Search

Objective: We investigated the respiratory and vastus lateralis oxygenation responses to exhaustive, constant-load cycling at two exercise intensities. Methods: Eight moderately-trained male randomly cycled to exhaustion at 75% and 85% of maximal work-load (CL75 and CL85, respectively) measured during a maximal incremental test. From continuous recordings of respiratory variables and near-infrared spectroscopy signals of the vastus lateralis muscle, VO2 slow component (SC) and deoxyhemoglobin (HHb) SC were calculated. Results: At exhaustion, VO2 (+19 ± 25%), VO2 SC (+59 ± 24%) and minute ventilation (+14 ± 14%) were significantly higher during CL85 vs. CL75, whereas oxyhemoglobin (-67 ± 22%) and total hemoglobin (-36 ± 3%) responses were lower (all p<0.05). Additionally, VO2 SC during CL75 and CL85 were strongly correlated (r=0.88, p<0.001). The HHb SC did not differ between CL75 and CL85 (3.10 ± 0.75 vs. 3.44 ± 1.1 A.U, respectively; p=0.60). HHb SC and VO2 SC during CL85 (r=0.94, p<0.001), but not during CL75 (r=-0.08, p=0.90), were correlated. Finally, HHb SC during CL75 and CL85 were unrelated (r=-0.20, p=0.70). Conclusion: Our results highlight that only the contribution of locomotor muscles to the VO2 SC magnitude is affected by the exercise intensity and not that of ventilation.

Objective: We investigated the respiratory and vastus lateralis oxygenation responses to exhaustive, constant-load cycling at two exercise intensities. Methods: Eight moderately-trained male randomly cycled to exhaustion at 75% and 85% of maximal work-load (CL75 and CL85, respectively) measured during a maximal incremental test. From continuous recordings of respiratory variables and near-infrared spectroscopy signals of the vastus lateralis muscle, VO2 slow component (SC) and deoxyhemoglobin (HHb) SC were calculated. Results: At exhaustion, VO2 (+19 ± 25%), VO2 SC (+59 ± 24%) and minute ventilation (+14 ± 14%) were significantly higher during CL85 vs. CL75, whereas oxyhemoglobin (-67 ± 22%) and total hemoglobin (-36 ± 3%) responses were lower (all p<0.05). Additionally, VO2 SC during CL75 and CL85 were strongly correlated (r=0.88, p<0.001). The HHb SC did not differ between CL75 and CL85 (3.10 ± 0.75 vs. 3.44 ± 1.1 A.U, respectively; p=0.60). HHb SC and VO2 SC during CL85 (r=0.94, p<0.001), but not during CL75 (r=-0.08, p=0.90), were correlated. Finally, HHb SC during CL75 and CL85 were unrelated (r=-0.20, p=0.70). Conclusion: Our results highlight that only the contribution of locomotor muscles to the VO2 SC magnitude is affected by the exercise intensity and not that of ventilation.

We assessed respiratory muscles oxygenation responses during a ramp exercise to exhaustion and further explored their relationship with the non-linear increase of VO2 (VO2 excess) observed above the gas-exchange threshold. Ten male cyclists completed a ramp exercise to exhaustion on an electromagnetically braked cycle-ergometer with a rate of increment of 30 W min−1 with continuous monitoring of expired gases (breath-by-breath) and oxygenation status of intercostal muscles. Maximal inspiratory and expiratory pressure measurements were taken at rest and at exhaustion. The VO2 excess represents the difference between VO2max observed and VO2max expected using linear equation between the VO2 and the intensity before gas-exchange threshold. The deoxyhemoglobin remained unchanged until 60% of maximal aerobic power (MAP) and thereafter increased significantly by 37 ± 18% and 40 ± 22% at 80% and 100% of MAP, respectively. Additionally, the amplitude of deoxyhemoglobin increase between 60 and 100% of MAP positively correlated with the VO2 excess (r = 0.69, p < 0.05). Compared to exercise start, the oxygen tissue saturation index decreased from 80% of MAP (−4.8 ± 3.2%, p < 0.05) onwards. At exhaustion, maximal inspiratory and expiratory pressures declined by 7.8 ± 16% and 12.6 ± 10% (both p < 0.05), respectively. In summary, our results suggest a significant contribution of respiratory muscles to the VO2 excess phenomenon.

We assessed respiratory muscles oxygenation responses during a ramp exercise to exhaustion and further explored their relationship with the non-linear increase of VO2 (VO2 excess) observed above the gas-exchange threshold. Ten male cyclists completed a ramp exercise to exhaustion on an electromagnetically braked cycle-ergometer with a rate of increment of 30 W min−1 with continuous monitoring of expired gases (breath-by-breath) and oxygenation status of intercostal muscles. Maximal inspiratory and expiratory pressure measurements were taken at rest and at exhaustion. The VO2 excess represents the difference between VO2max observed and VO2max expected using linear equation between the VO2 and the intensity before gas-exchange threshold. The deoxyhemoglobin remained unchanged until 60% of maximal aerobic power (MAP) and thereafter increased significantly by 37 ± 18% and 40 ± 22% at 80% and 100% of MAP, respectively. Additionally, the amplitude of deoxyhemoglobin increase between 60 and 100% of MAP positively correlated with the VO2 excess (r = 0.69, p < 0.05). Compared to exercise start, the oxygen tissue saturation index decreased from 80% of MAP (−4.8 ± 3.2%, p < 0.05) onwards. At exhaustion, maximal inspiratory and expiratory pressures declined by 7.8 ± 16% and 12.6 ± 10% (both p < 0.05), respectively. In summary, our results suggest a significant contribution of respiratory muscles to the VO2 excess phenomenon.