Competitive sports athletes frequently encounter various challenging training and competition environments, such as high temperature, high humidity, and hypoxic conditions. However, when the human body operates in these environments, it often experiences a decline in physical performance and an accelerated onset of exercise fatigue, among other negative effects (Osawa et al., 2017; Jung et al., 2021).

Hypoxia exposure, in comparison to normal environmental conditions, can restrict respiratory function and affect gas exchange in the human body. It can lead to a decrease in arterial oxygen saturation (SpO₂), capillary oxygen partial pressure, and ultimately limit oxygen supply to peripheral tissues (Twomey et al., 2017). Numerous studies have consistently demonstrated that hypoxia exposure leads to a decrease in exercise time, maximal oxygen uptake ( V ˙ O 2 ⁡ max ), and peak output power among athletes during incremental exhaustive exercise (Lawler et al., 1988; González-Alonso and Calbet, 2003; Subudhi et al., 2007). Furthermore, it induces a leftward shift in the Gas Exchange Threshold (GET) and Respiratory Compensation Point (RCP) (Zerbini et al., 2013; Bowen et al., 2016). Furthermore, research focusing on the impact of hypoxia exposure have demonstrated that during incremental exhaustive exercise, break point (BP) of active muscle deoxy-hemoglobin (HHb) undergoes a leftward shift under hypoxic conditions (Azevedo et al., 2020a). Additionally, when athletes engage in physical activities in high-temperature and humid environments, heat exposure can contribute to the acceleration of peripheral fatigue by influencing gas exchange and oxygen transport in skeletal muscle. The challenging conditions in such environments often lead to disruptions in heat dissipation, elevated core temperature (Tc), excessive dehydration, and impaired functional regulation of the cardiovascular, central nervous, and musculoskeletal systems (Périard et al., 2013; Yamaguchi et al., 2021). Consequently, these factors can restrict the capacity for oxygen transport and utilization in skeletal muscle tissue. As a result, athletes experience a leftward shift in the GET, along with a decrease in V ˙ O 2 ⁡ max and exercise time, when performing incremental exhaustive exercise under high-temperature and humid conditions (Tatterson et al., 2000; Sawka et al., 2011).

The dynamic characteristics of Oxygen Uptake ( V ˙ O 2 ) and HHb during incremental exercise, particularly in special environments such as high temperature and humidity, and hypoxic environments, have not been extensively studied. Previous research has shown that V ˙ O 2 exhibits a linear increase with exercise intensity, while HHb in skeletal muscle demonstrates a bilinear increase with exercise load (Vieth, 1989; Spencer et al., 2012). However, the specific differences in dynamic parameters between V ˙ O 2 and HHb during incremental exhaustive exercise under these special environments remain unclear. Exploring the dynamic changes of HHb in body gas exchange and skeletal muscle microcirculation during exercise can provide valuable insights into the mechanisms underlying premature peripheral fatigue in these environments.

Therefore, it is crucial to investigate the characteristics of oxygen supply in peripheral tissues and body gas exchange among athletes in high temperature, high humidity, and hypoxic environments. In our study, we utilized Near-Infrared Spectroscopy (NIRS) as a non-invasive method to assess oxygen levels in micro vessels. By comparing the characteristic parameters of oxygen uptake kinetics and deoxyhemoglobin kinetics in athletes during incremental exhaustive exercise under high temperature and high humidity, hypoxic, and normal environments, we aim to explore the influence of these different special environments on the dynamic changes of V ˙ O 2 and Muscle Oxygen Saturation (SmO₂) during exercise.

The aim of this study was to compare the effects of incremental exhaustive exercise on the dynamic changes of athletes’ V ˙ O 2 and HHb under different environments, in order to elucidate the relationship between the dynamic changes of V ˙ O 2 and HHb and peripheral fatigue in different environments. Our results demonstrate that compared to normal condition, both hypoxia exposure and heat exposure can lead to a reduction in exhaustion time and an acceleration of fatigue development, thereby negatively impacting aerobic capacity, such as gas exchange and oxygen supply in skeletal muscle tissue. Additionally, the dynamic changes of HHb in different modes indicated that hypoxic and heat stress might individually contribute to the reduction of athletes’ aerobic capacity.

