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

The purpose of the study was to determine whether neuromuscular electrical stimulation resistance training (NMES-RT)-evoked muscle hypertrophy is accompanied by increased Vo(2) 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 the leg Vo(2) peak, VE/Vco(2) ratio, and substrate utilization pre- and postintervention. 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 postintervention Vo(2) peak compared with baseline (Delta Vo(2) = 14%, P < 0.01) with no changes in the PMT group (Delta Vo(2) = 1.6%, P = 0.47). Similarly, thigh (Delta CSA(thigh) = 19%) and knee extensor (Delta 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 Vo(2) peak. Neither NMES-RT nor PMT changed mitochondrial complex tissue levels; however, changes in peak Vo l were related to complex I. In conclusion, in persons with SCI, NMES-RT-induced skeletal muscle hypertrophy was accompanied by increased peak Vo(2) consumption which may partially be explained by enhanced activity of mitochondrial complex I. NEW & NOTEWORTHY Leg oxygen uptake (Vo(2)) and ventilatory efficiency (VE/Vco(2) ratio) were measured during functional electrical stimulation cycling testing following 12-16 wk of either electrically evoked resistance training or passive movement training, and the respiration of mitochondrial complexes. Resistance training increased thigh muscle area and leg Vo(2) peak but decreased VE/Vco(2) ratio without changes in mitochondrial complex levels. Leg Vo(2) peak was associated with muscle hypertrophy and mitochondrial respiration of complex I following training.

Automated summary

In individuals with chronic spinal cord injury, neuromuscular electrical stimulation resistance training (NMES-RT) induced muscle hypertrophy is accompanied by an increase in peak Vo(2) consumption, possibly due to enhanced activity of mitochondrial complex I. This study highlights the association between muscle hypertrophy, peak Vo(2) consumption, and mitochondrial respiration of complex I in this population.