For football sport, Fardy [15
] has shown that soccer players made great strides in the cardiorespiratory endurance and VO2max
, and had about 15.5% increase in VO2max
after 10-week soccer training. Reilly and Thomas [16
] indicated that the vital capacity was increased, while the body fat, systolic blood pressure (SBP), diastolic blood pressure (DBP), peaceful HR and maximum HR were all decreased after a programme of pre-season training on the soccer players. Ostojic and Mazic [17
] suggested that soccer players should consume carbohydrate-electrolyte fluid throughout a game to help prevent deterioration in specific skill performance. Brites et al. [18
] showed that soccer players under regular training show an improved plasma antioxidant
status in comparison to sedentary controls. Hoff et al. [19
] showed that HR monitoring during soccer specific exercise is a valid indicator of actual exercise intensity. Unfortunately, few studies have addressed the autonomic nervous modulation of the football players. We found in this study that almost all HRV measures in the football group were significantly larger or smaller than those of normal controls except the nVLFP in the baseline measurement. However, there were no significant differences in SDRR
, TP, VLFP, and LFP between the football and control groups 60 min after the baseline measurement, and there were no significant differences in the SDRR
, VLFP, LFP, and nLFP between the football and control groups 90 min after the baseline measurement. This result suggested that a rest for 60 min can narrow down the difference in autonomic nervous modulation between football players and normal controls. Despite of this effect of rest on the autonomic nervous modulation in the control group, some HRV measures of the football players were still higher than those of normal controls after a rest for 60 to 90 min. This result suggested that even after a rest for 60 to 90 min, the autonomic nervous modulation of the sedentary controls still could not reach the same degree of relaxation as that of football players.
Ishida and Okada [20
] showed that there were significant differences in the spectral components of HRV during exercise between athletes and control subjects. Their results showed that physical training could possibly increase the parasympathetic activity (or decrease the sympathetic activity). Costa et al. [21
] indicated that higher power of both spectral bands (LF and HF) and higher amplitude of the respective peaks in athletes when compared with healthy sedentary subjects, with a clear predominance of the HF band in the total spectral power density, which suggested that the higher HRV observed in athletes reveals the predominance of parasympathetic activity, without reduction in the sympathetic tone. Shin et al. [22
] indicated that endurance training induces autonomic imbalance (i.e., the enhanced vagal activities and the attenuated sympathetic tone). Shin and his colleagues also demonstrated that the HR of athletes was significantly lower than that of non-athletes, and the HF power of athletes was significantly higher than that of non-athletes during rest and post-exercise period, indicating that vagal activity was enhanced by the adaptive changes in neural regulation produced by long-term physical training [23
]. Nagai and colleagues [24
] suggested that the 12-month moderate exercise training has a positive effect on cardiac ANS activity in the children who initially had low HRV. In accordance with these studies, we found that the indices of vagal modulation such as HFP and nHFP in the football group were significantly higher than those of normal controls, and the indices of sympathetic modulation such as nLFP and LHR in the football group were significantly lower than those of normal controls. Even after a rest for 60-90 minutes, many HRV measures of the football players such as HR, mRRI, rMSSD, HFP, nHFP, and LHR were still significantly different from those of the normal controls. Our observation suggested that football sports can increase the vagal modulation and decrease the sympathetic modulation of the subjects, similar to other kinds of sports or physical trainings, as compared to the non-athletes. Persistent strenuous exercise in the football training and game should be the reason why the HRV measures of the football group were so different from those of the non-athlete high in the baseline measurement.
Sixty and 90 min after baseline measurement, the HR was decreased while the mRRI, SDRR
, rMSSD, TP, VLFP, and HFP were increased in the control group. In the football group, however, a rest for 60 to 90 min could lead to slight decrease in HR and slight increase in mRRI only; no changes in other HRV measures could be found in the football group after a rest for 60 to 90 min. These results suggested that a rest for 60 to 90 min could result in increased overall HRV and decreased HR in the control subjects, but only slightly decreased HR and not changed overall HRV in the football group. It seems that football players at rest were already in a nearly full relaxation state which could not be relaxed further by taking more rest, while the non-athletes were not relaxed fully at rest and more rest could lead to further relaxation. This result seems to be in accordance with the finding of Rebelo et al. [25
] that in spite of the high intensity training period, there was no significant change in results from detraining condition to training condition in professional football players. Knoepï¬éi-Lenzin et al. [26
] showed that football training, consisting of high-intensity intermittent exercise, results in positive effects on blood pressure, body composition, stroke volume and supine heart rate variability, and elicits at least the same cardiovascular health benefits as continuous running exercise in habitually active men with mild hypertension. Mandigout et al. [27
] pointed out that an endurance training program had a positive effect on aerobic
potential, morphological and functional cardiac parameters and on nocturnal global HRV in healthy prepubertal children without inducing sympathetic and parasympathetic. In parallel with the finding of these studies, we found the PP and %FEV1
of the football players were larger than those of the controls. Our data suggested that the tracheobroncheal
tree of the football players might be more competent to allow more air to pass through, and the vascular resistance of the football players might be smaller than that of the non-athletes to facilitate a better blood circulation.
The frequency range of 0.003-0.04 Hz defined for the VLFP by the Task Force of the European Society of Cardiology and the North American Society of Pacing Electrophysiology [9
] is for the analysis of “entire 24 hours”. This definition of frequency range for VLFP cannot be applied to the present study because the ECG signals were recorded for only 15 minutes or so in this study. For analysis of short-term recordings (5 min), a frequency range of ≤ 0.04 Hz was defined for the frequency range of VLFP by the Task Force [9
]. Again, this definition of frequency range for VLFP cannot be applied to our study literally because the recording time of ECG in our study was 15 minutes or so which is longer than 5 minutes. In other words, there is currently “NO” standard definition for the frequency range of VLFP for ECG recording between 5 min and 24 hours. Therefore, we defined a frequency range of 0.01-0.04 Hz for VLFP in our studies. The upper limit of 0.04 Hz in our definition was the same as that of 24 hours and 5 min HRV analysis defined by the Task Force [9
]. Since a lower limit of 0.003 Hz for VLFP is too small to be defined for an ECG recording of 15 minutes or so; therefore, a lower limit of 0.01 Hz was chosen so that the counterpart of ultralow frequency power (ULFP) for 24 hours recording (≤0.003 Hz) could be calculated in an ECG recording of around 15 min or longer.
It was suspected that the Task Force [9
] might have not paid appropriate attention to the VLFP because the VLFP was not normalized by any power, and because the frequency range of the power used for the normalization of LFP and HFP did not cover that of VLFP in the definitions of the Task Force. We believe that this overlook of VLFP by the Task Force [9
] is an insufficiency to spectral HRV analysis because Taylor et al. [11
] have found that the VLF RR-interval oscillations
are very much dependent on vagal tone so that the VLFP can be used as the indices of renin-angiotensin-aldosterone system activity and vagal withdrawal in spectral HRV analysis. The vagal withdrawal here means that the vagus nerve is inhibited from slowing the activity of the sinoatrial node and from buffering the degree of contraction throughout the myocardium
. Thus, the VLFP and nVLFP cannot simply be downplayed. To remedy the insufficiency in the definitions of normalized powers by the Task Force, we used the power within the frequency range of 0.01-0.4 Hz (total power-ULFP) to normalize the VLFP, LFP and HFP in our studies. We believe that this way of definitions for nHFP, nLFP and nVLFP are improvements, rather than limitations, to spectral HRV analysis.
In this study, only 17 subjects per group were recruited for spectral HRV analysis. These are rather small groups, and thus the results obtained in this study should be interpreted with caution.