1. Introduction
The capacity for proper respiration, which includes supplying enough oxygen to the working muscles and removing carbon dioxide, depends on the efficiency of gas exchange during both external and internal respiration [
1,
2]. The gold standard for evaluating functional response through gas analysis is the cardiopulmonary exercise test (CPET), which helps identify functional and pathophysiological limitations [
1]. This test is particularly important for scuba divers, pilots, soldiers, and professional athletes who experience high levels of physical stress. During physical activity, lung ventilation increases to meet the oxygen needs of the skeletal muscles and activates the accessory respiratory muscles alongside the diaphragm [
3]. Respiratory muscle function depends on the strength and endurance of these muscles [
4]. Some studies have shown that inspiratory muscles can become fatigued after short periods of intense exercise. This phenomenon underscores the significant physiological demands placed on the respiratory system during vigorous physical activity [
5,
6] and after long periods of moderate-intensity exercise [
7]. Also, during these exercises, the respiratory muscles share the amount of oxygen consumed [
8,
9]. It has been determined that fatigue occurs in the diaphragm muscle with increased respiratory need during high-intensity exercises of 85% VO2max and above. Also, during these exercises, the respiratory muscles share the amount of oxygen consumed [
10]. The findings from previous studies mentioned above underscore the shared demand for cardiac output and oxygen consumption between active skeletal muscles and respiratory muscles during exercise.
Optimizing respiration plays a pivotal role in enhancing the efficiency of working skeletal muscles by facilitating the accelerated delivery of blood to the relevant regions. This interplay highlights the interconnectedness of respiratory and skeletal muscle function in supporting overall exercise performance and underscores the importance of respiratory optimization strategies in maximizing athletic potential [
11]. However, if the endurance of the respiratory muscles is not sufficient, it is predicted that exercise performance may decrease due to early fatigue of the diaphragm [
11]. High-intensity exercise causes peripheral vasoconstriction [
12]. In addition, it triggers the respiratory muscle metaboreflex, a high sympathetic nerve activity that limits blood flow to the working muscles and thus the energy output and consumption required for breathing [
12,
13].
The demanding work of the muscles used for inhalation has significant effects on the nervous system and the heart. In healthy people, voluntary resistance during inhalation that leads to muscle fatigue has been found to cause increases over time in muscle sympathetic nerve activity, heart rate, and mean arterial pressure. This is accompanied by a gradual decrease in arterial blood flow to inactive limbs [
14]. Research also suggests that the reflex triggered by the fatigue of the inspiratory muscles is activated during full-body exercise. Specifically, blood flow to the legs is inversely related to the effort of breathing during high-intensity exercise, and changes in leg blood vessel resistance are directly related to the amount of noradrenaline (norepinephrine) released [
15]. During prolonged intense full-body exercise, the response of the reflex associated with fatigue of the inspiratory muscles may limit exercise performance [
16]. However, training the inspiratory muscles can delay the activation of the respiratory muscle reflex, potentially improving performance [
12].
Our study represents a rare investigation that comprehensively evaluates both respiratory muscle parameters. The literature suggests that respiratory muscle fatigue typically does not manifest during exercise at intensities below approximately 80% of VO
2max [
17]. In another study, it was observed that during intense exercise (>85% of VO
2max) in highly trained individuals, respiratory muscles require approximately 15–16% of VO2max and cardiac output, whereas, in untrained individuals, this proportion is ≤10% [
18]. Considering these studies, our study aimed to investigate the impact of athletes’ respiratory muscle strength, as measured by maximal inspiratory and expiratory pressure, on aerobic endurance kinetics, specifically VO
2max. Given the widely acknowledged importance of respiratory muscle strength in athletic performance, understanding the association between respiratory muscle strength and aerobic endurance kinetics can inform training strategies aimed at optimizing performance and minimizing fatigue, ultimately enhancing athletes’ competitive edge. It is worth mentioning that MIP/MEP are also quasi-isometric and static measures and it was suggested that dynamic assessments may be more suitable in an athletic environment [
19]. Therefore, our study not only advances scientific knowledge but also has practical implications for enhancing athletic performance and improving training regimens in various sports contexts. In light of this information, we hypothesize that respiratory muscle strength will be associated with the kinetics of maximal oxygen consumption in athletes.
