Submaximal Cycle Exercise
The MST group improved their mechanical efficiency of cycling at 40 W by 31.3 ± 6.8%, with no other significant change in the measured variables. Perceived exertion in these patients while cycling at 40 W was also significantly reduced after MST, whereas this and all other physiological responses were unchanged by the 8-wk period in the controls (Fig. 2, Table 3). The O2 or CO2 ventilatory equivalents were not altered by the MST.
There were no significant changes in the control group. The MST group experienced a significant improvement in FEV1 from 0.92 ± 0.13 to 1.09 ± 0.13 L (~21.5%) (overall change in means = 0.23, CI = 0.1 to 0.4 L), which, in turn, improved FEV1 percentage predicted from 33 ± 3 to 40 ± 3% predicted (~21.2%). FVC also significantly increased from 1.99 ± 0.4 to 2.19 ± 0.3 L (~10%) (overall change in means = 0.44, CI = 0.12 to 0.76 L). Because both FEV1 and FVC increased after MST, the ratio of FEV1/FVC increased insignificantly from 49.9 ± to 5 to 52 ± 4% (overall change in means = 0.02, CI = −0.04 to 0.07%).
Maximal Exercise Cycle Tests
In agreement with the finding of improved mechanical efficiency in the MST group while cycling at 40 W, this group achieved a significantly greater maximal cycle work rate (~10%) with an unchanged V˙O2peak. This was not the case for the control group, whose only change between pre- and posttesting was an unexpected reduction in ventilation at WRmax (Fig. 2, Table 4). The O2 or CO2 ventilatory equivalents were not altered by the MST.
The improvement in 1RM correlated positively with the improvement in the rate of force development (r = 0.79, CI −0.06 to 0.98), mechanical efficiency (r = 0.65, CI −0.34 to 0.96), and FEV1 (r 2 = 0.67, CI −0.31 to 0.96). The improvement in the rate of force development correlated positively with the improvement in mechanical efficiency (r = 0.69, CI −0.28 to 0.96) and FEV1 (r = 0.76, CI −0.13 to 0.97). All were statistically significant correlations.
The major novel finding of this study is that MST significantly improved strength and rate of force development in patients with COPD, resulted in an approximately 32% increase in mechanical efficiency and a fall in perceived exertion during submaximal work. This improvement returned these patients to within the accepted normal range for cycling mechanical efficiency and is likely to translate into improved performance of daily activities and improved quality of life. In addition, MST significantly improved pulmonary function, as indicated by an approximately 22% increase in FEV1. On the basis of the clinical definition of severe COPD (i.e., FEV1 < 1.0 L), the improvement in FEV1 attained by these patients (0.92 ± 0.32 to 1.09 ± 0.34 L) returned them from a severe to a moderate diagnosis. This positive effect on pulmonary function, coupled with the increase in mechanical efficiency, supports a therapeutic role for MST as a useful treatment for patients with COPD.
MST and Mechanical Efficiency
There is now considerable evidence that COPD may be associated with attenuated mechanical efficiency (2,3,21,24,25). Most recently, the direct assessment of an isolated skeletal muscle model in patients with COPD revealed a concomitant reduction in the mechanical efficiency of and the number of type I fibers within this muscle group (24). Indeed, in contrast to healthy aging (16), older patients with moderate to severe COPD consistently demonstrate an increase in the proportion of type II fibers, assessed either histochemically (13) or by the expression of myosin heavy chain isoforms (18). As exercise intensity and or rate of force development increases, there is a growing reliance on type II muscle fibers that has been proposed to lead to less efficient muscular work (5). There are convincing data, both from in vitro (6) and in vivo (5,12) studies, that the energetic cost of force production is fiber-type specific. Although the current study did not directly assess the muscle structure of these patients with COPD, fiber-type differences may explain the documented attenuation in mechanical efficiency during cycling in this study (~15% vs normal (~23%)) (24,25).
The MST performed three times a week for 8 wk resulted in a 31.3 ± 6.8% (± SE) improvement in mechanical efficiency during submaximal cycle exercise, with no such changes apparent during the same time frame in the control group. The improvement in mechanical efficiency induced by MST correlated significantly with the increased rate of force development (r = 0.69) and peak force (r = 0.65). An increased rate of force development leads to longer atonic periods between contractions and enhanced muscle perfusion, whereas an increased peak force results in a reduction in the relative load placed on the muscle during submaximal efforts (19). Additionally, it was previously documented in humans that within 2-4 wk of an 8-wk strength-training program, there was a significant reduction in the percentage of type IIx fibers, with a concomitant trend toward an increase in the more fatigue-resistant type IIa fibers (28). Therefore, the consequences of MST, coupled with an increased reliance on type II fibers in patients with COPD, may explain some of the improvements observed in mechanical efficiency in these patients.
