The most important findings in the present study were that near significant and significant main effects and interactions provided evidence that a menthol based topical analgesic can increase ballistic hip flexion ROM of the treated and untreated contralateral limbs. Secondly, there was also evidence that static stretching contributed to greater ballistic ROM in both the stretched and non-stretched contralateral limbs. Finally, while static stretching improved passive static ROM over the testing period, active and ballistic stretching ROM was impaired. There was evidence for a positive effect of a menthol based analgesic on ballistic hip flexion ROM. The application of a menthol based topical analgesic on the hamstrings induced large and moderate magnitude, overall improvements in ballistic ROM in treated and contralateral (untreated) legs respectively (main effect for treatment). Furthermore, the topical analgesic counteracted the significant, small magnitude impairments in ballistic ROM induced by dynamic stretching in the treated and contralateral (untreated) legs respectively. There are no other studies in the literature that have examined the effects of a menthol based topical analgesic on flexibility nor its crossover effects. First suggested by Magnusson (Magnusson et al., 1996;1997) and supported in many other stretch-related studies (Behm, 2018b; Behm et al., 2016a; Behm and Chaouachi, 2011; Kay and Blazevich, 2012); the concept of stretch tolerance has been advocated as a significant contributing mechanism for acute and chronic increases in ROM. A meta-analysis by Freitas et al. (2017) examined 26 stretch training studies (durations ranged from 3-8 weeks with a weekly stretching duration of approximately 20 minutes) and reported that on average, the stretch training programs did not modify musculotendinous properties. Therefore, they purported that the enhanced extensibility must have been related to a greater stretch tolerance. Behm et al. (2016b) suggested that increased stretch tolerance would be a primary mechanism with the increased ROM of the shoulders after stretching the hip adductors and similarly the increased ROM of the hip flexors after stretching the shoulders. A similar mechanism was expounded by Chaouachi et al. (2017), with the improved ROM of the contralateral hip flexors following unilateral stretching of the hamstrings. Increased stretch tolerance could be related to changes in nociceptive sensitivity (Marchettini, 1993) that permits an accommodation of greater stretching-related discomfort or pain and a higher stretching intensity. Since menthol based topical analgesics act as counterirritants to decrease pain sensation (Galeotti et al., 2002; Macpherson et al., 2006), they could contribute to an increased stretch tolerance. Menthol inhibits transient receptor potential ion channels such as TRPA1 that evoke thermal and pain sensations (Macpherson et al., 2006) and inhibit neuronal membrane Ca++ channel currents enhancing analgesic properties (Galeotti et al., 2002). Hence with less discomfort or pain, the individuals might have been able to push themselves to greater ROM. This augmentation of ROM was seen in both the treated and untreated, contralateral legs. This crossover effect of a non-stretched contralateral leg would suggest that the increased stretch or pain tolerance had global consequences. Sigurdsson and Maixner (1994) suggested that the pain inhibition effects of noxious counterirritants can produce secondary hyperalgesia. Two foam rolling studies demonstrated that rolling the contralateral plantar flexors reduced muscle tender point pain (Aboodarda et al., 2015) and evoked tetanic stimulation pain (Cavanaugh et al., 2017) in the tested calf. The authors proposed a global pain modulatory system that might be related to the gate control theory of pain (Melzack and Wall, 1965; Moayedi and Davis, 2013) or the diffuse noxious inhibitory control model (Mense, 2000). With the gate control theory of pain, endogenous analgesia can result from descending signals to the opioid receptors, which would inhibit pain with serotonergic and noradrenergic neurons (Pud et al., 2009). Diffuse noxious inhibitory control is activated by nociceptive stimuli from a non-local tissue. The non-local receptor activity is transmitted to multi-receptive, wide dynamic range convergent neurons in the cortical subnucleus reticularis dorsalis where it inhibits pain transmission monoaminergically (Mense, 2000; Pud et al., 2009; Sigurdsson and Maixner, 1994) reducing pain perception not only locally but also at non-local sites (Pud et al., 2009; Sigurdsson and Maixner, 1994). However, in this study, this effect manifested small to large magnitude improvements with ballistic ROM only. The lack of topical analgesic effect on active ROM may be related to the substantially smaller ROM. Whereas, the overall ballistic