Yasunori Umemoto

Exercise Significantly Increases Plasma Adrenaline and Oxidized Low-Density Lipoprotein in Normal Healthy Subjects But Not in Persons With Spinal Cord Injury

OBJECTIVES To compare plasma concentrations of oxidized low-density lipoprotein (oxLDL) and adrenaline during exercise between persons with spinal cord injury (SCI) and able-bodied (AB) individuals. DESIGN Randomized controlled study. SETTING Human laboratory at a medical university. PARTICIPANTS Persons with SCI (n=7) and AB individuals (n=9). INTERVENTION Two-hour arm crank ergometer exercise at 60% maximum oxygen consumption. MAIN OUTCOME MEASURES Plasma oxLDL and adrenaline levels. RESULTS Exercise significantly increased plasma adrenaline levels in AB persons (mean ± SD: rest, 45.4±32.2 pg/mL; exercise, 200.9±113.7 pg/mL; P<.05) and persons with SCI; however; the magnitude of the increase in those with SCI was attenuated (mean ± SD: rest, 45.4±14.0 pg/mL; exercise, 83.0±55.8 pg/mL; P<.05). Exercise also significantly increased plasma oxLDL levels in AB persons (mean ± SD: rest, 102.2±30.2 U/L; exercise, 179.7±60.0 U/L; P<.05), but not in persons with SCI (mean ± SD: rest, 124.3±66.0 U/L; exercise, 138.9±59.5 U/L). CONCLUSIONS The results suggest that increases in plasma adrenaline levels during exercise contribute to the increase in plasma oxLDL levels.

The role of cardiac sympathetic innervation and skin thermoreceptors on cardiac responses during heat stress

The mechanism(s) for the changes in cardiac function during heat stress remain unknown. This study tested two unique hypotheses. First, sympathetic innervation to the heart is required for increases in cardiac systolic function during heat stress. This was accomplished by comparing responses during heat stress between paraplegics versus tetraplegics, with tetraplegics having reduced/absent cardiac sympathetic innervation. Second, stimulation of skin thermoreceptors contributes to cardiovascular adjustments that occur during heat stress in humans. This was accomplished by comparing responses during leg only heating between paraplegic versus able-bodied individuals. Nine healthy able-bodied, nine paraplegics, and eight tetraplegics participated in this study. Lower body (i.e., nonsensed area for para/tetraplegics) was heated until esophageal temperature had increased by ~1.0°C. Echocardiographic indexes of diastolic and systolic function were performed before and at the end of heat stress. The heat stress increased cardiac output in all groups, but the magnitude of this increase was attenuated in the tetraplegics relative to the able-bodied (1.3 ± 0.4 vs. 2.3 ± 1.0 l/min; P < 0.05). Diastolic function was maintained in all groups. Indexes of left atrial and ventricular systolic function were enhanced in the able-bodied, but did not change in tetraplegics, while these changes in paraplegics were attenuated relative to the able-bodied. These data suggest that the cardiac sympathetic innervation is required to achieve normal increases in cardiac systolic function during heat stress but not required to maintain diastolic function during this exposure. Second, elevated systolic function during heat stress primarily occurs as a result of increases in internal temperature, although stimulation of skin thermoreceptors may contribute.

Immediate Effects of Unaffected Arm Exercise in Poststroke Patients with Spastic Upper Limb Hemiparesis

Background: Spasticity is a major disabling symptom in stroke patients. Clinically, one of the goals of management of stroke patients should be to reduce spasticity. Recent evidence suggests that motor recovery after stroke comprises a hierarchical, dynamic framework of interacting mechanisms in brain cortex. We hypothesized that unaffected arm exercise can stimulate the ipsilateral motor cortex and change the affected upper limb function and spasticity in stroke patients. To test the hypothesis, we evaluated the effects of unaffected arm exercise on spasticity of the affected upper limb and motor function in stroke patients. Methods: The study was performed in 41 chronic stroke patients with upper limb hemiparesis. Affected upper limb spasticity and function were assessed at baseline and after each intervention by the modified Ashworth Scale and Fugl-Meyer Assessment, respectively. Patients were also evaluated clinically by the modified Rankin Scale, Functional Independence Measurement and National Institutes of Health Stroke Scale. Subjects stood for 10 min during the control period, and then cycled an arm crank ergometer at 50% of maximum work load for 10 min by the unaffected arm in standing position. Results: The mean age at study entry was 64.6 ± 1.7 years. The latency between onset of stroke and the study was 109.0 ± 17.0 months (range, 6-495). The cause of hemiparesis was cerebral infarction (n = 21), intracerebral hemorrhage (n = 17) or subarachnoid hemorrhage (n = 3). Exercise significantly improved the modified Ashworth Scale compared with baseline (p < 0.0001). No such change was noted after the control intervention. The Fugl-Meyer Assessment score did not change after exercise compared with baseline (p = 0.95). Conclusions: We conclude that 10 min of unaffected arm exercise improves the affected upper limb spasticity in stroke patients. Further studies are needed to determine the exact mechanism of such improvement and the long-term effects of unaffected arm exercise on motor performance.

