The reliability of back-extrapolation in estimating V ˙ O 2 p e a k in different swimming performances at the severe-intensity domain.

The amount of anerobic energy released during exercise might modify the initial phase of oxygen recovery (fast-O2debt) post-exercise. Therefore, the present study aimed to analyze the reliability of peak oxygen uptake ( V ˙ O 2 p e a k ) estimate by back-extrapolation ( B E - V ˙ O 2 p e a k ) under different swimming conditions in the severe-intensity domain, verifying how the alterations of the V ˙ O 2 recovery profile and anerobic energy demand might affect B E - V ˙ O 2 p e a k values. Twenty swimmers (16.7 ± 2.4 years, 173.5 ± 10.2 cm, and 66.4 ± 10.6 kg) performed an incremental intermittent step protocol (IIST: 6 × 250 plus 1 × 200 m, IIST_v200m) for the assessment of V ˙ O 2 p e a k . The V ˙ O 2 off-kinetics used a bi-exponential model to discriminate primary amplitude, time delay, and time constant (A1off, TD1off, and τoff) for assessment of fast-O2debt post IIST_v200m, 200-m single-trial (v200 m), and rest-to-work transition at 90% delta (v90%Δ) tests. The linear regression estimated B E - V ˙ O 2 p e a k and the rate of V ˙ O 2 recovery (BE-slope) post each swimming performance. The ANOVA (Sidak as post hoc) compared V ˙ O 2 p e a k to the estimates of B E - V ˙ O 2 p e a k in v200 m, IIST_v200 m, and v90%Δ, and the coefficient of dispersion (R2) analyzed the association between tests. The values of V ˙ O 2 p e a k during IIST did not differ from B E - V ˙ O 2 p e a k in v200 m, IIST_v200 m, and v90%Δ (55.7 ± 7.1 vs. 53.7 ± 8.2 vs. 56.3 ± 8.2 vs. 54.1 ± 9.1 ml kg-1 min-1, p > 0.05, respectively). However, the V ˙ O 2 p e a k variance is moderately explained by B E - V ˙ O 2 p e a k only in IIST_v200 m and v90%Δ (RAdj 2 = 0.44 and RAdj 2 = 0.43, p < 0.01). The TD1off and τoff responses post IIST_v200 m were considerably lower than those in both v200 m (6.1 ± 3.8 and 33.0 ± 9.5 s vs. 10.9 ± 3.5 and 47.7 ± 7.9 s; p < 0.05) and v90%Δ ( 10.1 ± 3.8 and 44.3 ± 6.3 s, p < 0.05). The BE-slope post IIST_v200m was faster than in v200 m and v90%Δ (-47.9 ± 14.6 vs. -33.0 ± 10.4 vs. -33.6 ± 13.8 ml kg-1, p < 0.01), and the total anerobic (AnaerTotal) demand was lower in IIST_v200 m (37.4 ± 9.4 ml kg-1) than in 200 m and 90%Δ (51.4 ± 9.4 and 46.2 ± 7.7 ml kg-1, p < 0.01). Finally, the τ1off was related to AnaerTotal in IIST_v200m, v200 m, and v90%Δ (r = 0.64, r = 0.61, and r = 0.64, p < 0.01). The initial phase of the V ˙ O 2 recovery profile provided different (although reliable) conditions for the estimate of V ˙ O 2 p e a k with BE procedures, which accounted for the moderate effect of anerobic release on V ˙ O 2 off-kinetics, but compromised exceptionally the V ˙ O 2 p e a k estimate in the 200-m single trial.

Physiological Responses During High-Intensity Interval Training in Young Swimmers.

