Biomedical Physiology and Kinesiology, Department of

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Subthreshold Stochastic Vestibular Stimulation Affects Balance-challenged Standing and Walking

Peer reviewed: 
Yes, item is peer reviewed.
Date created: 
2020-04-10
Abstract: 

Subthreshold stochastic vestibular stimulation (SVS) is thought to enhance vestibular sensitivity and improve balance. However, it is unclear how SVS affects standing and walking when balance is challenged, particularly when the eyes are open. It is also unclear how different methods to determine stimulation intensity influence the effects. We aimed to determine (1) whether SVS affects stability when balance is challenged during eyes-open standing and overground walking tasks, and (2) how the effects differ based on whether optimal stimulation amplitude is derived from sinusoidal or cutaneous threshold techniques. Thirteen healthy adults performed balance-unchallenged and balance-challenged standing and walking tasks with SVS (0–30 Hz zero-mean, white noise electrical stimulus) or sham stimulation. For the balance-challenged condition, participants had inflatable rubber hemispheres attached to the bottom of their shoes to reduce the control provided by moving the center of pressure under their base of support. In different blocks of trials, we set SVS intensity to either 50% of participants’ sinusoidal (motion) threshold or 80% of participants’ cutaneous threshold. SVS reduced medial-lateral trunk velocity root mean square in the balance-challenged (p < 0.05) but not in the balance-unchallenged condition during standing. Regardless of condition, SVS decreased step-width variability and marginally increased gait speed when walking with the eyes open (p < 0.05). SVS intensity had minimal effect on the standing and walking measures. Taken together, our results provide insight into the effectiveness of SVS at improving balance-challenged, eyes-open standing and walking performance in healthy adults.

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Scaling of Inertial Delays in Terrestrial Mammals

Peer reviewed: 
Yes, item is peer reviewed.
Date created: 
2020-02-04
Abstract: 

As part of its response to a perturbation, an animal often needs to reposition its body. Inertia acts to oppose the corrective motion, delaying the completion of the movement—we refer to this elapsed time as inertial delay. As animal size increases, muscle moment arms also increase, but muscles are proportionally weaker, and limb inertia is proportionally larger. Consequently, the scaling of inertial delays is complex. Our intent is to determine how quickly different sized animals can produce corrective movements when their muscles act at their force capacity, relative to the time within which those movements need to be performed. Here, we quantify inertial delay using two biomechanical models representing common scenarios in animal locomotion: a distributed mass pendulum approximating swing limb repositioning (swing task), and an inverted pendulum approximating whole body posture recovery (posture task). We parameterized the anatomical, muscular, and inertial properties of these models using literature scaling relationships, then determined inertial delay for each task across a large range of movement magnitudes and the full range of terrestrial mammal sizes. We found that inertial delays scaled with an average of M0.28 in the swing task and M0.35 in the posture task across movement magnitudes—larger animals require more absolute time to perform the same movement as small animals. The time available to complete a movement also increases with animal size, but less steeply. Consequently, inertial delays comprise a greater fraction of swing duration and other characteristic movement times in larger animals. We also compared inertial delays to the other component delays within the stimulus-response pathway. As movement magnitude increased, inertial delays exceeded these sensorimotor delays, and this occurred for smaller movements in larger animals. Inertial delays appear to be a challenge for motor control, particularly for bigger movements in larger animals.

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Article
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Modulation of hERG K+ Channel Deactivation by Voltage Sensor Relaxation

Peer reviewed: 
Yes, item is peer reviewed.
Date created: 
2020-02-28
Abstract: 

