Guillain-Barré syndrome (GBS) is the most common cause of acutely evolving motor and sensory deficits.1 By definition, GBS is an acute inflammatory demyelinating polyradiculoneuropathy that affects nerve roots and peripheral nerves leading to motor neuropathy and flaccid paralysis.1 This syndrome can affect people of all ages, but it is most prevalent in young adults and in persons in their fifth through eighth decades.1 The incidence of GBS is one to two cases per 100,000.1,2 In classic GBS, the time from onset to peak impairment is four weeks or less, but a recurrent form is reported in up to 10% of GBS cases. Additionally, a chronic form of GBS exists and is known as chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). The distinguishing feature of CIDP is the development of symptoms over eight weeks or longer.3 The incidence of CIDP is 0.8-1.9 cases per 100,000.3
Although the direct cause of GBS is unknown, it is reported that 73% of patients have a preceding illness.2 In 55% of patients, it is reported that pain precedes or exists early in the onset of GBS.2 The disease is characterized by ascending symmetric motor weakness progressing from the distal to proximal lower extremities, upper extremities, trunk, and face. Symptoms required for diagnosis of GBS are progressive weakness in more than one extremity and loss of deep tendon reflexes (DTRs).1 Symptoms supportive of diagnosis are presented in Table 1. Distal sensory impairments are common and can include hyperesthesia, paresthesia, numbness, and/or decreased vibratory or position sense, but these are not progressive or persistent.2 Additionally, 50% of patients will have cranial nerve involvement, 50% will have autonomic nervous system symptoms, and up to 30% of cases will require mechanical ventilation.1,2 Approximately 40% of patients who are hospitalized with GBS will require admission to an inpatient rehabilitation facility.4
The pathogenesis of GBS involves antibody-mediated demyelination, with myelin of Schwann cells as the primary target of attack. Lesions occur throughout the peripheral nervous system from the spinal nerve roots to the distal termination of both motor and sensory fibers. The earliest pathologic change in the peripheral nervous system is a generalized inflammatory response. Macrophages responding to the inflammatory signals initiate demyelination at the node of Ranvier. As products liberated by the macrophages strip the myelin, some degree of axonal degeneration occurs in most cases.1 Within two or three weeks of acute demyelinization, Schwann cells proliferate, inflammation resolves, and remyelinization begins.2
Management of GBS involves treatment of symptoms and prevention of secondary complications. Although rehabilitation is advocated for patients with GBS and CIDP, there is little evidence to support specific physical therapy (PT) interventions. Medical management for GBS and CIDP may include plasmapheresis, high-dose intravenous administration of immunoglobulin (IVIg), or corticosteroids.
Plasmapheresis involves the removal of plasma from circulation and filtering it to remove or dilute circulating antibodies. An investigation of plasmapheresis in GBS concluded that the time for patients to return to independent walking was less with plasmapheresis (53 days) compared with an untreated group (85 days).5 The treatment effect was stronger for patients treated within first week and for those with more severe disease.5 Additionally, plasma exchange begun later than two weeks into the illness did not result in any clear benefit to the patient.5
IVIg protein is normally used by the immune system to attack foreign organisms; thus, high-dose intravenous administration of IVIg is also thought to be effective in treating GBS. A randomized, controlled trial comparing IVIg and plasmapheresis treatments in GBS patients showed IVIg to be at least as effective as plasma exchange, with a lower incidence of complications.6
Because of the inflammatory nature of GBS, it would be expected that corticosteroids would be beneficial in treatment. However, substantial evidence shows that corticosteroids alone do not produce significant benefit or harm in the treatment of GBS.7 Nevertheless, corticosteroids may hasten GBS recovery when used in combination with IVIg treatment.7 Additionally, corticosteroids have been shown to be effective in the treatment of CIDP.3,8
This report presents the case of a 30-year-old male marathon runner who had a somewhat atypical presentation of acutely evolving motor and sensory deficits. Both GBS and CIDP were considered as diagnoses, and medical treatment included a combination of IVIg, plasmapheresis, and corticosteroids. Despite the uncertainty of prognosis and a relapse in function during the course of his care, this patient achieved a remarkable return to function. The focus of this case report is to describe the PT examination, intervention, and outcomes.
