It is well known that exercise produces analgesic effects (exercise-induced hypoalgesia (EIH)) in animal models and chronic pain patients, but the brain mechanisms underlying these EIH effects, especially concerning the emotional aspects of pain, are not yet fully understood. In this review, we describe drastic changes in the mesocorticolimbic system of the brain which permit the induction of EIH effects. The amygdala (Amyg) is a critical node for the regulation of emotions, such as fear and anxiety, which are closely associated with chronic pain. In our recent studies using neuropathic pain (NPP) model mice, we extensively examined the association between the Amyg and EIH effects. We found that voluntary exercise (VE) activated glutamate (Glu) neurons in the medial basal Amyg projecting to the nucleus accumbens (NAc) lateral shell, while it almost completely suppressed NPP-induced activation of GABA neurons in the central nucleus of the Amyg (CeA). Furthermore, VE significantly inhibited activation of pyramidal neurons in the ventral hippocampus-CA1 region, which play important roles in contextual fear conditioning and the retrieval of fear memory. This review describes novel information concerning the brain mechanisms underlying EIH effects as a result of overcoming the fear-avoidance belief of chronic pain.

Purpose: Brain-derived neurotrophic factor (BDNF) is an important neurotrophin. The present study investigated the effects of head-out water immersion (HOI) on serum BDNF concentrations. Methods: Eight healthy men performed 20 min head-out water immersion at 42 °C (hot-HOI) and 35 °C (neutral-HOI). These experimental trials were administered in a randomised order separated by at least 7 days. Venous blood samples were withdrawn at rest, immediately after the 20-min HOI, as well as at 15 and 30 min after the end of the HOI. Serum BDNF and S100β, plasma cortisol, platelet and monocyte counts, and core body temperature (T_cb) were measured. Results: T_cb was higher at the end of the hot-HOI and 15 min after hot-HOI (p < 0.01), but recovered to pre-HOI level at 30 min after hot-HOI. No change in T_cb was recorded during neutral-HOI. BDNF level was higher (p < 0.05) at the end of the hot-HOI and at 15 min after the end of hot-HOI, and returned to the baseline at 30 min after hot-HOI. S100β, platelet count and monocyte count remained stable throughout the study. Cortisol level was lower at the end of the hot-HOI and returned to pre-HOI level during the recovery period. BDNF and S100β, cortisol, and platelet and monocyte counts did not change throughout the neutral-HOI study. Conclusions: The present findings suggested that the increase in BDNF during 20-min hot-HOI was induced by hyperthermia through enhanced production, rather than by changes in permeability of the blood–brain barrier (BBB), platelet clotting mechanisms or secretion from monocytes.

Non-randomized study. Previous studies indicated that at least 2-h leg exercise at more than 60% maximum oxygen consumption (VO₂max) increased plasma interleukin (IL)-6 in able-bodied (AB) subjects. The purpose of the present study was to compare IL-6 response to arm exercise in AB subjects and persons with spinal cord injury (SCI). Wakayama Medical University in Japan. Six subjects with SCI between T6 and T10 and seven AB subjects performed 2-h arm crank ergometer exercise at 60%VO₂max. Plasma catecholamines, IL-6, tumor necrosis factor (TNF)-α and high-sensitivity C-reactive protein (hsCRP) were measured before exercise, 60-min exercise, immediately and 2 h after the completion of exercise. Arm exercise increased myoglobin and plasma IL-6 levels in SCI and AB (P<0.01), but there were no differences in them between the two groups throughout the study. Plasma levels creatine kinase, lactate dehydrogenase, TNF-α and hsCRP did not change throughout the study in both groups. These findings suggest neither significant muscle damage nor inflammatory response during exercise. The increase in plasma IL-6 in SCI was not unexpected, confirming that moderate intensity and relatively long-arm exercise is safe and beneficial for SCI subjects with regard to IL-6 excretion, as in AB subjects.

Clinical evidence suggests that early mobilization of patients with acute stroke improves activity of daily living (ADL). The purpose of this study was to compare the utility of the physiatrist and registered therapist operating acute rehabilitation (PROr) applied early or late after acute stroke. This study was prospective cohort study, assessment design. Patients with acute stroke (n = 227) admitted between June 2014 and April 2015 were divided into three groups based on the time of start of PROr: within 24 hours (VEM, n = 47), 24–48 hours (EM, n = 77), and more than 48 hours (OM, n = 103) from stroke onset. All groups were assessed for the number of deaths during hospitalization, and changes in the Glasgow Coma Scale (GCS), National Institute of Health Stroke Scale (NIHSS), and Functional Independence Measure (FIM) at hospital discharge. All patients were assessed by physiatrists, who evaluated the specific needs for rehabilitation, and then referred them to registered physical therapists and occupational therapists to provide early mobilization (longer than one hour per day per patient). The number of deaths encountered during the PROr period was 13 (out of 227, 5.7%), including 2 (4.3%) in the VEM group. GCS improved significantly during the hospital stay in all three groups, but the improvement on discharge was significantly better in the VEM group compared with the EM and OM groups. FIM improved significantly in the three groups, and the gains in total FIM and motor subscale were significantly greater in the VEM than the other groups. PROr seems safe and beneficial rehabilitation to improve ADL in patients with acute stroke.