Ergogenic effects of spinal cord stimulation on exercise performance following spinal cord injury.

Cervical or upper-thoracic spinal cord injury (SCI, ≥T6) often leads to low resting blood pressure (BP) and impaired cardiovascular responses to acute exercise due to disrupted supraspinal sympathetic drive. Epidural spinal cord stimulation (invasive, ESCS) and transcutaneous spinal cord stimulation (non-invasive, TSCS) have previously been used to target dormant sympathetic circuits and modulate cardiovascular responses. This case series compared the effects of cardiovascular-optimised ESCS and TSCS versus sham ESCS and TSCS on modulating cardiovascular responses and improving submaximal upper-body exercise performance in individuals with SCI. Seven males with a chronic, motor-complete SCI between C6 and T4 underwent a mapping session to identify cardiovascular responses to spinal cord stimulation. Subsequently, four participants (two ESCS and two TSCS) completed submaximal exercise testing. Stimulation parameters (waveform, frequency, intensity, epidural electrode array configuration, and transcutaneous electrode locations in the lumbosacral region) were optimised to elevate cardiovascular responses (CV-SCS). A sham condition (SHAM-SCS) served as a comparison. Participants performed arm-crank exercise to exhaustion at a fixed workload corresponding to above ventilatory threshold, on separate days, with CV-SCS or SHAM-SCS. At rest, CV-SCS increased BP and predicted left ventricular cardiac contractility and total peripheral resistance. During exercise, CV-SCS increased time to exhaustion and peak oxygen pulse (a surrogate for stroke volume), relative to SHAM-SCS. Ratings of perceived exertion also tended to be lower with CV-SCS than SHAM-SCS. Comparable improvements in time to exhaustion with ESCS and TSCS suggest that both approaches could be promising ergogenic aids to support exercise performance or rehabilitation, along with reducing fatigue during activities of daily living in individuals with SCI.

Effects of exercise on autonomic cardiovascular control in individuals with chronic, motor-complete spinal cord injury: an exploratory randomised clinical trial.

STUDY DESIGN: Secondary analysis of a clinical trial. OBJECTIVE: To assess the impact of 6 months of arm cycle ergometry training (ACET), or body weight-supported treadmill training (BWSTT), on autonomic cardiovascular responses to a laboratory sit-up test (SUT) in individuals with chronic (≥1-year post-injury) spinal cord injury (SCI). SETTING: Tertiary Rehabilitation Centre, Vancouver, Canada. METHODS: Sixteen individuals with motor-complete (American Spinal Injury Association Impairment Scale A-B) SCI between the fourth cervical and sixth thoracic spinal cord segments, aged 39 ± 11 years, were assessed. Participants were randomized to receive 72 sessions of moderate-to-vigorous intensity ACET (n = 8) or passive BWSTT (n = 8). Changes in mean arterial pressure (finger plethysmography), hemodynamics (Modelflow® method), and heart rate/heart rate variability (HR/HRV; electrocardiography) were measured in response to a  SUT before and after 6 months of exercise training. Spontaneous cardiovagal baroreflex sensitivity (cvBRS) was assessed using the sequence method. RESULTS: Neither ACET nor BWSTT impacted hemodynamic responses to SUT or the incidence of orthostatic hypotension (all P > 0.36). ACET increased HR (P < 0.01, ηp2 = 0.34) and high frequency (HF) power HRV responses (P < 0.01, ηp2 = 0.42) to SUT following 6 months of training while BWSTT did not. Consistent with this, cvBRS improved (P < 0.05, ηp2 = 0.16) only following ACET. Improvements in cvBRS were correlated with both the HR (r = 0.726, P < 0.0001) and HF power (r = -0.484, P < 0.01) responses to SUT. CONCLUSION: Six months of ACET, but not BWSTT, improved cardiovagal baroreflex control of HR but had no effect on BP responses to SUT in individuals with chronic, motor-complete SCI. SPONSORSHIP: Canadian Institutes of Health Research (CIHR) CLINICAL TRIAL REGISTRATION: NCT01718977.

