The sympathetic response to hypoxic exercise:
elevated but not prolonged

CAIYAN LI1, CHANSOL HURR1, SEUNG-RO LEE1, DONGWOO HAHN2, ANJIE WANG3

1Integrative Exercise Physiology Laboratory, Department of Physical Education, Jeonbuk National University, Jeonju South Korea; 2School of Health and Kinesiology, The University of Nebraska, Omaha, USA; 3Department of Physical Education, Anhui Polytechnic University, Wuhu, China.

Summary. Background. Hypoxic exercise has become an innovative approach to enhancing athletic performance and cardiovascular health. The response of sympathetic nerve activity (SNA) to hypoxia may offer unique benefits, although prolonged activation is associated with increased cardiovascular strain and delayed recovery. This study examined the effects of moderate-intensity aerobic exercise under normoxic (FiO2 = 20.9%) and hypoxic (FiO2 = 14%) conditions on SNA and physiological responses in healthy adults. Methods. This study employed a randomized crossover design. Eleven participants (eight males and three females) performed two 60-minute sessions of moderate-intensity aerobic exercise under normoxic and hypoxic conditions. SNA, mean arterial pressure (MAP), and heart rate (HR) were measured pre-exercise, immediately post-exercise, and during a 90-minute recovery period. Low-frequency (LF) and the LF/high -frequency (HF) ratio served as indicators of sympathetic activation. Results. After exercise, both LF and the LF/HF ratio were significantly higher in the hypoxic condition compared to the normoxic condition (LF: 0.532 ± 0.078 vs 0.461 ± 0.100 Hz, p = 0.021; LF/HF ratio: 0.918 ± 0.368 vs 1.172 ± 0.405, p = 0.018). Additionally, MAP was significantly lower under hypoxia than under normoxia (82.1 ± 7.7 vs 88.2 ± 6.2 mmHg, p = 0.008). No significant differences in these parameters were observed during the recovery period (all p > 0.05 from Post-30 to 90). Conclusions. These findings indicate that moderate-intensity hypoxic exercise transiently increases SNA and decreases MAP compared to normoxic exercise without prolonging recovery.

Key words. Sympathetic nerve activity, aerobic exercise, hypoxic exercise, recovery.

La risposta simpatica all’esercizio ipossico: elevata ma non prolungata

Riassunto. Background. L’esercizio fisico in condizioni di ipossia rappresenta un approccio innovativo per migliorare la performance atletica e la salute cardiovascolare. La risposta dell’attività nervosa simpatica (ANS) all’ipossia potrebbe offrire benefici specifici, sebbene un’attivazione prolungata sia associata a un aumento dello stress cardiovascolare e a un ritardo nei processi di recupero. Questo studio ha esaminato gli effetti dell’esercizio aerobico a intensità moderata svolto in condizioni normossiche (FiO₂ = 20,9%) e ipossiche (FiO₂ = 14%) sull’ANS e su altre risposte fisiologiche in adulti sani. Metodi. È stato adottato un disegno sperimentale crossover randomizzato. Undici partecipanti (otto uomini e tre donne) hanno eseguito due sessioni di esercizio aerobico di 60 minuti a intensità moderata, una in condizioni normossiche e una in condizioni ipossiche. L’ANS, la pressione arteriosa media (MAP) e la frequenza cardiaca (FC) sono state misurate prima dell’esercizio, immediatamente dopo e durante un periodo di recupero di 90 minuti. La componente a bassa frequenza (LF) e il rapporto LF/alta frequenza (HF) sono stati utilizzati come indicatori dell’attivazione simpatica. Risultati. Dopo l’esercizio, sia la componente LF che il rapporto LF/HF risultavano significativamente più elevati nella condizione ipossica rispetto a quella normossica (LF: 0,532 ± 0,078 vs 0,461 ± 0,100 Hz, p = 0,021; rapporto LF/HF: 0,918 ± 0,368 vs 1,172 ± 0,405, p = 0,018). Inoltre, la MAP era significativamente più bassa in ipossia rispetto alla normossia (82,1 ± 7,7 vs 88,2 ± 6,2 mmHg, p = 0,008). Non sono emerse differenze significative in questi parametri durante il periodo di recupero (tutti i p > 0,05 da Post-30 a 90 minuti). Conclusioni. Questi risultati indicano che l’esercizio ipossico a intensità moderata induce un aumento transitorio dell’attività simpatica e una riduzione della pressione arteriosa media rispetto all’esercizio normossico, senza tuttavia prolungare i tempi di recupero.