When comparing the dynamic changes of V ˙ O 2 during the process of incremental exhaustive exercise under different environments, our study revealed a significant reduction in Δ E V ˙ O 2 and OUES in HOT and HYP. These findings indicate that the gas exchange ability of athletes was inhibited in both environments. Specifically, during exercise in a high-temperature and high humidity environment, the V ˙ O 2 between 2 min and 10 min in the HOT was lower compared to the CON, which aligns with the research findings of Sawka (Sawka et al., 1985), González (González-Alonso and Calbet, 2003), and Wingo (Wingo et al., 2020). This can be attributed to the impact of heat stress on the cardiovascular system and oxygen delivery (Cheuvront et al., 2010). Heat stress reduces Cardiac Output (Q) and Mean Arterial Blood Pressure (MAP) by decreasing cardiac output, resulting in reduced skeletal muscle blood flow, oxygen delivery, and V ˙ O 2 during exercise. Heat stress can reduce blood flow in skeletal muscles during exercise by enhancing sympathetic nerve activity (Sawka et al., 1985). Therefore, during exercise under heat stress, athletes may reduce their oxygen consumption, which can result in a decrease in V ˙ O 2 and Δ E V ˙ O 2 . Additionally, our study observed a significant decrease in Δ E V ˙ O 2 and OUES of athletes under low-oxygen conditions, which aligns with the research findings of Wagner (Wagner et al., 1986) and Loeppky (Loeppky et al., 2020). However, it is important to note that these two studies did not specifically compare the slope of V ˙ O 2 before and after the GET. Nevertheless, our study found an increase in Δ E V ˙ O 2 ‐ 1 in the hypoxic environment. This finding may be attributed to the fact that the initial stage of exercise in a hypoxic environment effectively stimulates peripheral chemoreceptors, leading to increased depth and acceleration of respiration through reflex mechanisms. Furthermore, the utilization of oxygen reserves in the body results in a decrease in SpO₂. We believe that one of the reasons for the increase in △E_VO2-1 is the elevation in VE resulting from enhanced and accelerated respiration due to hypoxic exposure. Firstly, the decrease in oxygen reserve in the body during exercise affects oxygen kinetics. The increased VE under hypoxic conditions improves ventilation efficiency in the early stages of exercise, thereby offsetting the reduction in oxygen reserve (Engelen et al., 1996), resulting in an overall increase in VO₂ slope with decreasing blood oxygen saturation. Secondly, the elevated VE under hypoxic exposure leads to increased oxygen consumption of respiratory muscles and subsequently increased ventilation cost (Coast et al., 1993; Benoit et al., 1997), thereby influencing VO₂ production. Consequently, the V ˙ O 2 and working rate during the initial stage of exercise increase as the body ingests more oxygen to meet its normal work demands. Therefore, the results of V ˙ O 2 in HYP differ from those in HOT, with no significant decrease observed in V ˙ O 2 during the initial stage of exercise in HYP. However, as the duration of exercise increases, athletes may experience a decrease in blood perfusion to the respiratory muscles and limitations in gas diffusion. This can result in a mismatch between ventilation and perfusion, ultimately leading to a decrease in V ˙ O 2 . Therefore, the response of VE to exercise under hypoxic environment throughout the entire exercise process contributes to the reduction in Δ E V ˙ O 2 (Amann and Calbet, 2008).

