The intensity of lactate minimum (LM) has presented a good estimate of the intensity of maximal lactate steady-state (MLSS); however, this relationship has not yet been verified in the mouse model. We proposed validating the LM protocol for swimming mice by investigating the relationship among intensities of LM and MLSS as well as differences between sexes, in terms of aerobic capacity. Nineteen mice (male: 10, female: 9) were submitted to the evaluation protocols for LM and MLSS. The LM protocol consisted of hyperlactatemia induction (30 s exercise (13% body mass (bm)), 30 s resting pause and exhaustive exercise (13% bm), 9 min resting pause and incremental test). The LM underestimated MLSS (mice: 17.6%; male: 13.5%; female: 21.6%). Pearson's analysis showed a strong correlation among intensities of MLSS and LM (male (r = 0.67, p = 0.033); female (r = 0.86, p = 0.003)), but without agreement between protocols. The Bland-Altman analysis showed that bias was higher for females (1.5 (0.98) % bm; mean (MLSS and LM): 4.4%-6.4% bm) as compared with males (0.84 (1.24) % bm; mean (MLSS and LM): 4.5%-7.5% bm). The error associated with the estimated of intensity for males was lower when compared with the range of means for MLSS and LM. Therefore, the LM test could be used to determine individual aerobic intensity for males (considering the bias) but not females. Furthermore, the females supported higher intensities than the males. The differences in body mass between sexes could not explain the higher intensities supported by the females.

This study aims to propose and validate the tethered swimming lactate minimum test (TSLacmin) estimating aerobic and anaerobic capacity in one single test session, using force as measurement parameter. 6 male and 6 female young swimmers (age=15.7±1.1 years; height=173.3±9.5 cm; weight=66.1±9.5 kg) performed 4 sessions comprising i) an all-out 30 s test and incremental test (TSLacmin); ii) 30 min of tethered swimming at constant intensity (2 sessions); iii) free-swimming time trials used to calculate critical velocity. Tethered swimming sessions used an acquisition system enabling maximum (Fmax) and mean (Fmean) force measurement and intensity variation. The tethered all-out test lasting 30 s resulted in hyperlactatemia of 7.9±2.0 mmol·l. TSLacmin presented a 100% success applicability rate, which is equivalent to aerobic capacity in 75% of cases. TSLacmin intensity was 37.7±7.3 N, while maximum force in the all-out test was 105±27 N. Aerobic and anaerobic TSLacmin parameters were significantly related to free-swimming performance (r=-0.67 for 100 m and r=-0.80 for 200 m) and critical velocity (r=0.80). TSLacmin estimates aerobic capacity in most cases, and both aerobic and anaerobic force parameters are well related to critical velocity and free swimming performance.

This study investigated the effect of non-periodized training performed at 80, 100 and 120% of the anaerobic threshold intensity (AnT) and a linear periodized training model adapted for swimming rats on the gene expression of monocarboxylate transporters 1 and 4 (MCT1 and 4, in soleus and gastrocnemius muscles), protein contents, blood biomarkers, tissue glycogen, body mass, and aerobic and anaerobic capacities. Sixty Wistar rats were randomly divided into 6 groups (n = 10 per group): a baseline (BL; euthanized before training period), a control group (GC; not exercised during the training period), three groups exercised at intensities equivalent to 80, 100 and 120% of the AnT (G80, G100 and G120, respectively) at the equal workload and a linear periodized training group (GPE). Each training program lasted 12 weeks subdivided into three periods: basic mesocycle (6 weeks), specific mesocycle (5 weeks) and taper (1 week). Although G80, G100 and G120 groups were submitted to monotony workload (i.e. non-modulation at intensity or volume throughout the training program), rodents were evaluated during the same experimental timepoints as GPE to be able comparisons. Our main results showed that all training programs were capable to minimize the aerobic capacity decrease promoted by age, which were compared to control group. Rats trained in periodization model had reduced levels of lipid blood biomarkers and increased hepatic glycogen stores compared to all other trained groups. At the molecular level, only expressions of MCT1 in the muscle were modified by different training regimens, with MCT1 mRNA increasing in rats trained at lower intensities (G80), and MCT1 protein content showed higher values in non-periodized groups compared to pre-training and GPE. Here, training at different intensities but at same total workload promoted similar adaptations in rats. Nevertheless, our results suggested that periodized training seems to be optimize the physiological responses of rats.

We investigated the effects of the acute and chronic exercise, prescribed in different intensity zones, but with total load-matched on mitochondrial markers (COX-IV, Tfam, and citrate synthase (CS) activity in skeletal muscles, heart, and liver), glycogen stores, aerobic capacity and anaerobic index in swimming rats. For this, two experimental designs were performed (acute and chronic efforts). Load-matched exercises were prescribed below and above and on the anaerobic threshold (AnT), determined by the Lactate Minimum test. In chronic programs, two training prescription strategies were assessed (monotonous and linear periodized model). Results show changes in glycogen stores but no modification in the COX-IV and Tfam contents after acute exercises. In the chronic protocols, COX-IV and Tfam proteins and CS adaptations were intensity and tissue dependents. Monotonous training promoted better adaptations than the periodized model. Training at 80% of the AnT improved both performance variables, emphasizing the anaerobic index, concomitant to CS and COX-IV improvement (soleus muscle). The aerobic capacity and CS activity (gastrocnemius) were increased after 120% AnT training. In conclusion, acute exercise protocol did not promote responses in mitochondrial target proteins. An intensity and tissue dependence are reported in the chronic protocols, highlighting training at 80 and 120% of the AnT. Novelty: • Load-matched acute exercise did not enhance COX-IV and Tfam contents in skeletal muscles, heart, and liver. • In chronic exercise, COX-IV, Tfam, and citrate synthase activity adaptations were intensity and tissue dependents. •Monotonous training was more efficient than the periodized linear model in adaptations of target proteins and enzymatic activity.

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