To address the mechanisms underlying hatha yoga’s potential stress-reduction benefits, we compared inflammatory and endocrine responses of novice and expert yoga practitioners before, during, and after a restorative hatha yoga session, as well as in two control conditions. Stressors before each of the three conditions provided data on the extent to which yoga speeded an individual’s physiological recovery.
A total of 50 healthy women (mean age, 41.32 years; range, 30–65 years), 25 novices and 25 experts, were exposed to each of the conditions (yoga, movement control, and passive-video control) during three separate visits.
The yoga session boosted participants’ positive affect compared with the control conditions, but no overall differences in inflammatory or endocrine responses were unique to the yoga session. Importantly, even though novices and experts did not differ on key dimensions, including age, abdominal adiposity, and cardiorespiratory fitness, novices’ serum interleukin (IL)-6 levels were 41% higher than those of experts across sessions, and the odds of a novice having detectable C-reactive protein (CRP) were 4.75 times as high as that of an expert. Differences in stress responses between experts and novices provided one plausible mechanism for their divergent serum IL-6 data; experts produced less lipopolysaccharide-stimulated IL-6 in response to the stressor than novices, and IL-6 promotes CRP production.
The ability to minimize inflammatory responses to stressful encounters influences the burden that stressors place on an individual. If yoga dampens or limits stress-related changes, then regular practice could have substantial health benefits.
CRC = Clinical Research Center; CRP = C-reactive protein; HR = heart rate; hsCRP = high-sensitivity C-reactive protein; IL = interleukin; LPS = lipopolysaccharide; MASQ = Mood and Anxiety Symptom Questionnaire; PANAS = Positive and Negative Affect Scale; PBLs = peripheral blood leukocytes; sIL-6r = soluble IL-6 receptor; TEWL = transepidermal water loss; TNF = tumor necrosis factor; JOURNAL/psme/04.02/00006842-201002000-00002/ENTITY_OV0312/v/2017-07-26T061657Z/r/image-pngo2 max = maximum oxygen consumption.
From the Departments of Psychiatry (J.K.K.-G., L.C.), Medicine (W.B.M.), Psychology (J.K.K.-G., C.F.E., C.R.H.), Molecular Virology, Immunology, and Medical Genetics (W.B.M., R.G.), Institute for Behavioral Medicine Research (J.K.K.-G., L.C., W.B.M., C.F.E., R.G.), The Ohio State University, Columbus, Ohio.
Address correspondence and reprint requests to: Janice K. Kiecolt-Glaser, Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, 460 Medical Center Drive Rm130C, Columbus, OH 43210. E-mail: Janice.Kiecolt-Glaser@osumc.edu
Received for publication May 12, 2009; revision received October 23, 2009.
This research was supported, in part, by National Institutes of Health (NIH) grant AT00297 (J.K.-G., W.B.M., C.F.E., R.G.), NIH Training Grant AI55411 (L.C.; Virginia Sanders, PI), National Center for Research Resources Grant UL1RR025755 which funds the Clinical Research Center, and by Ohio State Comprehensive Cancer Center Core Grant CA16058.