Normobaric Hypoxia Exposure During Treadmill Aerobic Exercise After Stroke: A Safety and Feasibility Study

ObjectiveTo evaluate the safety and feasibility of performing treadmill aerobic exercise in moderate normobaric hypoxia among chronic hemiparetic stroke survivors.DesignObservational study using convenience sampling.SettingResearch laboratory in a tertiary rehabilitation hospital.ParticipantsChronic hemiparetic stroke survivors who could walk at least 10-m with or without assistance and had no absolute contraindications to exercise testing.InterventionParticipants (three male and four female) were asked to complete three normobaric hypoxia exposure protocols within a single session. First, they were passively exposed to normobaric hypoxia through gradual reductions in the fraction of inspired oxygen (FIO2 = 20.9, 17.0, and 15.0%) while seated (5-min at each level of FIO2). Participants were then exposed to the same reductions in FIO2 during constant-load exercise performed on a treadmill at 40% of heart rate reserve. Finally, participants completed 20-min of exercise while intermittently exposed to moderate normobaric hypoxia (5 × 2-min at FIO2 = 15.0%) interspaced with 2-min normoxia intervals (FIO2 = 20.9%).Outcome MeasuresThe primary outcome was occurrence of adverse events, which included standardized criteria for terminating exercise testing, blood oxygen saturation (SpO2) <80%, or acute mountain sickness score >2. The increased cardiovascular strain imposed by normobaric hypoxia exposure at rest and during exercise was evaluated by changes in SpO2, heart rate (HR), blood pressure, and rating of perceived exertion (RPE).ResultsOne participant reported mild symptoms of nausea during exercise in normobaric hypoxia and discontinued participation. No other adverse events were recorded. Intermittent normobaric hypoxia exposure was associated with reduced SpO2 (MD = −7.4%, CI: −9.8 to −5.0) and increased HR (MD = 8.2, CI: 4.6 to 11.7) compared to intervals while breathing typical room air throughout the 20-min constant-load exercise period. The increase in HR was associated with a 10% increase in relative effort. However, reducing FIO2 had little effect on blood pressure and RPE measurements.ConclusionModerate normobaric hypoxia appeared to be a safe and feasible method to increase the cardiovascular strain of submaximal exercise in chronic hemiparetic stroke survivors. Future studies evaluating the effects of pairing normobaric hypoxia exposure with existing therapies on secondary prevention and functional recovery are warranted.

Passive Properties of the Wrist and Fingers Following Chronic Hemiparetic Stroke: Interlimb Comparisons in Persons With and Without a Clinical Treatment History That Includes Botulinum Neurotoxin

Background: Neural impairments that follow hemiparetic stroke may negatively affect passive muscle properties, further limiting recovery. However, factors such as hypertonia, spasticity, and botulinum neurotoxin (BoNT), a common clinical intervention, confound our understanding of muscle properties in chronic stroke.Objective: To determine if muscle passive biomechanical properties are different following prolonged, stroke-induced, altered muscle activation and disuse.Methods: Torques about the metacarpophalangeal and wrist joints were measured in different joint postures in both limbs of participants with hemiparetic stroke. First, we evaluated 27 participants with no history of BoNT; hand impairments ranged from mild to severe. Subsequently, seven participants with a history of BoNT injections were evaluated. To mitigate muscle hypertonia, torques were quantified after an extensive stretching protocol and under conditions that encouraged participants to sleep. EMGs were monitored throughout data collection.Results: Among participants who never received BoNT, no significant differences in passive torques between limbs were observed. Among participants who previously received BoNT injections, passive flexion torques about their paretic wrist and finger joints were larger than their non-paretic limb (average interlimb differences = +42.0 ± 7.6SEM Ncm, +26.9 ± 3.9SEM Ncm, respectively), and the range of motion for passive finger extension was significantly smaller (average interlimb difference = −36.3° ± 4.5°SEM; degrees).Conclusion: Our results suggest that neural impairments that follow chronic, hemiparetic stroke do not lead to passive mechanical changes within the wrist and finger muscles. Rather, consistent with animal studies, the data points to potential adverse effects of BoNT on passive muscle properties post-stroke, which warrant further consideration.

Serial sarcomere number is substantially decreased within the paretic biceps brachii in individuals with chronic hemiparetic stroke

A muscle’s structure, or architecture, is indicative of its function and is plastic; changes in input to or use of the muscle alter its architecture. Stroke-induced neural deficits substantially alter both input to and usage of individual muscles. We combined in vivo imaging methods (second-harmonic generation microendoscopy, extended field-of-view ultrasound, and fat-suppression MRI) to quantify functionally meaningful architecture parameters in the biceps brachii of both limbs of individuals with chronic hemiparetic stroke and in age-matched, unimpaired controls. Specifically, serial sarcomere number (SSN) and physiological cross-sectional area (PCSA) were calculated from data collected at three anatomical scales: sarcomere length, fascicle length, and muscle volume. The interlimb differences in SSN and PCSA were significantly larger for stroke participants than for participants without stroke (P = 0.0126 and P = 0.0042, respectively), suggesting we observed muscle adaptations associated with stroke rather than natural interlimb variability. The paretic biceps brachii had ∼8,200 fewer serial sarcomeres and ∼2 cm2 smaller PCSA on average than the contralateral limb (both P < 0.0001). This was manifested by substantially smaller muscle volumes (112 versus 163 cm3), significantly shorter fascicles (11.0 versus 14.0 cm; P < 0.0001), and comparable sarcomere lengths (3.55 versus 3.59 μm; P = 0.6151) between limbs. Most notably, this study provides direct evidence of the loss of serial sarcomeres in human muscle observed in a population with neural impairments that lead to disuse and chronically place the affected muscle at a shortened position. This adaptation is consistent with functional consequences (increased passive resistance to elbow extension) that would amplify already problematic, neurally driven motor impairments.

