Although there was no significant difference in the HRV indicators among the three groups at rest, there was a discernible trend for the overweight group to exhibit lower HRV compared to the normal weight group and underweight group. The findings of Mitchelmore had similar results to the present study, the research revealed that SDNN at rest was not significantly different among the normal weight group (BMI 20–25 kg/m2), the overweight group (BMI 25–30 kg/m2), and the obese group (BMI > 30 kg/m2). [21]
After acute endurance exercise, SDNN showed a significant decrease in all three groups of subjects compared to its initial value. It can be inferred that shortly after engaging in exercise, there was a inhibition in vagus tone in all individuals. The same findings appear in previous reports on changes in time domain indicators of HRV after acute exercise. It has been demonstrated that a brief inhibition of vagus tone is witnessed after acute exercise. After an acute incremental loading exercise, SDNN, RMSSD, and pNN50 were significantly reduced in 12 male distance runners compared to their resting state. However, these parameters showed significant recovery 12 min after the end of the exercise. [22] In another study, 20 amateur distance runners performed 90 min of treadmill exercise at 95% of their individual anaerobic threshold intensity and found that 15 min after exercise, all time domain indicators were significantly lower than pre-exercise levels. However, after 6h of exercise, all indicators had recovered. [23]
All three groups exhibited a decrease in both LF and HF subsequent to engaging in acute endurance exercise (Fig. 2), indicating a decrease in both sympathetic and vagus tone. The results of this study were similar to those of other studies. Following the competition, it was found that the LF and HF of 13 male athletes were substantially reduced within a span of 10 min, in comparison to their resting state. [24] During acute bicycle incremental load exercise, 11 healthy young males exhibited a noteworthy reduction in both LF and HF. This trend persisted until the load reached 110W, after which HF remained relatively stable while LF continued to decrease. In particular, at 221 W, the R-R interval oscillations in the LF range were no longer present. [25] However, another study had different results. Following a 45 min bout of aerobic exercise at 80% HRmax intensity, a group of obese young males had their HRV indicators taken by Zhu and her associates at the 1h post-exercise time point, which indicated a reduction in HF and an elevation in LF when contrasted with their pre-exercise. [26] The current research on the impact of acute exercise on frequency domain indicators is inconclusive, and the variations may be attributed to differences in the subjects, exercise intensity, duration, type, HRV testing time points and instrumentation.
The brief decline in HRV that is brought about by acute exercise may serve as an indication of the physiological adaptation of the cardiovascular system to the stressors of exercise in individuals without cardiovascular disease. [23] Individual experience vasodilation and an increase in microvascular density in the early stages of exercise, which improves blood and oxygen supply to the heart and meets the increased oxygen demand of the heart during exercise. However, when individuals experience exercise fatigue and exhaustion, the secretion of cardiovascular regulatory factors leads to myocardial vasoconstriction and a decrease in myocardial microvascular density, which in turn leads to an insufficient blood supply/oxygen supply to the heart. [27] This may reduce the regulation of the ANS, resulting in a decrease in HRV. After acute endurance exercise, there was no significant difference in HRV in the underweight group compared with the normal weight group, whereas the overweight group had a deeper inhibition of HRV. This study seems to suggest the importance of maintaining a normal BMI in overweight males. However, the exact cause remains uncertain and requires further exploration. Sahar's study found that RMSSD, HFLn and HFnu were significantly lower in the overweight/obese group compared with the normal weight group in the baseline state, implying that an autonomic imbalance was already present in the overweight/obese group in a resting state, and this could have caused a delay in the recovery of vagal activity after 3 min step-length exercise in the overweight/obese group. [16] Nevertheless, this interpretation is not applicable in this study since the three groups did not show any significant differences in SDNN, LF, and HF at the baseline state. Another study have demonstrated that the amount of body fat in obese-inactive children is linked to a decrease in sympathetic and parasympathetic activity compared to lean-inactive children. [28] It is possible that the disparities in body fat between the three groups could have played a role in the result. In addition, exercise intensity can have an effect on HRV as well, [29] which could potentially affect the outcomes of this study. Since this study did not control the same relative intensity of exercise for different individuals, it is likely that individuals who are underweight, normal weight, and overweight were not exposed to the same load intensity when following the same exercise protocol.
In this study, we paid more attention to the relationship between BMI and post-exercise HRV. By monitoring the changes in HRV indicators after a short period of acute endurance exercise in people with different BMI, we were able to assess the differences in ANS function in people with different BMI after physiologic stress of CVS. The results of this study provide new data and insights for other researchers, further expanding the relationship between BMI and HRV, and contributing to the construction of a more comprehensive knowledge framework in the field of sports medicine and sports science, as well as playing an important role in the further promotion of healthy lifestyles.
There are also some limitations concerning this study. Firstly, this cross-sectional research design can only offer possible insights into the differences in autonomic function after acute endurance exercise in young males with different BMI, without establishing a causal relationship between them. Secondly, this study did not include young males with a BMI ≥ 30.0 Kg/m2, which led to incomplete conclusions from this study. Thirdly, this study did not involve subjects being exposed to the same exercise intensity, and the lack of multiple measurements of the findings reduced the reliability of the experimental results. Taking into account the strong correlation between physical activity levels and HRV, a more specialized tool is essential for obtaining reliable data on moderate-vigorous physical activity (MVPA) from subjects. Finally, the limited sample size in this study only allows for the results to be generalizable to young males. The existence of confounding variables that could potentially skew the results should also be considered. Lifestyle background investigations should be conducted in more detail on subjects in different BMI groups. Future research should use a larger sample size and a broader range of demographic data.