Wheelchair marathon creates a systemic anti-inflammatory environment in persons with spinal cord injury.

Objective:To investigate interleukin (IL)-6 and other inflammation markers in athletes with spinal cord injury (SCI) during a wheelchair marathon race. Design:Nonrandomized study in an actual race. Setting:The 28th Oita International Wheelchair Marathon Race, Japan. Participants:Twenty-eight men with SCI between T7 and L2 (16 full-marathon racers, full-group; and 12 half-marathon racers, half-group). Main Outcome Measures:Plasma IL-6, tumor necrosis factor (TNF)-&agr;, and high-sensitivity C-reactive protein (hsCRP) were measured the day before, immediately after the race, and 2 hours after the race. Results:Plasma IL-6 concentrations increased by 18.4-fold and by 9.4-fold (P < 0.05) in the full- and half-groups immediately after the race (P < 0.05), respectively, but returned to baseline at 2 hours of recovery. In contrast, plasma TNF-&agr; and hsCRP did not change throughout the race in both groups. The fold change in plasma IL-6 immediately after the race relative to the prerace was significantly higher in the full-group than the half-group (P < 0.05). In both groups, plasma IL-6 immediately after the race did not correlate with the average wheelchair speed. Interestingly, plasma IL-6 and hsCRP before the race in the full-group, but not in half-group, correlated negatively with the average wheelchair speed (P < 0.05). Conclusions:The study demonstrated that half- and full-marathon wheelchair races increased plasma IL-6, but not TNF-&agr; and hsCRP. Furthermore, the top athletes of the full-group had low plasma IL-6 and hsCRP at baseline. Wheelchair marathon competition, especially full-marathon, and daily training seem to have beneficial effects on SCI through the plasma IL-6 response.

Head-out immersion in hot water increases serum BDNF in healthy males

Abstract 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 (Tcb) were measured. Results: Tcb 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 Tcb 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.

Differences in serum IL-6 response after 1 °C rise in core body temperature in individuals with spinal cord injury and cervical spinal cord injury during local heat stress

Abstract Objectives: Passive rise in core body temperature achieved by head-out hot water immersion (HHWI) results in acute increases in serum interleukin (IL)-6 but no change in plasma adrenaline in patients with cervical spinal cord injury (CSCI). The purpose of the present study was to determine the mechanism of heat stress-induced increase in serum IL-6. Setting: A cross-sectional study. Methods: The study subjects were nine with CSCI, ten with thoracic and lumbar spinal cord injury (TLSCI) and eight able-bodied (AB) subjects. Time since injury was 16.1 ± 3.4 years in TLSCI and 16.4 ± 4.1 years in CSCI. Subjects were subjected to lower-body heat stress (LBH) by wearing a hot water-perfused suit until 1 °C increase in core temperature. The levels of serum IL-6, plasma adrenaline, tumour necrosis factor (TNF)-α, C-reactive protein (CRP), and counts of blood cells were measured at normothermia and after LBH. Results: Serum IL-6 concentrations increased significantly immediately after LBH in all the three groups. ΔIL-6% was lower in CSCI subjects compared with AB subjects. Plasma adrenaline concentrations significantly increased after LBH in AB and TLSCI subjects, but did not change throughout the study in CSCI subjects. Cardiac output and heart rate increased at the end of LBH in all three groups. Conclusions: Under a similar increase in core temperature, ΔIL-6% was lower in the CSCI group compared with the AB group. These findings suggest that the observed rise in IL-6 during hyperthermia is mediated, at least in part, by plasma adrenaline.