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Rationale: There have been a few reports on the early rehabilitation of patients with coronavirus disease (COVID-19), and none on the effectiveness and adverse events of early mobilization for mechanical ventilation patients (other than COVID-19) during deep sedation. This report indicates that sitting without adverse events is possible in patients with severe COVID-19 pneumonia during deep sedation with muscle relaxation., Patient Concerns: A 65-year-old man with a history of diabetes mellitus, lacunar infarction, and Parkinson's disease was admitted to a local hospital for pneumonia due to COVID-19. After admission, the patient was managed on a ventilator under deep sedation with muscle relaxants and sedatives. Twelve days after admission, the patient was transferred to our hospital due to his worsening respiratory status., Diagnosis: Pneumonia due to COVID-19 was diagnosed using a polymerase chain reaction-dependent method., Interventions: The day following transfer, a physical therapist started passive range of motion training and sitting., Outcomes: The period spanning his initial rehabilitation to muscle relaxant medication interruption was 9 days, and he underwent 7 rehabilitation sessions. The patient was unable to sit during only one of the 7 sessions due to pre-rehabilitation hypoxemia. In 5 of the 6 sitting sessions, PaO2/FiO2 transiently decreased but recovered by the time of subsequent blood sampling. The patient's PaCO2 decreased during all sessions. His blood pressure did not drastically decrease in any sitting session, except the first. Sputum excretion via sputum suction increased during sitting, and peak inspiratory pressure did not change., Lessons: The patient eventually died of pneumonia due to COVID-19. However, sitting during deep sedation with muscle relaxants did not cause any serious adverse events nor did it appear to cause obvious negative respiratory effects., Competing Interests: The authors have no funding and conflicts of interests to disclose., (Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.)

Objective: The aim of the present study was to compare the effects of acupuncture treatment on arterial blood pressure (BP) and heart rate (HR) in patients with mild hypertension with high sympathetic tone with those of normotensive patients and to examine the effects on cardiac sympathetic nerve activity (CSNA) and vagal activity using heart rate variability (HRV) analysis. Design: Eight male patients with prehypertension or stage I hypertension and eight normotensive age-matched patients were included in this study. All patients had their systolic BP (SBP), diastolic BP (DBP), HR, and HRV measured. In addition, the ratio of low-frequency (LF) to high-frequency (HF) HRV and the power of the HF of the HRV were recorded. The study was conducted at Kansai University of Health Sciences in Japan. Interventions: Each patient underwent a single, 15-min-long acupuncture session. Acupuncture was applied to PC6, LI4, ST36, LR3 on both sides, and GV20. Results: SBP and HR decreased significantly in the hypertensive group during and after acupuncture compared with the baseline SBP and HR ( p  < 0.05). LF/HF was significantly reduced during acupuncture ( p  < 0.05), and HF was significantly increased after acupuncture in the hypertensive group ( p  < 0.05). However, there were no significant changes in LF/HF or HF in the control group. Conclusions: Acupuncture may reduce the BP and HR in patients with mild hypertension. An HRV analysis suggests that acupuncture may suppress the enhanced basal CSNA activity and increase the vagal nerve activity in patients with mild hypertension. Clinical Trial Registration number: UMIN000041249.

Study Design: Acute experimental study., Objectives: To investigate the acute response of markers of lipid metabolism and interleukin (IL)-6 to dopamine infusion in people with a cervical spinal cord injury (CSCI)., Setting: Laboratory of Wakayama Medical University, Japan., Methods: Ten participants, four with CSCI and six AB individuals, underwent 50 min of dopamine infusion. Blood samples were collected prior to, immediately after and 1 h following cessation of dopamine infusion for the determination of circulating catecholamine, lipid, ketone body and IL-6 concentrations., Results: The adrenaline concentration following dopamine infusion was increased by 59 ± 7% in CSCI (p = 0.038, Cohen's d effect size (ES): 1.47), while this was not changed in AB (p = 0.223). Triglycerides and acetoacetic acid concentration were increased in both groups, immediately after and 1 h post-infusion (triglycerides p ≤ 0.042, ES CSCI: 1.00, ES AB: 1.12; acetoacetic acid p ≤ 0.030; ES CSCI: 1.72, ES AB: 1.31). 3-Hydroxybutyric acid concentration was increased in CSCI only (48 ± 15%, p = 0.039, ES: 1.44; AB p = 0.115). Dopamine infusion did not affect plasma IL-6 concentration in either group (p ≥ 0.368)., Conclusions: Dopamine infusion induced a sustained increase in triglyceride and ketone body concentrations in persons with CSCI. In contrast, cytokine concentrations were not affected by dopamine infusion. These findings suggest that circulating catecholamines can stimulate metabolism in people with CSCI despite the presence of autonomic dysfunction.

