Pulmonary Rehabilitation and Exercise Training Program Report (Assessment)

Introduction

Chronic obstructive pulmonary disease or COPD is a lung disease not fully reversible characterized by abnormal breathing caused by chronic obstruction of lung airflow (WHO, 2009). It is also known as “chronic bronchitis” and “emphysema” or a “smoker’s cough”, usually an under-diagnosed and life-threatening (WHO, 2009).

A COPD diagnosis is confirmed by a simple test called spirometry. The test measures how deeply a person can breathe and how fast air can move into and out of the lungs. Patients who have symptoms of cough, sputum production, or dyspnea or difficult or labored breathing, and a history of exposure to risk factors for the disease should consider diagnosis (WHO, 2009). In the absence of spirometry, the diagnosis of COPD should be done using all available tools. The clinical symptoms and signs that include abnormal shortness of breath and increased forced expiratory time help with the diagnosis (WHO, 2009). Likewise, a low peak flow is may be associated with COPD, but not always a COPD case but other lung diseases. While chronic cough and sputum production may precede the development of airflow limitation, not all individuals with cough and sputum production go on to develop COPD (WHO, 2009)

Discussion

COPD is almost always caused by cigarette smoking and medical science has not yet developed cures (ATS, 1995). Treatments, however, are of symptomatic benefit and it is highly suggested that stopping smoking can decrease the rate of deterioration of lung function.

In addition, bronchodilator and anti-inflammatory agents are helpful to many patients although reduction in airway obstruction is generally modest. Oxygen supplement adds length and improves quality of life in severely hypoxemic patients. Gaissert et al (1996) also noted that lung transplantation and lung volume reduction surgery may benefit a highly selected minority of patients.

Skeletal Muscle Dysfunction

Strength

Muscle strength is decreased in patients with COPD as compared normal same-age individuals specifically, the lower limb muscles are affected to a greater extent than are upper limb muscles (Bernard S, 1998). The reduction in lower limb strength is associated with the reduction in activity of the lower limbs amongst patients; quadriceps strength is also decreased by 20–30% in patients with moderate to severe COPD (Gosselink R, 1996), some patients have a reduction in strength of more than 50%.

Bernard (1998) suggested that quadriceps strength was correlated with the forced expiratory volume in 1 s (FEV1), i.e., the lower the FEV1, the weaker the quadriceps muscle.

Endurance

In Serres (1998) study that compared limb muscle endurance in patients with COPD and healthy control individuals, it was noted that endurance is particularly affected by motivational factors. A study found a significant reduction in quadriceps endurance in patients with COPD (Serres I, 1998) and another did not (Zattara-Hartmann MC, 1995). Small reductions in endurance of upper limb muscles (elbow flexors and adductor pollicis) have also been noted amongst patients with COPD (Zattara-Hartmann MC, 1995).

Fatigability

Patients with COPD become breathless when they exercise. This may discourage exercise due to breathlessness prior to stressing the muscle to develop fatigue. This is why most patients with COPD may develop contractile fatigue of the exercising muscle after performing exercise exceeding tolerance. Mador (2001) also suggested that patients with severe disease were as likely to develop exercise-induced quadriceps fatigue as those with milder disease; Healthy elderly individuals are also less likely to experience the muscle fatigue as compared to those with COPD.

Muscle fiber type

Biopsies have shown that the quadriceps muscle in patients with COPD has a reduced proportion of type I fibers and an increase in the proportion of type II fibers as compared against normal individuals (Whittom, 1998).

Muscle capillarity

Muscle capillarity is a basic component of the skeletal muscle oxidative capacity. Jobin (1998) found that the number of capillaries/mm² was significantly lower in patients with COPD than in healthy individuals. Likewise, the study indicated the ratio of the capillary to fiber was also significantly lower in patients with COPD. Likewise, the ratio of the capillary to fiber did not improve after a physical training program (Whittom F, 1998).

Muscle metabolism

Jakobsson’s (1995) study that biopsied the quadriceps muscle (Jakobsson P, 1995) showed a reduction in oxidative enzyme capacity in patients with COPD as compared with normal individuals.

Matthias (1998) also noted that blood lactate levels increase at very low work rates in patients with COPD, and because blood flow to the leg is within normal limits in patients with COPD, the increase in lactate is due to an increase in net lactate output across the leg. However, oxygen delivery to the exercising leg is also usual for those with COPD, suggesting that the increase in lactate production is due to an intrinsic muscle abnormality or decreased oxidative capacity resulting in early activation of anaerobic glycolysis (Matthias 1998).

