Abstract:
Purpose: Fatigue presents a major challenge for those living with spinal cord injury (SCI). Additionally, prolonged pulmonary oxygen uptake kinetics (VO2 on-kinetics) and reduced skeletal muscle oxidative capacity are experienced after SCI. These alterations may contribute to increased fatigability during walking if present in those with chronic motor-incomplete SCI (miSCI). The purpose of this study was to characterize fatigability, VO2 on-kinetics, and muscle oxygenation in individuals with chronic miSCI compared to an able-bodied reference group. Methods: Eight chronic miSCI participants and eight able-bodied participants completed a two constant work-rate walking bouts at a self-selected walking speed. Fatigability was calculated as the ratio of perceived fatigability and performance fatigability. VO2 on-kinetics was determined using a mono-exponential model in which a time constant (tp) and amplitude (∆VO2) was calculated during phase 2 of the biphasic kinetic response during bout 1 of walking. Concentration changes in resting deoxygenated myoglobin/hemoglobin capacity ([HHb]total) and halftime ([HHb] ½ time) were determined in the left lateral gastrocnemius during arterial occlusion using near-infrared spectroscopy (NIRS). Results: miSCI group experienced greater fatigability, perceived fatigability, and performance fatigability compared to the reference group (6.62 ± 4.86 vs 1.87 ± 0.98, p=0.017; 5.75 ± 0.71 vs 3.38 ± 1.77, p=0.006; and 1153.38 ± 529.47 vs 1800 ± 0.00 seconds, p=0.011, respectively). VO2 on-kinetic profiles of the miSCI were prolonged compared to the reference (41.2 ± 7.67 vs 23.3 ± 6.48; p<0.0001). Significant correlation was found between fatigability and (tp r = 0.56; p = 0.012). During resting arterial occlusion the miSCI group experienced slower [HHb] ½ time compared to the reference (185.9 ± 28.7 vs 157.9 ± 18.9 sec., p=0.047). Conclusion: These individuals living with chronic miSCI appeared to more fatigable as a result of higher levels of performance and perceived fatigability. The results suggest that poor cardiorespiratory function may be a mediator of fatigability and demonstrate that cardiorespiratory function measures can be used as physiological markers of fatigability in this population. Furthermore, reduced skeletal muscle oxidative capacity is implicated as a contributing mechanism to the observed slowed VO2 on-kinetics.
