The aim of this work was to implement combined spirometric and ³¹P MRS human muscle measurements by means of a commercial gas exchange system, which was adapted to perform dynamic acquisition of pulmonary ventilation during muscle exercise in a whole-body MR scanner. Its functionality was tested in healthy volunteers to evaluate the local, load induced changes in high energy phosphate metabolites (PCr and ATP) and muscular pH values as well as the corresponding global alterations of pulmonary parameters (O₂ and CO₂ volume flows)¹.In order to maintain the full functionality of the spirometric system within the magnetic field environment, the spirometer was placed outside the MR scanner room by extending the original 3 m gas sampling line to 5 m. Calibration measurements with 3 m and 5 m sampling lines were performed to assess the effects of longer lines on the spirometer functionality parameters delay (t_A time from mask to analyzer) and response time (t_10-90 record 90% of expected gas changes). Nine male subjects (28 ± 4 years) performed standardized, high-intense plantar flexions with a MR compatible pedal ergometer² (3 min load, 0.6 bar pedal resistance, 100 bpm frequency). Spirometric parameters (oxygen and carbogen fluxes, VO₂ and VCO₂) and ³¹P MR spectroscopic data (right calf muscle, TR = 290 ms) data were acquired simultaneously prior to, during and after the exercise. Dynamics of PCr and VO₂ during recovery were fitted with a mono- and bi-exponential function, respectively.Compared to 3 m line length, line extension was associated with an increase of t_A and t_10-90 from 0.29 ± 0.2 s to 0.31 ± 0.02 s and from 1.29 ± 0.12 s to 2.08 ± 0.01 s, respectively. With a typical maximum breathing frequency of 0.5 s-1, these changes are still in an appropriate range to avoid analyzing overlaps between consecutive breaths³. In the in vivo measurement the resting VO₂ (0.26 ± 0.07 l/min) and VCO₂ (0.24 ± 0.07 l/min) were relatively low due to the supine subject position. During the load phase, high pulmonary adaptions were attained (VO₂,load: 0.95 ± 0.17 l/min, VCO₂,load: 0.97 ± 0.19 l/min). Compared to VO₂, the VCO₂ revealed a distinctly higher increase (Fig. 1) indicating accumulation of non-metabolic CO₂ (excess-CO₂: 0.5 ± 0.3 l/min). All subjects showed strong PCr depletion below 20% of its resting level 70 s after onset of exercise (Fig. 2) followed by a noticeable slow recovery (recovery time constant 324 ± 170 s) after the exercise, which goes along with a low end-exercise pH of 6.45 ± 0.19 due to high tissue acidification. In terms of the interactions of pH with the creatine kinase equilibrium the PCr time constant revealed, except for one subject, a negative correlation with end-exercise pH (R² = 0.96, p < 0.001, Fig. 3 left). PCr recovery showed also a positive correlation with the time constant of the slow VO₂ recovery component (R² = 0.63, p < 0.01, Fig. 3 right).This work describes the successful implementation of combined spiroergometry and functional ³¹P MRS in exercised human calf muscles by using a properly modified commercial spirometry system. The positive correlation between PCr and VO₂ recovery time constants supports the expected effects of adaption in ventilation on the oxidatively driven PCr resynthesis¹. However, this correlation should be taken with caution, since globally measured VO₂ as well as local O₂ supply in muscles can also be affected by other physiological factors, for example by heavy muscle acidification. In our in vivo study, the latter was reflected in a VCO₂ overshoot corresponding to non-metabolic CO₂, which is formed during lactate buffering with bicarbonate. Therefore, verification of these interrelations requires additional acquisition of e.g. lactate accumulation, metabolic acidosis as well as buffer capacity.