Mechanisms of skeletal muscle dysfunction

Disuse

Casaburi (1996) noted that patients with COPD reduce their level of physical activity because exertion causes unpleasant results, this vicious cycle in the reduction of physical activity leads to deconditioning, and more impairment in skeletal muscle function leading to additional symptoms at lower levels of work. Casaburi (1996) also noted that inactivity produces a number of structural and biochemical changes and decrease in oxidative capacity and muscle atrophy are seen amongst COPD patients.

Medications

It was reported that short courses of high-dose corticosteroids are used to treat acute exacerbations in patients with COPD, while low-dose oral corticosteroids had been used chronically to treat some patients with COPD; the efficacy is much disputed (Decramer M, 1996). Steroid-induced myopathy has been well accepted despite the initial doubts.

Histologically, both myopathic changes and generalized fibre atrophy are seen (Decramer M, 1996). In Decramer’s (1996) study, survival of patients with steroid-induced myopathy was significantly lower than that in a matched group of patients with COPD and a similar degree of airflow obstruction.

Hypoxia

Chronic hypoxia adversely affects skeletal muscles, with prolonged exposure to high-altitude hypoxia, glycolytic enzyme (which is active in anaerobic metabolism) activity increases, whereas oxidative enzyme activity decreases (Corbucci GG, 1995). Hypoxia also increases oxidative stress, which can adversely affect muscle performance (Corbucci GG, 1995).

Hypercapnia

Mador (1997) have noted that short-term exposure to hypercapnia leads to muscle weakness but has no effect in fatigability (Mador MJ, 1997). There had also been a significant reduction noted in acute hypercapnic respiratory failure in energy metabolism, also reduced ATP and phosphocreatine concentrations (Fiaccadori E, 1987). Fiaccadori (1987) also suggested that acute hypercapnia also contributes to intracellular acidosis in patients with acute respiratory failure.

Nutrition

Nutritional depletion is normal occurrence amongst patients with COPD. Most commonly noted nutritional depletion is the bodyweight less than 90% of ideal body weight (Schols AMWJ, 1993). 35% of patients entering a pulmonary rehabilitation program were nutritionally depleted when the above premise is taken into consideration (Schols AMWJ, 1993). Prolonged under-nutrition results in a reduction in muscle strength and endurance (McLoughlin DM, 1998), reduction in muscle mass and fibre atrophy (McLoughlin DM, 1998).

Oxidative stress

Oxidative stress may contribute to the skeletal muscle dysfunction of patients with COPD. Plasma concentrations of lipid peroxidation increased in patients with COPD during acute exacerbations (Rahman I, 1996) and it has been noted that the main source of the oxygen free radicals is mitochondria (Ji LL, 1996).

Likewise, skeletal-muscle dysfunction is already recognized as a symptom of advanced COPD (Celli BR, 2004). Some studies already pointed out that exercise causes skeletal-muscle dysfunction and other morphological and metabolic changes seen amongst COPD patients (Mador MJ, 2001).

A substantial variation in exercise-training programs may employ training of the lower-extremity muscles, upper-extremity muscles, respiratory muscles, or some combination of these three although debate optimal exercise protocol and the intensity, duration, and frequency of training for various muscle groups that should be applied in COPD is still highly contested (Casaburi, 1991). Others suggest that endurance exercise for the lower extremities should be the primary exercise modality while the roles of upper-body, respiratory-muscle, and strength training remain undefined (Gosselink R, 1997; ACCP/AACVPR, 1997)

Lower-Extremity Training

Pulmonary rehabilitation programs include education, psychosocial intervention and support, physical and occupational therapy, training in self-management, and the acquisition of dyspnea-reduction skills (ACCP/AACVPR). In addition, lower-extremity training is also included. Some evidence-based reviews (ACCP/AACVPR, 1997) noted the benefits of lower-extremity training and have suggested its inclusion in all rehabilitation programs.

However, the frequency, intensity, and duration of exercise are suggested as individualized but exercise should be performed at submaximal work capacity. Intensity may be increased every fifth session and it should last a minimum of 30 minutes per session. By the end of the program, exercise duration should increase to an hour per session (Puhan MA, 2005).

One research focused on high-intensity exercise carried out at 60% to 80% of the patient’s maximum workload, significant physiological training effects were noted. These included increase in maximum oxygen consumption, a delay in reaching the anaerobic threshold, a decrease in heart rate, and an increase in the skeletal muscles’ oxidative capacity (Casaburi, 1991). It should be noted, however, that patients in this study had moderate COPD; results may not be applicable to patients with severe COPD.

Upper-Extremity Training

Sivori (1998) suggested that upper-extremity training may be used for patients with COPD, This can be conducted using either a supported modality such as an arm ergometer or an unsupported modality such as dowels and weights. Upper-extremity training improves arm endurance and strength, increase sense of well-being, and reduce metabolic demands of arm movement (Sivori 1998).