Parole chiave. Attività nervosa simpatica, esercizio aerobico, esercizio ipossico, recupero.

Introduction

Hypoxic exercise, or exercise conducted under reduced oxygen levels, has been gaining attention as an innovative strategy for enhancing health outcomes1, particularly for managing chronic conditions like obesity2 and hypertension3. By increasing physiological stress, hypoxic environments have been shown to promote greater adaptations compared to normoxic conditions4. These adaptations include improved cardiovascular efficiency3,4, enhanced metabolic responses2, and increased muscle endurance5. As a result, hypoxic training has become increasingly popular among athletes and in clinical settings alike1. The physiological demands of hypoxic exercise offer therapeutic potential by enhancing metabolic health and cardiovascular function, making it a promising tool for addressing modern health challenges1,4.

A key aspect of the body’s response to hypoxia is the activation of the autonomic nervous system, particularly through increased sympathetic nerve activity (SNA)6,7. Hypoxia triggers a range of autonomic responses to maintain oxygen delivery to tissues8. The SNA responds by increasing heart rate, vasoconstriction, and systemic vascular resistance to compensate for reduced oxygen availability9,10. This activation is critical to maintain homeostasis during acute hypoxic exposure9. Both exercise and hypoxia independently elevate SNA, but their combined effects may result in a more pronounced and sustained sympathetic response11,12. Although these autonomic responses are essential for managing oxygen deficiency, the impact of elevated SNA under hypoxic conditions warrants further exploration10.

While triggering of the SNA by hypoxia can enhance oxygen delivery and performance in the short term, sustained elevation of SNA can lead to negative physiological consequences13. Prolonged SNA activation has been associated with increased cardiovascular strain, higher blood pressure, and delayed recovery14,15. Furthermore, chronic overactivation of the SNS can result in sleep disruption, loss of appetite, and increased systemic inflammation, all of which can impair recovery and overall health16,17. Despite these concerns, the effects of elevated SNA in hypoxic exercise protocols have not been extensively studied. Current research has largely focused on the beneficial adaptations of hypoxic exercise, often overlooking possible autonomic side effects18. Understanding this balance is crucial for optimizing hypoxic training, particularly for individuals with cardiovascular risk factors19.

This study aims to evaluate the effects of aerobic exercise under both normoxic and hypoxic conditions on SNA and recovery. Specifically, we aim to determine whether hypoxic exercise induces greater and more sustained increases in SNA compared to normoxic exercise. We hypothesize that while hypoxic exercise will elevate SNA more than exercise in normoxia, the recovery of sympathetic activity following exercise will be more prolonged under hypoxic conditions than under normoxic conditions.

Materials and methods

Participants

Eleven healthy young subjects participated in this study, consisting of eight males (age: 27.1 ± 3.7 yrs, height: 179.4 ± 6.2 cm, body weight: 77.5 ± 8.2 kg, BMI: 24.1 ± 2.2 kgm-2) and three females (age: 27.4 ± 4.6 yrs, height: 161.3 ± 7.6 cm, body weight: 55.8 ± 3.5 kg, BMI: 21.5 ± 1.5 kgm-2). All participants were nonsmokers and engaged in regular aerobic training (>1 hour per day, at least 5 days per week). This study protocol was approved by the Jeonbuk National University Ethics Committee (IRB #: JBNU 2022-02-010-001) on 10 February 2022. The experiments were adhered to the standards set by the Declaration of Helsinki (2013). All participants were verbally informed of the risks and potential discomforts associated with the experimental trials, and written informed consent was obtained from all subjects prior to their participation.

