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Purpose: This study investigates if co-ingestion of cluster dextrin (CDX) augments the appearance of intrinsically labeled meat protein hydrolysate-derived amino acid (D5-phenylalanine), Akt/mTORC1 signaling, and myofibrillar protein fractional synthetic rate (FSR). Methods: Ten moderately trained healthy males (age: 21.5 ± 2.1 years, body mass: 75.7 ± 7.6 kg, body mass index (BMI): 22.9 ± 2.1 kg/m2) were included for a double-blinded randomized controlled crossover trial. Either 75 g of CDX or glucose (GLC) was given in conjunction with meat protein hydrolysate (0.6 g protein * FFM−1) following a whole-body resistance exercise. A primed-continuous intravenous infusion of L-[15N]-phenylalanine with serial muscle biopsies and venous blood sampling was performed. Results: A time × group interaction effect was found for serum D5-phenylalanine enrichment (P < 0.01). Serum EAA and BCAA concentrations showed a main effect for group (P < 0.05). Tmax serum BCAA was greater in CDX as compared to GLC (P < 0.05). However, iAUC of all serum parameters did not differ between CDX and GLC (P > 0.05). Tmax serum EAA showed a trend towards a statistical significance favoring CDX over GLC. The phosphorylation of p70S6KThr389, rpS6Ser240/244, ERK1/2Thr202/Tyr204 was greater in CDX compared to GLC (P < 0.05). However, postprandial myofibrillar FSR did not differ between CDX and GLC (P = 0.17). Conclusion: In moderately trained younger males, co-ingestion of CDX with meat protein hydrolysate does not augment the postprandial amino acid availability or myofibrillar FSR as compared to co-ingestion of GLC during the recovery from a whole-body resistance exercise despite an increased intramuscular signaling. Trial registration: ClinicalTrials.gov ID: NCT03303729 (registered on October 3, 2017).

The purpose of this study was to examine the effects of blood lactate level (La) on oxygen uptake ( ·VO2) kinetics during recovery after short-term exercise with maximal effort (sprint). Three sprints were performed on a cycle ergometer with a load of 8% of body weight at maximal rotation rate. ·VO2 kinetics and oxygen debt were determined after three sprint tests: one 10-s cycling sprint, five repeated 10-s cycling sprints with 6-min intervals and one 30-s cycling sprint. There was no significant difference between peak power outputs in the 10-s sprint and five sprints. There was no difference in ·VO2 kinetics during recovery from one sprint and during recovery after five sprints. La peaked at 5 min. The peak value of La was significantly lower in one sprint (4.41 ± 0.9 mM) than in five sprints (7.01 ± 2.2 mM). Thus, despite a difference in La, there was no difference between ·VO2 kinetics during recovery after one sprint and after five sprints. There was a significant difference in ·VO2 between the five sprints and 30-s sprint from 70 s to 320 s during recovery, but there were no significant differences in La after 5 min of recovery. There were two phases in ·VO2. They consisted of fast oxygen debt and slow oxygen debt. There were also no differences in slow and fast oxygen debts between the two 10-s sprints despite significant differences in blood lactate during recovery. Peak La in the five sprints was not significantly different from that in the 30-s sprint (8.68 ± 1.2 mM). However, slow oxygen debt was significantly greater in the 30-s sprint than in the five sprints. It is concluded that · VO2 kinetics during recovery are not affected by an increase in blood lactate.

To determine that whether arterial carbon dioxide (PaCO2) affects ventilation (VE) during recovery from impulse-like exercises of various intensities, subjects performed four impulse-like tests with different workloads. Each test consisted of a 20-sec impulse-like exercise at 80 rpm and 60-min recovery. Blood samples were collected at rest and during recovery to measure blood ions and gases. VE was measured continuously during rest, exercise and recovery periods. A significant curvilinear relationship was observed between VE and pH during recovery from the 300 and 400 watts tests in all subjects. VE was elevated during recovery from the 100 watts test despite no change in any of the humoral factors. Arterialized carbon dioxide (PaCO2) kinetics showed fluctuation, being increased at 1 min and decreased at 5 min during recovery, and this fluctuation was more enhanced with increase in exercise intensity. There was a significant relationship between VE and PaCO2 during recovery from the 300 and 400 watts tests in all subjects. The results of the present study demonstrate that pH and neural factors drive VE during recovery from impulse-like exercise and that fluctuation in PaCO2 controls VE as a feedback loop and this feedback function is more enhanced as the work intensity increases.

In order to test our hypothesis that muscle condition has an effect on the cognition of self-motion and consequently on the ventilatory response during exercise, six healthy subjects performed a moderate incremental exercise test (IET) on a cycle ergometer under two conditions [resistance exercise condition (REC) and control condition (CC)]. In the REC, resistance exercise (30 incline leg presses) was conducted during two sessions scheduled at 48 and then 24 h prior to the IET. For the CC, the subjects were instructed to refrain from participating in strenuous exercise for a period of 2 days prior to the IET. In the IET, the workload was increased from 78 to 118 W in steps of 8 W every 3 min. Although the ventilatory response during the IET was significantly higher in the REC than in the CC, there were no significant differences in cognitive indexes (RPE and awareness of change in workload) between the two conditions. In addition, the magnitude of muscle soreness was significantly higher in the REC than in the CC. However, the level of soreness in the REC was very low, and there were no significant differences in blood lactate concentration and integrated EMG between the two conditions. These results suggest that a change in peripheral neural reflex is the primary cause of increased ventilatory response to moderate exercise after resistance exercise, although the role of a cognitive element cannot be absolutely excluded.

The aim of this study was to determine whether a 350-s recovery period allows recovery of peak power output (PPO) to its initial value under the condition of a blood lactate (La) concentration higher than 10 mmol·L-1 during repeated cycling sprints (RCS). RCS (10×10-s cycling sprints) were performed under two conditions. Under one condition, the recovery period of RCS was fixed at 35 s (RCS35), and under the other condition, a 350-s recovery period was set before the 5th and 9th sets, and a 35-s recovery period was set before the other sets (RCScomb). In RCScomb, PPO in the 5th set recovered to that in the 1st set, but PPO in the 9th set did not. Under both conditions, blood La concentration progressively increased and reached approximately 14 mmol·L-1 at the end of the RCS. In RCScomb, VO2 immediately before the 5th set was not significantly different from that immediately before the 9th set. Mean power frequency (MPF) values estimated by a surface electromyogram from the vastus lateralis in the 5th and 9th sets were significantly higher in RCScomb than in RCS35. In conclusion, a 350-s recovery period does not allow recovery of PPO to its initial value under the condition of a blood La concentration of 14 mmol·L-1 during RCS.

The purpose of this study was to determine whether neuromuscular activation is affected by blood lactate concentration (La) and the level of oxygen uptake immediately before a cycling sprint (preVO2). The tests consisted of ten repeated cycling sprints for 10 sec with 35-sec (RCS35) and 350-sec recovery periods (RCS350). Peak power output (PPO) was not significantly changed despite an increase in La concentration up to 12 mmol/L in RCS350. Mean power frequency (MPF) of the power spectrum calculated from a surface electromyogram on the vastus lateralis showed a significantly higher level in RCS350. In RCS35, preVO2 level and La were higher than those in RCS350 in the initial stage of the RCS and in the last half of the RCS, respectively. Thus, neuromuscular activation during exercise with maximal effort is affected by blood lactate concentration and the level of oxygen uptake immediately before exercise, suggesting a cyclic system between muscle recruitment pattern and muscle metabolites.