**2. Link between segmental spinal stability and upright sagittal spinal motor control on Earth**

Non-specific LBP is experienced in the lower region of the spine and is not attributable to a known cause or specific pathology such as infection, systemic disease, fracture or cauda equina syndrome [8]. Non-specific LBP is often multifactorial in its origin; this makes it complex to treat. Panjabi [9] was one of the first to recognise that abnormal spinal mechanics may be a common factor in people with back pain. He identified several potential triggers and causes of abnormal mechanics, including inflammation, biochemical and nutritional changes, immunological factors, structural changes in discs and endplates.

Atrophy [4, 10–13] and altered motor control [4] of the LM and TrA muscles are linked with the common symptom of altered mechanics. Both muscles have a substantial body of evidence linking their dysfunction and atrophy with LBP on Earth [4, 6, 14–18]. Similar patterns of muscle atrophy and LBP have also been observed in those who are exposed to microgravity [5, 6, 19, 20].

#### **2.1. Deep and superficial lumbopelvic muscles in spinal stability**

The paraspinal muscles can be divided into deep and superficial muscles based on a structural model of the spine presented by Bergmark [21] who provided the following definitions. **Deep muscles** have their origin and/or insertion at the vertebrae and have an action that includes controlling the curvature and/or structural stiffness of spine. Deep muscles include the LM and TrA muscles. The LM muscle controls and stabilises lumbar lordosis [22] during force transfer through the spine [23, 24] and provides segmental stiffness [25, 26]. The TrA muscle provides a transverse force, therefore increasing stiffness and extrinsic stability of the spine [4] by increasing intra-abdominal pressure [14, 27]. **Superficial muscles** control the large spinal movements and transfer loads between the thorax and pelvis, they do not directly increase stiffness or stability of the spine at a segmental level [21] but can increase global trunk stiffness [28]. Superficial muscles include erector spinae, the internal and external oblique muscles, rectus abdominis, quadratus lumborum and psoas.

Bergmark [21] also defined stability in engineering terms as the ability of a structure to maintain its equilibrium under loading. This definition was extended to define clinical spinal stability as the ability of the spine, under physiological loads, to limit structural displacement so as to prevent damage to spinal structures including the discs, ligaments and neural structures. The spine gains passive stability from bones, ligaments, tendons and fascia, while it was suggested that active stability is provided by deep muscles [21]. Studies using in vitro cadaveric specimens of human spinal segments found that the specimens became mechanically unstable at loads much less than those experienced by in vivo spines [25]. This finding highlighted the importance of the stabilising force provided by the LM and TrA muscles in allowing the spine to function under everyday loading.

### **2.2. Spinal stabilising system and motor control**

and transversus abdominis (TrA) muscles, resulting from periods of deconditioning, are linked to non-specific LBP and spinal injury risk in both post-flight astronauts and general populations [3–6]. However, voluntary recruitment of these two key muscles is difficult and

This chapter discusses the key factors contributing to lumbopelvic deconditioning in spaceflight and shows how exercise countermeasures against deconditioning can be developed to

Non-specific LBP is experienced in the lower region of the spine and is not attributable to a known cause or specific pathology such as infection, systemic disease, fracture or cauda equina syndrome [8]. Non-specific LBP is often multifactorial in its origin; this makes it complex to treat. Panjabi [9] was one of the first to recognise that abnormal spinal mechanics may be a common factor in people with back pain. He identified several potential triggers and causes of abnormal mechanics, including inflammation, biochemical and nutritional changes,

Atrophy [4, 10–13] and altered motor control [4] of the LM and TrA muscles are linked with the common symptom of altered mechanics. Both muscles have a substantial body of evidence linking their dysfunction and atrophy with LBP on Earth [4, 6, 14–18]. Similar patterns of muscle atrophy and LBP have also been observed in those who are exposed to microgravity

The paraspinal muscles can be divided into deep and superficial muscles based on a structural model of the spine presented by Bergmark [21] who provided the following definitions. **Deep muscles** have their origin and/or insertion at the vertebrae and have an action that includes controlling the curvature and/or structural stiffness of spine. Deep muscles include the LM and TrA muscles. The LM muscle controls and stabilises lumbar lordosis [22] during force transfer through the spine [23, 24] and provides segmental stiffness [25, 26]. The TrA muscle provides a transverse force, therefore increasing stiffness and extrinsic stability of the spine [4] by increasing intra-abdominal pressure [14, 27]. **Superficial muscles** control the large spinal movements and transfer loads between the thorax and pelvis, they do not directly increase stiffness or stability of the spine at a segmental level [21] but can increase global trunk stiffness [28]. Superficial muscles include erector spinae, the internal and external oblique

Bergmark [21] also defined stability in engineering terms as the ability of a structure to maintain its equilibrium under loading. This definition was extended to define clinical spinal

**2. Link between segmental spinal stability and upright sagittal** 

immunological factors, structural changes in discs and endplates.

