This study demonstrates the absence of limitations in either cardiorespiratory or metabolic variables during jogging regardless of types of breast support used. The slightly diminished respiratory flow rates after immediate donning the JB can be compensated during jogging. In addition, JB shows an earlier recovery of some metabolic and cardiorespiratory variables (V̇O2, EE, V̇E, and SVR) in comparison with CB. As jogging without breast support causes the risks of repeated motions of soft tissues around the chest [18], we recommend active females to jog with bras to enhance cardiorespiratory recovery during training.
Results from this study show that elastic compression of bras, from either CB or JB, will not cause any difficulties in cardiorespiratory and metabolic functions during jogging. Thus, intensity-dependent characteristics likely dominate most of the cardiorespiratory and metabolic responses, not the compressive force from bra elastic properties. It was reported that the difficulty of breathing in association with uncomfortable feeling will only from the tight chest wall restriction [17]. Indeed, it has been shown that high chest wall compressive pressures of over 75 mmHg (101 cm H2O) [19] or up to -20% of chest circumference [20] can cause deteriorations in lung function with reductions in VC and expiratory flow rates. According to previous finding [21], we observed minimal skin furrows from chest straps, which indicate minimal pressure generated from either CB or JB. However, this minimal pressure is possibly the cause of immediate unfamiliar feelings [22] which lower some respiratory variables. In addition, women subjects with statures of 160 cm and 60 kg body weight have small chest wall area compared to the whole body surface area [23] which approximately corresponds to about 0.3 m2 [24]. Thus, the bra types used in this study cover minimal chest surface area and would not induce high chest wall restriction.
Ventilatory responses to exercise in the present study confirm the intensity dependent characteristics. This exercise-induced ventilation was observed immediately after the exercise activity was started, of which ventilatory changes were similar regardless types of breast support. An immediate ventilatory response is initially derived from neural drives and later from blood-borne mediators from exercising muscles [25]. Thus, exercise-induced ventilation via neural and chemical drives could overcome any pressure-induced respiratory limitations from breast supports. Neural and chemical components were the main ventilatory drives [26], we believe that the diminutions, as well as the fluctuations, of these components after exercise explain the differences of cardiorespiratory patterns during recovery. During exercise, plateaus in VT appeared earlier where RR gradually increased across all conditions. This suggests that further increases in V̇E at higher intensities were mainly a result of the increase in RR.
Similar to other Asian women, Thai female adolescents determine the smaller bra sizes with various styles [27]. It was notified that wearing an inappropriate breast support for many hours a day is possibly associated with increased risk of breast cancer [28]. In the present study, there were variations in CB sizes and cup types (B and C), however, JB participants had correct sizes and cups fitting by the professional staffs. Even if minimal, both bras may induce some compression from the elastic recoil of garments. Consequently, the self-determined breast support causes higher V̇E during recovery.
Metabolism during exercise showed intensity-dependent patterns in all conditions. It appears that the effects of exercise intervention seem likely to override effects of breast supports. A previous study reported that high external chest wall restriction resulted in minimal reductions in maximum oxygen uptake (41.9 ± 1.3 to 39.4 ± 1.3 ml/kg/min) [29]. In the present study, we observed no changes in oxygen consumption in all conditions. Thus, this indicates that there are no limitations in metabolism despite NB or breast support types during exercise.
An immediate metabolic recovery was primarily observed only in the NB condition. In fact, full recovery appears within 3–4 min post-exercise, which is a common characteristic. Metabolism remained slightly elevated across all conditions during recovery, indicating that despite the exercise cessation, biochemical processes remain active [30]. This was documented by the elevated rate of high glucose uptake in working muscles during recovery [31]. This may have occurred in all conditions during recovery. However, we believe that breast support pressures, even slight, possibly reflect higher metabolic processes during recovery.
The RER values during exercise indicated that all conditions utilized glycolytic processes as the main energy substrate. During recovery, we found significant differences in V̇O2, V̇CO2, RER, and EE compared with resting values only in two breast support conditions. With minimum pressure, we believe that this will additionally induce higher rates of excess post-exercise oxygen consumption and even higher carbon dioxide production [32] because biochemical activation remains [31]. We also observed the remaining high RER, > 1.00, in all conditions condition during recovery. This may hypothetically indicate the interference of anaerobic processes. However, as we did not measure any blood chemistry (e.g. lactate), this will be our concern for the next investigation. Looking back at respiratory rate (RR), values across all conditions at 80% MHR (Fig. 1B) approached the nearest maximum respiratory rate of 45–50 bpm which adults can attain during exercise [33]. As RR becomes limited, this will predict involvement of anaerobic processes thereafter. Unlike other studies [34], the 5-min recovery period in the present study is not appropriate for exercise at moderate to high intensities, i.e., > 80% MHR.
Likewise, the similar changes in cardiovascular variables across all conditions confirm that the effects of exercise intensity overcome the effects of breast support upon wearing. The present study and previous report [35] confirm that physical activity induces higher ventricular contraction, which in turn results in increasing stroke volume and cardiac output. This will occur with the reduction in total peripheral vascular resistance via vasodilation mechanism [36]. This is due to changes in intrathoracic pressure. These cardiac compensatory conditions may be impaired only when chest wall restriction is extremely high [35].
We also explored the evidence of compressive forces related to the bras’ shoulder straps and found that the JB induced only 6 g/cm2 (data from manufacturer side). This minimal external pressure may not affect the hemodynamics within the thorax [20]. Since body surface area is constant, increasing CI is mainly due to increases in CO. This suggests that cardiac compensation during exercise can sufficiently provide hemodynamics to all body parts [37].
The increases in SV and CO during exercise are most likely due to higher RR, HR and venous return (VR) from changes in intrathoracic pressure. The volume of blood being ejected or remaining in the heart are unique parts of our investigation. Since the EDV mainly depends on end-diastolic duration and VR, thus the longer the end-diastolic duration at sub-maximum workload, the higher blood volume will be filled in the heart chamber [38]. Accordingly, heart rates across all exercise intensities were in the same ranges among conditions, thus presumably resulting in similar EDV. Ejection fraction (EF) normally ranges from 55 to 70% and may rise up to approximately 80% during maximum exercise to adapt to the higher physical workload [39]. In healthy individuals during exercise, higher EF would represent an increase in ventricular function, whereas a decrease in EF would represent impairment of ventricular function [38]. The above has been used as a clinical indicator [38], in which it is generally known that sympathetic activation during exercise will stimulate greater cardiac contraction in parallel with a faster cardiac rhythm. Moreover, the reductions in vascular resistance are due to exercise-induced vasodilation via an increased secretion of nitric oxide, a local vasodilator, and other agonists, which are involved in endothelium-dependent pathways [40].