Abstract
The purpose of the study was to determine whether neuromuscular electrical stimulation resistance training (NMES-RT)-evoked muscle hypertrophy is accompanied by increased V̇o(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 V̇o(2) peak, V̇E/V̇co(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 V̇o(2) peak compared with baseline (ΔV̇o(2) = 14%, P < 0.01) with no changes in the PMT group (ΔV̇o(2) = 1.6%, P = 0.47). Similarly, thigh (ΔCSA(thigh) = 19%) and knee extensor (ΔCSA(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 V̇o(2) peak. Neither NMES-RT nor PMT changed mitochondrial complex tissue levels; however, changes in peak V̇o(2) were related to complex I. In conclusion, in persons with SCI, NMES-RT-induced skeletal muscle hypertrophy was accompanied by increased peak V̇o(2) consumption which may partially be explained by enhanced activity of mitochondrial complex I.NEW & NOTEWORTHY Leg oxygen uptake (V̇o(2)) and ventilatory efficiency (V̇E/V̇co(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 V̇o(2) peak but decreased V̇E/V̇co(2) ratio without changes in mitochondrial complex levels. Leg V̇o(2) peak was associated with muscle hypertrophy and mitochondrial respiration of complex I following training.