Blood pressure response to head-up tilt (HUT) in 7 healthy subjects and 9 patients before and after coronary artery bypass grafting (CABG) was measured during supine and 15-min 60° HUT. Stroke volume (SV) and ejection fraction (EF) were assessed by echocardiography. Baseline mean arterial pressure (MAP) and heart rate (HR) in patients before CABG were similar to healthy subjects. MAP in patients decreased by 6 (4-9) mmHg [median (1st-3rd quartiles)] during 7-12 mmHg of HUT with decreased cardiac output (CO = SV × HR) while HR remained unchanged. MAP in healthy subjects remained unchanged during HUT with increased HR. Body weight decreased by 3.5 (2.5-3.7) kg and MAP decreased by 6 (2-13) mmHg during the last 3-min HUT while HR increased after CABG. Decreases in SV and CO during HUT disappeared after CABG. Blood pressure decreased during HUT in patients before and after CABG regardless of HR response.

Study Design: Experimental study., Objective: Individuals with spinal cord injuries (SCI) may present with impaired sympathetic control over thermoregulatory responses to environmental and exercise stressors, which can impact regional core temperature (T core ) measurement. The purpose of this study was to investigate whether regional differences in T core responses exist during exercise in individuals with SCI., Setting: Rehabilitation centre in Wakayama, Japan., Methods: We recruited 12 men with motor-complete SCI (7 tetraplegia, 5 paraplegia) and 5 able-bodied controls to complete a 30-min bout of arm-cycling exercise at 50% V̇O 2 peak reserve. T core was estimated using telemetric pills (intestinal temperature; T int ) and esophageal probes (T eso ). Heat storage was calculated from baseline to 15 and 30 min of exercise., Results: At 15 min of exercise, elevations in T eso (Δ0.39 ± 0.22 °C; P < 0.05), but not T int (Δ0.04 ± 0.18 °C; P = 0.09), were observed in able-bodied men. At 30 min of exercise, men with paraplegia and able-bodied men both exhibited increases in T eso (paraplegia: Δ0.56 ± 0.30 °C, P < 0.05; able-bodied men: Δ0.60 ± 0.31 °C, P < 0.05) and T int (paraplegia: Δ0.38 ± 0.33 °C, P < 0.05; able-bodied men: Δ0.30 ± 0.30 °C, P < 0.05). T eso began rising 7.2 min earlier than T int (pooled, P < 0.01). Heat storage estimated by T eso was greater than heat storage estimated by T int at 15 min (P = 0.02) and 30 min (P = 0.03) in men with paraplegia. No elevations in T eso , T int , or heat storage were observed in men with tetraplegia., Conclusions: While not interchangeable, both T eso and T int are sensitive to elevations in T core during arm-cycling exercise in men with paraplegia, although T eso may have superior sensitivity to capture temperature information earlier during exercise.

Ventral tegmental area (VTA) dopamine (DA) neurons are the primary source of dopamine in target structures that constitute the mesolimbic reward system. Previous studies demonstrated that voluntary wheel running (VWR) by neuropathic pain (NPP) model mice produces exercise-induced hypoalgesia (EIH), and that activation of mesolimbic reward system may lead to EIH. However, the neuronal mechanism by which the mesolimbic reward system is activated by VWR is unknown. Here, we found that VWR produces EIH effects and reverses the marked reduction in activated lateral VTA (lVTA)-DA neurons induced by NPP. The proportions of activated laterodorsal tegmental nucleus (LDT)-cholinergic and lateral hypothalamus-orexin neurons were significantly enhanced by VWR. Retrograde tracing and dual immunostaining revealed that VWR activates lVTA-projecting LDT-cholinergic/non-cholinergic and lateral hypothalamic area (LHA)-orexin/non-orexin neurons. Therefore, EIH effects may be produced, at least in part, by activation of the mesolimbic reward system via activation of LDT and LHA neurons.