The hERG (human-ether-à-go-go-related gene) channel underlies the rapid delayed rectifier current, Ikr, in the heart, which is essential for normal cardiac electrical activity and rhythm. Slow deactivation is one of the hallmark features of the unusual gating characteristics of hERG channels, and plays a crucial role in providing a robust current that aids repolarization of the cardiac action potential. As such, there is significant interest in elucidating the underlying mechanistic determinants of slow hERG channel deactivation. Recent work has shown that the hERG channel S4 voltage sensor is stabilized following activation in a process termed relaxation. Voltage sensor relaxation results in energetic separation of the activation and deactivation pathways, producing a hysteresis, which modulates the kinetics of deactivation gating. Despite widespread observation of relaxation behaviour in other voltage-gated K+ channels, such as Shaker, Kv1.2 and Kv3.1, as well as the voltage-sensing phosphatase Ci-VSP, the relationship between stabilization of the activated voltage sensor by the open pore and voltage sensor relaxation in the control of deactivation has only recently begun to be explored. In this review, we discuss present knowledge and questions raised related to the voltage sensor relaxation mechanism in hERG channels and compare structure-function aspects of relaxation with those observed in related ion channels. We focus discussion, in particular, on the mechanism of coupling between voltage sensor relaxation and deactivation gating to highlight the insight that these studies provide into the control of hERG channel deactivation gating during their physiological functioning.

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Article
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Intermittent Calf Compression Delays the Onset of Presyncope in Young Healthy Individuals

Peer reviewed: 
Yes, item is peer reviewed.
Date created: 
2020-01-23
Abstract: 

Orthostatic fluid shifts reduce the effective circulating volume and thus contribute to syncope susceptibility. Recurrent syncope has a devastating impact on quality of life and is challenging to manage effectively. To blunt orthostatic fluid shifts, static calf compression garments are often prescribed to patients with syncope, but have questionable efficacy. Intermittent calf compression, which mimics the skeletal muscle pump to minimize pooling and filtration, holds promise for the management of syncope. We aimed to evaluate the effectiveness of intermittent calf compression for increasing orthostatic tolerance (OT; time to presyncope). We conducted a randomized single-blind crossover study, in which participants (n = 21) underwent three graded 60° head-up-tilt tests to presyncope with combined lower body negative pressure on separate days. Low frequency intermittent calf compression (ICLF; 4 s on and 11 s off) at 0–30 and 0–60 mmHg was applied during two tests and compared to a placebo condition where the garment was fitted, but no compression applied. We measured continuous leg circumference changes (strain gauge plethysmography), cardiovascular responses (finger plethysmography; Finometer Pro), end tidal gases (nasal cannula), and cerebral blood flow velocity (CBFv, transcranial Doppler). The 0–60 mmHg ICLF increased OT (33 ± 2.2 min) compared to both placebo (26 ± 2.4 min; p < 0.001) and 0–30 mmHg ICLF (25 ± 2.7 min; p < 0.001). Throughout testing 0–60 mmHg ICLF reduced orthostatic fluid shifts compared to both placebo and 0–30 mmHg ICLF (p < 0.001), with an associated improvement in stroke volume (p < 0.001), allowing blood pressure to be maintained at a reduced heart rate (p < 0.001). In addition, CBFv was higher with 0–60 mmHg ICLF than 0–30 mmHg ICLF and placebo (p < 0.001). Intermittent calf compression is a promising novel intervention for the management of orthostatic intolerance, which may provide affected individuals renewed independence and improved quality of life.

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Article
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Glaucoma-Related Differences in Gaze Behavior When Negotiating Obstacles

Peer reviewed: 
Yes, item is peer reviewed.
Date created: 
2018-07-24
Abstract: 

Purpose: Safe navigation requires avoiding objects. Visual field loss may affect how one visually samples the environment, and may thus contribute to bumping into objects and falls. We tested the hypothesis that gaze strategies and the number of collisions differ between people with glaucoma and normally sighted controls when navigating around obstacles, particularly under multitasking situations.

Methods: Twenty persons with moderate–severe glaucoma and 20 normally sighted controls walked around a series of irregularly spaced vertical obstacles under the following three conditions: walking with obstacles only, walking and counting backward to simulate a conversation, and walking while performing a concurrent visual search task to simulate locating a landmark. We quantified gaze patterns and the number of obstacle contacts.

Results: Compared with controls, people with glaucoma directed gaze closer to their current position (P < 0.05). They also directed a larger proportion of fixations (in terms of number and duration) to obstacles (P < 0.05). Despite this finding, considerably more people with glaucoma contacted an obstacle (P < 0.05). Multitasking led to changes in gaze behavior in both groups, and this was accompanied by a large increase in obstacle contacts among those with glaucoma (P < 0.05).

