RESUMEN
The purpose of the study was to determine whether neuromuscular electrical stimulation resistance training (NMES-RT)-evoked muscle hypertrophy is accompanied by increased VÌo2 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 VÌo2 peak, VÌE/VÌco2 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 VÌo2 peak compared with baseline (ΔVÌo2 = 14%, P < 0.01) with no changes in the PMT group (ΔVÌo2 = 1.6%, P = 0.47). Similarly, thigh (ΔCSAthigh = 19%) and knee extensor (ΔCSAknee = 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 VÌo2 peak. Neither NMES-RT nor PMT changed mitochondrial complex tissue levels; however, changes in peak VÌo2 were related to complex I. In conclusion, in persons with SCI, NMES-RT-induced skeletal muscle hypertrophy was accompanied by increased peak VÌo2 consumption which may partially be explained by enhanced activity of mitochondrial complex I.NEW & NOTEWORTHY Leg oxygen uptake (VÌo2) and ventilatory efficiency (VÌE/VÌco2 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 VÌo2 peak but decreased VÌE/VÌco2 ratio without changes in mitochondrial complex levels. Leg VÌo2 peak was associated with muscle hypertrophy and mitochondrial respiration of complex I following training.
Asunto(s)
Terapia por Estimulación Eléctrica , Entrenamiento de Fuerza , Traumatismos de la Médula Espinal , Estimulación Eléctrica , Femenino , Humanos , Masculino , Músculo Esquelético , Oxígeno , Traumatismos de la Médula Espinal/terapiaRESUMEN
Many drugs, hormones, components of herbal medicines, environmental pesticides and toxins are Solute Carrier family 22 (SLC22) substrates. The last twenty years has seen great progress in determining SLC22 tissue expression profiles, membrane localization, energetics, substrate profiles and biopharmaceutical significance. However, much still remains to be answered in terms of SLC22 family member's roles in 'normal' physiology as compared to pathophysiological states, as well as in drug interactions that impact pharmacokinetics, efficacy and toxicity. This review begins with a brief synopsis of SLC22 family discovery, function and tissue expression. Subsequent sections provide examples establishing a role for SLC22 transporters in food-drug, herbal supplement-drug, endogenous substrate-drug and drug-drug interactions.