Experimental design

This study employed a randomized crossover design, in which participants were blind to the environmental conditions (i.e., normobaric hypoxia or normoxia). Subjects visited the laboratory for two sessions, spaced one week apart. Participants were randomly assigned to the hypoxic or normoxic condition using a computer-generated random sequence in Excel, ensuring equal probability of allocation. They were instructed to maintain their regular diet but to avoid eating within 2 hours before each visit. Additionally, they were asked to refrain from strenuous physical activity, alcohol, and caffeine for 24 hours prior to each session. To minimize the impact of diurnal variations on exercise performance, all testing sessions were scheduled at the same time of day (±1 hour).

Each session consisted of 60 minutes of moderate-intensity aerobic exercise in either normoxic (FiO2 = 20.9%) or hypoxic (FiO2 = 14%) conditions. Upon arrival at the laboratory, participants rested for 10 minutes in a climate-controlled chamber, followed by a 5-minute seated period for baseline measurements, including heart rate (HR), arterial blood pressure, and resting sympathetic nerve activity (SNA). The exercise protocol included a 5-minute warm-up, 50 minutes of low to moderate-intensity cycling on a recumbent bike (266R, Egojin Company, China), and a 5-minute cooldown. After exercising, a 90-minute recovery period commenced, during which HR, mean arterial pressure (MAP), and SNA were recorded pre-exercise (Pre), 5 minutes post-exercise (Post-5), and at 30-minute intervals (Post-30, Post-60, and Post-90).

All sessions took place in a climate chamber (7 m length × 4 m width × 3 m height). The hypoxic environment was regulated using a hypoxic generator (JAY-60H, Longfian, Baoding, China). The chamber’s environmental temperature was maintained at a constant ~21°C with a humidity of ~50%. The targeted fraction of inspired oxygen levels for the normoxic and hypoxic conditions were set at 20.9% and 14%, respectively, and FiO2 levels during the sessions were continuously monitored using a wireless oxygen gas analyzer (AR8100, Smart Sensor, Dongwan, China).

Measurements

Arterial blood pressure was measured using an electronic sphygmomanometer (HEM-770A, Omron Healthcare, Kyoto, Japan) for diastolic (DBP) and systolic blood pressure (SBP). Participants were seated quietly, and the blood pressure cuff was wrapped tightly around the upper arm, positioned 2-3 cm above the elbow. Measurements were taken three times, with the average being recorded. MAP was calculated as one-third the sum of SBP plus two times DBP. These data were recorded at baseline, immediately post-exercise, and every 30 minutes during recovery.

Heart rate (HR) was continuously recorded with a Polar transmitter (OH1, Polar Electro, Kempele, Finland) and averaged over the last 30 seconds of each phase. Exercise intensity, defined as 50-60% of HRmax, was determined based on previous research results, with HRmax and target HR calculated by the formulas20,21:

HRmax = 220-age

Target HR = [(HRmax-HRrest) × % Intensity] + HRrest

Autonomic function was assessed using the dry electrode Quick-20 Cognionics headset (Cognionics, CA, USA), which measured heart rate variability indices, including the low-frequency (LF) and high-frequency (HF) components, to evaluate sympathetic and parasympathetic contributions. The LF/HF ratio served as a primary indicator of sympathetic nerve activity22. Participants were seated in a quiet environment, and LF and the LF/HF ratio were recorded at the end of baseline, after exercise, and every 30 minutes during recovery.

Statistical analyses

Data are expressed as means ± SD. A two-way repeated measures ANOVA was used to determine the main effects of condition, time, and the interaction between condition and time, followed by Tukey’s post hoc analysis. Statistical significance was set at p < 0.05. Consistent with an a priori sample-size calculation (G*Power 3.1) conducted in a previous study23, 11 participants per condition were required to achieve the targeted statistical power of β = 0.80 at α = 0.05 for the repeated sprint tests (actual power = 0.84 at n = 11). To account for potential dropouts, 12 participants were recruited.

Partial eta-squared (η2) was calculated to estimate the effect size of the two-way ANOVA (main effects and interaction), with values of 0.01, 0.06, and above 0.14 representing small, medium, and large effects, respectively. Additionally, Cohen’s conventions for effect size (ES) were applied when a significant difference (P < 0.05) was detected between conditions, where an ES of 0.2, 0.5, and 0.8 was considered a small, medium, and large effect, respectively. All statistical calculations were performed using Prism 10 software (GraphPad Software, San Diego, CA, USA).

