In this exploratory analysis, PEs evoked significant safe-magnitude metabolic and cardiovascular responses; the stress may be greater in CPE. The responses were not significant until 40% of the CPE duration or the second session of IPE. Additionally, La increased, and RERs were over 1; neither the %VO2max/kg nor %HRmax exceeded the %VO2AT/kg or %HRAT, respectively.
Prior research suggests that HR, VO2/kg, and BP increase during lower-extremity IEs [17, 18]. While similar results were observed in the presented study, the magnitudes of VO2/kg were much higher [10, 13]. The reason for the larger metabolic response may be that compared with previously investigated exercises, PEs require higher levels of neuromuscular activation to meet the increasing demands of muscle oxygenation and energy supply . The presented results of EE were also consistent with this statement. Increased HR and BP during small- and large-muscle IEs have been widely reported [12,13,14, 19] due to the increased cardiac output, circulating norepinephrine, and metaboreflex activation . The magnitudes of HR and BP elevation were similar to those reported in previous studies of small- and large-muscle IEs [12,13,14], which may strengthen the statement that cardiovascular responses to IEs were irrespective of the types and mass of muscle contraction due to the decreased cardiac preload and increased afterload [6, 20].
Both responses were greater in CPE, and similar results were reported in studies comparing IEs and isotonic exercises [6, 14]. Larger-magnitude increase in CPE may be caused by a longer duration of Valsalva-like physiological changes and autonomic nervous activation. During IEs, the Valsalva maneuver is easily performed and the PE-induced responses are similar to performing Valsalva maneuver for 15–20 s; intrathoracic pressure (ITP) and systemic vascular resistance (SVR) increase, followed by a decrease in venous return and stroke volume [6, 14, 21]. To maintain the cardiac output for exercise, HR was proportionally increased in compensation [6, 14]. These physiological changes may take minimum 30 s to reach a steady state after the onset of SVR strain and increased ITP . For the PE is not a Valsalva maneuver, the time to steady state may be not 30 s and will be discussed in the following part. Steady state may be achievable for CPE, but not IPE, which demands 1-min exercise followed by rest. Moreover, higher exercise volume in may have led to longer exposure to circulating norepinephrine and metaboreflex activation . Apart from these, the IPE allows for greater muscle reperfusion,  which may mitigate the Valsalva-like effects of CPE. The lower DBP observed during recovery in the present study was also reported during limb remote ischemic conditioning . This may be attributed to the regulation of the autonomic nervous system and increased secretion of vasodilatory substances (e.g., nitric oxide) amongst distal limbs. Another reason may be a sudden drop of central venous pressure and expansion of the superior and inferior vena cavae induced by the decreased ITP . These physiological changes result in a decrease of the peripheral venous pressure and DBP [21, 22]. However, the underlying mechanisms remain understudied. Nevertheless, neither the HR nor BP during PEs exceeded the exercise-termination limits, suggesting a wider application of PEs in youth patients with borderline or mild CVDs.
In our study, differences in %HRmax were nonsignificant compared with the rest values until over 40% of the exercise duration of PEs. In the following exercise timepoints, the differences were not significant from the %HRmax at 40%. Combined with the total plank duration in our study, it suggests the time to steady state may around 1–2 min, and it was interrupted by the rest intervals in IPE. The phase effects of %VO2max/kg was consistent with those in %HRmax, but the time was delayed in RER and EE. These results were not reported by prior studies. During the first 1–2 min of exercise, energy was mainly supplied by adenosine triphosphate-phosphocreatine and glycolysis, and prolonged exercises relies on aerobic metabolism, characterized by evident increased in VO2/kg and RER . In this case, the causes of the advance steady state of VO2/kg may be the response of sudden raise in norepinephrine secretion and restricted right ventricular output [6, 21]. For RER was a parameter describing the pathways of energy supplied, the time to steady state in this study was also consistent with the energy metabolism sequence and features . These cardiovascular and metabolic features were studied based on the constant workload exercises, and the similar results in this study also implied PE is a constant workload exercise [23, 24].  Based on the features of constant workload exercises, a light workload may evoke a slighter increase in HR and VO2/kg, and the variables are maintained at steady states until exercise termination after minutes of increase . In this regard, combining the concerns of time effects and the implied physiological changes, cardiovascular stress may be higher if performing a prolong PE. The IPE may be more friendly for youth patients with borderline or mild CVDs with similar training-induced responses, and the extended exercise duration or augmented sets could be individualized.
Interestingly, none of the %VO2max/kg and %HRmax over the %VO2AT/kg and %HRAT accompanied by RER over 1 with increased La. The reasons are still unexplained. The anaerobic threshold was measured by CPET, during which respiration depth, rate, HR, and stroke volume were increased to meet the incremental muscular oxidation . Exercise over the anaerobic threshold (RER = 1) in CPET suggests that the energy supplied by oxidative system is inadequate to maintain the required activity level; thus, glycolysis is activated with La accumulation [25, 26]. La accumulation could decrease plasma pH, suppress muscle contraction, and facilitate peripheral and central fatigue . Consequently, adjusted by the central nervous system, the expired CO2 concentration increases to maintain the blood plasma’s acid-base equilibrium .
Essentially, failure to maintain the PE may be caused by impeded respiration, oxygen delivered, and La clearance, leading to suppressed muscle contraction. PEs share the same muscles around the rib cage and abdomen [5, 29]; thus, identical to other IEs, PEs could increase the ITP . The diaphragm must modulate the ITP for respiration when the diaphragm and abdominal muscles contract concurrently . The range of motion in the rib cage was also restricted, and the flow-generating function of the diaphragm decreased . As a result, the peak VO2/kg was affected . Conversely, increased muscle pump and vasodilation are significant during CPET [2, 6]. However, during IEs, the muscles tend to impede capillary vasodilation, thereby increasing the SVR . Muscle exercise-induced perfusion was impeded, leading to relative ischemia . This phenomenon is also consistent with the higher exercise DBP, increased %VO2max/kg at CPE recovery, and rest intervals of IPE in our study. La could not be promptly removed from the muscles due to the impeded perfusion leading to decreased muscle contraction and exacerbated muscle fatigue [2, 26, 27]. La may accumulate within the contracted muscles and be removed during the IPE’s rest intervals, leading to a lower La than CPE. In this regard, energy may be mainly supplied by anaerobic metabolism during PEs, and enhanced lactate tolerance and skeletal muscle capillary density may prolong the plank duration.
Overall, there were some limitations in our study. First, only 11 subjects were included in our study as participants were required to perform at least 3 min of the PE. Nevertheless, previous studies in this field recruited 7–20 subjects, and the power had been checked was satisfactory by the prior and posteriori sample size calculations. Second, the exercise volumes were not equal for each participant; the responses to completing a 1-min PE session may be mild in subjects with longer CPE durations. The metabolic and cardiovascular responses may be less significant; however, the relationship between exercise intensity and plank duration is still unknown, and we wanted to guarantee that subjects could complete all three IPE sessions. Additionally, the IPE was selected to include rest intervals, similar to a typical training session. Third, whole-body muscle contraction was required, and noninvasive BP measurement was difficult under this circumstance. Although the random error may be greater, it should affect all subjects in both PEs in the same way. Finally, the effectiveness and safety of applying PE in patients with CVDs could not be entirely guaranteed only by our study, but this study could be a starting investigation in expanding the application of large-muscle IE to patients with CVDs. At the present stage, further studies in applying PEs to youth patients with borderline or mild CVDs and elder healthy population is worth exploring.