# Effect of PEMF on Muscle Oxygen during Cycling:
## 4 Discussion
Importantly, accelerating the time course of the matching between muscle O\({}_{2}\) delivery to O\({}_{2}\) utilization can speed up the rate of adjustment when the time constant is longer than 20 s; nevertheless, when it is less than 20 s, it would appear that the modifications of VO\({}_{2}\) are principally administered by intracellular processes [30]. The amplitude of the HHb primary component is interrelated to muscle O\({}_{2}\) release and homogeneity of perfusion. Based on a previous study [4], we hypothesized that PEMF stimulation enhanced microcirculation through an increase in arteriole diameter. In addition, we supposed that the interaction between stimulation and Ca\({}^{2+}\) /NO/cGMP/protein kinase G led to a modulation of nitric oxide (NO) signal, which facilitates the release of O\({}_{2}\) in muscles during contraction by enhancing muscle microvascular oxygenation [7; 33]. As postulated by [PERSON]'s law of diffusion, the oxygen pressure in the microvasculature (i.e., muscle PO\({}_{2}\)mv) is the driving force for blood-myocyte O\({}_{2}\) transfer. During metabolic demand, the skeletal muscle PO\({}_{2}\)mv on-kinetics is determined by the dynamic matching between oxygen delivery and utilization (i.e., Q\({}_{02}\)/V\({}_{02}\) ratio) [34]. Previous reports show that changes in NO levels influence muscle PO\({}_{2}\)mv during transitions of metabolic demand, suggesting that augmented NO-mediated function could, at least in part, enhance muscle microvascular oxygenation in trainers [35]. More recently, [PERSON] et al. [36] found that betroot juice (supplements rich of NO\({}_{3}\)\({}^{-}\)) has no effect on TOI, VO\({}_{2}\) kinetics, and exercise tolerance when severe intensity exercise (similar to our results; 3.49 vs. 3.46 L/min) occurred in normoxia with respect to hypoxia. The authors concluded that NO supplementation during severe exercise is related to the level of muscle deoxygenation sustained during such exercise intensity. Besides, it is probable that NO supplementation has a major role during exercise conducted in altitude, in persons with higher type II muscle fibers, and in populations with impairments in muscle oxygen delivery. The possible release of NO is a significant factor of the metabolic inertia to the VO\({}_{2}\) dynamics during exercise conducted at a higher intensity. The specific mechanism by which NO contributes to the metabolic inertia at exercise onset is unclear but, in vitro, it has been verified that NO competes with O\({}_{2}\) at the mitochondrial level [37]. Although our results cannot discriminate between \"metabolic\" and \"O\({}_{2}\) delivery\" factors, which reduce VO\({}_{2}\) on-kinetics, we can suppose that intracellular features would slow the VO\({}_{2}\) on-kinetics to the level detected in the present study, but more studies are needed to explore this phenomenon. Blood lactate level, recorded at the third minute of exercise, was significantly higher during stimulation, suggesting a possible influence of PEMF on muscle activity and on the glycolytic metabolism of type-II muscular fibers [38]. This effect could be caused by the change of membrane permeability and Ca\({}^{2+}\) channel conduction, enhancing ion flux and cellular concentrations [39] that improve contraction mechanisms during exercise. A recent study [40] has showed that NO\({}_{3}\)\({}^{-}\) changes contractile properties and metabolic and/or vascular control in fast-twitch muscle fibers. Precisely, it has been found that NO supplementation speeds up pulmonary VO\({}_{2}\) and muscle HHb kinetics during the transition from moderate to severe exercise intensity compared to placebo juice. Given that this intensity would be expected to recruit type II muscle fibers, [PERSON] et al. concludedthat NO supplementation could have precise effects on metabolic and/or vascular control in fast-twitch human muscle fibers, in accordance with previous research in rodents [41]. Surprisingly, this was not associated with a reduced blood lactate level.