Study Design: Experimental study., Objectives: To characterize static and dynamic cerebral autoregulation (CA) of individuals with cervical spinal cord injury (SCI) compared to able-bodied controls in response to moderate increases in mean arterial pressure (MAP) caused by mild whole-body cold stress., Setting: Japan METHODS: Five men with complete autonomic cervical SCI (sustained > 5 y) and six age-matched able-bodied men participated in hemodynamic, temperature, catecholamine and respiratory measurements for 60 min during three consecutive stages: baseline (10 min; 33 °C water through a thin-tubed whole-body suit), mild cold stress (20 min; 25 °C water), and post-cold recovery (30 min; 33 °C water). Static CA was determined as the ratio between mean changes in middle cerebral artery blood velocity and MAP, dynamic CA as transfer function coherence, gain, and phase between spontaneous changes in MAP to middle cerebral artery blood velocity., Results: MAP increased in both groups during cold and post-cold recovery (mean differences: 5-10 mm Hg; main effect of time: p = 0.001). Static CA was not different between the able-bodied vs. the cervical SCI group (mean (95% confidence interval (CI)) of between-group difference: -4 (-11 to 3) and -2 (-5 to 1) cm/s/mm Hg for cold (p = 0.22) and post-cold (p = 0.24), respectively). At baseline, transfer function phase was shorter in the cervical SCI group (mean (95% CI) of between-group difference: 0.6 (0.2 to 1.0) rad; p = 0.006), while between-group differences in changes in phase were not different in response to the cold stress (interaction term: p = 0.06)., Conclusions: This pilot study suggests that static CA is similar between individuals with cervical SCI and able-bodied controls in response to moderate increases in MAP, while dynamic CA may be impaired in cervical SCI because of disturbed sympathetic control.

Background: Lumbar spondylolysis is a defect in the pars interarticularis that is common in young athletes; the stress distribution at the pars interarticularis is the highest in extension and rotation movements. The paraspinal muscles play an important role in stabilization of the lumbar spine; however, no study has assessed the properties of paraspinal muscles in athletes with lumbar spondylolysis., Objective: To evaluate the properties of paraspinal muscles in athletes with lumbar spondylolysis., Design: Cross-sectional study., Setting: Laboratory., Participants: Six high school baseball players with terminal-stage lumbar spondylolysis and 11 high school baseball players without organic lumbar lesions of similar anthropometric characteristics., Methods: All subjects performed the unsupported trunk holding test combined with surface electromyographic (EMG) power spectral analysis until exhaustion. The results of EMG power spectral analysis were compared between the spondylolysis and control groups., Main Outcome Measurements: The median frequency (MF) was computed from the raw EMG signal of the erector spinae and multifidus during trunk holding test using fast Fourier transform spectrum analysis. The initial MF and MF slope were calculated., Results: No significant differences in endurance time were found between the spondylolysis and control groups. The initial MF and the MF slopes of the erector spinae and multifidus were significantly lower in the spondylolysis group than in the control group., Conclusions: The results suggest lower fast-twitch motor unit recruitment in the erector spinae and multifidus of high school baseball players with terminal-stage lumbar spondylolysis compared with the control., Level of Evidence: IV., (Copyright © 2018 American Academy of Physical Medicine and Rehabilitation. Published by Elsevier Inc. All rights reserved.)

Physical exercise, such as forced treadmill running and swimming, can sufficiently improve mechanical allodynia and heat hyperalgesia in animal models of neuropathic pain (NPP), including partial sciatic nerve ligation, chronic constriction injury, and spinal nerve ligation models. Thus, physical exercise has been established as a low-cost, safe, and effective way to manage NPP conditions, but the exact mechanisms underlying such exercise-induced hypoalgesia (EIH) are not fully understood. A growing body of evidence has identified several factors that work at different levels of the nervous system as playing important roles in producing EIH in animal models of NPP. The objective of this review is to provide an overview of key players associated with EIH, and then to discuss our current understanding of the mechanisms underlying EIH. Relevant studies have demonstrated that physical exercise can dramatically alter the levels of inflammatory cytokines, neurotrophins, neurotransmitters, endogenous opioids, and histone acetylation at various sites in the nervous system, such as injured peripheral nerves, dorsal root ganglia, and spinal dorsal horn in animal models of NPP, thereby contributing to the production of EIH. These results suggest that EIH is produced through multiple cellular and molecular events in the pain pathway.