The patient was a 30-year-old male with no significant medical history. He was employed as a sales representative for a computer storage firm. He reported that he was training for a marathon during the time in which his symptoms began. This patient was of interest for this case report because he had an above-average preexisting level of fitness. He experienced a significant decline in function as a result of an atypical presentation and course of GBS. Despite a prolonged course from the onset of symptoms to maximal impairment, the patient was able to make a remarkable functional recovery during his course of acute rehabilitation and was able to return to running within six months of the initial onset of symptoms.
The patient reported an initial onset of flulike symptoms during a vacation out of state. This was followed one to two weeks later by the onset of severe myalgias and arthralgias in the legs and unexplained fatigue. The patient sought care from both the emergency department and his primary care physician, undergoing many tests to determine the cause of his illness. The patient was given a diagnosis of GBS one month after the initial onset of symptoms, at which time he was unable to heel or toe walk, felt very fatigued, and had experienced a 15-lb weight loss. He was admitted to the hospital for IVIg treatment one week later, at which time he was experiencing difficulty walking. After a week of inpatient treatment, his mobility improved, and he was transferred to acute rehabilitation. Upon admission to acute rehabilitation, the patient experienced a progression to severe weakness that required inpatient readmission for plasmapheresis and corticosteroid treatment. At this time, the diagnosis of CIDP was considered, and the prognosis for return of function was uncertain. After three weeks in inpatient care, the patient was readmitted to the acute rehabilitation unit with stabilizing condition and improving function. A timeline of these events as obtained through hospital chart review is presented in Table 2.
At the time of the initial interview, it had been 10 weeks since the patient’s initial onset of flulike symptoms. The patient was unable to walk, required moderate assistance for bathing and dressing, and required minimal assistance for grooming, toileting, and transfers. His goals for his stay in acute rehabilitation were to return to living independently and hopefully to return to walking.
At the time of the initial interview, the patient denied current fever, chills, or sweating, and his vital signs were stable. He reported a 20- to 30-lb weight loss since the onset of disease but had already consulted with a staff nutritionist. He also reported weakness and fatigue related to the GBS. His cardiopulmonary examination was unremarkable, and he denied chest pain or shortness of breath. He showed good skin color and no signs of redness or swelling, and no scars or incisions were noted. It was evident that the patient’s musculoskeletal system required further investigation, as difficulty with bed mobility, feeding, and transfers were observed, and he was unable to stand or ambulate. His neuromuscular system also required further examination, as DTRs were absent for patellar tendon and Achilles tendon reflexes. In terms of psychosocial and cognitive systems, the patient was alert and oriented, had good out-of-town family support, and showed excellent knowledge of his illness and motivation to participate in rehabilitation.
Functional mobility was assessed using the Functional Independence Measure (FIM). The FIM has well-established reliability9–11 and is valid in a variety of populations.12–15 The FIM has been shown to be sufficiently sensitive in detecting disability and change over time during rehabilitation of GBS patients.16 At initial examination, the patient’s FIM score was 80/126, with a motor subscore was 45/91 (refer to Figure 1 for the complete FIM). Observation revealed that the patient required supervision with bed mobility tasks of sit to supine and supine to sit. In transferring from bed to wheelchair, the patient required supervision and set up for placement when using a slideboard and required minimal assistance without the slideboard. He was unable to ambulate but was able to propel a wheelchair 30 feet with modified independence. The patient reported fatigue with this task.
Muscle performance was assessed using manual muscle testing (MMT). This method has been shown to be reliable in a variety of populations.17–19 MMT revealed significant symmetrical weakness, with distal muscle groups more affected than proximal muscles (Table 3). It was also noted that the patient substituted trunk and shoulder muscles for upper extremity muscles to perform functional activities. For example, he used his abdominals for supine-to-sit activities because of triceps weakness.
Neurologic testing involved a gross assessment of coordination, in which both rapid alternating movement and heel-to-shin movements were found to be intact. Dermatome sensory testing for light touch revealed that sensation was impaired in a glove-and-stocking pattern. DTRs were assessed as these are criteria for the diagnosis of GBS and are a highly reproducible measure.20 At initial evaluation, the patient’s DTRs were 1+ for bilateral biceps and brachioradialis and trace for bilateral triceps. Patellar and Achilles DTRs were absent.
