The sustainability of VO2max: effect of decreasing the workload.

The study examined the maintenance of VO(2max) using VO(2max) as the controlling variable instead of power. Therefore, ten subjects performed three exhaustive cycling exercise bouts: (1) an incremental test to determine VO(2max) and the minimal power at VO(2max) (PVO(max)), (2) a constant-power test at PVO(max) and (3) a variable-power test (VPT) during which power was varied to control VO(2) at VO(2max). Stroke volume (SV) was measured by impedance in each test and the stroke volume reserve was calculated as the difference between the maximal and the average 5-s SV. Average power during VPT was significantly lower than PVO(max) (238 ± 79 vs. 305 ± 86 W; p < 0.0001). All subjects, regardless of their VO(2max) values and/or their ability to achieve a VO(2max) plateau during incremental test, were able to sustain VO(2max) for a significantly longer time during VPT compared to constant-power test (CPT) (958 ± 368 s vs. 136 ± 81 s; p < 0.0001). Time to exhaustion at VO(2max) during VPT was correlated with the power drop in the first quarter of the time to exhaustion at VO(2max) (r = 0.71; p < 0.02) and with the stroke volume reserve (r = 0.70, p = 0.02) but was not correlated with VO(2max). This protocol, using VO(2max) rather than power as the controlling variable, demonstrates that the maintenance of exercise at VO(2max) can exceed 15 min independent of the VO(2max) value, suggesting that the ability to sustain exercise at VO(2max) has different limiting factors than those related to the VO(2max) value.

NMR metabolomics for assessment of exercise effects with mouse biofluids.

Exercise modulates the metabolome in urine or blood as demonstrated previously for humans and animal models. Using nuclear magnetic resonance (NMR) metabolomics, the present study compares the metabolic consequences of an exhaustive exercise at peak velocity (Vp) and at critical velocity (Vc) on mice. Since small-volume samples (blood and urine) were collected, dilution was necessary to acquire NMR spectra. Consequently, specific processing methods were applied before statistical analysis. According to the type of exercise (control group, Vp group and Vc group), 26 male mice were divided into three groups. Mice were sacrificed 2 h after the end of exercise, and urine and blood samples were drawn from each mouse. Proton NMR spectra were acquired with urine and deproteinized blood. The NMR data were aligned with the icoshift method and normalised using the probabilistic quotient method. Finally, data were analysed with the orthogonal projection of latent-structure analysis. The spectra obtained with deproteinized blood can neither discriminate the control mice from exercised mice nor discriminate according to the duration of the exercise. With urine samples, a significant statistical model can be estimated when comparing the control mice to both groups, Vc and Vp. The best model is obtained according to the exercise duration with all mice. Taking into account the spectral regions having the highest correlations, the discriminant metabolites are allantoin, inosine and branched-chain amino acids. In conclusion, metabolomic profiles assessed with NMR are highly dependent on the exercise. These results show that urine samples are more informative than blood samples and that the duration of the exercise is a more important parameter to influence the metabolomic status than the exercise velocity.

Cardiac output and performance during a marathon race in middle-aged recreational runners.

PURPOSE: Despite the increasing popularity of marathon running, there are no data on the responses of stroke volume (SV) and cardiac output (CO) to exercise in this context. We sought to establish whether marathon performance is associated with the ability to sustain high fractional use of maximal SV and CO (i.e, cardiac endurance) and/or CO, per meter (i.e., cardiac cost). METHODS: We measured the SV, heart rate (HR), CO, and running speed of 14 recreational runners in an incremental, maximal laboratory test and then during a real marathon race (mean performance: 3 hr 30 min ± 45 min). RESULTS: Our data revealed that HR, SV and CO were all in a high but submaximal steady state during the marathon (87.0 ± 1.6%, 77.2 ± 2.6%, and 68.7 ± 2.8% of maximal values, respectively). Marathon performance was inversely correlated with an upward drift in the CO/speed ratio (mL of CO × m(-1)) (r = -0.65, P < 0.01) and positively correlated with the runner's ability to complete the race at a high percentage of the speed at maximal SV (r = 0.83, P < 0.0002). CONCLUSION: Our results showed that marathon performance is inversely correlated with cardiac cost and positively correlated with cardiac endurance. The CO response could be a benchmark for race performance in recreational marathon runners.

A new incremental test for VO2max accurate measurement by increasing VO2max plateau duration, allowing the investigation of its limiting factors.

The purpose of this study was to (1) validate a new exercise protocol for accurate measurement of VO(2max) by obtention of a VO(2max) plateau for all subjects fit and unfit (2) test the hypothesis that VO(2max) plateau duration is not correlated with VO(2max) and (3) verify that limiting factors of VO(2max) plateau duration are different from those of VO(2max) amplitude. Therefore, 14 subjects performed two incremental cycling tests: (1) a classical incremental test (CIT) to determine VO(2max), the power at VO(2max) (PVO(2max)) and at the lactate threshold (PLT) (2) a new incremental test (NIT) in which the power was decreased just after the subject reached VO(2max). During both protocols, heart rate, stroke volume, cardiac output, the arterio-venous difference and the oxygen blood saturation were recorded. The results showed that, with the NIT, subject could maintain a long VO(2max) plateau (6 ± 3 min), even those who could not reach VO(2max) plateau at the end of CIT (n = 5). The VO(2max) plateau duration was not correlated with VO(2max) amplitude which was correlated with the power at SV(max) (r = 0.888, p < 0.001). The VO(2max) plateau duration was correlated with the power decrease (W/s) during the VO(2max) plateau (r = -0.72, p = 0.003) but not with cardiac-related factors nor with PVO(2max). In conclusion, these experiments showed that it was possible to get a long VO(2max) plateau at the end of NIT whatever the individual VO(2max) amplitude was. The limiting factor of VO(2max) duration was the power output.