Background: Brain-derived neurotrophic factor (BDNF) has been implicated in enhancing neuronal health. Exercise and noninvasive positive-pressure ventilation (NPPV) are known to independently alter BDNF levels in patients with depression, dementia, type 2 diabetes, chronic obstructive pulmonary disease, and obstructive sleep apnea syndrome. However, the combined effects of exercise and NPPV on serum BDNF in normal subjects are unknown., Objective: To determine the effects of the combination of acute aerobic exercise under NPPV on serum BDNF in normal adults., Design: Cross-over design study., Setting: Wakayama Medical University., Participants: Ten healthy young men., Intervention: The subjects exercised on a cycle ergometer at 60% of pretraining maximal oxygen uptake (V.O 2max ) for 30 minutes daily for 5 consecutive days with or without NPPV (12 cmH 2 O). The 5-day exercise protocol was repeated after a 3-week washout period with or without NPPV., Main Outcome Measurements: Serum BDNF, plasma cortisol, and platelet, lymphocyte, and monocyte counts were measured at 24 hours before the first day exercise with or without NPPV and 24 hour after last day exercise with or without NPPV at resting condition. Measurements were also made on the first day exercise; serum BDNF level was measured immediately before and immediately after exercise, as well as at 1, 2, and 3 hours after exercise with or without NPPV., Results: The 5-day exercise protocol significantly (P < .05) increased serum BDNF when combined with NPPV, but not without NPPV, and did not change plasma cortisol level, platelet, or lymphocyte counts, with or without NPPV. The 5-day exercise protocol also significantly (P < .05) decreased monocyte count without NPPV, but not with NPPV, relative to baseline. Changes noticed immediately after the first day of exercise included significant (P < .05) increase in serum BDNF compared with immediately before the exercise, with or without NPPV., Conclusions: The results indicated that a 5-day exercise protocol combined with NPPV increased serum BDNF, suggesting that NPPV synergistically enhances the effect of aerobic exercise on serum BDNF level., Level of Evidence: II., (Copyright © 2016 American Academy of Physical Medicine and Rehabilitation. Published by Elsevier Inc. All rights reserved.)

Unlabelled: Physical exercise can attenuate neuropathic pain (NPP), but the exact mechanism underlying exercise-induced hypoalgesia (EIH) remains unclear. Recent studies have shown that histone hyperacetylation via pharmacological inhibition of histone deacetylases in the spinal cord attenuates NPP, and that histone acetylation may lead to the production of analgesic factors including interleukin 10. We intended to clarify whether histone acetylation in microglia in the spinal dorsal horn contributes to EIH in NPP model mice. C57BL/6J mice underwent partial sciatic nerve ligation (PSL) and PSL- and sham-runner mice ran on a treadmill at a speed of 7 m/min for 60 min/d, 5 days per week, from 2 days after the surgery. PSL-sedentary mice developed mechanical allodynia and heat hyperalgesia, but such behaviors were significantly attenuated in PSL-runner mice. In immunofluorescence analysis, PSL surgery markedly increased the number of histone deacetylase 1-positive/CD11b-positive microglia in the ipsilateral superficial dorsal horn, and they were significantly decreased by treadmill-running. Moreover, the number of microglia with nuclear expression of acetylated H3K9 in the ipsilateral superficial dorsal horn was maintained at low levels in PSL-sedentary mice, but running exercise significantly increased them. Therefore, we conclude that the epigenetic modification that causes hyperacetylation of H3K9 in activated microglia may play a role in producing EIH., Perspective: This article presents the importance of epigenetic modification in microglia in producing EIH. The current research is not only helpful for developing novel nonpharmacological therapy for NPP, but will also enhance our understanding of the mechanisms and availability of exercise in our daily life., (Copyright © 2016 American Pain Society. Published by Elsevier Inc. All rights reserved.)