Evaluation and Diagnosis
From a rehabilitation perspective, the synthesis of physical findings was as follows: the patient presents with inability to participate in work and recreational activities and requires assistance with mobility, dressing, and transfers because of severe upper and lower extremity weakness from an inflammatory demyelinating polyneuropathy. This was consistent with Practice Pattern 5G; impaired motor function and sensory integrity associated with acute or chronic polyneuropathies.21
The prognosis, anticipated goals, and expected outcomes for this patient were uncertain as a result of the ambiguity of diagnosis. According to hospital records, the patient’s medical diagnosis was most often listed as GBS, but the diagnosis of CIDP was also recorded on several occasions. With CIDP, there is a poorer prognosis for the complete return of function than with GBS.
GBS has a mortality rate of 5%.22 In 50% of cases, progression ceases in two weeks, and in 90% of cases, progression ceases in four weeks.1 Recovery can take months to years, and 50% of patients have remaining minor neurologic deficits such as diminished or absent DTRs. Persistent residual deficits that have significant effect on function are present in 15% of patients, with the most common long-term deficits being weakness of anterior tibialis musculature and less often weakness of intrinsics in foot and hand, quadriceps, and gluteal muscles.2 However, it is reported that 80% of patients with GBS are ambulatory within six months of the initial onset of symptoms.2,22
Factors that predict a poor outcome include the need for mechanical ventilation, onset at an older age, and significantly reduced evoked motor potential amplitude.23,24 Mechanical ventilation and older age are not applicable in this patient’s case. However, electromyographic studies conducted seven weeks after the onset of symptoms indicated a reduction in peroneal motor amplitudes, which suggested some degree of superimposed axonal injury. It was expected that this may contribute to a poorer functional prognosis for the patient.
It is unclear whether time to peak impairment or a protracted time before recovery begins are poor prognostic indicators. A recent study found a strong negative correlation between the duration of both acute and plateau phases of GBS and muscle force recovery slope.25 Because this patient had a prolonged acute phase, it was expected that muscle force recovery rate may be slow. However, a study of rehabilitation outcomes in GBS found that while the length of acute care is longer with a prolonged time to peak impairment, the length of rehabilitation stay was not significantly affected by the time to reach the disease nadir.26
An additional consideration in the prognosis was the patient’s extremely high level of previous function. His experience as a marathon runner increased his motivation and ability to participate in rehabilitation and therefore gave him higher expectations for recovery.
Plan of Care
In accordance with the protocols for the acute rehabilitation facility, the patient was treated with a total of 18 hours of therapy per week. This included one hour each daily of PT, occupational therapy, and group activity led by a physical or occupational therapist. During the course of his three-week stay, the patient was actively involved in all scheduled therapy sessions and never failed to meet total weekly hour requirements.
The patient’s goals for acute rehabilitation were to return to living independently, prepare for return to work, and to eventually return to walking. Short-term goals (one week) were for the patient to tolerate three hours of activity per day to meet the standards of the acute rehabilitation facility, to transfer independently from the bed to the wheelchair and from the wheelchair to the toilet using the slideboard to facilitate independence with toileting and to propel the wheelchair independently 300 feet to attend therapy sessions. Long-term goals (four weeks) for the patient were to ascend and descend four steps using the least restrictive assistive device to safely enter and exit his home at time of discharge, to ambulate safely 50 feet using the least restrictive assistive device to have independent household mobility, and to tolerate six hours of activity per day to prepare for return to work in computer sales.
The PT intervention involved a progressive program of functional exercise while monitoring for overuse and fatigue.2 It is understood that strengthening attained is proportional to number of intact motor units.27 Thus, advances in strength were expected to be limited by the level of existing damage in the motor system. As recommended for peripheral neuropathy conditions, increases in activity or exercise level were implemented only if there was improvement or no decline after one week at a given intensity.28
With the volatility of the disease and the potential for excessive fatigue, exercises were directed at strengthening for function rather than strength itself.28 Activities were progressed from passive range of motion, to gravity-eliminated active range of motion (AROM), to antigravity AROM, to resisted exercise in functional patterns for the upper extremity, lower extremity, and trunk. Exercises were performed with low volume, typically five to 10 repetitions, and always terminated before the patient reported fatigue. Frequent rest periods were provided, and the patient’s response to exercise was consistently monitored for shortness of breath or other signs of fatigue. A typical 60-minute therapy session is outlined in Appendix A.
