No abstract

To characterize the determinants of the power-duration (W-t) relationship in patients with chronic obstructive pulmonary disease (COPD), we evaluated 8 nonhypoxemic patients (FEV(1) = 1.27 +/- 0.26 L) and 10 healthy controls. After an initial maximum-incremental exercise test on cycle ergometer (peak), the subjects underwent four high-intensity constant-load tests to the limit of tolerance (t), each on different days. The W-t relationship was found to be hyperbolic in both groups. Absolute values of both the critical power asymptote (theta(F)) and the curvature constant (W') were lower in patients than in control subjects. However, when expressed as percentage of peak work rate theta(F) was significantly higher in patients compared with control subjects (81.8 +/- 3.3% versus 67.5 +/- 3.7%, respectively, p < 0.01). There were severe reductions in t in the patients that were consistently associated with higher breathlessness scores and V E/MVV ratios. Interestingly, all patients were able to sustain exercise at theta(F) for 20 min despite near-maximum physiological and subjective stresses. We conclude that the reductions of both parameters of the hyperbolic W-t relationship (theta(F) and W') in patients with COPD were due to the ventilatory constraints and their sensory consequences. Importantly, theta(F) separated a "sustainable" from a "nonsustainable" exercise-intensity domain: this parameter consistently occurred closer to peak work rate in patients than the healthy control subjects.

SUMMARYFor moderate work rates (i.e. below the lactate threshold, OL), oxygen uptake (VO2) approaches the steady state mono-exponentially. At higher work rates, the VO2 kinetics are more complex, reflecting the delayed superimposition of an additional, slow component. The mechanisms of this 'slow' component are poorly understood. It has been demonstrated, however, that while a prior bout of supra-OL cycling (with a 6 min recovery) does not significantly affect the VO. time course for a subsequent sub-OL bout, it significantly speeds the VO2 response to a subsequent supra-OL bout (Gausche, Harmon, Lamarra & Whipp, 1989;Gerbino, Ward & Whipp, 1996). These investigators proposed that this speeding was a result of improved muscle perfusion during the exercise transient, possibly related to the residual metabolic acidaemia still present at the start of the subsequent exercise bout. To determine whether speeding of the VO2 kinetics could also be induced by a bout of prior high-intensity exercise performed at a remote site (e.g. the arms), subjects each performed two 6 min bouts of high-intensity cycling (leg exercise: LE) at a work rate equivalent to 50% of 'ALE' (the difference between maximum 1VO2LE and oLLE). On one occasion this was preceded by a 6 min period of cycling at 50 % ALE and, on another, by a similar period of arm-crank exercise (arm exercise: AE) at 50% AAE; in each case, the work bouts were separated by 6 min of unloaded pedalling. Pulmonary gas exchange variables were derived breath-by-breath. During unloaded pedalling and at minute 6 of each work bout, arterialized venous blood samples were drawn from the dorsum of the heated hand or at the wrist for analysis of pH, lactate, pyruvate, noradrenaline (NAdr), adrenaline (Adr), and potassium (K+). The difference in V02 between minute 6 and 3 of each work bout (AVO ) and the 'partial' 02 deficit (02 Def) provided indices of the slow phase of V02 kinetics. The initial AE and LE bouts resulted in similar degrees of metabolic (lactic) acidaemia; the residual acidaemia at the end of the subsequent 6 min recovery phase was also similar for the two protocols, as were [K+], [Adr] and [NAdr]. The subsequent LE bouts were associated with reductions in both A1!02, and 02 Def, relative to control, with the effect being more marked when the work was preceded by a prior LE bout than a prior AE bout: AV02, averaging 32 and 56 % of control, respectively, and 02 Def 71 and 81 %. Consequently, the increase in [lactate] and decrease in pH induced in this second LE bout were smaller when preceded by prior leg exercise than prior arm exercise. It is therefore concluded that while metabolic acidaemia induced at a site remote from the legs is associated with a less prominent slow phase of the V0 kinetics for high-intensity leg exercise, a component specific to the involved contractile units appears to exert the dominant effect. The mechanisms underlying this response are, however, presently uncertain.