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Functional rearrangements of the cardiorespiratory system in swimmers as a marker of professional adaptation stages
https://doi.org/10.47183/mes.2026-527
Abstract
Introduction. Given the continuously increasing complexity of modern sports, rising training intensity, and growing demands at competitions, studying the mechanisms of swimmers’ adaptation to extreme physical loads has become particularly relevant. The obtained data may serve as a scientific basis for optimizing training programs and individualizing load distribution.
Objective. To characterize adaptive responses to maximal-intensity exercise in swimmers across different qualification levels.
Materials and methods. Adaptive changes in the autonomic nervous, cardiovascular, and respiratory systems were studied in swimmers performing high-intensity swimming over a 500-m freestyle distance. The experiment involved 81 participants, who were divided into three groups of 27 individuals each, according to their professional level: low, moderate, and high. To assess the cardiovascular system, systolic and diastolic blood pressure and heart rate (HR) were measured in the subjects before and after completing the trial. HR was recorded using a portable cardiac monitor placed on the left upper arm and on the index finger of the right hand. To evaluate the pulmonary circulation, the exhaled nitric oxide (NO) level was measured with a NOBreath V2 nitric oxide analyzer. The following parameters were calculated: pulse pressure, mean arterial pressure, stroke volume, cardiac output, total peripheral vascular resistance, Quaas index, Kerdo index, Robinson index, and adaptive capacity.
Results. The results demonstrated a direct relationship between the time to complete the 500-m freestyle swimming trial and the athletes’ professional level: group 1 – 792 ± 25.2 s, group 2 – 655 ± 30.2 s, and group 3 – 468 ± 24.6 s. In swimmers with a high professional level, the following post-exercise changes were observed: a 90.8% increase in cardiac output (p < 0.05), driven by a 41.9% rise in stroke volume (p < 0.05) and a moderate 33.5% HR elevation (p < 0.05); a 47.2% reduction in total peripheral resistance (p < 0.05); and an 11.2% increase in NO levels (p < 0.05). Correlation analysis revealed an association between swimming trial performance and adaptive capacity, HR, and the Robinson index. In swimmers with low and moderate professional levels, the changes reflected an exhaustive response pattern. A pronounced HR increase was observed with a relatively modest rise in stroke volume. Exhaled NO levels decreased by 10.1% (p < 0.05) in the low-level group and by 3.7% (p < 0.05) in the moderate-level group. The increases in cardiac output were substantially lower – 49.1% (p < 0.05) and 75.4% (p < 0.05), respectively – than those observed in the high-level swimmers.
Conclusions. With increasing professional level, athletes develop a complex of adaptive changes that enable them to cope more effectively with high loads during intense swimming. In swimmers with low and moderate professional levels, the response to exercise was exhaustive in nature: a pronounced HR increase was observed alongside a negligible rise in stroke volume and a decrease in NO levels. In contrast, swimmers with a high professional level demonstrated a n economical adaptive response: a balanced increase in cardiac output was achieved through elevated stroke volume and a moderate rise in HR; additionally, exhaled NO levels increased and autonomic regulation was optimized. Collectively, these adaptations support greater efficiency in overcoming high-intensity loads when swimming a 500-m distance.
Keywords
For citations:
Klenkov I.R., Pokrovskaya D.F., Tsybina G.M., Salnikov M.V., Shakaev Zh.Zh. Functional rearrangements of the cardiorespiratory system in swimmers as a marker of professional adaptation stages. Extreme Medicine. 2026;28(3):394-399. https://doi.org/10.47183/mes.2026-527
INTRODUCTION
Swimming in a training mode induces persistent physiological changes in swimmers’ bodies. The horizontal body position in water facilitates venous return to the heart, increasing preload, which leads to an elevated stroke volume [1][2]. Over time, this enables a further increase in stroke volume, thereby improving athletic performance. The cooling effect of water triggers peripheral vasoconstriction, primarily to reduce heat loss. Prolonged training promotes the development of endothelium-dependent vasodilation, which also contributes to enhanced athletic achievements.
During swimming, the specific breathing pattern (exhalation into water and breath-holding during turns) creates a hypoxic stimulus that activates autonomic mechanisms of heart rate regulation [1][3]. This triggers a cascade of adaptive responses, including increased chemoreceptor sensitivity and enhanced sympathetic activity of the autonomic nervous system. These adaptations improve endurance during cardiorespiratory loads and contribute to better swimming performance [4][5].
The adaptive capacity of the organism is largely determined by the state of the autonomic nervous, cardiovascular, and respiratory systems [6]. The training regimen triggers a complex of adaptive changes, including an increase in stroke volume, the development of endothelium-dependent vasodilation, and the activation of autonomic mechanisms of heart rate regulation [7][8]. Assessment of the functional state of these systems can provide a basis for developing optimal training regimens for professional swimmers.