Functional activity progression was focused toward independent mobility, with the ultimate goal of living in a home that had four stairs to enter and traveling to and from work. Mobility and transfer activities were addressed concurrently in treatment sessions.
Over the three-week acute rehabilitation stay, transfer activities progressed from supervised slideboard transfers to modified independent lateral transfers without the use of a slideboard, to standing pivot transfers using a walker, to standing pivot transfers without use of the walker. Transfer activities also involved sit to stand from varying surfaces, vehicle transfers, and floor recovery.
Mobility activities involved wheelchair propulsion on varied surfaces and gait with progressively decreased reliance on assistive devices. Week 1 mobility activities included wheelchair propulsion of 30-100 feet using the upper and lower extremities, use of a standing frame with weight shifting, and walking six steps in the parallel bars wearing bilateral ankle-foot orthoses (AFOs). During week 2, mobility activities progressed to wheelchair propulsion of 200 feet using the upper extremities, walking four to six feet forward and backward in the parallel bars wearing bilateral AFOs, and walking 30-125 feet with a front-wheeled walker and bilateral AFOs. By week 3, gait training included walking 50-250 feet using a front-wheeled walker and bilateral AFOs, walking 40 feet in the parallel bars without AFOs, walking 50 feet using forearm crutches and bilateral AFOs, ascending and descending four to 12 stairs using a handrail and wearing AFOs, and ambulating over grass, uneven sidewalks, ramps, and curbs with front-wheeled walker and bilateral AFOs.
Functional mobility improved significantly over the course of the acute rehabilitation stay. At the time of discharge, the patient’s FIM score was 113/126, with a motor subscore of 78/91 (refer to Figure 1 for the complete FIM). Observation revealed that the patient was independent with all bed mobility tasks. He was able to transfer with modified independence to and from sit to stand and to and from a wheelchair and could perform floor recovery with stand by assist. The patient could independently propel a wheelchair 500 feet using the upper extremities. He was able to ambulate 250 feet using a front-wheeled walker and bilateral AFOs and could negotiate curbs, stairs, ramps, and uneven surfaces. The patient was also able to ascend and descend 12 stairs using one handrail and wearing bilateral AFOs.
Muscle performance also improved considerably, although distal muscle groups continued to be more affected than proximal muscles (Table 4). The patient continued to have strength gains after discharge from acute rehabilitation, as evidenced by improved MMT scores in all lower extremity muscle groups at the time of discharge from outpatient therapy (Table 4). The emphasis of PT treatment in the acute rehabilitation and outpatient settings was on the lower extremities; thus, strength data are presented accordingly.
Light touch remained impaired in a glove-and-stocking pattern, although the patient reported this to be less noticeable than before. DTRs in the lower extremities were trace to 1+ in patellar tendons and absent in Achilles tendons.
At nearly three months after the initial onset of symptoms, the patient was independent in functional mobility activities with the use of bilateral AFOs and a front-wheeled walker. He continued PT on an outpatient basis for the next two months to address persistent distal weakness and decreased endurance to activity. Outpatient discharge reports indicated that the patient was able to ambulate 45 minutes without an assistive device before fatigue. A follow-up phone call to the patient six months after the initial onset of symptoms revealed that he was ambulating functional community distances without any assistive device, living independently at home, driving a car, and beginning to return to jogging.
The focus of this case report was to describe the PT examination, intervention, and outcome in an atypical presentation of GBS. The patient in this case was never given a definitive diagnosis for his illness. His onset to maximum impairment was longer than the four-week period typically seen with GBS; thus, CIDP was considered. However, it is reported that 8%-16% of patients with GBS have one or more deteriorations after initial improvement or stabilization after treatment with plasma exchange or IVIg.29 A retrospective study by Ruts et al29 found these treatment-related fluctuations in GBS to occur within 11 weeks of the onset of disease. Interestingly, in a study of seven adult patients with GBS who were given IVIg for their initial treatment, five deteriorated one to 16 days after treatment, and relapse rates of 2%-26% were reported with plasma exchange.30 Acute-onset CIDP patients were also found to have exacerbations resulting in deterioration of function; however, 92% of these occurred more than nine weeks after the onset of symptoms.29 Odaka et al31 studied 663 patients initially with a diagnosis of GBS and found that 13 had a relapse within eight weeks of initial treatment and were later given a diagnosis of CIDP. The clinical course of eight of the 13 patients who received maintenance treatment showed remission after six to 12 months with no further deterioration, two recovered slowly after six months, and the other three had relapses after six to 10 months.