Temporal Changes of Cardiac Structure, Function, and Mechanics During Sub-acute Cervical and Thoracolumbar Spinal Cord Injury in Humans: A Case-Series.

Individuals with cervical spinal cord injury (SCI) experience deleterious changes in cardiac structure and function. However, knowledge on when cardiac alterations occur and whether this is dependent upon neurological level of injury remains to be determined. Transthoracic echocardiography was used to assess left ventricular structure, function, and mechanics in 10 male individuals (median age 34 years, lower and upper quartiles 32-50) with cervical (n = 5, c-SCI) or thoracolumbar (n = 5, tl-SCI) motor-complete SCI at 3- and 6-months post-injury. Compared to the 3-month assessment, individuals with c-SCI displayed structural, functional, and mechanical changes during the 6-month assessment, including significant reductions in end diastolic volume [121 mL (104-139) vs. 101 mL (99-133), P = 0.043], stroke volume [75 mL (61-85) vs. 60 mL (58-80), P = 0.042], myocardial contractile velocity (S') [0.11 m/s (0.10-0.13) vs. 0.09 m/s (0.08-0.10), P = 0.043], and peak diastolic longitudinal strain rate [1.29°/s (1.23-1.34) vs. 1.07°/s (0.95-1.15), P = 0.043], and increased early diastolic filling over early myocardial relaxation velocity (E/E') ratio [5.64 (4.71-7.72) vs. 7.48 (6.42-8.42), P = 0.043]. These indices did not significantly change in individuals with tl-SCI between time points. Ejection fraction was different between individuals with c-SCI and tl-SCI at 3 [61% (57-63) vs. 54% (52-55), P < 0.01] and 6 months [58% (57-62) vs. 55% (52-56), P < 0.01], though values were considered normal. These results demonstrate that individuals with c-SCI exhibit significant reductions in cardiac function from 3 to 6 months post-injury, whereas individuals with tl-SCI do not, suggesting the need for early rehabilitation to minimize cardiac consequences in this specific population.

Spinal cord injury impairs cardiac function due to impaired bulbospinal sympathetic control.

Spinal cord injury chronically alters cardiac structure and function and is associated with increased odds for cardiovascular disease. Here, we investigate the cardiac consequences of spinal cord injury on the acute-to-chronic continuum, and the contribution of altered bulbospinal sympathetic control to the decline in cardiac function following spinal cord injury. By combining experimental rat models of spinal cord injury with prospective clinical studies, we demonstrate that spinal cord injury causes a rapid and sustained reduction in left ventricular contractile function that precedes structural changes. In rodents, we experimentally demonstrate that this decline in left ventricular contractile function following spinal cord injury is underpinned by interrupted bulbospinal sympathetic control. In humans, we find that activation of the sympathetic circuitry below the level of spinal cord injury causes an immediate increase in systolic function. Our findings highlight the importance for early interventions to mitigate the cardiac functional decline following spinal cord injury.

Cardiac arrhythmias six months following traumatic spinal cord injury.

OBJECTIVE: To investigate the incidence of cardiac arrhythmias at six months following traumatic spinal cord injury (SCI) and to compare the prevalence of arrhythmias between participants with cervical and thoracic SCI. DESIGN: A prospective observational study using continuous twenty-four-hour Holter monitoring. SETTING: Inpatient rehabilitation unit of a university research hospital and patient home setting. PARTICIPANTS: Fifty-five participants with acute traumatic SCI were prospectively included. For each participant, the SCI was characterized according to the International Standards for Neurological Classification of SCI by the neurological level and severity according to the American Spinal Injury Association Impairment Scale. OUTCOME MEASURES: Comparisons between demographic characteristics and arrhythmogenic occurrences as early as possible after SCI (4 ± 2 days) followed by 1, 2, 3, 4 weeks and 6 month time points of Holter monitoring. RESULTS: Bradycardia (heart rate [HR] <50 bpm) was present in 29% and 33% of the participants with cervical (C1-C8) and thoracic (T1-T12) SCI six months after SCI, respectively. The differences in episodes of bradycardia between the two groups were not significant (P < 0.54). The mean maximum HR increased significantly from 4 weeks to 6 months post-SCI (P < 0.001), however mean minimum and maximum HR were not significantly different between the groups at the six-month time point. There were no differences in many arrhythmias between recording periods or between groups at six months. CONCLUSIONS: At the six-month timepoint following traumatic SCI, there were no significant differences in occurrences of arrhythmias between participants with cervical and thoracic SCI compared to the findings observed in the first month following SCI.