Conclusions: Glaucoma alters gaze patterns when negotiating a series of obstacles and increases the likelihood of collisions. Multitasking in this situation exacerbates these changes.

Translational Relevance: Understanding glaucoma-related changes in gaze behavior during walking in cluttered environments may provide critical insight for orientation and mobility specialists and guide the design of gaze training interventions to improve mobility.

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Comparison of Autonomic Control of Blood Pressure During Standing and Artificial Gravity Induced via Short-Arm Human Centrifuge

Peer reviewed: 
Yes, item is peer reviewed.
Date created: 
2018-06-25
Abstract: 

Autonomic control of blood pressure is essential toward maintenance of cerebral perfusion during standing, failure of which could lead to fainting. Long-term exposure to microgravity deteriorates autonomic control of blood pressure. Consequently, astronauts experience orthostatic intolerance on their return to gravitational environment. Ground-based studies suggest sporadic training in artificial hypergravity can mitigate spaceflight deconditioning. In this regard, short-arm human centrifuge (SAHC), capable of creating artificial hypergravity of different g-loads, provides an auspicious training tool. Here, we compare autonomic control of blood pressure during centrifugation creating 1-g and 2-g at feet with standing in natural gravity. Continuous blood pressure was acquired simultaneously from 13 healthy participants during supine baseline, standing, supine recovery, centrifugation of 1-g, and 2-g, from which heart rate (RR) and systolic blood pressure (SBP) were derived. The autonomic blood pressure regulation was assessed via spectral analysis of RR and SBP, spontaneous baroreflex sensitivity, and non-linear heart rate and blood pressure causality (RR↔SBP). While majority of these blood pressure regulatory indices were significantly different (p < 0.05) during standing and 2-g centrifugation compared to baseline, no change (p > 0.05) was observed in the same indices during 2-g centrifugation compared to standing. The findings of the study highlight the capability of artificial gravity (2-g at feet) created via SAHC toward evoking blood pressure regulatory controls analogous to standing, therefore, a potential utility toward mitigating deleterious effects of microgravity on cardiovascular performance and minimizing post-flight orthostatic intolerance in astronauts.

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The Critical Power Model as a Potential Tool for Anti-doping

Peer reviewed: 
Yes, item is peer reviewed.
Date created: 
2018-06-06
Abstract: 

Existing doping detection strategies rely on direct and indirect biochemical measurement methods focused on detecting banned substances, their metabolites, or biomarkers related to their use. However, the goal of doping is to improve performance, and yet evidence from performance data is not considered by these strategies. The emergence of portable sensors for measuring exercise intensities and of player tracking technologies may enable the widespread collection of performance data. How these data should be used for doping detection is an open question. Herein, we review the basis by which performance models could be used for doping detection, followed by critically reviewing the potential of the critical power (CP) model as a prototypical performance model that could be used in this regard. Performance models are mathematical representations of performance data specific to the athlete. Some models feature parameters with physiological interpretations, changes to which may provide clues regarding the specific doping method. The CP model is a simple model of the power-duration curve and features two physiologically interpretable parameters, CP and W′. We argue that the CP model could be useful for doping detection mainly based on the predictable sensitivities of its parameters to ergogenic aids and other performance-enhancing interventions. However, our argument is counterbalanced by the existence of important limitations and unresolved questions that need to be addressed before the model is used for doping detection. We conclude by providing a simple worked example showing how it could be used and propose recommendations for its implementation.

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Evaluation of Forearm Vascular Resistance during Orthostatic Stress: Velocity Is Proportional to Flow and Size Doesn’t Matter

Peer reviewed: 
Yes, item is peer reviewed.
Date created: 
2019-11-15
Abstract: 

Background

The upright posture imposes a significant challenge to blood pressure regulation that is compensated through baroreflex-mediated increases in heart rate and vascular resistance. Orthostatic cardiac responses are easily inferred from heart rate, but vascular resistance responses are harder to elucidate. One approach is to determine vascular resistance as arterial pressure/blood flow, where blood flow is inferred from ultrasound-based measurements of brachial blood velocity. This relies on the as yet unvalidated assumption that brachial artery diameter does not change during orthostatic stress, and so velocity is proportional to flow. It is also unknown whether the orthostatic vascular resistance response is related to initial blood vessel diameter.