3. Results
The statistical analyses of the VO2max, VE, VO2, and VCO2 parameters are presented in tables below.
According to
Table 2, the parameters indicate a strong and significant relationship with VO
2max/kg (R = 0, 715, R
2 = 0.511,
p < 0.05). The above-mentioned variables together explain 51% of the total variance in VO2max/kg (
Figure 1). According to the standardized regression coefficient (β), mid-axilla circumference, MEP and inspiratory subcostal circumference values have a significant effect on VO
2max, while the other predictor variables do not seem to have a significant effect on VO
2max. When examining the bilateral and partial correlations between the predictor variables and VO
2max, we found a negative correlation between the MIP, mid-axilla, and axilla circumference measurements during inspiration and expiration, and the mid-subcostal and subcostal circumference measurements during inspiration and expiration. Also, a positive relationship was determined between MEP and MVV values (
Figure 1)
According to
Table 3, the parameters show a strong and significant relationship with VE (R = 0.760, R
2 = 0.577,
p < 0.05). The mentioned variables together explain 57% of the total variance in VE (
Figure 2). According to the standardized regression coefficient (β), the values of MEP and inspiratory subcostal circumference measurement have a significant effect on VE, while the other predictor variables do not seem to have a significant effect on VE. When the bilateral and partial correlations between the predictor variables and VE were examined, low-level correlations were found between MIP and VE, and moderate and positive correlations with other parameters.
Table 4 demonstrates that the parameters have a strong and significant relationship with VO
2 (R = 0.814, R
2 = 0.663,
p < 0.05). The mentioned variables together explain 66% of the total variance in VO2 (
Figure 3).According to the standardized regression coefficient (β), the values of MEP and subcostal circumference on inspiration have a significant effect on VO
2, while the other predictor variables do not seem to have a significant effect on VO
2. When the bilateral and partial correlations between predictor variables and VO
2 were examined, low-level correlations were found between MIP and VO
2, and moderate and positive correlations with other parameters.
In
Table 5, there is a strong and significant relationship with VCO2 (R = 0.802, R
2 = 0.643,
p < 0.05). These variables combined account for 64% of the total variance in VCO2 (
Figure 4). According to the standardized regression coefficient (β), the values of MEP and inspiratory subcostal circumference measurement have a significant effect on VCO
2, while other predictor variables do not seem to have a significant effect on VCO
2. When the bilateral and partial correlations between the predictor variables and VCO
2 were examined, low-level correlations were found between MEP and VCO
2, and moderate and positive correlations with other parameters.
In
Table 6, a multiple linear regression analysis with interaction terms was conducted to explore the relationship between VO
2max (VO
2/kg) and respiratory muscle strength (MIP, MEP), along with physiological factors (VE, VO
2, and VCO
2). The model was statistically significant and explained approximately 89.9% of the variance in VO
2max (R
2 = 0.899, adjusted R
2 = 0.859, F
(11, 28) = 22.60,
p < 0.001). The interaction between MIP and VE was found to be significant (β = −0.084,
p = 0.006), indicating that the effect of inspiratory muscle strength on VO
2max is moderated by ventilatory efficiency. Specifically, as VE increases, the impact of MIP on VO
2max becomes more pronounced. Additionally, the interaction between MEP and VE was also significant (B = 0.072,
p = 0.012), suggesting that expiratory muscle strength interacts positively with VE to influence VO2max. However, other interaction terms, such as MIP with VO
2 (B = 0.002,
p = 0.315) and MIP with VCO
2 (B = 0.001,
p = 0.608), were not statistically significant. Similarly, no significant interactions were found between MEP with VO
2 or VCO
2. This suggests that while respiratory muscle strength interacts with ventilatory efficiency, it does not interact significantly with oxygen consumption or carbon dioxide production to affect VO
2max.
