We assessed the linearity of oxygen uptake (VO2) kinetics for several work intensities in four trained cyclists. VO2 was measured breath by breath during transitions from 33 W (baseline) to work rates requiring 38, 54, 85, and 100% of maximal aerobic capacity (VO2max). Each subject repeated each work rate four times over 8 test days. In every case, three phases (phases 1, 2, and 3) of the VO2 response could be identified. VO2 during phase 2 was fit by one of two models: model 1, a double exponential where both terms begin together close to the start of phase 2, and model 2, a double exponential where each of the exponential terms begins independently with separate time delays. VO2 rose linearly for the two lower work rates (slope 11 ml.min-1 W-1) but increased to a greater asymptote for the two heavier work rates. In all four subjects, for the two lighter work rates the double-exponential regression reduced to a single value for the time constant (average across subjects 16.1 +/- 7.7 s), indicating a truly monoexponential response. In addition, one of the responses to the heaviest work rate was monoexponential. For the remaining seven biexponential responses to the two heaviest work rates, model 2 produced a significantly better fit to the responses (P less than 0.05), with a mean time delay for the slow component of 105 +/- 46 s.(ABSTRACT TRUNCATED AT 250 WORDS)

Other than during sleep and contrived laboratory testing protocols, humans rarely exist in prolonged metabolic steady states; rather, they transition among different metabolic rates (V O2). The dynamic transition of V O2 (V O2 kinetics), initiated, for example, at exercise onset, provides a unique window into understanding metabolic control. This brief review presents the state-of-the art regarding control of V O2 kinetics within the context of a simple model that helps explain the work rate dependence of V O2 kinetics as well as the effects of environmental perturbations and disease. Insights emerging from application of novel approaches and technologies are integrated into established concepts to assess in what circumstances O2 supply might exert a commanding role over V O2 kinetics, and where it probably does not. The common presumption that capillary blood flow dynamics can be extrapolated accurately from upstream arterial measurements is challenged. From this challenge, new complexities emerge with respect to the relationships between O2 supply and flux across the capillary-myocyte interface and the marked dependence of these processes on muscle fiber type. Indeed, because of interfiber type differences in O2 supply relative to V O2, the presence of much lower O2 levels in the microcirculation supplying fast-twitch muscle fibers, and the demonstrated metabolic sensitivity of muscle to O2, it is possible that fiber type recruitment profiles (and changes thereof) might help explain the slowing of V O2 kinetics at higher work rates and in chronic diseases such as heart failure and diabetes.

No abstract

To determine the change in muscle oxygenation in response to progressively increasing work rate exercise, muscle oxyhemoglobin + oxymyoglobin saturation was measured transcutaneously with near infrared spectroscopy in the vastus lateralis muscle during cycle ergometry. Studies were done in 11 subjects while gas exchange was measured breath-by-breath. As work rate was increased, tissue oxygenation initially either remained constant near resting levels or, more usually, decreased. Near the work rate and metabolic rate where significant lactic acidosis was detected by excess CO2 production (lactic acidosis threshold, LAT), muscle oxygenation decreased more steeply. As maximum oxygen uptake (VO2max) was approached, the rate of desaturation slowed. In 8 of the 11 subjects, tissue O2 saturation reached a minimum which was sustained for 1-3 min before VO2max was reached. The LAT correlated with both the VO2 (r = 0.95, P < 0.0001) and the work rate (r = 0.94, P < 0.0001) at which the rate of tissue O2 desaturation accelerated. These results describe a consistent pattern in the rate of decrease in muscle oxygenation, slowly decreasing over the lower work rate range, decreasing more rapidly in the work rate range of the LAT and then slowing at about 80% of VO2max, approaching or reaching a minimum saturation at VO2max.