Results

Changes in low frequency and LF/HF ratio are presented in figure 1.




Significant main effects of time and interaction on low frequency were observed (p = 0.031 and p = 0.006, respectively; η² = 0.138 and η² = 0.165, respectively). However, no significant main effect of condition was detected (p = 0.566, η² = 0.034). Low frequency in the hypoxic condition was higher than in the normoxic condition immediately after exercise (Post-5, 0.461 ± 0.100 vs 0.532 ± 0.078 Hz, p = 0.021, ES = 0.37). For the LF/HF ratio, significant main effects of time and interaction were also noted (p = 0.046 and p = 0.008, respectively; η² = 0.113 and η² = 0.157, respectively), though no significant main effect of condition was found (p = 0.633, η² = 0.019). The LF/HF ratio in the hypoxic condition was higher than in the normoxic condition immediately after exercise (Post-5, 0.918 ± 0.368 vs 1.172 ± 0.405, p = 0.018, ES = 0.31). During the recovery phase, no significant differences were observed between conditions for either low frequency or LF/HF ratio.

Changes in SBP, DBP, and MAP levels are presented in figure 2.




Significant main effects of time and interaction were observed on SBP and MAP separately (SBP: p < 0.001 and p = 0.017, respectively; η² = 0.347 and η² = 0.139, respectively; MAP: p < 0.001 and p = 0.029, respectively; η² = 0.275 and η² = 0.125, respectively). A main effect of time was noted for DBP (p = 0.073, η² = 0.106), but no significant main effect for condition was detected for SBP, DBP, or MAP (all p > 0.05). Post-exercise SBP was significantly lower in the hypoxic condition compared to the normoxic condition (Post-5, 127.5 ± 9.9 vs 114.1 ± 9.6 mmHg, p = 0.040, ES = 0.56). Similarly, MAP was lower in the hypoxic condition than in the normoxic condition after exercise (Post-5, 88.2 ± 6.2 vs 82.1 ± 7.7 mmHg, p = 0.008, ES = 0.40).

No significant differences in target HR between normoxia and hypoxia conditions were found (normoxia: 129.9 ± 5.3 vs Hypoxia: 130.9 ± 5.9 beats·min-1, p > 0.05). The changes in HR levels are shown in figure 3.




Statistical analysis revealed a significant main effect of time on HR (p < 0.001, η² = 0.978), but no significant main effects for condition or interaction were observed (p = 0.473 and p = 0.705, respectively; η² = 0.101 and η² = 0.026, respectively).

Discussion

This study explored the effects of moderate-intensity hypoxic exercise (FiO2 = 14%) on sympathetic nerve activity (SNA) and cardiovascular responses, providing insight into how hypoxic conditions influence autonomic regulation during exercise and recovery. Our findings indicate that while SNA increased following exercise in both hypoxic and normoxic conditions, hypoxia elicited significantly higher low-frequency (LF) power and LF/HF ratio immediately post-exercise. Additionally, mean arterial pressure (MAP) was lower in hypoxia compared to normoxia, suggesting distinctive cardiovascular adaptations to reduced oxygen availability. Importantly, SNA recovery did not differ between conditions, indicating that moderate hypoxic exercise does not impose additional recovery demands.

The sympathetic nervous system is activated during exercise18. The elevated LF power and LF/HF ratio following hypoxic exercise suggest an acute increase in sympathetic drive under hypoxic stress10,12. Hypoxia likely activates peripheral chemoreceptors, which trigger sympathetic activation to maintain oxygen delivery to essential tissues6. This response may serve as an adaptive mechanism, ensuring adequate circulation and oxygen distribution despite reduced oxygen availability24. Moderate, HR-matched hypoxic exercise appears to elicit a similar cardiac autonomic and physiological response to normoxic exercise, but with a reduced mechanical load and delayed parasympathetic reactivation11.

Our study demonstrated a significant increase in sympathetic activity immediately post-exercise in hypoxic conditions compared to normoxic conditions. Previous research has shown that hypoxia increases sympathetic activity and reduces parasympathetic regulation12. However, in our study, no significant differences in recovery were observed between conditions. A plausible explanation is that the moderate-intensity exercise employed may not have induced a severe hypoxic response. Higher exercise intensities19,25, and challenging environmental conditions have been shown to cause greater homeostatic disruptions, leading to slower post-exercise recovery of SNA and HR14, 26. Further research should investigate whether high-intensity training in hypoxia delays SNA recovery.