4. Discussion
This study aimed to investigate the relationships between athletes’ respiratory muscle strength, assessed via MIP and maximal expiratory pressure MEP, and aerobic endurance, as characterized by maximal oxygen consumption kinetics. It is noteworthy that approximately 16% of oxygen intake during exercise is utilized by the respiratory muscles. During maximal exercise (85% and above of maximum heart rate), approximately 14–16% of cardiac output is directed to the respiratory muscles [
15]. Considering this aspect, the impact of respiratory muscles on performance is significant and cannot be ignored [
26]. Our study found a negative correlation between VO
2max and measurements of the circumference at the mid-axilla and axilla during both inspiration and expiration, as well as at the mid-subcostal and subcostal regions during inspiration and expiration.
In our study, we observed positive correlations between MEP and MVV, suggesting an augmented ventilatory response during exercise, where greater MEP and MVV capacity result in increased respiratory frequency. There are studies indicating an increase in maximum minute ventilation due to CO
2 elevation during exercise [
27,
28]. This, in turn, facilitates the swift elimination of carbon dioxide and enhanced oxygen uptake during physical exertion.
Furthermore, Dempsey et al. (2008) found that the respiratory muscle load during maximal exercise has a significant impact on tidal volume and CO in healthy trained individuals [
29]. Another study conducted by Johnson et al. (2007) reported improvements in cycling performance following specific inspiratory muscle training, accompanied by an increase in anaerobic work capacity [
30]. Additionally, Vasiccova et al. (2017) reported that improving inspiratory muscle strength through respiratory muscle training led to an enhancement in swimmers’ maximum underwater swimming distance [
31]. Lastly, differences in respiratory muscles between sports disciplines may result from variations in anaerobic or aerobic demands. The diverse nature of the group was crucial for enhancing the study’s quality and diversity. In the literature, Klusiewicz (2014) could not find a correlation between the MIP value and absolute or relative VO
2max values in male athletes but did find a correlation between the MIP value and absolute or relative VO
2max values in female athletes. In our study, no significant relationship could be found between relative VO
2max and MIP measurement results, which suggests that the athletes in our study reached their VO
2max value before reaching their maximum inspiratory muscle strength potential [
32].
Previous studies in the literature have mainly focused on explaining the impact of respiratory muscle strengthening training on VO2max. For instance, Lomax et al. (2011) found that a 4-week program of inspiratory muscle training enhanced the performance of the Yo-Yo test for two groups of 12 male football players competing in the national league. The training involved one set of 30 breaths twice daily at 50% of maximal inspiratory mouth pressure (PImax) and a pre-training inspiratory muscle warm-up of two sets of 30 breaths at 40% of PImax. This improvement was reported to be significant when compared to a control group [
33]. In another study, Volianitis et al. (2001) reported a study they conducted on 14 female competitive rowers at the commencement of rowing which found that the athletes’ VO
2max value after respiratory muscle warm-up exercise performed with branch-specific general warm-up was higher than that of the experimental group [
34]. In contrast, Amonette and Dupler (2002) reported in a study conducted on 12 male competitive triathletes and marathon runners (N = 8 research, N = 4 control group) that breathing exercises (MIP 15%, performed twice a day for a maximum of 30 breaths for 4 weeks) did not cause an improvement in VO
2max capacity [
35]. In another study conducted on young football players, it was reported that there was no significant change in VO
2max values after a four-week respiratory muscle training program [
36]. Likewise, Romer et al. (2002) conducted a study on 16 trained male cyclists (age = 29 ± 3.3 research group, age = 30 ± 2.6 control group), and they showed that inspiratory muscle training (6 weeks) caused no significant change in the VO
2max values of the subjects after respiratory muscle training. However, there is evidence that maximal increasing exercise attenuates the perceptual response to exercise, and there is evidence of improved performance in competitive cyclists after inspiratory muscle training [
9].
During high-intensity endurance exercise, there is increased production of metabolic CO
2. This excess CO
2 needs to be removed by increasing ventilation. If the respiratory muscles are not strong or enduring enough to meet the increased demand for ventilation, the levels of CO
2 in the tissues and blood will rise, leading to metabolic acidosis. This can cause both skeletal and respiratory muscles to fail. Therefore, expiratory muscle strength is important in this context [
36]. We found a moderate positive correlation between MEP and VCO
2 in our study, demonstrating the significance of expiratory muscle strength. Our study also revealed that subcostal circumference measurements in MEP during inspiration significantly affected VE. In line with these findings, it is predicted that increased development of respiratory muscles will result in higher air intake into the lungs per minute, leading to improved sports performance [
37].