The aim of the study was to identify the mechanisms underlying the adaptation of the cardiovascular, respiratory, and autonomic nervous systems to maximal-intensity loads in swimmers of different training levels during a 500-m freestyle swim.
MATERIALS AND METHODS
The study included 81 male participants with a mean age of 21.1 ± 0.6 years. They were divided into three equal groups of 27 individuals each, according to their swimming expertise level:
- Group 1 — low level (no systematic training);
- Group 2 — moderate level (systematic training for up to 3 years);
- Group 3 — high level (systematic training for more than 3 years, including 9 international-class swimmers).
All participants completed a 500-m swimming trial at maximal intensity using the freestyle technique. Cardiovascular and respiratory parameters were recorded before and after the trial.
To assess the cardiovascular system, systolic (SBP) and diastolic (DBP) blood pressure and heart rate (HR) were measured in all subjects using a portable monitor placed on the left upper arm (Mindray BeneView N1, China). To evaluate pulmonary circulation, exhaled nitric oxide (NO) levels were measured before and after the trial using a nitric oxide analyzer (NOBreath V2, Bedfont Scientific Ltd, UK). The following parameters were calculated: pulse pressure (PP), mean arterial pressure (MAP), stroke volume (SV) using the Starr formula, cardiac output (CO), total peripheral vascular resistance (TPVR), Quaas index, Kerdo index, Robinson index, and adaptive capacity (AC)1,2.
The obtained results were subjected to statistical analysis using IBM SPSS Statistics software. The normality of the distribution of quantitative variables was assessed using the Shapiro–Wilk test. To evaluate statistically significant changes (p < 0.05) in related samples (pre- and post-exercise periods), the Wilcoxon signed-rank test was applied. The relationship between parameters was examined using correlation analysis with calculation of the Spearman’s rank correlation coefficient.
RESULTS AND DISCUSSION
Changes in hemodynamic parameters in swimmers during the 500-m freestyle trial across groups with different levels of professional training are presented in the table. The mean trial time was 792 ± 25.2 s in group 1, 655 ± 30.2 s in group 2, and 468 ± 24.6 s in group 3. Athletes in group 3 (high professional level) demonstrated better performance compared to groups 1 and 2 by 69.2% and 40.1%, respectively. These findings clearly demonstrate a direct relationship between professional level and trial completion time.
Table. Hemodynamic parameter changes during a 500-m freestyle swim
|
Parameter |
Group 1 (n = 27) |
Group 2 (n = 27) |
Group 3 (n = 27) |
||||||
|
Before swimming M ± SЕ |
After swimming M ± SЕ |
Δ, % |
Before swimming M ± SЕ |
After swimming M ± SЕ |
Δ, % |
Before swimming M ± SЕ |
After swimming M ± SЕ |
Δ, % |
|
|
Systolic blood pressure, mmHg |
134.0 ± 3.2 |
132.6 ± 2.6 |
0.2 |
133.5 ± 2.6 |
128.3 ± 2.2 |
-2.9 |
132.6 ± 1.8 |
136.4 ± 2.3 |
3.1 |
|
Diastolic blood pressure, mmHg |
76.3 ± 1.3 |
73.6 ± 2.6 |
-2.9 |
77.6 ± 1.6 |
66.4 ± 1.5* |
-13.6 |
79.1 ± 1.4 |
68 ± 1.4* |
-13.5 |
|
Heart rate, bpm |
85.3 ± 2.1 |
109 ± 2.4* |
29.5 |
81.4 ± 2.3 |
103.8 ± 3.1* |
29.7 |
81.3 ± 2 |
106.6 ± 2.3* |
33.5 |
|
Pulse pressure, mmHg |
59.1 ± 2.9 |
57.7 ± 2.7 |
2.3 |
54.5 ± 2.7 |
61.1 ± 2.8* |
16.6 |
53.3 ± 2.2 |
68.3 ± 1.6* |
32.7 |
|
Stroke volume, mL |
70.8 ± 1.7 |
79.1 ± 3* |
13.6 |
67.8 ± 1.9 |
89 ± 2.2* |
34.5 |
66.3 ± 1.7 |
92.6 ± 1.9* |
41.9 |
|
Cardiac output, mL |
6060 ± 232 |
8604 ± 354* |
49.1 |
5553 ± 258 |
9243 ± 380* |
75.4 |
5365 ± 158 |
9852 ± 291* |
90.8 |
|
Exhaled nitric oxide level, ppb |
23.8 ± 2.3 |
20.3 ± 2* |
-10.1 |
29 ± 4.5 |
