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

José P Morgado; Catarina N Matias; Joana Filipa Reis; Dalia Curto; Francisco Bessone Alves; Cristina P Monteiro

doi:10.3389/fphys.2020.00471

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

Front Physiol. 2020 May 12:11:471. doi: 10.3389/fphys.2020.00471. eCollection 2020.

Authors

José P Morgado^{1

2

3}, Catarina N Matias^{1

4}, Joana Filipa Reis^{1

3

4}, Dalia Curto¹, Francisco Bessone Alves^{1

4}, Cristina P Monteiro^{1

4}

Affiliations

¹ Laboratory of Physiology and Biochemistry of Exercise, Faculdade de Motricidade Humana, Universidade de Lisboa, Lisbon, Portugal.
² Instituto Superior de Ciências Educativas, Lisbon, Portugal.
³ Universidade Europeia, Lisbon, Portugal.
⁴ Interdisciplinary Center for the Study of Human Performance (CIPER), Faculdade de Motricidade Humana, Universidade de Lisboa, Lisbon, Portugal.

Abstract

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.

Keywords: leukocytes; lymphocytes subsets; swimmers; training season; upper respiratory symptoms.