Exercise training
As with able-bodied individuals, there is strong evidence in support for the use of exercise training for improving cardiovascular health among people with SCI (see Cardiovascular chapter). This is important because there is a high incidence of physical inactivity in individuals with SCI and as such, they are at increased risk of secondary conditions such as cardiovascular disease, diabetes, osteoporosis and obesity. There is clear evidence that the cardiovascular and skeletal muscle systems adapt positively to exercise training in both able-bodied and SCI people. However, the lungs and airways do not change appreciably in response to exercise training. It is likely that exercise is not sufficiently stressful to warrant an adaptive response. This may be even more so when considering the small muscle mass used in wheelchair propulsion or arm cranking exercise. On the other hand, respiratory muscles are both metabolically and structurally plastic and they respond to exercise training. This statement is based largely on direct evidence from animal models and indirect evidence from able-bodied humans.
Exercise training may influence the control of breathing and respiratory sensations (i.e., dyspnea). It is generally accepted that exercise training results in a lower minute ventilation at any given absolute oxygen consumption or power output. This is likely due to a reduction in one or more of the mechanisms (neural and/or humoral) purported to cause the hyperpnea (increased respiratory rate) associated with exercise. As such, the positive effects of exercise training in SCI may reside in an increase in respiratory muscle strength and endurance as well as a reduced ventilatory demand during exercise. A lower ventilation and/or sensation of dyspnea during exercise would lower the work of breathing and prevent early termination of exercise, respectively.
Author Year; Country |
Methods |
Outcome |
Jung et al. 2014; South Korea Randomized Controlled Trial PEDro=5 N=20 |
Population: N=20 with SCI (12M, 8F) |
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Effect Sizes: Forest plot of standardized mean differences (SMD ± 95%C.I.) as calculated from pre- and post-intervention data
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Brurok et al. 2013; Norway Cross-over repeated measures N=15 |
Population: N=15 AIS-A SCI individuals |
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Tiftik et al., 2015; Turkey Controlled Trial |
Population: N=52 with SCI (40M, 12F) |
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Taylor et al. 2014; United States |
Population: N=14 SCI individuals (13M 1F) |
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Terson de Paleville et al. 2013; United States |
Population: N=8 AIS-A tetraplegic SCI (7M, 1F) individuals |
**Cough, inspiration/expiration tasks |
Moreno et al. 2013; Brazil |
Population: N=15 male tetraplegic individuals with SCI divided into control (n=7) and rugby players (n=8) groups. |
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Lee et al. 2012; Korea Prospective cohort |
Population: N=38 C-SCI patients divided into experimental (Mechanical Insufflation-Exsufflation [MI- E] Feedback Resistive training) (n=19) and control groups (n=19). MI-EFRT group: 17M 2F; mean (SD) age: 45.7 (3.4) yrs; DOI: 20.0(1.5) months. |
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Jacobs 2009; USA Prospective Controlled Trial |
Population: N=18 SCI participants with complete motor paraplegia (level of injury T6-T10); participants were assigned either resistjve training (RT) or endurance training (ET): RT group: 6M 3F; mean(SD) age: 33.8 (8.0) yrs |
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Janssen & Pringle 2008; The Netherlands Pre-Post |
Population: N=12 men with SCI (6 with tetraplegia and 6 paraplegia), including 4 participants (mean (SD) age: 44(14) yrs, DOI: 13(8) yrs) who had previous training on ES-LCE |
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Valent et al 2008; The Netherlands Cohort |
Population: N=137 SCI participants; C5 or lower; aged 18-65 years. Hand cycling group: 35 participants with paraplegia, 20 with tetraplegia. Non-hand cycling group: 56 with paraplegia, 26 with tetraplegia. |
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de Carvalho et al. 2006; Brazil |
Population: (1) Treatment group: 11 males with complete tetraplegia, ages 22-50, C4-C7, 25-180 months post-injury |