In the current study, a possible limitation in terms of cycling efficiency was the regular exposure to cycling as a warm-up in the strength-training group, but not in the controls. However, the minimal load and duration of this cycling exposure, combined with our inability to improve mechanical efficiency with cycling-specific training in other COPD patients (unpublished observations), refutes this as a major limitation of the present study.
MST and Pulmonary Function
The MST group revealed a clear improvement in both FEV1 and FVC. Although MST did not involve any specific expiratory muscle training, it is well accepted that the biomechanics of leg press exercise demands an integral involvement and, therefore, training adaptation of the abdominal muscles (15,29). Acknowledging the negative impact of COPD on lung elastic recoil and airway resistance, but also recognizing the concomitant weakening of the respiratory muscles, it is possible that functional improvements of the expiratory muscles (abdominal wall, internal intercostals) may have led to improved pulmonary function, as measured by forced expiration. Indeed, several indications in the literature suggest that a relationship between peripheral strength-training responses and pulmonary function in COPD may exist (27,30). Most recently, Kongsgaard et al. (14) added to this trend by recognizing that their control group of patients with COPD who only performed breathing exercises had a fall in FEV1 during a 12-wk period, whereas the strength-trained patients maintained their prestudy levels. In the current study, with only an 8-wk duration, the FEV1 of the control subjects remained constant, but the MST group revealed an approximately 20% increase in FEV1, which correlated well with their improvements in the rate of force development (r 2 = 0.58) and 1RM (r 2 = 0.45). Although the improvements in FEV1 and FVC are in a positive direction, and FEV1 correlates well with many indices of COPD disease severity, the clinical impact of these improvements in pulmonary function on patient health still need to be determined.
MST, Strength, and Rate of Force Development
There is clear evidence that COPD is associated with attenuated muscle strength (9). In fact, up to 70% of patients demonstrate lower quadriceps-muscle strength than their healthy age-matched counterparts, and disease severity, as assessed by symptom intensity and pulmonary function, is well correlated with this loss of strength (4). The muscle-mass wasting that accompanies COPD, perhaps as a simple consequence of inactivity, seems to explain these findings in that the ratio of quadriceps strength/muscle CSA is preserved (4,7). Although not the major goal of this study, the improvements in muscle strength attained by the current patients with COPD (Fig. 2, Table 4) are in agreement with the findings of Simpson et al. (27), who revealed that more traditional strength training could improve muscle strength in such patients and lead to higher exercise capacities in terms of time to exhaustion at submaximal workload. It should be noted that in these studies and in the current research, there are always considerable, unavoidable learning effects that are probably as important, in terms of the strength changes, as the physiological adaptations in the muscle itself. Additionally, test-retest data were not collected in the present study, which may also limit the interpretation of the recorded strength changes. However, in our hands, these tests have revealed excellent test-retest data.
COPD is the most common chronic pulmonary disease, with more than 14 million North Americans living with this diagnosis (8). It is universally accepted that a substantially reduced exercise capacity accompanies COPD, with a subsequent attenuation in maximal work rate. However, it is also becoming increasingly apparent that, in addition to the degradation of pulmonary function, a reduction in skeletal muscle mechanical efficiency may also contribute to the challenge of physical work performed by these patients (2,3,24,25). These multiple factors combine, leading to inactivity, muscle disuse, and a downward spiral toward even more exaggerated ill health.
The current findings reveal that because MST is minimally taxing to the ventilatory and cardiac systems, it is well suited to patients with COPD, not resulting in the normal dyspnea-associated discomfort experienced by this population during conventional exercise such as walking. This is highlighted in the current patients by the 100% compliance and completion of training in the MST group. The inclusion of MST in a cardiopulmonary rehabilitation program could, according to the current data, result in an approximately 32% increase in mechanical efficiency. In the real world, this translates to either having the potential to perform significantly more work or to perform the same work with a reduced effort, which is likely an important result with practical implications for patients with COPD.
We express our sincere thanks to the subjects who participated in the study. This study was funded in part by the Norwegian Research Council by providing a Professor II position for Dr. Richardson. Additional support was provided by National Heart, Lung, and Blood Institute Grant HL-17731 and Tobacco Related Disease Research Program Grant # 15RT-0100.
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Keywords:©2007The American College of Sports Medicine
CHRONIC OBSTRUCTIVE PULMONARY DISEASE; SKELETAL MUSCLE; RATE OF FORCE DEVELOPMENT; EXERCISE; EFFICIENCY