Experimental knee pain impairs joint torque and rate of force development in isometric and isokinetic muscle activation.
Level 3 - non-randomized controlled study
Non-randomized within-subject experimental laboratory study in healthy humans
PubMed 31332518 · doi:10.1007/s00421-019-04195-6
What was done
Twenty healthy individuals received a hypertonic saline injection into the right knee to induce acute experimental joint pain. Researchers measured maximum knee extensor torque and electromyography (EMG) across isometric, concentric, and eccentric contractions using a Biodex dynamometer. The rate of force development (RFD) and rate of EMG rise were assessed during isometric contractions. Measurements were collected at baseline, during the pain state, and after pain resolution.
What was found
The abstract reports directional outcomes without exact numerical values. Maximum joint torque and peak quadriceps EMG decreased significantly during pain, with similar reductions observed across isometric, concentric, and eccentric contractions. Maximum RFD and rate of EMG rise were significantly reduced during pain primarily during the early phase (50-100 ms after contraction onset), but remained largely unaffected at later intervals (150-200 ms).
Why it matters
These findings indicate that acute nociceptive input impairs rapid neuromuscular activation and torque production similarly across distinct contraction modes. This early-phase force deficit helps explain sudden joint instability and impaired functional performance in clinical knee pain.
Limits
The study tested acute, chemically induced pain via hypertonic saline in 20 healthy volunteers, which may not replicate the pathophysiology, central sensitization, or chronicity of clinical musculoskeletal disorders. The abstract does not provide exact numerical effect sizes, variance, or p-values.
Cited by
- supports Pain and structural damage inhibit the central nervous system from maximally activating and recruiting muscles.