For example, Mannelli and coworkers recently overstressed knee joint where their release of the anti inflammatory cytokines, IL 10 and TGF B reverse the catabolic changes caused by strenuous exertion. In addition, the IL 10 and TGF B produced by these during T regulators may tilt the TH balance in the knee joint towards TH2 responses which preferentially result in IL 4 production further fostering a shift in chondrocyte metabolism towards ECM replenishment. Several additional tests were used in this study to as sess overall Inhibitors,Modulators,Libraries joint function, QoL, and physical activity. The additional parameters and tests measured included a six minute timed walk plus the Stanford exercise scale and KOOS survey. With respect to the KOOS survey, both cohorts were statistically significant versus baseline for symptoms, pain, daily function, recreational activities and QoL but were not significant from each other.
This is not an unexpected finding given that this study was carried out with healthy subjects who do not present with any joint issues at rest. It is Inhibitors,Modulators,Libraries only when the knee is stressed via the stepmill do subjects report any joint dis comfort. Under these conditions, and as indicated Inhibitors,Modulators,Libraries above, the UC II group appears to experience less joint discom fort and greater joint flexibility. No difference in clinical outcomes between groups was seen in the six minute timed walk, the daily distance walked, or the Stanford exercise scale questionnaire. Once again we are not sur prised by these results given that these tests and ques tionnaires are designed and clinically validated to assess the severity of arthritic disease in unhealthy populations.
No clinical biomarkers associated with arthritic dis eases were assessed in this study. Healthy subjects would not be expected to present with significant alterations in their inflammatory biomarker profile as they lack clinical disease. In addition, it should be noted that the joint discomfort Inhibitors,Modulators,Libraries measured in this study is acute pain induced by a stressor rather than due to an ongoing inflamma tory event. Therefore, any elevation in inflammation markers that might occur in these healthy subjects may simply be due to the physiological impact of strenuous exercise. There are two study limitations to consider when reviewing these results. The first, time to onset of initial pain, was limited to a 10 minute interval.
The current study design did not address the Inhibitors,Modulators,Libraries possibility that subjects might cease to experience pain on the stepmill. Future studies example should allow for an extension of the exertion interval in order to gauge how much longer a subject can exercise be fore reporting pain. In this way better defined parameters can be placed upon the degree to which UC II supplemen tation results in the cessation of joint pain due to strenuous exercise in healthy subjects.