22.7 ± 2* |
-3.7 |
29.7 ± 3.3 |
31.8 ± 3.9* |
11.2 |
|
Adaptive capacity, arbitrary units |
2.56 ± 0.06 |
2.78 ± 0.05 |
10.0 |
2.51 ± 0.06 |
2.66 ± 0.04* |
7.2 |
2.51 ± 0.04 |
2.65 ± 0.06* |
5.8 |
|
Mean arterial pressure, mmHg |
95.5 ± 1.6 |
96.3 ± 1.7 |
1.4 |
96.2 ± 1.5 |
89.4 ± 0.8 |
-6.6 |
97 ± 1.2 |
89.9 ± 1.4 |
-7.0 |
|
Total peripheral vascular resistance, mmHg × s/mL |
1.3 ± 0.05 |
0.93 ± 0.07* |
-25.1 |
1.46 ± 0.06 |
0.78 ± 0.03* |
-43.2 |
1.49 ± 0.06 |
0.75 ± 0.02* |
-47.2 |
|
Quaas index, arbitrary units |
15.8 ± 0.1 |
19.9 ± 1.3* |
34.1 |
15.3 ± 0.1 |
17.6 ± 0.7* |
21.8 |
15.9 ± 0.5 |
16 ± 0.6 |
6.7 |
|
Kerdo index, arbitrary units |
9.3 ± 2.6 |
31.9 ± 2.6* |
165.2 |
2.9 ± 3.2 |
34.3 ± 2.7* |
56.4 |
1.2 ± 2.8 |
35.7 ± 1.4* |
50.7 |
|
Robinson index, arbitrary units |
114.9 ± 4.8 |
145.2 ± 3.8* |
31.0 |
109.5 ± 4.6 |
140.8 ± 3.9* |
33.3 |
107.7 ± 2.9 |
145.7 ± 4.6* |
37.6 |
Table prepared by the authors based on their own data
Note. * — p < 0.05; M — arithmetic mean of the group; SЕ — standard error of the arithmetic mean; Δ — change relative to the baseline value.
In group 1, the following statistically significant changes in parameters were observed after the trial: an increase in HR (29.5%, p < 0.05), SV (13.6%, p < 0.05), CO (49.1%, p < 0.05), Quaas index (34.1%, p < 0.05), Kerdo index (165.2%, p < 0.05), and Robinson index (31.0%, p < 0.05). A decrease in exhaled NO (10.1%, p < 0.05) and TPVR (25.1%, p < 0.05) was also detected post-exercise. Two statistically significant correlations between the studied parameters and trial performance were identified: SV (r = –0.381, p < 0.01) and AC (r = 0.287, p < 0.05) measured after the trial. These findings indicate a relationship between trial success and cardiac contractile function. Although the mean SV increase in group 1 was relatively modest, individuals exhibiting a positive inotropic effect (i.e., an increase in SV) demonstrated better trial performance.
CO increased as a result of increases in both HR and SV. A TPVR reduction was also observed. The Quaas, Kerdo, and Robinson indices increased in group 1 athletes. These changes indicate an adaptive cardiovascular response during the trial.
The decline in NO levels is associated with depletion of NO synthesis reserves caused by hypoxia under maximal exercise load, leading to local vasospasm in the pulmonary circulation.
In group 2, the following statistically significant post-trial changes were observed: an increase in HR (29.7%, p < 0.05), PP (16.6%, p < 0.05), SV (34.5%, p < 0.05), CO (75.4%, p < 0.05), AC (7.2%, p < 0.05), Quaas index (21.8%, p < 0.05), Kerdo index (56.4%, p < 0.05), and Robinson index (33.3%, p < 0.05). A decrease was also detected in DBP (13.6%, p < 0.05), NO (3.7%, p < 0.05), and TPVR (43.2%, p < 0.05). Correlation analysis revealed a statistically significant relationship between trial performance and AC measured after the trial (r = 0.294, p < 0.05), indicating the importance of adaptive responses during trial execution.
In group 2 athletes, the mean SV increased several-fold more than in group 1, which may have contributed to their trial performance. CO also rose due to concurrent increases in HR and SV. A pronounced reduction in TPVR was observed. The Kerdo index showed a less pronounced increase compared to group 1, indicating a more stabilized autonomic nervous system function. This process directly influences the body’s adaptive capacity, which is consistent with the demonstrated effect of AC on trial success. The Quaas and Robinson indices increased to a similar extent as in group 1. A modest decline in NO levels may suggest a minor vascular spasm in the pulmonary circulation and reflect a compensatory adaptation to the aquatic environment.