Heart rate (HR) increased during exercise and declined during recovery in both conditions, with no significant differences observed. The post-exercise increase in HR is driven by sympathetic activation to maintain oxygen delivery to tissues9. During recovery, the reduction in HR depends on parasympathetic reactivation and a gradual decrease in sympathetic drive27. Previous studies suggest that hypoxia elevates HR during exercise due to compensatory responses to reduced oxygen availability28. Although some evidence indicates that the same absolute intensity of exercise under hypoxia is associated with greater exercise-induced metabolic stress and delayed cardiac autonomic recovery11, the lack of HR differences in our study may be attributed to the moderate exercise intensity used, which may not have induced the same level of stress as higher intensities documented in other research.

Regardless of whether in normoxic or hypoxic conditions, exercise leads to an increase in MAP24. This rise in blood pressure results from increased cardiac output, driven by elevated heart rate and stroke volume, along with sympathetic nervous system activation9,14. Interestingly, our results showed that post-exercise MAP under hypoxic conditions was lower than under normoxic conditions. This reduction can be attributed to the vasodilatory effects of hypoxia, particularly due to the release of nitric oxide (NO), which serves as a key vasodilator to enhance blood flow and improve oxygen delivery 5. Consequently, while exercise generally raises blood pressure, the sustained effects of hypoxia induce vascular adaptations that result in a lower MAP compared to normoxia.

Overall, our study results suggest that in moderate-intensity exercise, lower MAP and higher SNA are observed in hypoxia compared to normoxia immediately after exercise, but not during the recovery period. Additionally, moderate-intensity exercise did not produce differences in HR between hypoxic and normoxic conditions. For most of the indices examined, similar trends were observed when comparing mean responses, end-of-exercise responses, and successive exercise bouts across the different conditions. In recent years, hypoxic training has been recognized as an effective method to enhance performance in sports requiring high levels of aerobic and/or anaerobic endurance29. Beyond its impact on exercise performance, recent evidence suggests that intermittent hypoxia training may have clinical applications30. Previous studies have demonstrated that hypoxic training could serve as an alternative therapeutic strategy for patients with hypertension31. However, few studies have examined the potential side effects of hypoxic training, particularly regarding recovery.

Higher exercise intensity delays post-exercise recovery of impedance-derived cardiac sympathetic activity14. Future studies should explore the effects of different exercise intensities in hypoxic conditions to better understand the thresholds that may delay recovery. The present findings were obtained in healthy, active subjects; therefore, further research is needed to investigate the impact of hypoxic exercise on different special populations1. Examining these effects in diverse groups, including those with cardiovascular or respiratory conditions, could provide valuable insights into the therapeutic potential of hypoxic exercise.

Conclusions

Our findings indicate that moderate-intensity hypoxic exercise elevates SNA and reduces MAP immediately after exercise without affecting HR or SNA recovery. For sports and clinical applications, these results suggest that moderate hypoxic exercise could enhance sympathetic activation and vasodilation without extending recovery time, potentially benefiting hypertensive patients and athletes who require efficient recovery protocols. Nevertheless, higher-intensity hypoxic exercise may delay SNA recovery, warranting further investigation.

Conflict of interest. The authors declare that there is no conflict of interest.

Funding. This research was supported by National University Development Project at Jeonbuk National University in 2024. This research was also supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF), funded by the Ministry of Education (RS-2023-00243082).

Authors’ contributions. Conceptualization, SL and CH; Methodology, CL and CH; Software, SL, AW and CH; Validation, CL and CH; Formal analysis, SL and CH; Investigation, SL; Resources, CH; Data curation, SL; Writing-original draft preparation, AW; Writing-review and editing, CH; Visualization, AW; Supervision, CH; Project administration, CH. All authors have read and agreed to the published version of the manuscript. CL and CH contributed equally.

Acknowledgment. We would like to express our appreciation to all participants for their involvement in the study.

Availability of data and materials. The data presented in this study are available on reasonable request from the corresponding author.

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