Methods

We determined beat-to-beat heart rate (ECG), blood pressure (Portapres) and vascular resistance (Doppler ultrasound) during a combined orthostatic stress test (head-upright tilting and lower body negative pressure) continued until presyncope. Participants were 16 men (aged 38.4±2.3 years) who lived permanently at high altitude (4450m).

Results

The supine brachial diameter ranged from 2.9–5.6mm. Brachial diameter did not change during orthostatic stress (supine: 4.19±0.2mm; tilt: 4.20±0.2mm; -20mmHg lower body negative pressure: 4.19±0.2mm, p = 0.811). There was no significant correlation between supine brachial artery diameter and the maximum vascular resistance response (r = 0.323; p = 0.29). Forearm vascular resistance responses evaluated using brachial arterial flow and velocity were strongly correlated (r = 0.989, p<0.00001) and demonstrated high equivalency with minimal bias (-6.34±24.4%).

Discussion

During severe orthostatic stress the diameter of the brachial artery remains constant, supporting use of brachial velocity for accurate continuous non-invasive orthostatic vascular resistance responses. The magnitude of the orthostatic forearm vascular resistance response was unrelated to the baseline brachial arterial diameter, suggesting that upstream vessel size does not matter in the ability to mount a vasoconstrictor response to orthostasis.

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Association between Sedentary Behaviour and Physical, Cognitive, and Psychosocial Status among Older Adults in Assisted Living

Peer reviewed: 
Yes, item is peer reviewed.
Date created: 
2017-08-24
Abstract: 

Objective. Identification of the factors that influence sedentary behaviour in older adults is important for the design of appropriate intervention strategies. In this study, we determined the prevalence of sedentary behaviour and its association with physical, cognitive, and psychosocial status among older adults residing in Assisted Living (AL). Methods. Participants (, mean age = 86.7) from AL sites in British Columbia wore waist-mounted activity monitors for 7 consecutive days, after being assessed with the Timed Up and Go (TUG), Montreal Cognitive Assessment (MoCA), Short Geriatric Depression Scale (GDS), and Modified Fall Efficacy Scale (MFES). Results. On average, participants spent 87% of their waking hours in sedentary behaviour, which accumulated in 52 bouts per day with each bout lasting an average of 13 minutes. Increased sedentary behaviour associated significantly with scores on the TUG (, ) and MFES (, ), but not with the MoCA or GDS. Sedentary behaviour also associated with male gender, use of mobility aid, and multiple regression with increased age. Conclusion. We found that sedentary behaviour among older adults in AL associated with TUG scores and falls-related self-efficacy, which are modifiable targets for interventions to decrease sedentary behaviour in this population.

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Depolarization Of The Conductance-Voltage Relationship In The Nav1.5 Mutant, E1784K, Is Due To Altered Fast Inactivation

Peer reviewed: 
Yes, item is peer reviewed.
Date created: 
2017-09-12
Abstract: 

E1784K is the most common mixed long QT syndrome/Brugada syndrome mutant in the cardiac voltage-gated sodium channel NaV1.5. E1784K shifts the midpoint of the channel conductance-voltage relationship to more depolarized membrane potentials and accelerates the rate of channel fast inactivation. The depolarizing shift in the midpoint of the conductance curve in E1784K is exacerbated by low extracellular pH. We tested whether the E1784K mutant shifts the channel conductance curve to more depolarized membrane potentials by affecting the channel voltage-sensors. We measured ionic currents and gating currents at pH 7.4 and pH 6.0 in Xenopus laevis oocytes. Contrary to our expectation, the movement of gating charges is shifted to more hyperpolarized membrane potentials by E1784K. Voltage-clamp fluorimetry experiments show that this gating charge shift is due to the movement of the DIVS4 voltage-sensor being shifted to more hyperpolarized membrane potentials. Using a model and experiments on fast inactivation-deficient channels, we show that changes to the rate and voltage-dependence of fast inactivation are sufficient to shift the conductance curve in E1784K. Our results localize the effects of E1784K to DIVS4, and provide novel insight into the role of the DIV-VSD in regulating the voltage-dependencies of activation and fast inactivation.

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