Neuromuscular electrical stimulation resistance training enhances oxygen uptake and ventilatory efficiency independent of mitochondrial complexes after spinal cord injury: a randomized clinical trial

Abstract

The purpose of the study was to determine whether neuromuscular electrical stimulation resistance training (NMES-RT) evoked muscle hypertrophy is accompanied by increased VO2 peak, ventilatory efficiency and mitochondrial respiration in individuals with chronic spinal cord injury (SCI). Thirty-three men and women with chronic, predominantly traumatic, SCI were randomized to either NMES-RT (n=20) or passive movement training (PMT; n=13). Functional electrical stimulation-lower extremity cycling (FES-LEC) was used to test leg VO2 peak, VE/VCO2 ratio and substrate utilization prior to and post-intervention. Magnetic resonance imaging was used to measure muscle cross-sectional area (CSA). Finally, muscle biopsy was performed to measure mitochondrial complexes and respiration. The NMES-RT group showed a significant increase in post-intervention VO2 peak compared to baseline (∆ VO2 = 14%, P < 0.01) with no changes in the PMT group (∆ VO2 = 1.6%, P= 0.47). Similarly, thigh (∆ CSA Thigh = 19%) and knee extensor (∆ CSA Knee = 30.4 %, P < 0.01) CSAs increased following NMES-RT but not after PMT. The changes in thigh and knee extensor muscle CSAs were positively related with the change in VO2 peak. Neither NMES-RT nor PMT changed mitochondrial complex tissue levels; however, changes in peak VO2 were related to complex I. In conclusion, in persons with SCI, NMES-RT-induced skeletal muscle hypertrophy was accompanied with increased peak VO2 consumption which may partially be explained by enhanced activity of mitochondrial complex I.

Exoskeleton Training and Trans-Spinal Stimulation for Physical Activity Enhancement After Spinal Cord Injury (EXTra-SCI): An Exploratory Study

“…Conclusions that can be drawn from this study are limited by the small sample size, and some outcomes are limited to sub-groups of participants. The use of multiple imputation in limited sample size is a valid technique to fill in missing data (40) and similar to what our group has published previously (41). The authors recognize, however, that even with multiple imputation, data in this study were limited and the significant findings for anthropometrics and body composition must be confirmed in larger sample sizes.…”

Assessment of mitochondrial respiratory capacity using minimally invasive and noninvasive techniques in persons with spinal cord injury

“…These results suggest that improved muscle function may be mediated by mitochondrial capacity and highlights the need for clinical evaluation tools to assist in monitoring skeletal muscle function in this population [15]. An improved understanding of the cellular response of skeletal muscles in chronic SCI may help clinicians better formulate therapeutic and rehabilitative regimens for improving the long-term health and quality of life for persons living with SCI [13,16].…”

“…Due the presence of fat infiltration that is associated in individuals with SCI, an excess amount of muscle was utilized [7]. The plasma membrane of muscle fibers was permeabilized by gentle agitation for 20 min at 4˚C in BioPS containing 50 μg/ml saponin [40] followed by two 4-min washes in mitochondrial respiration buffer (miR05, 0.5 mM EGTA, 3 mM MgCl 2 6H 2 O, 60 mM lactobionic acid, 20 mM taurine, 10 mM KH 2 PO 4 , 20 mM HEPES, 110 mM D-sucrose, 1g/L bovine serum albumin, pH 7.1) [13].…”

“…Oxygen concentration and flux were recorded with DatLab software (Oroboros, Innsbruck, Austria). Respiration was measured using the following protocol: 10 mM glutamate + 5 mM malate (complex I substrates), followed by sequential additions of 0.1 and 1 mM ADP, 10 μM cytochrome c (to test for membrane integrity), 1 μM rotenone (complex I inhibitor), 10 mM succinate (complex II substrate), 40 μM 2-thenoyltrifluoroacetone (TTFA) (complex II inhibitor), 0.5 mM tetramethyl-p-phenylenediamine (TMPD)-10 mM sodium ascorbate (complex IV substrates), and 10 mM sodium azide (complex IV inhibitor); Oxygen flux was expressed as pmol�sec -1 normalized to mg weight of the fiber bundle [13]. Mitochondrial respiration rates were determined after correcting for non-mitochondrial oxygen consumption following the addition of the corresponding inhibitor for complex I, II, and IV.…”

“…However, it is still unclear whether mitochondrial dysfunction contributes to this observed pattern of substrate utilization after SCI. Multiple studies have shown that electrical stimulation training of muscle may yield increased muscle endurance, function increases in oxidative enzyme activity and gene expression [11][12][13][14]. These results suggest that improved muscle function may be mediated by mitochondrial capacity and highlights the need for clinical evaluation tools to assist in monitoring skeletal muscle function in this population [15].…”