Efficient utilization of the respiratory muscles plays a critical role in sustaining prolonged aerobic activities. Enhanced respiratory muscle efficiency is commonly associated with improved exercise performance and overall endurance capacity [
38]. Numerous studies within the literature have explored the efficacy of respiratory muscle training (RMT) as a means to augment exercise performance and optimize athletic outcomes, indicating its potential value in both elite and recreational athletes. For instance, Illi et al. (2012) conducted a comprehensive systematic review and meta-analysis, demonstrating the significant benefits of RMT in improving exercise performance among healthy individuals [
39]. Building upon this foundation, Kowalski et al. (2024) explored the practical applications of RMT specifically within the context of endurance sports, shedding light on its potential implications for athletes [
40]. Additionally, Haj Ghanbari et al. (2013) conducted meta-analyses, providing compelling evidence for the efficacy of RMT in enhancing athletic performance across various disciplines [
41]. Another study conducted by Shei (2018) contributed to the body of knowledge by reviewing the ergogenic effects of RMT in healthy individuals, further substantiating its potential benefits in exercise settings [
42]. Likewise, Lazovic et al. (2015) investigated respiratory adaptations in athletes across different sports disciplines, highlighting the versatility and applicability of RMT strategies [
43]. Lastly, Hackett (2020) conducted a study focusing on specific respiratory muscle adaptations in males engaged in both endurance and strength training, providing valuable insights into the physiological mechanisms underlying RMT benefits [
44]. The studies mentioned above emphasize that RMT is an effective strategy for improving exercise performance and athletic outcomes in diverse populations and settings. Endurance training is thought to delay the onset of respiratory muscle fatigue and improve the efficiency of oxygen utilization. As respiratory muscle development progresses, it is expected to increase air intake volume, leading to a positive impact on sports performance [
3]. Additionally, enhancing the strength of respiratory muscles not only enhances performance but also helps in preventing injuries. For instance, previous studies demonstrate significant improvements in respiratory muscle strength and functional outcomes, indicating potential benefits for injury prevention and recovery [
45]. Increased respiratory muscle strength can assist athletes in maintaining proper breathing mechanics during intense exercise, reducing the risk of fatigue-related injuries and respiratory distress [
46].
Furthermore, research has found inconsistencies in the effects of inspiratory muscle training on athletic performance. Some studies show significant benefits, while others do not demonstrate meaningful improvements. These discrepancies may be due to the use of standard inspiratory muscle training protocols without considering individual differences [
47]. Additionally, RMT is associated with extra stress and training load. Therefore, such training methods should not be unconditionally recommended without considering the broader context [
48].
Lastly, our study found a negative correlation between VO
2max and chest circumference measurements at rest, during inspiration, and expiration, as well as diaphragm circumference measurements at rest, during inspiration, and expiration. In contrast, positive correlations were observed between MEP and MVV values. In a resting state, the diaphragm or external intercostal muscles alone are sufficient for adequate respiration. However, during intense exercise, the effectiveness of the diaphragm decreases, and accessory muscles such as the scalene muscles, pectoralis minor, and sternocleidomastoid muscles gradually come into play to assist with inspiration [
49]. During calm breathing, expiration is passive because the chest wall and lungs tend to return to their original state due to their elastic properties. During exercise, the internal intercostal muscles become active, responsible for forceful expiration. The contraction of these expiratory muscles, which reduces intrathoracic volume, increases lung compression [
50]. Hence, this suggests that when exercising, the respiratory system is more active. This may be due to stronger expiratory muscles and a higher maximum voluntary ventilation, leading to a faster breathing rate. This helps in quicker removal of carbon dioxide and faster absorption of oxygen.