The patient in this case report experienced a decline in function seven weeks after his initial onset of symptoms. Because he was medically treated with a combination of IVIg, plasma exchange, and corticosteroids, it is difficult to discern what aspects of his relapse and his subsequent return to function were related to medical treatment. It is also difficult to determine the role that PT interventions may have played in the relapse and subsequent return to function.
Given the uncertainty of diagnosis and the episode of deterioration in function, it was also difficult to predict the potential functional outcomes with rehabilitation for this patient. Full recovery was not expected at the time of discharge from acute rehabilitation, as 50% of patients with GBS have remaining minor neurologic deficits and 15% have persistent residual deficits in function.2 As anticipated, the patient had residual weakness in his distal musculature. However, the patient showed rapid improvement in muscle performance and FIM scores over his three-week stay and had not reached a plateau in muscle performance or functional performance by the time of his discharge. Additionally, the patient was able to ambulate somewhat sooner than predicted, considering that only 80% of GBS patients are ambulatory within six months of the onset of symptoms.2
Throughout his rehabilitation, the patient’s exercise intensity was moderated to avoid fatigue. A limitation to this case report is the lack of objective measurement of fatigue. Because the patient was a marathon runner, he had excellent awareness of his body’s response to exercise; thus, self-reported fatigue was used to determine the intensity and duration of exercise. However, it is unknown whether he pushed himself past fatigue at times in hopes of a quicker recovery or if his previous level of conditioning enabled him to work harder before feeling fatigued. Specific guidelines for PT interventions involving patients with GBS have not been examined in the literature. However, recent studies involving other neuromuscular conditions have demonstrated benefits of moderate to intense therapeutic exercise with no deleterious effects. A recent study involving adults with multiple sclerosis concluded that a progressive resistance exercise program led to improved muscle performance and physical activities without adverse events.32 In a randomized, controlled trial of strength training in postpolio patients, it was found that progressive resistance training did not adversely affect motor unit survival and that the magnitude of strength gains was greater than that seen in a healthy elderly control group.33 Although the mechanisms for disease progression are different for GBS, patients with GBS may also benefit from an increased intensity of exercise without detrimental consequences. The patient’s previous level of physical activity and motivation to regain his previous level of function facilitated a more aggressive progression of exercise intensity that may have positively influenced his functional outcomes. However, further research using objective measures of fatigue is needed to determine the optimal training intensity and frequency of exercise in rehabilitation of this patient population and whether progressive resistance training has any detrimental effects on physical recovery after GBS.
1. Goodman CC, Fuller KS, Boissonnault WG. Pathology: Implications for the Physical Therapist.
2nd ed. Philadelphia, PA: Saunders; 2003.
2. Umphred DA. Neurological Rehabilitation.
4th ed. St. Louis, MO: Mosby; 2001.
3. Lewis RA. Chronic inflammatory demyelinating polyradiculoneuropathy. emedicine.com WebMD
4. Meythaler JM. Rehabilitation of Guillain-Barre syndrome. Arch Phys Med Rehabil.
5. Plasmapheresis and acute Guillain-Barre syndrome. The Guillain-Barre Syndrome Study Group. Neurology.
6. Bril V, Ilse WK, Pearce R, et al. Pilot trial of immunoglobulin versus plasma exchange in patients with Guillain-Barre syndrome. Neurology.
7. Hughes RA, Swan AV, van Koningsveld R, et al. Corticosteroids for Guillain-Barre syndrome. Cochrane Database Syst Rev.
8. Rentzos M, Anyfanti C, Kaponi A, et al. Chronic inflammatory demyelinating polyneuropathy: a 6-year retrospective clinical study of a hospital-based population. J Clin Neurosci.
9. Ottenbacher KJ, Hsu Y, Granger CV, et al. The reliability of the functional independence measure: a quantitative review. Arch Phys Med Rehabil.
10. Roth E, Davidoff G, Haughton J, et al. Functional assessment in spinal cord injury: a comparison of the Modified Barthel Index and the ‘adapted’ Functional Independence Measure. Clin Rehabil.
