The interactive effect of pain and topical analgesic on motor pathway excitability of the biceps brachii

Stefanelli, Lucas (2017) The interactive effect of pain and topical analgesic on motor pathway excitability of the biceps brachii. Masters thesis, Memorial University of Newfoundland.

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Abstract

Delayed onset muscle soreness (DOMS) is muscle pain that arises 24-72 hours after exercise involving unfamiliar strenuous muscle loading. DOMS is commonly induced by eccentric muscle contractions and may signify exercise-induced muscle damage including impaired excitation-contraction coupling and injury to cytoskeletal proteins in the sarcomere. During DOMS, muscle pain is transmitted via A-delta and C-fibre afferents (group III/IV afferents) to the central nervous system (CNS). While it has been shown that muscle force production is significantly diminished in DOMS, there is limited evidence on the influence of DOMS on corticospinal excitability or inhibition. Furthermore, to date no work has investigated how the application of topical analgesic interacts with DOMS to modulate corticospinal excitation. The current thesis employed a model of DOMS involving fatiguing eccentric elbow flexor contraction exercise. We investigated the effect of DOMS on indices of corticospinal excitability (motor evoked potential [MEP] and cervicomedullary evoked potential [CMEP] area and latency) and inhibition (silent period), peripheral motor excitability (Mmax area and latency), and pain pressure threshold (PPT) in the dominant biceps brachii muscle, as well as how application of a menthol-based topical analgesic (Biofreeze®) influenced these outcomes. Two experiments were employed to test the effects of topical analgesic in participants with and without DOMS. In the first experiment (Experiment A: No DOMS), 16 young healthy adults (F = 8, M = 8; age = 23 ± 1.1 yr; body mass = 71.9 ± 9.1 kg; height = 174.2 ± 8.2 cm) were randomly allocated to receive either a menthol-based topical analgesic gel (Topical Analgesic, n = 8) or a placebo gel (Placebo, n = 8) in a double-blind fashion, during a single session; DOMS was not induced. Prior to the application of gel (pre-gel), as well as 5 (post-5 min), 15 (post-15 min), 30 (post-30 min), and 45 (post-45 min) minutes after the application of gel, MEP area, latency, and silent period; CMEP area and latency; and Mmax area and latency were measured. Participants’ MEP and CMEP areas were normalized to Mmax area. Neither group showed a statistically significant change in these outcome measures at any post-gel time-point compared to pre-gel (p > .05). In the second experiment (Experiment B: DOMS), 16 young healthy male adults (age = 26 ± 5.1 yr; body mass = 81.9 ± 9.1 kg; height = 179.8 ± 6.1 cm) completed two experimental sessions. During the first session participants completed a fatiguing eccentric elbow flexor contraction protocol to induce DOMS. Participants returned 48 hours later and were randomly allocated to Topical Analgesic (n = 8) or Placebo (n = 8) in a double-blind fashion. During the second session MEP area/Mmax area, MEP latency, silent period, CMEP area/Mmax Area, CMEP latency, Mmax area, and Mmax latency were measured at the same time-points as above. Additionally, PPT was measured during session one (pre-DOMS), as well as at the above time-points. Both groups exhibited a statistically significant decrease in PPT from pre-DOMS to pre-gel (Topical Analgesic, pre-DOMS = 7.03 ± 2.48 kg, pre-gel = 3.12 ± 1.26 kg, p <0.001 Placebo, pre-DOMS = 5.77 ± 2.35 kg, pre-gel = 3.51 ± 1.58 kg, p = .005). Following the application of gel there was a significant increase in PPT at post-15 min (3.70 ± 1.69 kg, t₍₇₎ = -2.619, p = .034), post-30 min (3.92 ± 1.67 kg, t₍₇₎ = -3.987, p = .005), and post-45 min (4.33 ± 1.65 kg, t₍₇₎ = -4,566, p = .003) compared to pre-gel (3.12 ± 1.26 kg) in the Topical Analgesic group only. Under the Placebo group, there was no statistically significant change in PPT values (p > .05). Regarding neurophysiological changes there was a statistically significant increase in silent period compared to pre-gel (85.67 ± 19.65 ms) at both post-30 min (96.08 ± 26.62 ms, p = .045) and post-45 min (94.23 ± 22.32 ms, p = .029), in the Topical analgesic Group. The Placebo group did not exhibit a statistically significant change in silent period at any time-point (p > .05). No other measures of corticospinal (MEP area/Mmax area, MEP latency, CMEP area/Mmax area, CMEP latency) or peripheral motor excitability (Mmax area, Mmax latency) were significantly different after the application of topical analgesic or placebo gel (p > .05). When comparing pre-gel neurophysiological outcomes in participants from Experiment A: No DOMS (n = 16) and Experiment B: DOMS (n = 16), there were statistically significant differences in MEP area/Mmax area (Experiment A = 0.222 ± 0.169; Experiment B = 0.097 ± 0.057, p = .011), CMEP area/Mmax area (Experiment A = 0.186 ± 0.148; Experiment B = 0.077 ± 0.045; p = .012), and silent period (Experiment A = 77.41 ± 31.05 ms; Experiment B = 100.85 ± 32.29 ms; p = .045). No other neurophysiological measures were significantly different across experiments (p > .05). The present findings suggest that DOMS imposes changes in the neuromuscular system that result in increased pain, reduced corticospinal excitability, and elevated corticospinal inhibition. Following the administration of menthol-based topical analgesic, but not a placebo gel, there is a reduction in pain which is accompanied by further increases in corticospinal inhibition. These results provide novel information on the neurophysiological effects of DOMS, as well as the influence on topical analgesic on DOMS-induced neurophysiological changes.

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