Abstract
To determine the autonomic effects of sub‐occipital release (SOR) during experimentally induced pain, 16 healthy subjects (8 women, 8 men) experienced ischemic (forearm post‐exercise muscle ischemia; PEMI) and cold (hand cold pressor test; CPT) pain. Heart rate (HR; ECG) and mean arterial blood pressure (MAP; photoplethysmography) were measured. SOR or a sham control (modified yaw; 30 cycles/min) was performed in the final min of experimental pain. PEMI caused increases in MAP of 23±2 and 20±2 mmHg, but no differences were observed with the addition of either SOR or yaw. PEMI modestly elevated HR during ischemia, followed by a significant reduction with SOR (‐3±2 bpm) and yaw (‐4±2 bpm) from baseline, but no differences were observed between treatment and sham. CPT increased MAP (11±1 and 9±2 mmHg) and HR (10±2 and 8±3 bpm) prior to SOR and yaw. Neither treatment nor sham blunted MAP increases (SOR = 25±2, yaw = 22±2 mmHg) to CPT, but both decreased HR (SOR = 3±2, yaw = 2±2 bpm) from baseline. To further probe potential mechanisms, systemic acetylsalicylic acid (ASA; 967 mg) was given 60 min prior to testing to reduce prostaglandin (PG) synthesis. ASA blunted pain perception but did not alter cardiovascular changes to PEMI and did not interact with SOR or yaw. These data indicate that that both SOR and sham may be affecting the parasympathetic nervous system via a non‐PG mechanism.Grant Funding Source: Supported by a grant from the American Osteopathic Association
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