In this exploratory analysis, PEs evoked significant metabolic and cardiovascular responses within a safe magnitude; 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 > 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. [15–17] While similar results were observed in the presented study, the magnitudes of VO2/kg were much higher. [9, 12] 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. [16] 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 [11–13, 18] due to the increased cardiac output, circulating norepinephrine, and metaboreflex activation. [6] The magnitudes of HR and BP elevation were similar to those reported in previous studies of small- and large-muscle IEs [11–13] that were considered safe, [18] which may strengthen the statement that cardiovascular responses to IEs were irrespective of the types and mass of muscle contraction due to the cardiac preload reduction and increased afterload. [6, 19] Both responses were greater in CPE, and similar results were reported in studies comparing IEs and isotonic exercises. [6, 13]
During IEs, the Valsalva maneuver is easily performed; intrathoracic pressure (ITP) and systemic vascular resistance (SVR) increase, followed by a decrease in venous return and stroke volume. [6, 13] To maintain the cardiac output for exercise, HR was proportionally increased in compensation. [6, 13] Moreover, the exercise volume was higher in the CPE than IPE, which may have led to longer exposure to circulating norepinephrine and metaboreflex activation. [6] Apart from these, the IPE allows for greater muscle reperfusion, [6] 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. [20] 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 [20]; 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 patients with borderline or mild CVDs.
In our study, differences were nonsignificant compared with the rest values until over 40% of the training duration of PEs. This result was not reported by prior studies investigating the whole process of IEs. It may suggest that 2–3 minutes were required for significant cardiovascular and metabolic responses to emerge, consistent with the process of adenosine triphosphate and creatine phosphate glycolysis activation during exercise. [21] These physiological changes occurred to activate the aerobic metabolism, during which an exercise could be performed with less lactate accumulation. [21] Nonsignificant differences in HR and VO2/kg among time points after the 40% duration during both PEs were similar to those observed during constant workload exercises. [22, 23] A light workload in constant workload exercise may evoke a slighter increase in HR and VO2/kg, and the variables are maintained at steady levels until exercise termination after minutes of increase. [23] In this regard, considering the higher BP elevation and risk of performing the prolonged Valsalva maneuver in the CPE, the IPE may be more friendly for patients with borderline or mild CVDs with similar training-induced responses.
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. [24] Exercise over the anaerobic threshold (RER = 1) in CPET suggests that the energy supplied by aerobic oxidation is inadequate to maintain the required activity level; thus, glycolysis is activated with La accumulation. [24, 25] La accumulation could decrease plasma pH, suppress muscle contraction, and facilitate peripheral and central fatigue. [26] Consequently, adjusted by the central nervous system, the expired CO2 concentration increases to maintain the blood plasma’s acid-base equilibrium. [27]
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, 28]; thus, identical to other IEs, PEs could increase the ITP. [6] The diaphragm must modulate the ITP for respiration when the diaphragm and abdominal muscles contract concurrently. [29] The range of motion in the rib cage was also restricted, and the flow-generating function of the diaphragm decreased. [29] As a result, the peak VO2/kg was affected. [29] 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. [2] Muscle exercise-induced perfusion was impeded, leading to relative ischemia. [2] 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, 25, 26] 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. However, because the acute, safe responses during IPE were reported in a healthy population, the acute and long-term training-induced effects on patients with borderline or mild CVDs require further research.
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 minutes of the PE. Nevertheless, previous studies in this field recruited 7–20 subjects, and the power was checked by the prior and posteriori sample size calculations. Second, the exercise volumes were not equal for each participant; the responses to completing a 1-minute 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.