It is of note that some patients may experience more dyspnea during arm exercise than during leg exercise at a comparable level. Likewise, unsupported arm exercise involving eight to 10 repetitions for a total of 30 minutes per session results in decreased dyspnea cases and improve health-related quality of life as compared to those produced by high-intensity lower-extremity training (Normandin EA, 2002).

Respiratory-Muscle Training

Controversies exists with regards to the effects of respiratory-muscle training for patients with COPD. Some guidelines provide that respiratory-muscle training should be used for certain patients with COPD, particularly those who exhibit respiratory-muscle weakness (Casaburi, 1991). A study by Sturdy (2003) evaluated a protocol of 2 minutes of training at 70% of maximal inspiratory pressure (measured using a handheld breathing valve) followed by 1 minute of rest, repeated six times, showed that respiratory-muscle training can be used successfully as part of a comprehensive pulmonary rehabilitation program, Aside from tolerable, the therapy improved respiratory-muscle strength and endurance, whole-body exercise capacity, and quality of life.

Maintenance

There had been found beneficial effects of exercise training for patients who complete comprehensive pulmonary rehabilitation programs. Guell (2000) found the beneficial effects of lower-extremity training continuing up to 2 years if the patient is active in maintenance program. The program recommends a weekly patient contact with the training staff and monthly supervised exercise. Weiner’s study (2004) of inspiratory respiratory-muscle training showed that continued training over a one-year period resulted in increased inspiratory-muscle strength, inspiratory-muscle endurance, and distance walked.

It is obvious that maintaining exercise training improves muscular performance because, depending on the training program, strength, endurance, or both improve (McComas AJ, 1996). In general, maintaining endurance training leads to increased percentages of type I and IIa fibers accompanied with greater oxidative capacity, resulting in higher fatigue resistance (McComas AJ, 1996). Therefore, considering that fatigue is the main limiting factor in peripheral muscle performance, maintaining endurance training protocol may be most suitable for improving the exercise capacity of limb muscles in COPD patients. This is also illustrated by the fact that in COPD patients, maintaining quadriceps endurance training shows a larger improvement with training than does strength (O’Donnell DE, 1998). Maintaining regular physical exercise involves a regular increase in exposure of muscle tissue to oxygen and training thus probably reduces the risk of oxidative stress (Sen CK, 1994).

The common complaints amongst COPD patients include dyspnoea, less exercise tolerance and reduced quality of life. While medication may improve pulmonary function in COPD, it does not necessarily affect positive exercise capacity (Grove A, 1996). Peripheral muscle weakness, deconditioning and impaired gas exchange also reduce exercise tolerance (Gosselink R, 1996).

Exercise intolerance appear important to COPD patients as it leads to muscle weakness and may disable patients with a high utilization of healthcare resources (Decramer M, 1997). Quality of life suffers as they avoid work due to the disease and become isolated. An alarming addition is that poor exercise capacity contribute to early mortality (Decramer M, 1997).

Pulmonary rehabilitation programmes aim at reversing the negative impacts of COPD to improve exercise capacity, activities of daily living, quality of life and even survival. Comprehensive and flexible programmes are advised to address each patient’s needs and should include smoking cessation, optimal medical treatment, exercise training, breathing exercises, nutritional intervention, psychosocial support and health education (Donner CF, 1997).

Exercise training is considered an important part of the treatment but the best methods of exercise training are still debated (Donner CF, 1997).

Conclusion

Skeletal muscle dysfunction, common in patients with COPD, plays vital role in limiting exercise performance. While its importance cannot be ignored, individualized programmes that address to improving muscle endurance, exercise tolerance and quality of living must be recommended and applied to COPD patients to halt their debilitating situation.

Together with medication, an effective pulmonary rehabilitation program cannot delete the consequences of COPD to an individual and the health team or family working with them but it could help arrest or even improve a less desirable living condition.

Exercise is vital in rehabilitation and may involve lower extremities, the upper extremities, and the respiratory muscles. This improves skeletal muscle function, enhance endurance, improve quality of life, and lessen the level of dyspnea for patients with COPD. As mentioned earlier, the ideal training regimen is yet to be fully defined but a regular, sustained exercise program should be part of the comprehensive therapy for patients with COPD.

Various researchers have defined the mechanisms of the dysfunction, investigate the consequences, quantify the dysfunction, and some tried to reverse skeletal muscle dysfunction. Nevertheless, there is a need for further investigation and experimentation to refine the mechanisms of skeletal dysfunction and the consequences for exercise performance. Likewise, more insight in clinical tools to diagnose skeletal dysfunction and establish treatment modalities to reverse or to prevent skeletal muscle dysfunction in COPD is still needed.

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