ROM values were 114.5° ± 10.3 and 110.4° ± 11.5 for topical analgesic and placebo respectively, the active ROM averaged 82.4° ± 10.4 and 80.9° ± 12.5 respectively. The active ROM was limited not only by the extensibility of the hamstrings musculotendinous units, but also the force output or strength of the hip flexor muscles (i.e. quadriceps, iliopsoas). Since the active ROM was approximately 300 less than ballistic ROM, the effect of the topical analgesic on hamstrings stretch-related discomfort would not have played a major role. In contrast, the passive static ROM was similar to ballistic ROM with 117.9° ± 14.4 and 119.3° ± 15.1 for the topical analgesic and placebo conditions respectively and yet there was no significant topical analgesic effect on passive static ROM. The passive ROM was achieved with the aid of the researcher rather than an active contraction of the hip flexors as with active and ballistic ROM. Hence with ballistic ROM, the ROM was constrained by the propulsive force of the hip flexors, which may have influenced to a greater degree, the tolerable stretch limit of the participants. Furthermore, with the passive static ROM, the Hawthorne effect could have played a role whereby the participants may have consciously or subconsciously tried to please the researcher and surpassed their typical zone of (dis)comfort (Sedgwick and Greenwood, 2015; Ulmer, 1976). Therefore, if the researcher surpassed the participant’s typical level of discomfort, the researcher may have inadvertently exceeded the stretch tolerance, minimizing the effect of the topical analgesic. A second major finding was that unilateral static stretching contributed to small magnitude, greater ballistic ROM in both the stretched and non-stretched contralateral limbs (3.4-4.6%; d = 0.31-0.35). It has been reported that static stretching may have a greater impact on increasing muscle compliance (decreasing stiffness) (Behm, 2018a; Behm et al., 2016a; Blazevich et al., 2012; Kay and Blazevich, 2012; Kay et al., 2015). As mentioned previously, the limits of the active ROM were approximately 300 less than the ballistic ROM and thus muscle compliance issues would not have impacted active ROM to a substantial degree. Secondly as already mentioned, the passive static and active ROM would have been constrained by the researcher and the hip flexor muscle force output respectively. While the ballistic ROM would also be constrained by hip flexor muscle force output, the force-velocity relationship indicates that forces decrease at higher velocities (Pertuzon and Bouisset, 1973; Thorstensson et al., 1976; Trafton, 1951). Thus potential hip flexor muscle forces would have been less than the slower active ROM forces or the researcher assisted passive static ROM. Therefore in attempting to achieve maximal ballistic ROM (only 3-90 difference between passive static and ballistic ROM), with a reduced force output, the advantage of increased musculotendinous compliance with static stretching may have permitted a greater ballistic ROM. The main effects for time illustrated that while static stretching improved passive static ROM over the testing period, active and ballistic stretching ROM were impaired. While at first glance this finding may be perplexing, it must be remembered that the main effect for time combines dynamic and static stretching as well as topical analgesic and placebo conditions. Whereas, the static stretching intervention was conducted while lying supine with a researcher performing the stretching movements, the dynamic stretching intervention was performed while standing erect and performing 3 sets of 30 active contractions. Furthermore, when tested, the participants had the tested leg strapped to the electronic goniometer and thus had to stand on one leg while tested. The combination of active contractions during both the dynamic stretch intervention and the testing could have induced some fatigue and negatively impacted the ROM test that necessitated active contractions (active and ballistic ROM). While the menthol based topical analgesic effect augmenting stretch tolerance to increase ROM could be of benefit for athletes and others interested in improving joint flexibility, there must be some caution exercised. Individuals who are not accustomed to moving their limbs through a full range of joint motion, or individuals with compromised muscle and tendon strength (rehabilitation) could possibly stretch beyond their tensile limit leading to muscle or tendon strain. Hence, surpassing the normal stretch tolerance should only be attempted by trained and experienced individuals. While including both sexes could be considered a strength of the study, a limitation would be that there were only seven participants for each sex. Thus, the lack of significant sex-related findings may be related to a lack of statistical power for this factor. |