Regarding the oxygen supply to skeletal muscles, our findings are consistent with previous literature reports (Zhang et al., 2010), indicating a positive correlation between BP and GET. In terms of selecting the appropriate linear fitting model for HHb, Spencer (Spencer et al., 2012) have noted that the bilinear model provides a more accurate description of the potential physiological response of HHb in subjects compared to the S-type regression model. Thus, we employed the bilinear model to assess the dynamic changes in HHb in VL during exercise. To evaluate the HHb response throughout the entire exercise process, we also calculated the slope of HHb from the onset of exercise to the point of exhaustion. Interestingly, our observations demonstrate that the ΔE_HHb in the HOT is higher than that in the CON, and the significance of SmO₂ is lower in the HOT compared to the CON at the 10-min mark during exercise. Previous research by Dennis (Dennis et al., 2023) has shown that exercise at 35°C and 40°C, compared to a single exercise at 20°C, can enhance the deoxygenation reaction in skeletal muscles. Girard (Girard et al., 2016) have highlighted that high-intensity exercise in a high temperature and humidity environment can affect the efficiency of output power and accelerate peripheral fatigue. Our study indicates that the efficiency of output power of skeletal muscles increases during the initial stage of exercise in the high-temperature and high-humidity environment, offsetting some of the negative effects (Racinais et al., 2017). Consequently, we did not observe a significant decrease in SmO₂ in the VL during the initial stage of exercise. However, as exercise intensity and duration increased, along with an increase in Tc, peripheral fatigue eventually set in. Throughout the entire exercise process, the significant increase in ΔE_HHb may be attributed to the rightward shift of the oxygen dissociation curve caused by a decrease in Hb affinity for oxygen as temperature rises, promoting oxygen release (Webb et al., 2022). Simultaneously, in the analysis of V ˙ O 2 and HHb, the Δ V ˙ O 2 /ΔHHb value in the HOT also revealed an enhancement in skeletal muscle Hb deoxygenation reaction. In particular, during the initial stage of exercise, we observed an increase in E_HHb-1 in the HOT condition compared to the CON condition, while E_VO2-1 remained unchanged. This observation aligns with the findings of Nybo et al. (Nybo et al., 2001), who reported that heat stress did not influence the oxygen uptake rate in the early stages of exercise but led to a reduction in oxygen uptake and oxygen pulse. It has been suggested that oxygen uptake kinetics are influenced by both the rise in skin temperature and core temperature (Rowell et al., 1966; José et al., 1997), although they do not increase simultaneously during the early stages of exercise. Despite the acceleration of skeletal muscle deoxygenation in these early stages, compensatory mechanisms appear to address the lack of oxygen delivery. Our investigation revealed an increase in HR in the HOT condition, accompanied by an elevation in cardiac output within a certain heart rate range to compensate for the mismatch between oxygen intake and utilization. As heart rate increased within a specific range, cardiac output(Q) also rose to compensate for the discrepancy between oxygen intake and utilization. Additionally, it has been noted that higher Q, hemoconcentration, and enhanced O₂ extraction contribute to a similar initial rate of rise in V ˙ O 2 (González-Alonso and Calbet, 2003). Therefore, the early-stage mismatch between oxygen uptake and utilization in exercise under high temperature and high humidity may result from various factors. Furthermore, the correlation results showed that ΔE_HHb in the HOT was negatively correlated with V ˙ O 2 ⁡ max , suggesting that the increase in Hb deoxygenation reaction during exercise, resulting from the aforementioned mechanism, may be associated with a decrease in exercise duration. Hence, athletes engaging in physical activity within high-temperature, high-humidity environments conditions may potentially influence the interplay between oxygen uptake in skeletal muscles and lungs.

Hypoxia exposure negatively affects athletes during incremental exhaustive exercise, resulting in decreased SpO₂, SmO₂, and VO_2max at the point of exhaustion. This is consistent with findings from previous studies (Osawa et al., 2011; Azevedo et al., 2020a). Osawa (Osawa et al., 2017) and Bowen (Bowen et al., 2016) have also demonstrated that the SmO₂ curve of skeletal muscle decreases while the HHb curve increases during incremental exhaustive exercise in a hypoxic environment. However, these studies did not compare the slope of HHb during exercise. In the initial stage of incremental exhaustive exercise in a hypoxic environment, the metabolism is immediately affected. Hypoxia exposure causes the anaerobic energy supply system to be utilized earlier to maintain ATP demand (Linnarsson et al., 1974), leading to a left shift in BP and GET. Previous studies have shown that the value of ΔE_HHb during incremental exhaustive exercise can be influenced by factors such as body position (DiMenna et al., 2010) and metabolic diseases (Gildea et al., 2019). In our study, we observed a significant increase in ΔE_HHb-1 before BP, indicating that as skeletal muscle deoxygenation accelerates, the ability to increase peripheral oxygen delivery and meet the increased oxygen demand decreases. However, in the study by Azevedo (Azevedo et al., 2020b), only the leftward shift of BP and the increase in HHb during exercise under hypoxia were observed, without affecting ΔE_HHb-1. In comparison, our study employed a lower FiO₂ for exercise, which may explain the enhanced skeletal muscle deoxygenation response. Acute hypoxia exposure leads to a significant reduction in oxygen delivery to skeletal muscles during exercise, but this can be compensated by increased oxygen uptake in the body (Calbet et al., 2009). The increase in Δ E V ˙ O 2 ‐ 1 and Δ V ˙ O 2 /ΔHHb before GET reflects the relationship between the decrease in oxygen reserve and the increase in oxygen uptake. The earlier deployment of the anaerobic energy supply system causes the slope of HHb to rise rapidly in the initial stage, and impaired hemodynamic response can be considered a potential mechanism for decreased exercise capacity (Gildea et al., 2019). Additionally, the decrease in muscle O₂ flow may potentially limit the possibility of V ˙ O 2 kinetics during exercise (Koga et al., 2007). The observed correlation between ΔE_HHb-1 and V ˙ O 2 ⁡ max in the HYP group supports this perspective.