Accidental boosting in an individual with tetraplegia - considerations for the interpretation of cardiopulmonary exercise testing.

CONTEXT: Autonomic dysreflexia (AD), characterized by a transient increase in systolic blood pressure (BP), is experienced by individuals with spinal cord injury (SCI) and can be purposefully induced ('boosting') to counteract autonomic dysfunction that impairs cardiovascular responses to exercise. Herein, we demonstrate the impact of unintentional boosting observed during cardiopulmonary exercise testing (CPET) in an inactive male with SCI (C5, motor-complete). FINDINGS: On two separate occasions the individual performed a standard arm-crank CPET (1-min stages, 7W increase in resistance) following by a longer CPET (4-min stages, 12W increase in resistance), both to volitional exhaustion. The second CPET was performed to confirm the accuracy of exercise intensity prescription and verify peak exercise parameters. Immediately following the second CPET on the initial visit, the individual reported symptoms of AD, verified as a 58mmHg increase in systolic BP from baseline. Relative to the first CPET, performed only 35 min earlier, there were pronounced differences in peak exercise responses. In comparison to the longer CPET performed on the second visit without a concomitant episode of AD (thereby controlling for the type of CPET protocol administered), peak exercise outcomes were considerably elevated: power output (Δ19W), oxygen uptake (Δ3.61 ml·â€…kg·-1min-1), ventilation (Δ11.4 L ·min-1) and heart rate (Δ9 b·min-1). CONCLUSION/CLINICAL RELEVANCE: This case raises important considerations around the nuances of CPET in this population. In individuals susceptible to BP instability, the physiologically boosted state may explain a significant proportion of the variance in peak aerobic capacity and should be closely monitored before and after clinical CPET.

Associations between left ventricular structure and function with cardiorespiratory fitness and body composition in individuals with cervical and upper thoracic spinal cord injury.

STUDY DESIGN: Cross-sectional. OBJECTIVE: It is known that left ventricular mass (LVM) and cardiorespiratory fitness (CRF) are associated to fat-free mass (FFM).  It is unknown if these factors associated with left ventricular (LV) structure and function outcomes in individuals with spinal cord injury (SCI). SETTING: University-based laboratory.Vancouver, BC, Canada. METHODS: Thirty-two individuals (aged 40 ± 11 years) with chronic, motor-complete SCI between the fourth cervical and sixth thoracic levels were recruited. Echocardiographic LV parameters and body composition were assessed at rest, as per the recommended guidelines for each technique. CRF was assessed during an incremental arm-cycle exercise test until volitional fatigue. The appropriate bivariate correlation coefficients [i.e., Pearson's (r) and Spearman's rank (Rs)] tests were used for normal and non-normal distributed variables, respectively. RESULTS: LV structure and function parameters were not associated with the indexed peak oxygen consumption (V̇O2peak) [i.e., relative to body weight or FFM] (Rs values ranged from -0.168 to 0.134, all P values > 0.223). The association between peak oxygen pulse and the resting echocardiographic-obtained SV was medium sized (Rs = 0.331, P = 0.069). The LVM associations with FFM and fat mass (FM) were large and small (r = 0.614, P < 0.001 and r = 0.266, P = 0.141, respectively). Associations of absolute V̇O2peak were medium- positive with FFM (Rs = 0.414, P = 0.021) but negative with FM (Rs = -0.332, P = 0.068). CONCLUSION: LV parameters measured at rest are not associated with V̇O2peak in individuals with cervical and upper-thoracic SCI. Given the observed associations between LVM and V̇O2peak with FFM, future studies may consider utilizing FFM for indexing cardiovascular measures following SCI.