Abstract:Reproductive hormones are implicated in moderating pain. Animal studies support both pronociceptive and antinociceptive actions of oestradiol and progesterone suggesting that the net effect of these hormones on pain is complex and likely depends on the interaction between hormones and the extent of fluctuation rather than absolute hormone levels. Several clinical pain conditions show variation in symptom severity across the menstrual cycle. Though, there is still no consensus on whether the menstrual cycle inf… Show more
“…In support of the current findings, a previous study reports greater perception of pain and rating of perceived exertion during exercise in women during the EF phase compared with the LF or ML phase [43]. The influence of the menstrual cycle on pain perception is complicated and not clearly described [44]. In fact, oestrogen and progesterone receptors occur on central and peripheral nerves and have been reported to induce both pronociceptive and antinociceptive affects where the overall effect may be dependent on the receptor type and relative presence of oestrogen and progesterone [44].…”
Section: Discussionsupporting
confidence: 84%
“…In fact, oestrogen and progesterone receptors occur on central and peripheral nerves and have been reported to induce both pronociceptive and antinociceptive affects where the overall effect may be dependent on the receptor type and relative presence of oestrogen and progesterone [44]. Nevertheless, most evidence suggests the occurrence of reduced perception of clinical pain in the ML phase and heighted pain when oestrogen concentrations are low such as in EF phase or when oestrogen concentrations reduce rapidly [44]. Moreover, patients with rheumatoid arthritis report greater joint pain and stiffness during the LF phase [44].…”
Section: Discussionmentioning
confidence: 99%
“…Nevertheless, most evidence suggests the occurrence of reduced perception of clinical pain in the ML phase and heighted pain when oestrogen concentrations are low such as in EF phase or when oestrogen concentrations reduce rapidly [44]. Moreover, patients with rheumatoid arthritis report greater joint pain and stiffness during the LF phase [44]. …”
Serum creatine kinase (CK) activity reflects muscle membrane disruption. Oestrogen has antioxidant and membrane stabilising properties, yet no study has compared the CK and muscle soreness (DOMS) response to unaccustomed exercise between genders when all menstrual phases are represented in women. Fifteen eumenorrhoeic women (early follicular, EF (n = 5); late follicular, LF (n = 5); mid-luteal, ML (n = 5) phase) and six men performed 20 min of downhill running (−10% gradient) at 9 km/h. Serum CK activity and visual analogue scale rating of perceived muscle soreness were measured before, immediately, 24-h, 48-h and 72-h after exercise. The 24-h peak CK response (relative to pre-exercise) was similar between women and men (mean change (95% confidence interval): 58.5 (25.2 to 91.7) IU/L; 68.8 (31.3 to 106.3) IU/L, respectively). However, serum CK activity was restored to pre-exercise levels quicker in women (regardless of menstrual phase) than men; after 48-h post exercise in women (16.3 (−4.4 to 37.0) IU/L; 56.3 (37.0 to 75.6) IU/L, respectively) but only after 72-h in men (14.9 (−14.8 to 44.6) IU/L). Parallel to the CK response, muscle soreness recovered by 72-h in men. Conversely, the women still reported muscle soreness at 72-h despite CK levels being restored by 48-h; delayed recovery of muscle soreness appeared mainly in EF and LF. The CK and DOMS response to downhill running is gender-specific. The CK response recovers quicker in women than men. The CK and DOMS response occur in concert in men but not in women. The DOMS response in women is prolonged and may be influenced by menstrual phase.