In our study, we also observed that ΔE_HHb-2 in the HHb plateau after BP appeared to be unaffected by the environmental factors, supporting the notion that the increase in HHb near the critical exercise intensity is not limited by the oxygen diffusion capacity (Murias et al., 2013). Iannetta (Iannetta et al., 2018) have indicated that an oxygen reserve can still be observed in the deep layer of the VL during incremental exhaustive exercise, and this is not influenced by gender or training level (Inglis et al., 2019). Therefore, the presence of an HHb plateau does not indicate the upper limit of oxygen extraction. After reaching BP, the diffusion capacity of oxygen from the capillaries to the muscle fibers may have reached its peak, and the subsequent increase in oxygen uptake depends more on increased oxygen delivery. In our study, we did not observe any difference in Δ E V ˙ O 2 ‐ 2 among the three environments, which consequently led to no difference in ΔE_HHb-2. This suggests that the oxygen extraction capacity during the HHb plateau phase is not influenced by the environmental conditions.

Some criticisms persist regarding the use of near-infrared spectroscopy in the determination of tissue oxygenation. NIRS signals capture changes in hemoglobin Hb and Mb oxygenation, enabling a robust assessment of muscle oxygenation status throughout all exercise stages with high precision (Lucero et al., 2018). Muscle oxygenation reflects the equilibrium between oxygen delivery and oxygen utilization (Koga et al., 2007). However, the contributions of Hb and Mb to NIRS signals differ during muscle contraction (Spires et al., 2011). Other factors, including hematocrit, blood volume, arterioles, capillaries, and venous distribution, can also influence the interpretation of NIRS dynamics in oxygenation and deoxygenation (Koirala et al., 2021). With increased blood flow during exercise, THb may be affected (Alvares et al., 2020). However, even when skin and muscle blood flow increase simultaneously, changes in NIRS-derived oxygenation signals (SmO₂, HHb) can still accurately reflect alterations in muscle oxygenation (Tew et al., 2010). Some studies have suggested that the oxygenated signal is influenced by increased skin blood flow, while the deoxygenation signal is not sensitive to changes in blood volume (Grassi et al., 2003; Grassi and Quaresima, 2016). Additionally, Koirala et al.'s study (Koirala et al., 2021) found that changes in blood volume have an additional impact on oxygenation Hb-Mb, primarily associated with capillary oxygenation Hb. In contrast, the effect on deoxidation HHb-Mb is less pronounced, given its association with abundant O₂ delivery due to the high O₂ saturation of Hb and Mb. Therefore, based on the aforementioned evidence, we maintain confidence in exploring deoxyhemoglobin dynamics in athletes during increasing load exercises under different environments.

When athletes engage in incremental exhaustive exercise in a hypoxic environment or a high temperature and high humidity environment, the gas exchange in the body and the oxygen supply to skeletal muscle tissue can be compromised. This can have implications for athletes, as accelerated deoxygenation of skeletal muscle during increasing load exercise under high temperature and high humidity, and excessive deoxygenation of skeletal muscle before the break point of deoxygenated hemoglobin under hypoxic environments, may contribute to peripheral fatigue in different conditions.

In high temperature and high humidity environments, exercise intensity can negatively impact the skeletal muscle deoxygenation response. On the other hand, low to moderate load training in a hypoxic environment can accelerate the skeletal muscle deoxygenation response. Therefore, coaches should take into account the specific characteristics of peripheral fatigue during training or competition in different environments and design appropriate training or competition programs accordingly. It is important to consider the limitations imposed by these environments and develop strategies to optimize performance and mitigate the negative effects of reduced oxygen availability and increased heat and humidity.