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Fukuoka et al. 2006; Japan |
Population: N=8 (7M 1F); mean(SD) age: 46.5(8.3) |
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Sutbeyaz et al. 2005; Turkey |
Population: N=20 people with SCI (12 men, 8 1. women), 14 complete, 6 incomplete (T6-T12), mean(SD) age: 31.3(8.2) yrs; DOI: 3.8(5.8) yrs. |
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Le Foll-de-Moro et al. 2005; France |
Population: N=6 participants (5M 1F), T6- & T11/12, mean (SD) age: 29 (14) yrs; mean DOI: 94 days. |
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Silva et al. 1998; Brazil Pre-post N=24 |
Population: N=24 participants (12 people with 1. paraplegia, 12 able-bodied individuals), median age SCI: 31 yrs (range 22-54), control: 30 (range 22-52), T1-T12, all ASIA A, >3 yrs after injury. |
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Hooker & Wells 1989; USA |
Population: N=8 SCI (4M 4F); Low intensity group: C5-T7 (age range 26-36yrs); Moderate Intensity group: C5-T9 (age range 23-36yrs) |
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Discussion
Evidence for exercise training for the respiratory management of the SCI person includes 2 experimental, non-randomized controlled trials and 9 lower-level studies. Studies describing the acute responses to exercise in people with SCI were not included nor were studies that investigated competitive athletes with SCI. Included studies were difficult to interpret because of relatively small sample sizes, differences in exercise modality (wheelchair, arm crank exercise, body weight supported treadmill training) as well as inconsistency in the frequency, intensity and duration of exercise training. Four studies included a control group (Silva et al. 1998; de Carvalho et al. 2006; Lee et al. 2012; Moreno et al. 2013), and the control groups in the studies by de Carvalho et al. (2006), Lee et al. (2012) and Moreno et al. (2013) included subjects comparable to those in the treatment group. This is in contrast to the control group used in Silva and colleagues study that consisted of able-bodied subjects only. While healthy controls may be used for the normative values, they cannot be considered a true control group for SCI subjects.
There is insufficient evidence to strongly support exercise training as a means to improve pulmonary function or ventilatory responses to exercise in SCI people. Some evidence (Le Foll-de-Moro et al. 2005) indicated that following exercise training, peak VE, VT and ventilatory reserve improve. However, the training intensity needs to be relatively high (70-80% of maximum heart rate at a minimum of 3x/week for 6 weeks) whereas lower intensities did not show similar efficacy (Hooker & Wells 1989). Other studies, including one with level 2 evidence, show no change in pulmonary function or ventilation during exercise (Valent et al. 2008; Jacobs 2009). Although 6 months of body-weight supported treadmill training in conjunction with neuromuscular electrical stimulation was shown to be effective for improving peak measures of respiration, the intensity at which subjects worked to achieve these outcomes is unclear, as each performed according to their individual capacity (de Carvalho et al. 2006). Additional well-designed randomized controlled trials are necessary to elucidate if exercise training is an effective means by which to improve pulmonary function at rest and during exercise. Nonetheless, from the limited SCI data and the well-known able-bodied response to upper limb training, it appears that changes to exercise ventilation and ventilatory efficiency can be positively influenced.
Conclusion
There is level 2 evidence (based on 2 prospective controlled trials: de Carvalho et al. 2006; Tiftik et al. 2015) and level 4 evidence (based on 5 pre-post studies: Silva et al. 1998; Sutbeyaz et al. 2005; Le Foll-de-Moro et al. 2005; Fukuoka et al. 2006; Terson de Paleville et al. 2013) to support exercise training as an intervention that might improve resting and exercising respiratory function in people with SCI.
There is level 4 evidence (based on 1 pre-post study: Janssen and Pringle 2008) that computer controlled electrical stimulation induced leg cycle ergometry (ES-LCE) increases the peak values of oxygen uptake, carbon dioxide production, and pulmonary ventilation.