During heavy and severe constant-load exercise, VO2 displays a slow component (VO2sc) typically interpreted as a loss of efficiency of locomotion. In the ongoing debate on the underpinnings of the VO2sc, recent studies suggested that VO2sc could be attributed to a prolonged shift in energetic sources rather than loss of efficiency. We tested the hypothesis that the total cost of cycling, accounting for aerobic and anaerobic energy sources, is affected by time during metabolic transitions in different intensity domains. Eight active men performed 3 constant load trials of 3, 6, and 9 min in the moderate, heavy, and severe domains (i.e., respectively below, between, and above the two ventilatory thresholds). VO2, VO2 of ventilation and lactate accumulation ([La−]) were quantified to calculate the adjusted oxygen cost of exercise (AdjO2Eq, i.e., measured VO2 − VO2 of ventilation + VO2 equivalent of [La−]) for the 0–3, 3–6, and 6–9 time segments at each intensity, and compared by a two-way RM-ANOVA (time × intensity). After the transient phase, AdjO2Eq was unaffected by time in moderate (ml*3 min−1 at 0–3, 0–6, 0–9 min: 2126 ± 939 < 2687 ± 1036, 2731 ± 1035) and heavy (4278 ± 1074 < 5121 ± 1268, 5225 ± 1123) while a significant effect of time was detected in the severe only (5863 ± 1413 < 7061 ± 1516 < 7372 ± 1443). The emergence of the VO2sc was explained by a prolonged shift between aerobic and anaerobic energy sources in heavy (VO2 − VO2 of ventilation: ml*3 min−1 at 0–3, 0–6, 0–9 min: 3769 ± 1128 < 4938 ± 1256, 5091 ± 1123, [La−]: 452 ± 254 < 128 ± 169, 79 ± 135), while a prolonged metabolic shift and a true loss of efficiency explained the emergence of the VO2sc in severe.

Introduction This study aimed to model the dissociation in the V˙O2/power output (PO) relationship between ramp incremental (RI) and constant work rate (CWR) exercise and to develop a novel strategy that resolves this gap and enables an accurate translation of the RI V˙O2 response into a constant PO. Methods Nine young men completed two RI tests (30 and 15 W·min−1) and CWR tests at seven intensities across exercise intensity domains. The V˙O2/PO relationship for RI and CWR exercise was modeled, and the dissociation was compared in terms of PO. The accuracy of three translation strategies was tested in the moderate-intensity (i.e., zone 1) and heavy-intensity (i.e., zone 2) domain. Strategy 1 comprised a simple mean response time correction, whereas strategies 2 and 3 accounted for the loss of mechanical efficiency in zone 2 by applying an extra correction that was based on, respectively, the difference between s 2 − CWR and s 2 − ramp and the ratio s 2/s 1. Results For all intensities, differences in PO were found between CWR and RI exercise (P < 0.001). Overall, these differences were smaller for the 15-W·min−1 compared with the 30-W·min−1 protocol (P = 0.012). Strategy 1 was accurate for PO selection in zone 1 (bias = 0.4 ± 7.3 W), but not in zone 2 (bias = 17.1 ± 15.9 W). Only strategy 2 was found to be accurate for both intensity zones (bias = 2.2 ± 14.2 W) (P = 0.107). Conclusion This study confirmed that a simple mean response time correction works for PO selection in the moderate-intensity but not in the heavy-intensity domain. A novel strategy was tested and validated to accurately prescribe a constant PO based on the RI V˙O2 response in a population of young healthy men.

The data confirm the specificity in the physical requirements of rugby in individual playing positions at all competitive levels and document significant differences among elite and 1st- and 2nd-division players in the same positional role. These differences may reflect the variable technical abilities, selection, training practices, and requirements of the game among these categories.

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The interplay between chronic constraint and advanced aging on blood flow, shear-rate, vascular function, nitric oxide (NO)-bioavailability, microcirculation, and vascular inflammation factors is still a matter of debate. Ninety-eight individuals (Young, n = 28, 23 ± 3 yrs; Old, n = 36, 85 ± 7 yrs; Bedridden, n = 34, 88 ± 6 yrs) were included in the study. The bedridden group included old individuals chronically confined to bed (3.8 ± 2.3 yrs). A blood sample was collected and analyzed for plasma nitrate, and vascular inflammatory markers. Hyperemic response (∆peak) during the single passive leg movement (sPLM) test was used to measure vascular function. Skeletal muscle total hemoglobin was measured at the vastus lateralis during the sPLM test, by means of near infrared spectroscopy (NIRS). Bedridden subjects revealed a depletion of plasma nitrates compared with Old (−23.8%) and Young (−31.1%). Blood flow was lower in the Bedridden in comparison to Old (−20.1%) and Young (−31.7%). Bedridden presented lower sPLM ∆peak compared Old (−72.5%) and the Young (−83.3%). ∆peak of NIRS total hemoglobin was lower in the Bedridden compared to that in the Young (−133%). All vascular inflammatory markers except IL-6 were significantly worse in the Bedridden compared to Old and Young. No differences were found between the Old and Young in inflammatory markers. Results of this study confirm that chronic physical constraint induces an exacerbation of vascular disfunction and differential regulation of vascular-related inflammatory markers. The mechanisms involved in these negative adaptations seems to be associated with endothelial dysfunction and consequent diminished NO-bioavailability likely caused by the reduced shear-rate consequential to long-term reduction of physical activity.