Interleukin-6 and Delayed Onset Muscle Soreness Do Not Vary during the Menstrual Cycle
Chaffin, Morgan E., Berg, Kris E., Meendering, Jessica R., Llewellyn, Tamra L., French, Jeffrey A., Davis, Jeremy E., Research Quarterly for Exercise and Sport
The purpose of this study was to determine if a difference in interleukin-6 (IL-6) and delayed onset muscles soreness (DOMS) exists in two different phases of the menstrual cycle. Nine runners performed one 75-min high-intensity interval running session during the early follicular (EF) phase and once during the midluteal (ML) phase of the menstrual cycle. Estrogen and progesterone levels were significantly reduced in the EF phase when compared to the ML phase. IL-6 levels increased from pre- to postexercise in the EF and ML phases (p < .001). There was no relationship between the IL-6 level and DOMS. The results suggest that menstruating female runners need not vary training throughout the month to reduce DOMS.
Key words: estrogen, high-intensity exercise, progesterone
Cytokines are low-molecular weight proteins involved in the interactions between immune and nonimmune cells (Gomez-Merino et al., 2006; Nieman et al., 2001). Cytokines are responsible for the influx of lymphocytes, neutrophils, monocytes, and other inflammatory cells into injured tissue at the site of inflammation (Pedersen et al., 2001; Petersen & Pedersen, 2005). It has been proposed that the inflammatory marker interleukin-6 (IL-6) is a product of the muscle cell myoblasts and satellite cells in response to muscle injury. Plasma IL-6 increases at a constant rate during exercise and is correlated to exercise intensity, duration, the muscle mass recruited, and the athlete's endurance capacity (Petersen & Pedersen, 2005). Furthermore, endurance exercise is known to induce pro-inflammatory cytokines that have negative effects on performance (Bruunsgaard et al., 1997; Nieman et al., 2005).
The large number of women participating in endurance events warrants study of the impact of female physiology on these inflammatory responses. Much research on female endurance athletes has focused on menstrual disturbances associated with bone mineral density, body weight, body temperature, and menstrual abnormalities (Bonen et al., 1983; Burrows & Bird, 2000; Garcia et al., 2006; Jurkowski, 1982; Lebrun, McKenzie, Prior, & Taunton, 1995). However, limited research has focused on how the menstrual cycle affects muscle damage, exercise-induced inflammation, and delayed onset muscle soreness (DOMS). Hormonal fluctuations during different phases of the menstrual cycle may influence cytokine production during exercise (Timmons, Hamadeh, Devries, & Tarnopolsky, 2005), but research is needed to determine if this hormonal variation is associated with inflammation and DOMS.
The fluctuation of sex hormones across the menstrual cycle may affect production of these inflammatory markers. The menstrual cycle has two different phases: follicular and luteal. In the early follicular (EF) phase, estrogen and progesterone levels are low, and in the midluteal (ML) phase both are elevated. Angstwurm, Gartner, and Ziegler-Heitbrock (1997) reported that resting IL-6 levels are lowest in the luteal phase, when progesterone levels are elevated, and highest in the follicular phase during normal menstruation, when estrogen and progesterone are low. In contrast, the luteal phase has been associated with an increase in the immune cells leukocytes and lymphocytes, which are associated with cytokine production (Bouman, Moes, Heineman, de Leij, & Faas, 2001; Faas et al., 2000).
Several studies suggested that increased 17[beta]-estradiol levels have a protective effect against inflammation and nmscle damage. E2 may provide protection through its membrane stabilizing capabilities and antioxidant properties (B. Kendall & Eston, 2002). Previous research also found that estrogen may significantly impair the inflammatory cascade through gene regulation by reducing the molecule adhesion expression and suppressing neutrophil and macrophage production (B. Kendall & Eston, 2002). As a membrane stabilizer, estrogen may decrease neutrophil free radical production by limiting the fluctuations of intracellular calcium homeostasis (Tiidus, 2000). …