Charcot-Marie-Tooth disease (CMT) is one of the most commonly inherited neuromuscular diseases causing progressive muscle weakness; contracture; deformity in the feet, legs, and hands; and impairments of ambulation and handgrip. Reduced physical ability can be attributed not only to the disease but also to physical deconditioning. Previously, most physicians in the field of rehabilitation were anxious about the hypothesis of overwork weakness in CMT, and did not conduct intensive exercise programs for patients with CMT. However, recent studies have reported that progressive resistance strengthening programs for lower extremities are feasible, safe, beneficial, and improve exercise intolerance and undue fatigue in patients with CMT. Although the improvement in exercise tolerance may be partly due to the reversal of deconditioning effect of related sedentary lifestyle, progressive resistance training and physical fitness can improve walking function, activities of daily living, and subjective perception of pain and fatigue in patients with CMT. To increase the daily physical function, some studies described the potential benefits of ankle-foot orthoses (AFOs); however, no control study supported it. So far, the training programs on CMT have been dependent on the exercise programs for able-bodied individuals. To increase the effects of rehabilitation, optimal programs that combine the training protocol and AFO strategies will have to be designed for patients with CMT.

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., (Copyright © 2015 the American Physiological Society.)

The purpose of this study was to define common carotid blood flow (CBF), cardiovascular and endocrine responses during head-up tilt (HUT) in patients with acute cerebrovascular diseases (CVD). In 31 male patients with acute CVD (damage of the supratentorial area) and 21 age-matched control male subjects, we measured CBF, mean blood pressure (MBP), heart rate, stroke volume and cardiac output responses before (baseline), during and after HUT. We also measured plasma levels of antidiuretic hormone, adrenaline, noradrenaline, aldosterone and plasma renin activity. After obtaining baseline measurements during 3-minutes horizontal position, HUT was performed for 5 minutes, followed by continuation of recording for 3 more minutes in the horizontal position. During HUT, CBF decreased significantly and equally in both groups. MBP did not change during HUT in both groups. The endocrine responses were also not different between the two groups. The results suggest that damage to the supratentorial area in patients with acute CVD do not alter the CBF, cardiovascular and endocrine responses. In other words, HUT does not predispose patients with acute CVD to serious falls in MBP and CBF at upright posture.

Objective: To investigate the longitudinal changes in physical capacity over 20 years in athletes with spinal cord injury (SCI)., Design: Longitudinal study (20-y follow-up)., Setting: Laboratory setting., Participants: Persons with SCI (N=7)., Interventions: Not applicable., Main Outcome Measures: Maximum oxygen consumption Vo(2)max) measured in 1986-1988 and in 2006., Results: Subjects with SCI maintained stable Vo(2)max in 2006. Six of the 7 continued various wheelchair sports activities, while 1 person quit sports activities 1 year after the baseline study. The latter person showed reduced Vo(2)max by 53%, while 2 persons who continued strenuous wheelchair sports activities showed increased Vo(2)max by 43% and 45% after 20 years., Conclusion: The results indicated that physical capacity reflected the level of sports activity in subjects with SCI who maintained sports activities.

The purpose of the present study was to investigate the relationship between bowel maneuvers and autonomic dysreflexia (AD) in patients with cervical spinal cord injuries (CSCI). Fifteen consecutive, clinically stable patients with CSCI participated. We evaluated changes in blood pressure (BP), pulse rate (PR) and classic symptoms of AD before, during and after a bowel program involving the manual removal of stool in lateral recumbency. The insertion of rectal medication induced a significant increase in systolic BP, which persisted during additional digital rectal stimulation. Furthermore, the manual removal of stool induced AD, with maximal increases of systolic BP (169.1(+-)19.5 mmHg, mean(+-)SD). However, the insertion of a finger into the anus after the end of stool flow did not cause a further increase in systolic BP. Systolic BP recovered to pre-program values within 5 min after defecation. Our study demonstrated that the combined effects of rectal and/or anal sphincter distension and uninhibited rectal contraction in response to the manual removal of stool might induce AD. We recommend avoiding, if at all possible, the manual removal of stool in order to prevent AD in patients with CSCI.