This study analyzed whether 100- and 200-m interval training (IT) in swimming differed regarding temporal, perceptual, and physiological responses. The IT was performed at maximal aerobic velocity (MAV) until exhaustion and time spent near to maximalVO2 peak oxygen uptake (⩒O2peak), total time limit (tLim), peak blood lactate [La-] peak, ⩒O2 kinetics (⩒O2K), and rate of perceived exertion (RPE) were compared between protocols. Twelve swimmers (seven males 16.1 ± 1.1 and five females 14.2 ± 1 years) completed a discontinuous incremental step test for the second ventilatory threshold (VT2), ⩒O2peak, and MAV assessment. The swimmers subsequently completed two IT protocols at MAV with 100- and 200-m bouts to determine the maximal ⩒O2 (peak-⩒O2) and time spent ≥VT2, 90, and 95% of ⩒O2peak for the entire protocols (IT100 and IT200) and during the first 800-m of each protocol (IT8x100 and IT4x200). A portable apparatus (K4b2) sampled gas exchange through a snorkel and an underwater led signal controlled the velocity. RPE was also recorded. The Peak-⩒O2 attained during IT8x100 and IT4x200 (57.3 ± 4.9 vs. 57.2 ± 4.6 ml·kg-1·min-1) were not different between protocols (p = 0.98) nor to ⩒O2peak (59.2 ± 4.2 ml·kg-1·min-1, p = 0.37). The time constant of ⩒O2K (24.9 ± 8.4 vs. 25.1 ± 6.3-s, p = 0.67) and [La-] peak (7.9 ± 3.4 and 8.7 ± 1.5 mmol·L-1, p = 0.15) also did not differ between IT100 and IT200. The time spent ≥VT2, 90, and 95%⩒O2peak were also not different between IT8x100 and IT4x200 (p = 0.93, 0.63, and 1.00, respectively). The RPE for IT8x100 was lower than that for IT4x200 (7.62 ± 2 vs. 9.5 ± 0.7, p = 0.01). Both protocols are considered suitable for aerobic power enhancement, since ⩒O2peak was attained with similar ⩒O2K and sustained with no differences in tLim. However, the fact that only the RPE differed between the IT protocols suggested that coaches should consider that nx100-m/15-s is perceived as less difficult to perform compared with nx200-m/30-s for the first 800-m when managing the best strategy to be implemented for aerobic power training.

The Cellular Composition of the Innate and Adaptive Immune System Is Changed in Blood in Response to Long-Term Swimming Training.

Competitive swimming requires high training load cycles including consecutive sessions with little recovery in between which may contribute to the onset of fatigue and eventually illness. We aimed to investigate immune changes over a 7-month swimming season. Fifty-four national and international level swimmers (25 females, 29 males), ranging from 13 to 20 years of age, were evaluated at rest at: M1 (beginning of the season), M2 (after the 1st macrocycle's main competition), M3 (highest training load phase of the 2nd macrocycle) and M4 (after the 2nd macrocycle's main competition) and grouped according to sex, competitive age-groups, or pubertal Tanner stages. Hemogram and the lymphocytes subsets were assessed by automatic cell counting and by flow cytometry, respectively. Self-reported Upper Respiratory Symptoms (URS) and training load were quantified. Although the values remained within the normal range reference, at M2, CD8+ decreased (M1 = 703 ± 245 vs. M2 = 665 ± 278 cell µL-1; p = 0.032) and total lymphocytes (TL, M1 = 2831 ± 734 vs. M2 = 2417 ± 714 cell µL-1; p = 0.007), CD3+ (M1 = 1974 ± 581 vs. M2 = 1672 ± 603 cell µL-1; p = 0.003), and CD4+ (M1 = 1102 ± 353 vs. M2 = 929 ± 329 cell µL-1; p = 0.002) decreased in youth. At M3, CD8+ remained below baseline (M3 = 622 ± 245 cell µL-1; p = 0.008), eosinophils (M1 = 0.30 ± 0.04 vs. M3 = 0.25 ± 0.03 109 L-1; p = 0.003) and CD16+56+ (M1 = 403 ± 184 vs. M3 = 339 ± 135 cell µL-1; p = 0.019) decreased, and TL, CD3+, and CD4+ recovered in youth. At M4, CD19+ were elevated (M1 = 403 ± 170 vs. M4 = 473 ± 151 cell µL-1; p = 0.022), CD16+56+ continued to decrease (M4 = 284 ± 131 cell µL-1; p < 0.001), eosinophils remained below baseline (M4 = 0.29 ± 0.05 109 L-1; p = 0.002) and CD8+ recovered; monocytes were also decreased in male seniors (M1 = 0.77 ± 0.22 vs. M4 = 0.57 ± 0.16 109 L-1; p = 0.031). The heaviest training load and higher frequency of URS episodes happened at M3. The swimming season induced a cumulative effect toward a decrease of the number of innate immune cells, while acquired immunity appeared to be more affected at the most intense period, recovering after tapering. Younger athletes were more susceptible at the beginning of the training season than older ones.