Post-contractile BOLD contrast in skeletal muscle at 7 T reveals inter-individual heterogeneity in the physiological responses to muscle contraction

Muscle blood oxygenation‐level dependent (BOLD) contrast is greater in magnitude and potentially more influenced by extravascular BOLD mechanisms at 7 T than it is at lower field strengths. Muscle BOLD imaging of muscle contractions at 7 T could, therefore, provide greater or different contrast than at 3 T. The purpose of this study was to evaluate the feasibility of using BOLD imaging at 7 T to assess the physiological responses to in vivo muscle contractions. Thirteen subjects (four females) performed a series of isometric contractions of the calf muscles while being scanned in a Philips Achieva 7 T human imager. Following 2 s maximal isometric plantarflexion contractions, BOLD signal transients ranging from 0.3 to 7.0% of the pre‐contraction signal intensity were observed in the soleus muscle. We observed considerable inter‐subject variability in both the magnitude and time course of the muscle BOLD signal. A subset of subjects (n = 7) repeated the contraction protocol at two different repetition times (TR: 1000 and 2500 ms) to determine the potential of T1‐related inflow effects on the magnitude of the post‐contractile BOLD response. Consistent with previous reports, there was no difference in the magnitude of the responses for the two TR values (3.8 ± 0.9 versus 4.0 ± 0.6% for TR = 1000 and 2500 ms, respectively; mean ± standard error). These results demonstrate that studies of the muscle BOLD responses to contractions are feasible at 7 T. Compared with studies at lower field strengths, post‐contractile 7 T muscle BOLD contrast may afford greater insight into microvascular function and dysfunction. Postcontractile muscle BOLD responses measured at 7 T in the soleus muscles of four subjects following a brief, 2 s maximal contraction. Panels A–D highlight the between subject variability in the magnitude and time course of the postcontractile muscle BOLD response. These differences are likely due to differences in the magnitude and timing of the post‐contractile increase in blood flow, the on‐kinetics of mitochondrial respiration, and/or the architecture of the microvasculature in the muscle.