Factors related to daily use of the paretic upper limb in patients with chronic hemiparetic stroke–A retrospective cross-sectional study

Aims The present study aimed to determine factors associated with the frequency of paralyzed upper extremity (UE) use in chronic stroke patients with severe UE functional deficiency. Methods We retrospectively reviewed the medical records of 138 consecutive patients, and 117 was analyzed (median age, 55 [range, 18–85] years; median stroke duration, 24.5 [range, 7–302] months) with chronic hemiparetic stroke who were admitted to our hospital for intensive upper extremity rehabilitation. The mean Fugl-Meyer Assessment (FMA) UE score was 28.6. All of them are independent in their activity of daily living (ADL) and without remarkable cognitive deficits. Amount-of-use score of Motor Activity Log-14 (MAL-AOU) was applied as the index of daily use of affected UE. The following parameters were examined as the explanatory variables: demographics, proximal and distal sub-scores of FMA UE, Modified Ashworth Scale (MAS), and sensory function scores in the Stroke Impairment Assessment Set (SIAS). Results The median MAL-AOU score was 0.57 [range, 0.28–0.80]. Ordinal regression analysis revealed that FMA proximal, FMA distal, and SIAS sensory function (touch) were associated with AOU score of MAL-14 (Pseudo R-square = 0.460). Conclusion Not only motor but also sensory function, especially tactile sensation, play a crucial role in the daily use of affected UE in chronic stroke patients with severe UE hemiparesis.

Immediate Effects of Kinesio Taping of Tibialis Anterior and Ankle Joint on Mobility and Balance Ability for Chronic Hemiparesis: Randomized Controlled Cross-Sectional Design

Background Stroke patients with hemiparesis are generally described as being slow and suffering a balance disability. Objective The purpose of this cross-sectional single-blind study was to evaluate the immediate effects of Kinesio taping of tibialis anterior and quadriceps on the mobility and balance ability in individuals with chronic hemiparetic stroke. Methods Thirty-three subjects participated in this study. Participants were divided into 3 groups: Ankle Kinesio taping (AKT) group, a placebo (PKT) group, and a control (NKT) group. The AKT group underwent Kinesio tapping of ankle joint and tibialis muscle, PKT group underwent placebo taping, and NKT group underwent no Kinesio taping. All participants were assessed before and after taping training using timed up and go test (TUG), timed up and down stairs test (TUDS), and balance ability. Results After taping training, the AKT group showed significant improvement in mobility and balance ability compared to the PKT group and NKT group (p < 0.05). The results of this study confirmed that Kinesio taping was effective to the balance and mobility abilities of patients with chronic hemiparetic stroke. Conclusions This study suggested Kinesio taping as an effective intervention to increase the mobility and balance abilities of patients with chronic hemiparetic stroke. Therefore, this study are believed to provide the baseline information to effectively improve the balance and mobility abilities of patients with chronic hemiparetic stroke during the rehabilitation treatment in the future.

Serial sarcomere number is substantially decreased within the paretic biceps brachii in individuals with chronic hemiparetic stroke

ABSTRACTA muscle’s structure, or architecture, is indicative of its function and is plastic; changes in input to or use of the muscle alter its architecture. Stroke-induced neural deficits substantially alter both input to and usage of individual muscles. Here, we combined novel in vivo imaging methods (second harmonic generation microendoscopy, extended field-of-view ultrasound, and fat-supression MRI) to quantify functionally meaningful muscle architecture parameters in the biceps brachii of both limbs of individuals with chronic hemiparetic stroke and in age-matched, unimpaired controls. Specifically, serial sarcomere number and physiological cross-sectional area were calculated from data collected at three anatomical scales: sarcomere length, fascicle length, and muscle volume. Our data indicate that the paretic biceps brachii had ~8,500 fewer serial sarcomeres compared to the contralateral limb (p=0.0044). In the single joint posture tested, the decreased serial sarcomere number was manifested by significantly shorter fascicles (10.7cm vs 13.6cm; p<0.0001) without significant differences in sarcomere lengths (3.58μm vs. 3.54μm; p=0.6787) in the paretic compared to the contralateral biceps. No interlimb differences were observed in unimpaired controls, suggesting we observed muscle adaptations associated with stroke rather than natural interlimb variability. This study provides the first direct evidence of the loss of serial sarcomeres in human muscle, observed in a population with neural impairments that lead to disuse and chronically place the affected muscle at a shortened position. This adaptation is consistent with functional consequences (increased passive resistance to elbow extension) that would amplify already problematic, neurally driven motor impairments.SIGNIFICANCE STATEMENTSerial sarcomere number determines a muscle’s length during maximum force production and its available length range for active force generation. Skeletal muscle length adapts to functional demands; for example, animal studies demonstrate that chronically shortened muscles decrease length by losing serial sarcomeres. This phenomenon has never been demonstrated in humans. Integrating multi-scale imaging techniques, including two photon microendoscopy, an innovative advance from traditional, invasive measurement methods at the sarcomere scale, we establish that chronic impairments that place a muscle in a shortened position are associated with the loss of serial sarcomeres in humans. Understanding how muscle adapts following impairment is critical to the design of more effective clinical interventions to mitigate such adaptations and to improve function following motor impairments.