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Abstract
We examined the relationship between grip strength declines and muscle-tendon responses induced by long-term
performance of a high-repetition, low-force (HRLF) reaching task in rats. We hypothesized that grip strength declines would
correlate with inflammation, fibrosis and degradation in flexor digitorum muscles and tendons. Grip strength declined after
training, and further in weeks 18 and 24, in reach limbs of HRLF rats. Flexor digitorum tissues of reach limbs showed lowgrade
increases in inflammatory cytokines: IL-1b after training and in week 18, IL-1a in week 18, TNF-a and IL-6 after training
and in week 24, and IL-10 in week 24, with greater increases in tendons than muscles. Similar cytokine increases were
detected in serum with HRLF: IL-1a and IL-10 in week 18, and TNF-a and IL-6 in week 24. Grip strength correlated inversely
with IL-6 in muscles, tendons and serum, and TNF-a in muscles and serum. Four fibrogenic proteins, TGFB1, CTGF, PDGFab
and PDGFbb, and hydroxyproline, a marker of collagen synthesis, increased in serum in HRLF weeks 18 or 24, concomitant
with epitendon thickening, increased muscle and tendon TGFB1 and CTGF. A collagenolytic gelatinase, MMP2, increased by
week 18 in serum, tendons and muscles of HRLF rats. Grip strength correlated inversely with TGFB1 in muscles, tendons and
serum; with CTGF-immunoreactive fibroblasts in tendons; and with MMP2 in tendons and serum. Thus, motor declines
correlated with low-grade systemic and musculotendinous inflammation throughout task performance, and increased
fibrogenic and degradative proteins with prolonged task performance. Serum TNF-a, IL-6, TGFB1, CTGF and MMP2 may
serve as serum biomarkers of work-related musculoskeletal disorders, although further studies in humans are needed.