in COPD is the result
of central restraints rather than peripheral skeletal muscle dysfunction, w
hile the beneficial effect of 100% O-2 (with no change in maximum ventilati
on) suggests that the respiratory system is not the sole constraint to oxyg
en consumption.