In group 3, the following statistically significant post-trial changes were observed: an increase in HR (33.5%, p < 0.05), PP (32.7%, p < 0.05), SV (41.9%, p < 0.05), CO (90.8%, p < 0.05), NO (11.2%, p < 0.05), AC (5.8%, p < 0.05), Kerdo index (50.7%, p < 0.05), and Robinson index (37.6%, p < 0.05). A decrease was also detected in DBP (13.5%, p < 0.05) and TPVR (47.2%, p < 0.05). Correlation analysis revealed several statistically significant relationships between post-trial parameters and trial performance: AC (r = 0.509, p < 0.01), HR (r = 0.381, p < 0.05), and Robinson index (r = 0.415, p < 0.01). The relationship between performance success and adaptive capacity demonstrates a moderate correlation (0.5 < r < 0.75) and is more pronounced compared to group 2.
A strong positive correlation was observed between HR and the Robinson index (r = 0.835, p < 0.001), indicating a unidirectional response pattern. The relationship between HR and trial performance suggests that at a more advanced stage of training adaptation, swimmers exhibit a more pronounced chronotropic effect in heart rate regulation. AC, MAP, TPVR, and the Kerdo and Robinson indices showed significantly greater increases compared to group 2.
It should be noted that NO levels were elevated compared to groups 1 and 2, indicating vasodilation in the pulmonary circulation. This facilitates efficient oxygenation of tissues that experience hypoxic stress during swimming. The higher exhaled NO level, together with the marked TPVR reduction — also observed in group 2 — is likely a result of adaptive mechanisms aimed at increasing circulating blood volume during swimming [9].
Notably, the Quaas index remained virtually unchanged in group 3 participants, reflecting a high level of training and manifesting as enhanced cardiovascular resistance to hypoxia and improved hemodynamic economy.
The PP increase indicates enhanced myocardial contractility, which likely contributed to the SV rise and, consequently, CO.
Thus, swimming as part of a training regimen induces changes in the cardiorespiratory system of swimmers. At the initial stage, these changes manifest as an enhanced inotropic effect of cardiac regulation [10]. Over time, an adaptive shift occurs, accompanied by the engagement of the chronotropic regulatory mechanism, which becomes pronounced at a high level of training (group 3). At the final stage of adaptation, alterations in the vascular system (both pulmonary and systemic circulation) develop; these changes enable the body to meet the high oxygen demand as rapidly as possible.
CONCLUSION
- In swimmers with low and moderate professional levels, the observed changes indicated an exhaustive pattern of response: a pronounced HR increase was accompanied by a relatively modest SV rise. The NO level decreased by 10.1% and 3.7%, respectively, while the CO increases were considerably lower (49.1% and 75.4%) compared to those in swimmers with a high professional level.
- In swimmers with a high professional level, a balanced and economical response pattern was observed: CO increased by 90.8%, primarily due to a rise in SV (41.9%) coupled with a moderate HR increase (33.5%). A pronounced reduction in TVPR (47.2%) was accompanied by an increase in NO levels (11.2%), indicating the development of endothelium-dependent vasodilation.
- Correlation analysis confirmed that, in swimmers with a high professional level, successful performance of the standardized task was associated with the AC, HR, and the Robinson index.
- With an increase in professional level, swimmers develop a complex of adaptive rearrangements: the inotropic function of the heart is enhanced, and vascular tone and autonomic regulation are optimized. This improves the efficiency of performing maximal loads during swimming.
- Further clinical and experimental studies are required to systematize the adaptive changes that occur in swimmers during the training process.
Authors’ contribution. All authors confirm that their contributions meet the ICMJE criteria for authorship. The primary contributions are distributed as follows: Ilyas R. Klenkov — study design, study conduct, data analysis, text writing; Daria F. Pokrovskaya — manuscript drafting, statistical analysis; Galina M. Tsybina — manuscript drafting, statistical analysis; Maxim V. Salnikov — study conduct, data analysis; Zhenis Zh. Shakaev — data analysis.
1. Diagnostic indices and physiological exercise tests: A manual for physicians. Murmansk: Sever; 2008.
2. Zagryadsky VP, Sulimo-Samuyllo ZK. Methods of research in work physiology: A methodological manual. Leningrad: Military Medical Academy named after S.M. Kirov; 1991.
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About the Authors
I. R. KlenkovRussian Federation
Ilyas R. Klenkov, Cand. Sci. (Med.)
St. Petersburg
D. F. Pokrovskaya
Russian Federation
Daria F. Pokrovskaya
St. Petersburg
G. M. Tsybina
Russian Federation
Galina M. Tsybina
St. Petersburg
M. V. Salnikov
Russian Federation
Maxim V. Salnikov
St. Petersburg
Zh. Zh. Shakaev
Russian Federation
Zhenis Zh. Shakaev
St. Petersburg
Review
For citations:
Klenkov I.R., Pokrovskaya D.F., Tsybina G.M., Salnikov M.V., Shakaev Zh.Zh. Functional rearrangements of the cardiorespiratory system in swimmers as a marker of professional adaptation stages. Extreme Medicine. 2026;28(3):394-399. https://doi.org/10.47183/mes.2026-527
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