It is well-documented that there are two distinct phases of respiratory increase when physical activity begins. Initially, there is a sudden and noticeable rise in respiration, followed by a more gradual increase in both the depth and frequency of breathing. During the onset of exercise, even before chemical signals are released, the cerebral motor cortex becomes more active, sending neural signals to the respiratory center. This neural activation is responsible for the initial spike in respiration. The second phase of respiratory increase is driven by physiological changes in the arterial blood, such as temperature elevation and alterations in chemical composition. As exercise duration progresses, factors such as increased temperature, CO
2, and hydrogen ion (H+) concentrations stimulate greater oxygen consumption in the muscles and an expansion of the arteriovenous oxygen difference (a-v O
2 difference). This, in turn, activates chemoreceptors and the respiratory center, leading to enhanced respiratory frequency and depth [
51].
During intense exercise, tidal volume can increase by up to 50% of vital capacity. However, as maximal workload is approached, tidal volume begins to decline, and the increase in minute VE becomes dependent on an elevated breathing frequency. Individuals naturally adjust both the depth and frequency of respiration to maintain optimal ventilatory efficiency. Well-trained athletes can utilize up to 95% of their MVV during exercise, whereas untrained individuals typically reach only 60–70% of their MVV. These interconnected physiological responses underscore the critical role of respiratory muscles during maximal exertion. Following prolonged exercise, fatigue may develop in the diaphragm and other respiratory muscles, further emphasizing their importance in sustaining performance [
52].
Despite the valuable insights gained from this study, several limitations should be acknowledged. First, the uneven distribution of participants across the sports groups in the study may limit the generalizability of the findings. However, the impact of this on the analysis results has been carefully considered, and the findings have been interpreted with these limitations in mind. Future research with a more homogeneous sample within each sport can support these findings and enhance generalizability. Second, all participants in this study were of Caucasian descent. While this was a homogeneous sample that allowed for controlled comparisons within this group, it limits the external validity of the findings. Research has shown that physiological factors, including respiratory function and oxygen consumption, can vary across ethnicities. As a result, caution should be exercised when applying these findings to athletes of different ethnic backgrounds, and future studies should aim to include more ethnically diverse populations to determine whether similar associations hold across various groups. Third, although the measurement techniques used—such as respiratory function tests, maximal oxygen consumption (VO2max), and diaphragmatic circumference assessments—are widely accepted and validated in general athletic populations, the specific validation of these methods for athletes in sports such as biathlon, judo, and cross-country skiing was not conducted. It is important to ensure that the methods used are reliable and valid for the specific populations being studied, as variations in sport-specific respiratory and aerobic demands could impact the accuracy of the measurements. Moreover, considering the potential interactions observed in our study, key outcomes such as MIP, MEP, and various physiological measurements—including VO2max, VE, and VCO2 are interrelated. These associations are influenced by factors such as training level, age, gender, and exercise intensity. A more detailed examination of these complex interactions may yield a deeper understanding of the mechanisms underlying respiratory and metabolic performance. The way these variables interact has significant implications for the development of personalized training programs aimed at optimizing athletic performance.
To address the lack of specific recommendations for coaches and athletes, the study’s findings suggest several practical applications. Coaches could focus on improving the efficiency of respiratory mechanics, rather than solely aiming for increased chest expansion, by incorporating breathing exercises that target both inspiratory and expiratory muscles, such as diaphragmatic breathing and controlled exhalation. Athletes should consider integrating RMT into their routine to enhance MEP, which was positively correlated with VO2max and VE. Additionally, individualized assessments of respiratory patterns and chest mobility could help tailor training programs to optimize oxygen uptake and endurance, especially in athletes engaged in high-intensity or endurance sports. Finally, environmental factors such as altitude and temperature should be considered during training, as they might influence the relationship between respiratory parameters and performance.
Coaches can enhance athletes’ respiratory muscle strength by integrating targeted RMT into their programs. For endurance sports, focus on exercises that improve both inspiratory and expiratory muscle strength, while strength and power sports may benefit from shorter, intense breathing exercises aimed at boosting expiratory strength. Tailor RMT to the athlete’s competition level, using moderate resistance for beginners and advanced resistance for elite athletes. Individual assessments of lung capacity and respiratory patterns should guide adjustments to training programs. Additionally, adapt training to environmental factors like altitude and temperature to optimize respiratory performance.