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Purpose This study examined the relationship of physiological and anthropometric characteristics with parameters of the critical power (CP) model, and in particular the reconstitution of W′ following successive bouts of maximal exercise, amongst trained and untrained cyclists. Methods Twenty male adults (trained nine; untrained 11; age 39 ± 15 year; mass 74.7 ± 8.7 kg; V̇O2max 58.0 ± 8.7 mL kg−1 min−1) completed three incremental ramps (20 W min−1) to exhaustion interspersed with 2-min recoveries. Pearson’s correlation coefficients were used to assess relationships for W′ reconstitution after the first recovery (W′rec1), the delta in W′ reconstituted between recoveries (∆W′rec), CP and W′. Results CP was strongly related to V̇O2max for both trained (r = 0.82) and untrained participants (r = 0.71), whereas W′ was related to V̇O2max when both groups were considered together (r = 0.54). W′rec1 was strongly related to V̇O2max for the trained (r = 0.81) but not untrained (r = 0.18); similarly, ∆W′rec was strongly related to V̇O2max (r = − 0.85) and CP (r = − 0.71) in the trained group only. Conclusions Notable physiological relationships between parameters of aerobic fitness and the measurements of W′ reconstitution were observed, which differed among groups. The amount of W′ reconstitution and the maintenance of W′ reconstitution that occurred with repeated bouts of maximal exercise were found to be related to key measures of aerobic fitness such as CP and V̇O2max. This data demonstrates that trained cyclists wishing to improve their rate of W′ reconstitution following repeated efforts should focus training on improving key aspects of aerobic fitness such as V̇O2max and CP.

This study tested the hypothesis that the respiratory compensation point (RCP) and breakpoint in deoxygenated [heme] [deoxy[heme]BP, assessed via near-infrared spectroscopy (NIRS)] during ramp incremental exercise would occur at the same metabolic rate in the upright (U) and supine (S) body positions. Eleven healthy men completed ramp incremental exercise tests in U and S. Gas exchange was measured breath-by-breath and time-resolved-NIRS was used to measure deoxy[heme] in the vastus lateralis (VL) and rectus femoris (RF). RCP (S: 2.56 ± 0.39, U: 2.86 ± 0.40 L·min−1, P = 0.02) differed from deoxy[heme]BP in the VL in U (3.10 ± 0.44 L·min−1, P = 0.002), but was not different in S in the VL (2.70 ± 0.50 L·min−1, P = 0.15). RCP was not different from the deoxy[heme]BP in the RF for either position (S: 2.34 ± 0.48 L·min−1, U: 2.76 ± 0.53 L·min−1, P > 0.05). However, the deoxy[heme]BP differed between muscles in both positions ( P < 0.05), and changes in deoxy[heme]BP did not relate to ΔRCP between positions (VL: r = 0.55, P = 0.080, RF: r = 0.26, P = 0.44). The deoxy[heme]BP was consistently preceded by a breakpoint in total[heme], and was, in turn, itself preceded by a breakpoint in muscle surface electromyography (EMG). RCP and the deoxy[heme]BP can be dissociated across muscles and different body positions and, therefore, do not represent the same underlying physiological phenomenon. The deoxy[heme]BP may, however, be mechanistically related to breakpoints in total[heme] and muscle activity.

We hypothesize that the V̇O(2) time constant (τ(V̇O2)) determines exercise tolerance by defining the power output associated with a “critical threshold” of intramuscular metabolite accumulation (e.g. inorganic phosphate), above which muscle fatigue and work inefficiency are apparent. Thereafter, the V̇O(2) “slow component”, and its consequences (increased pulmonary, circulatory and neuromuscular demands) determine performance limits.

Purpose We tested the hypothesis that incremental ramp cycling exercise performed in the supine position (S) would be associated with an increased reliance on muscle deoxygenation (deoxy[heme]) in the deep and superficial vastus lateralis (VLd and VLs, respectively) and the superficial rectus femoris (RFs) when compared to the upright position (U). Methods 11 healthy men completed ramp incremental exercise tests in S and U. Pulmonary $$\dot{V}$$ V ˙ O2 was measured breath-by-breath; deoxy[heme] was determined via time-resolved near-infrared spectroscopy in the VLd, VLs and RFs. Results Supine exercise increased the overall change in deoxy[heme] from baseline to maximal exercise in the VLs (S: 38 ± 23 vs. U: 26 ± 15 μM, P S: 36 ± 21 vs. U: 25 ± 15 μM, P S: 32 ± 23 vs. U: 29 ± 26 μM, P > 0.05). Conclusions The present study supports that the impaired balance between O2 delivery and O2 utilization observed during supine exercise is a regional phenomenon within superficial muscles. Thus, deep muscle defended its O2 delivery/utilization balance against the supine-induced reductions in perfusion pressure. The differential responses of these muscle regions may be explained by a regional heterogeneity of vascular and metabolic control properties, perhaps related to fiber type composition.

Critical power is a fundamental parameter defining high‐intensity exercise tolerance, and is related to the phase II time constant of pulmonary oxygen uptake kinetics (τV˙O2). Whether this relationship is causative is presently unclear. This study determined the impact of raised baseline work rate, which increases τV˙O2, on critical power during upright cycle exercise. Critical power was determined via four constant‐power exercise tests to exhaustion in two conditions: (1) with exercise initiated from an unloaded cycling baseline (U→S), and (2) with exercise initiated from a baseline work rate of 90% of the gas exchange threshold (M→S). During these exercise transitions, τV˙O2 and the time constant of muscle deoxyhemoglobin kinetics (τ [HHb + Mb]) (the latter via near‐infrared spectroscopy) were determined. In M→S, critical power was lower (M→S = 203 ± 44 W vs. U→S = 213 ± 45 W, P = 0.011) and τV˙O2 was greater (M→S = 51 ± 14 sec vs. U→S = 34 ± 16 sec, P = 0.002) when compared with U→S. Additionally, τ [HHb + Mb] was greater in M→S compared with U→S (M→S = 28 ± 7 sec vs. U→S = 14 ± 7 sec, P = 0.007). The increase in τV˙O2 and concomitant reduction in critical power in M→S compared with U→S suggests a causal relationship between these two parameters. However, that τ [HHb + Mb] was greater in M→S exculpates reduced oxygen availability as being a confounding factor. These data therefore provide the first experimental evidence that τV˙O2 is an independent determinant of critical power. Keywords critical power, exercise tolerance, oxygen uptake kinetics, power‐duration relationship, muscle deoxyhemoglobin kinetics, work‐to‐work exercise.

Little evidence exists with regard to the effect that exercise training has upon oxygen uptake kinetics in adolescent females. The aim of the study was to compare $$\dot{V}{\text{O}}_{2}$$ and muscle deoxygenation kinetics in a group of trained (Tr) and untrained (Utr) female adolescents. Twelve trained (6.4 ± 0.9 years training, 10.3 ± 1.4 months per year training, 5.2 ± 2.0 h per week) adolescent female soccer players (age 14.6 ± 0.7 years) were compared to a group (n = 8) of recreationally active adolescent girls (age 15.1 ± 0.6 years) of similar maturity status. Subjects underwent two, 6-min exercise transitions at a workload equivalent to 80 % of lactate threshold from a 3-min baseline of 10 W. All subjects had a passive rest period of 1 h between each square-wave transition. Breath-by-breath oxygen uptake and muscle deoxygenation were measured throughout and were modelled via a mono-exponential decay with a delay relative to the start of exercise. Peak $$\dot{V}{\text{O}}_{2}$$ was significantly (p