The main finding was that heavy elastic resistance training induces a normal physiological response and is safe in COPD patients. In most of the cases, at least a two-level resistance increase was needed to obtain a significant nRMS increase during knee extensions in COPD patients. In fact, a real nRMS increase was only evident at the VL and RF, revealing that in spite of increasing the elastic resistance, the VM was not further stimulated.
The nRMS changes were mostly observed during low-moderate resistance levels, while during the three heaviest elastic resistances (black, silver, gold colors) there were no changes, in contrast with a similar previous study in patients with haemophilia 30. In fact, the greatest between-resistance mean differences in our study were found during the first resistance level. This might be explained by a greater opportunity window for increasing nRMS during the lower resistances and lower accumulated neuromuscular fatigue. Differences in muscle strength between the investigated patient groups can thus affect the increase. In addition, intrinsic muscle changes in COPD patients due to early metabolite accumulation 31 and reduced fiber conduction velocity 32 while exercising may have caused early fatigue and reduced the possibility of increasing nRMS after this point. It must also be considered that the firing rates and motor-unit recruitment thresholds may occur below 100 % of the MVIC 33, which would also be difficult to achieve further nRMS increments.
It is worth mentioning that some differences across the quadriceps muscles were noted. For instance, it seems that the VL needs a greater resistance increment than the RF to increase its nRMS. Conservely, the VL increased its nRMS during the knee extension with the blue color (4th heaviest resistance) while nRMS at the RF was no further increased after the green color (5th heaviest resistance). In line with our findings, a recent similar study conducted among patients with severe haemophilia reported that increasing 2–3 elastic resistance levels was needed to increase nRMS in the quadriceps muscle 30. Unfortunately, there are no similar studies conducted among COPD patients.
Another between-muscle difference was that VL and VM had greater general nRMS than RF. Comparable results have been found in patients with COPD during an isometric knee extension 34 or in healthy adults during dynamic knee extensions 35. This greater muscle activation at least at the VL could be partially explained by a stronger force-generating capacity 36. Specifically, it was estimated that the VL and VM had a contribution of 40% and 25% of the quadriceps strength respectively, while the RF and vastus intermedius contributed 35% 36. This, in conjunction with the more linear EMG/force relationship at the VL compared with the RF and VM 37 might explain why this muscle was the only one showing some differences between the heaviest elastic resistance levels. In addition, a shift from fiber type I to II in the VL is a typical skeletal muscle alteration among COPD patients 38. Moreover, the VL has reduced pennation angle and muscle thickness in these patients when compared with age-matched healthy people 39 and is more affected than the VM by age-related fiber atrophy 40 or muscle disuse after short immobilization 41. Hence, if any of these aforementioned events would be present in our patients, it could be plausible that the VL would need a greater extent of nRMS to overcome the same relative resistance than the other quadriceps muscles. All these findings highlight the need for tailored quadriceps training. To our knowledge, this is the first study demonstrating specific nRMS values for different quadriceps muscles during a typical rehabilitative exercise with progressive resistance, which may help to individualize exercise dosing.
Another relevant finding of our study is the absence of nRMS changes in the VM in spite of the progressive resistance provided, in contrast with a similar article in patients with haemophilia.30 This is likely due to the altered neuromuscular response present in COPD patients and some of the above-mentioned dissimilarities between quadriceps muscles 32. For instance, VL muscle oxygen consumption increased with increasing cadence during constant load cycling, whereas VM remained unchanged 42.
Our correlations between the color of the band or the relative resistance and VM nRMS were weak, but moderate for VL nRMS and RF nRMS. Likewise, VL nRMS and RF nRMS were more correlated with RPE, dyspnea and quadriceps fatigue than VM nRMS. This might have relevant clinical implications, especially for those with more advanced disease and less exercise tolerance. For example, in this specific case and muscle, a lower resistance could be used to provide similar nRMS but with lower RPE, dyspnea and quadriceps fatigue, which may facilitate training and adherence. Dyspnea or muscle fatigue usually limit or stop exercise practice among COPD patients before the skeletal muscles are maximally stressed 19. In our case, dyspnea, quadriceps fatigue and RPE increased in a dose-response fashion while progressing resistance. We found that quadriceps fatigue and especially RPE were more correlated with the resistance progressions than dyspnea, which did not increase to the same extent, suggesting that these variables can especially limit resistance training and should be monitorized. However, achieving a sufficient level of muscle fatigue during training can be relevant, since COPD patients who developed training-induced quadriceps fatigue had greater functional exercise capacity and health-related quality of life than patients without fatigue 43. Interestingly, authors 43 found similar quadriceps force and maximal exercise capacity improvements in both subgroups. Taking these findings and ours together, it could be suggested that in the absence of nRMS differences and when patients can tolerate it, heavier elastic resistances causing higher muscle fatigue could be desirable to maximize exercise benefits. This shows the relevance of evaluating acute quadriceps fatigue together with dyspnea during the training session to individualize exercise dosing. In addition, RPE could also be relevant during COPD rehabilitation. Based on our results, RPE was the acute symptom with the greatest and more consistent increase likely due to its association with nRMS, dyspnea and especially muscle fatigue. Nevertheless, RPE has demonstrated being associated with other variables in this cohort of patients, such as perceived exercise self-efficacy and exercise capacity 44. Despite the absence of similar electromyographical studies among COPD patients, a moderate-very strong association between RPE and nRMS has been reported during shoulder exercises in healthy adults 45. Notably, a study among COPD patients reported no cardiorespiratory changes (i.e., blood pressure, heart rate, oxygen saturation, minute ventilation and oxygen uptake) during knee extensions at low and high intensities, but RPE did increase with the latter 46. In accordance, we found that heart rate and oxygen saturation were stable during the different resistance levels, whereas the other acute symptoms and especially RPE increased. Interestingly, a recent study suggested that RPE, rather than muscle fatigue and exercise-induced muscle pain, was the main exercise stopper during high-intensity aerobic exercise 47. Further studies are needed to understand better those variables limiting exercise practice among COPD and whether RPE correlates with other relevant outcomes.
It must be taken into account that our results cannot be extrapolated to other exercises or exercise variations (e.g., performing knee extensions with both limbs at a time). It also needs to be considered that all the measurements were conducted during three repetitions per condition which may differ when targeting higher volumes. However, this approach is appropriate and is usually used in literature to evaluate nRMS during multiple resistances/intensities to avoid accumulated fatigue 28,30,45, which can be especially relevant in COPD patients 32.
In conclusion, heavy elastic resistance training seems to be feasible in COPD patients, without causing high dyspnea increments and with a stable cardiorespiratory response. In general, COPD patients need to increase at least two elastic resistance levels to obtain a real RF and VL nRMS increase during knee extensions, while there is no nRMS progression for the VM. There is no nRMS progression between the three heaviest elastic resistances, although these levels could be used to increase muscle fatigue or RPE. Dyspnea, quadriceps fatigue and especially RPE increase in a dose-response fashion and are correlated with the relative resistance, the resistance level and nRMS.