# Effect of PEMF on Muscle Oxygen during Cycling:
## 4 Discussion  
The main result of this study is that PEMF stimulation, applied during heavy constant-load exercise, increases the velocity and the quantity of muscle O\({}_{2}\) available. The greater muscle O\({}_{2}\) extraction induced by stimulation accelerated the HHb kinetics without affecting the tissue oxygenation index or the pulmonary VO\({}_{2}\) kinetics. Different studies have established the incidence of a good correlation between the HHb signal recorded with NIRS and the fractional O\({}_{2}\) extraction in animals and in exercising human muscles, and the concept is further strengthened only if the tissue oxygenation index remains constant. This is because TOI includes oxyhemoglobin (HbO\({}_{2}\)), which is more significantly influenced by skin blood flow, occurring for thermoregulatory reasons due to exercise with respect to HHb (for a review see [16]). During PEMF stimulation, we observed a tendency toward a greater change and faster kinetic of HHb concentration. PEMF was able to induce a muscle O\({}_{2}\) availability, but at the same time, the stimulation was not sufficient enough to speed up and change the pulmonary VO\({}_{2}\) on-transition kinetics. These variations at the muscle level were not accompanied by an improvement in endurance performance, such as the changes of the VO\({}_{2}\) on-kinetics (speeding up of its phase II with the decrease in the slow component). This result can be clarified by the fact that the maximal cardiac output places a limitation on muscle blood flow and oxygen delivery to muscles employed during high intensity constant-load exercise that involves large muscle mass (i.e., during cycling), whereas PEMF might act only at the local level. Some authors found that the lack of faster oxygen kinetics in conditions where oxygen transport has been augmented is evidence that a metabolic mechanism, independent of oxygen, limits oxidative phosphorylation at the exercise onset (for more information see [28]). Given that our data demonstrate an accelerated O\({}_{2}\) release at muscle level, the higher metabolism and/or the recruitment of type II muscle fibers at the onset of heavy exercise could be the procedure responsible for the slower oxygen kinetics [29]. Type II muscle fibers exhibit higher O\({}_{2}\) costs during cycling and show slower VO\({}_{2}\) on-kinetics in comparison to type I oxidative fibers, which might explain the slower  
Figure 3: Vastus lateralis tissue oxygenation index (TOI) kinetics following acute PEMF stimulation (ON) and sham condition (OFF). Vertical dotted line at time 0 represents the transition from unloaded pedaling (baseline at 0 W) to constant-load exercise. Data points are average values (%) calculated each second. VO\({}_{2}\) responses. These results reinforce the concept that slower VO\({}_{2}\) on-kinetics may be linked not only to the intracellular components related to aerobic metabolism, but also connected to the divergence between oxygen delivery and utilization at tissue level [30]. A faster modification of blood flow or the removal of limitations related to O\({}_{2}\) diffusion at the periphery did not accelerate the VO\({}_{2}\) kinetics response in isolated muscle [31]. According to [PERSON] et al. [30], our findings propose that when \(\uptau\)s is fewer than 20 s, oxygen delivery and utilization are well-matched, so additional provision of O\({}_{2}\) may not result in quicker VO\({}_{2}\) kinetics. In fact, when the rate of adjustment in pulmonary VO\({}_{2}\) on-kinetics was reduced to the level that it became comparable to the rate of adjustment of HHb on-kinetics, no additional accelerating of VO\({}_{2}\) kinetics was detected with supplementary training [32]. Together, these values support the role of microvascular O\({}_{2}\) delivery as a constraint to muscle O\({}_{2}\) utilization, meaning that there could be a point above which VO\({}_{2}\) kinetics is limited primarily by the rate of adjustment of O\({}_{2}\) delivery within the tissues.