“…In support of the current findings, a previous study reports greater perception of pain and rating of perceived exertion during exercise in women during the EF phase compared with the LF or ML phase [43]. The influence of the menstrual cycle on pain perception is complicated and not clearly described [44]. In fact, oestrogen and progesterone receptors occur on central and peripheral nerves and have been reported to induce both pronociceptive and antinociceptive affects where the overall effect may be dependent on the receptor type and relative presence of oestrogen and progesterone [44].…”
Section: Discussionsupporting
confidence: 84%
“…In fact, oestrogen and progesterone receptors occur on central and peripheral nerves and have been reported to induce both pronociceptive and antinociceptive affects where the overall effect may be dependent on the receptor type and relative presence of oestrogen and progesterone [44]. Nevertheless, most evidence suggests the occurrence of reduced perception of clinical pain in the ML phase and heighted pain when oestrogen concentrations are low such as in EF phase or when oestrogen concentrations reduce rapidly [44]. Moreover, patients with rheumatoid arthritis report greater joint pain and stiffness during the LF phase [44].…”
Section: Discussionmentioning
confidence: 99%
“…Nevertheless, most evidence suggests the occurrence of reduced perception of clinical pain in the ML phase and heighted pain when oestrogen concentrations are low such as in EF phase or when oestrogen concentrations reduce rapidly [44]. Moreover, patients with rheumatoid arthritis report greater joint pain and stiffness during the LF phase [44]. …”
Serum creatine kinase (CK) activity reflects muscle membrane disruption. Oestrogen has antioxidant and membrane stabilising properties, yet no study has compared the CK and muscle soreness (DOMS) response to unaccustomed exercise between genders when all menstrual phases are represented in women. Fifteen eumenorrhoeic women (early follicular, EF (n = 5); late follicular, LF (n = 5); mid-luteal, ML (n = 5) phase) and six men performed 20 min of downhill running (−10% gradient) at 9 km/h. Serum CK activity and visual analogue scale rating of perceived muscle soreness were measured before, immediately, 24-h, 48-h and 72-h after exercise. The 24-h peak CK response (relative to pre-exercise) was similar between women and men (mean change (95% confidence interval): 58.5 (25.2 to 91.7) IU/L; 68.8 (31.3 to 106.3) IU/L, respectively). However, serum CK activity was restored to pre-exercise levels quicker in women (regardless of menstrual phase) than men; after 48-h post exercise in women (16.3 (−4.4 to 37.0) IU/L; 56.3 (37.0 to 75.6) IU/L, respectively) but only after 72-h in men (14.9 (−14.8 to 44.6) IU/L). Parallel to the CK response, muscle soreness recovered by 72-h in men. Conversely, the women still reported muscle soreness at 72-h despite CK levels being restored by 48-h; delayed recovery of muscle soreness appeared mainly in EF and LF. The CK and DOMS response to downhill running is gender-specific. The CK response recovers quicker in women than men. The CK and DOMS response occur in concert in men but not in women. The DOMS response in women is prolonged and may be influenced by menstrual phase.
The discrepancy between pain models using healthy volunteers and drug trials under real acute and chronic pain conditions in patients as well as methodological aspects may have contributed to this result. The impact of these findings questions the general use of pain models as predictors for early decision making during drug development. The study was registered in ClinicalTrials.gov (NCT01615510).
“…Women often have a higher incidence of pain (Amandusson and Blomqvist, 2013; Fillingim and Maixner, 2000; Iacovides et al, 2015; Sherman and LeResche, 2006) and women report orofacial pain more often than men (Koopman et al, 2009). Polymorphisms in the estrogen receptor will increase the risk of women developing various orofacial pain conditions supporting a biological basis for estradiol (Kang et al, 2007; Ribeiro-Dasilva et al, 2009).…”
Pain can vary over the estrous cycle as a result of changes in estradiol concentration but the mechanism causing this variation is unclear. Because the thalamus is important in pain control, gene expression in the lateral thalamus (ventral posteromedial, ventral posterolateral, reticular thalamic nuclei) was screened at different phases of the estrous cycle. Gene expression changes in Sprague-Dawley rats were further analyzed by real-time PCR and ELISA and plasma estradiol levels were measured by RIAs at different phases of the estrous cycle. Our results indicated that both the RNA and protein expression of glutamate decarboxylase 1 and 2 (GAD1, GAD2), GABA(A) receptor-associated protein like 1 (GABARAPL1) and vesicular GABA transporter (VGAT) significantly increased in the lateral thalamus when plasma estradiol levels were elevated. Estradiol levels were elevated during the proestrus and estrus phases of the estrous cycle. Estrogen receptor α (ERα) was observed to be co-localized in thalamic cells and thalamic infusion of an ERα antagonist significantly reduced GAD1 and VGAT transcript. GAD1, GAD2 GABARAPL1 and VGAT have been shown to effect neuronal responses suggesting that modulation of pain during the estrous cycle can be dependent, in part, through estradiol induced changes in thalamic gene expression.
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