11. Stineman MG, Shea JA, Jette A, et al. The Functional Independence Measure: tests of scaling assumptions, structure, and reliability across 20 diverse impairment categories. Arch Phys Med Rehabil.
12. Corrigan JD, Smith-Knapp K, Granger CV. Validity of the functional independence measure for persons with traumatic brain injury. Arch Phys Med Rehabil.
13. Granger CV, Deutsch A, Linn RT. Rasch analysis of the Functional Independence Measure (FIM) Mastery Test. Arch Phys Med Rehabil.
14. Pollak N, Rheault W, Stoecker JL. Reliability and validity of the FIM for persons aged 80 years and above from a multilevel continuing care retirement community. Arch Phys Med Rehabil.
15. Whiteneck GG. A Functional Independence Measure trial in SCI model systems. Paper presented at: ASIA Proceedings, 1982.
16. Prasad R, Hellawell DJ, Pentland B. Usefulness of the Functional Independence Measure (FIM), its subscales and individual items as outcome measures in Guillain Barre syndrome. Int J Rehabil Res.
17. Mayhew JE, Florence JM, Mayhew TP, et al. Reliable surrogate outcome measures in multicenter clinical trials of Duchenne muscular dystrophy. Muscle Nerve.
18. Ottenbacher KJ, Branch LG, Ray L, et al. The reliability of upper- and lower-extremity strength testing in a community survey of older adults. Arch Phys Med Rehabil.
19. Pollard H, Lakay B, Tucker F, et al. Interexaminer reliability of the deltoid and psoas muscle test. J Manipulative Physiol Ther.
20. McCombe PF, Fairbank JC, Cockersole BC, et al. Volvo Award in clinical sciences. Reproducibility of physical signs in low-back pain. Spine.
21. APTA. Guide to Physical Therapist Practice.
American Physical Therapy Association; 2001.
22. Ropper AH. The Guillain-Barre syndrome. N Engl J Med.
23. Dhar R, Stitt L, Hahn AF. The morbidity and outcome of patients with Guillain-Barre syndrome admitted to the intensive care unit. J Neurol Sci.
24. McKhann GM. Guillain-Barre syndrome: clinical and therapeutic observations. Ann Neurol.
25. El Mhandi L, Calmels P, Camdessanche JP, et al. Muscle strength recovery in treated Guillain-Barre syndrome: a prospective study for the first 18 months after onset. Am J Phys Med Rehabil.
26. Meythaler JM, DeVivo MJ, Braswell WC. Rehabilitation outcomes of patients who have developed Guillain-Barre syndrome. Am J Phys Med Rehabil.
27. Herbison GJ, Jaweed MM, Ditunno JF Jr. Exercise therapies in peripheral neuropathies. Arch Phys Med Rehabil.
28. Bensman A. Strenuous exercise may impair muscle function in Guillain-Barre patients. JAMA.
29. Ruts L, van Koningsveld R, van Doorn PA. Distinguishing acute-onset CIDP from Guillain-Barre syndrome with treatment related fluctuations. Neurology.
30. Irani DN, Cornblath DR, Chaudhry V, et al. Relapse in Guillain-Barre syndrome after treatment with human immune globulin. Neurology.
31. Odaka M, Yuki N, Hirata K. Patients with chronic inflammatory demyelinating polyneuropathy initially diagnosed as Guillain-Barre syndrome. J Neurol.
32. Taylor NF, Dodd KJ, Prasad D, et al. Progressive resistance exercise for people with multiple sclerosis. Disabil Rehabil.
33. Chan KM, Amirjani N, Sumrain M, et al. Randomized-controlled trial of strength training in post-polio patients. Muscle Nerve.
Sample PT Session
Exercise session during week 2 of acute rehabilitation stay
* Warm-up/cardiovascular training○ Lower extremity stationary cycling—six minutes▪ Three minutes forward▪ Three minutes backward
* Pregait activities○ Standing knee bend in parallel bars—one set of 10 repetitions○ Lateral weight shifts in parallel bars—one set of 10 repetitions○ Ambulate four feet in parallel bars with bilateral AFOs and PT assistance to block knees as needed
* Transfer activities○ Sit to stand in parallel bars—two sets of five repetitions○ Stand to sit in parallel bars—two sets of five repetitions