The results of this study show that marathon runners have significantly increased T2 and T1rho values directly after the competition and that T2 values decreased back to baseline after 3 months, while T1rho values remained at a high level. These findings suggest that using T1rho and T2 measurements, biochemical meniscal matrix changes occur after a marathon that may reflect meniscal injury and may not be completely reversible.
Our results agree with previous studies that marathon running does not induce focal knee MR abnormalities. Also, no significant differences in the prevalence of knee abnormalities in the marathon runner group and control group were found. In an early MR study Shellock et al. also reported that the prevalence of meniscal tears in marathon runners is not higher than the prevalence reported for sedentary persons, and that runners have the same amount of meniscal degeneration as non-runner athletes [12
]. While some studies described mild changes in knee joint structures after marathon running, no severe changes were reported: Hohmann et al. examined marathon runners before and after the marathon using MRI and recorded no focal damage at the knee joint due to long distance running [10
]. Kursunoglu-Brahme et al. [11
] reported an increased prevalence of joint effusion that developed in 5 of the 10 subjects after long distance running. In addition, 5 of the 10 subjects had mildly increased signal intensity within their menisci after jogging. These investigators suggested that jogging frequently leads to acute changes in the knee, which could be demonstrated with MR imaging. The significance of these changes was unknown at that time. Schueller-Weidekamm et al. [14
] also reported joint effusions and increased intrameniscal signal after marathon running. However, they concluded that marathon running does not cause severe, acute lesions of cartilage, ligaments, or bone marrow of the knee in well-trained runners. Similar to these results, Krampla et al. [9
] performed an MRI study of the knee in marathon runners before and after competition, and reported that minor meniscal signal alterations were slightly more noticeable soon after running, but had returned to normal 6 weeks after the competition. Without exception the increase in pre-existing low-grade signal alterations were transient. These results correspond to our results where T2 values decreased after 3 months as a sign of decreased water content and swelling.
To the best of our knowledge, however, no study has been performed to date that has obtained quantitative T2 or T1rho measurements of the meniscus in marathon runners. Mosher et al. [29
] examined knee cartilage T2 values of 7 subjects before and immediately after 30 min of running. There was a statistically significant decrease in T2 of the superficial 40% of weight-bearing femoral cartilage after exercise. These investigators assumed that cartilage compression might result in greater anisotropy of superficial collagen fibers. In contrast, we found an increase in T2 values at the meniscus after running, but the examinations after competition in our study were carried after 48–72 h.
T2 relaxation time mapping is currently most frequently used to study the biochemical composition of cartilage: it is sensitive to a wide range of water interactions in tissue and in particular depends on the content, orientation, and anisotropy of collagen [30
]. The correlation between T2 and PG is not yet clear. Some studies showed that the depletion of PG had little influence on T2 [32
]; Watrin-Pinzano et al., however, found significantly increased T2 with hyaluronidase-induced PG degeneration [35
]. Compared with cartilage, meniscus has higher type 1 collagen concentration, which explains the lower T2 values in meniscus compared with hyaline cartilage T2 values [16
T1rho describes the spin-lattice relaxation in the rotating frame, and changes in the extracellular matrix of cartilage, like the loss of PG, may be reflected in the measurements of T1rho because of the less restricted motion of water protons [16
]. T1rho correlates highly with the PG content of the cartilage [36
]. The concentration of PG in hyaline cartilage is much higher than the PG amount in the meniscus [37
]; also, the factors that contribute to T1rho changes in the meniscus are not clear and need further investigation. In cartilage, changes in collagen and hydration may affect T1rho. However, even with the current spin-lock frequency (500 Hz) of clinical MR imagers, T1rho values are approximately 30% higher than T2 values in cartilage and approximately 20% higher in the menisci [16
]. Spin-locking reduces dipolar interaction, which dominates T2 relaxation. Previous studies showed that chemical exchanges between bulk water and the hydroxyl and amine groups of PG may be important relaxation mechanisms for T1rho in articular cartilage [38
]. Studies have also explained that T1rho is more sensitive to PG changes than is T2 in degenerated cartilage [20
]. Given that after 3 months T1rho values remained at a high level in our study, one might conclude that running a marathon might induce persisting changes in the meniscal matrix.
Rauscher et al. analyzed meniscal T1rho and T2 values in healthy subjects and patients with osteoarthritis [16
]. The results of this study demonstrated that meniscal matrix measurements may be used to differentiate healthy subjects from individuals with early OA. Matrix measurements increased consistently with higher OA grade. In addition, significant correlations between matrix measurements in the meniscus and clinical scores (WORMS) were found. Krishnan et al. [21
] analyzed the T1 values of gadolinium-based contrast material in the meniscus and the relationship between this parameter and the T1 of delayed gadolinium-based contrast material in the articular cartilage. Their study results showed that the T1 in the meniscus correlated significantly with that in the articular cartilage (delayed gadolinium-enhanced magnetic resonance imaging of cartilage (dGEMRIC)), potentially demonstrating associated degenerative processes in the knee joint. Using the dGEMRIC technique the PG concentration can be quantified [22
]. In an experimental study Pap et al. [40
] found similar results. They examined the influence of an excessive running load on the development of knee OA in male Wistar rats. Histological assessment of the knee joint sections revealed a significant increase in osteoarthritic changes with a higher running load.
Limitations of our study have to be acknowledged. The number of subjects recruited to our study is relatively low; only 13 marathon runners could be examined before and after marathon running and only 9 marathon runners completed the follow-up MRI examination after 3 months. As a consequence of this, our study was not able to investigate the influence of marathon running in general on meniscal structure. Although the number of study subjects was low, statistical significance was achieved as the results were consistent and nearly every study subject showed the same longitudinal T2 and T1rho changes in each compartment. To better understand whether a persisting increase in T1rho values 3 months after the marathon might be a sign of irreversible changes in the matrix decomposition long-term follow-up examination after 1 or 2 years would be required to monitor the T1rho values. Also, a histological correlation of the T2 and T1rho values would be interesting, but obviously not possible in a clinical study. T1rho may represent a change in the meniscus matrix, but it is not clear what the factors are that contribute to T1rho changes in the meniscus and needs further investigation.