**2.1. Deep and superficial lumbopelvic muscles in spinal stability**

muscles, rectus abdominis, quadratus lumborum and psoas.

presents a rehabilitation challenge [7].

**spinal motor control on Earth**

[5, 6, 19, 20].

aid both astronauts and people on Earth with LBP.

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To achieve spinal stability, the deep muscles must be controlled by precise coordination of activation and timing. The complete spinal stabilising system was, therefore, conceptualised by Panjabi [29] as having a neural control element, a passive spinal column (and ligaments) and an active system of deep muscles. The control system assesses and directs the deep muscles to provide varying levels of extrinsic stability while the passive elements of the spinal column provide intrinsic stability. To successfully provide control, actions are based on feedback from both the active and passive components. Mechanoreceptors in the passive structures indicate levels of force and stress, while feedback on muscle activation patterns and stretch are provided by the active system. In addition to the muscle feedback system, there is now strong evidence that LM and TrA are ideally activated in a feedforward mechanism, that is, they act in anticipation of changing loads. Importantly, the dysfunction of this feedforward control system has been linked with LBP [28].

#### **2.3. Segmental stability and the neutral zone**

During dynamic loads into spinal flexion and extension, there is displacement of each vertebra, which allows flexibility. At low loads, the spine was observed to be highly flexible and then stiffening as loads increased. A neutral zone was defined as the range of segmental displacement within which there is a minimal resistance to the displacement [29]. This is represented graphically in **Figure 1** with the neutral zone being represented by a ball in a bowl. The motion of the ball represents the displacement motion of the vertebral segment, while the steepness of the sides represents varying stability with steeper sides demonstrating increased resistance to displacement. As segmental spinal stability increases, the neutral zone becomes smaller, demonstrated by placing the ball in a wine glass. As segmental spinal stability decreases, the neutral zone gets larger, demonstrated by placing the ball in a flat bowl (**Figure 1**).

It was hypothesised that decreased stability may be caused either by damage to the passive stability system and/or abnormal activity or control of the active system that leads to a larger neutral zone [29]. An increase in the neutral zone is likely to be associated with increased stress on spinal structures so, it results in pain. Therefore, interventions were suggested for unstable painful spines which aimed at reducing the neutral zone through retraining control of the active stability system or through the use of spinal fusion [29].

which found reduced cross-sectional area of LM in the lower lumbar spine. In the study, 32 clinical participants were compared with 23 matched no-LBP volunteers, and the LM crosssectional area was measured using CT scans. A study in pigs by Hodges et al. [12] found that induced L4 spinal disc lesions resulted in LM cross-sectional area decreases at the same level of the injury within 3 days, compared to no change in no-LBP controls. Injury to the L3 nerve root resulted in LM cross-sectional area reduction at the affected level and down to L4, L5 and S1 levels in 15 induced injury pigs compared to six controls. The controls were, however, still subjected to a sham surgical procedure that involved all the same steps as the injured pigs apart from the inducing of the injury. A comparison study by Hides et al. [3] of 26 first episode acute unilateral low back pain patients with 51 healthy controls, found that LM asymmetry in the people with back pain, isolated to the symptomatic level compared to symmetrical LM muscles in the no-LBP controls. A comparison study by Hodges and Richardson [4] of 15 LBP patients with 15 no-LBP matched controls used electromyography to assess the activation and timing of TrA in response to upper limb movements. It was observed that TrA activation was consistently delayed in the people with back pain. A comparison study by Ferreira and Hodges [13], in which 10 low back pain patients compared with 10 healthy matched controls, found consistently reduced changes in TrA thickness in their group with back pain during lower limb

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While Panjabi's theories were seminal to improve our understanding of lumbopelvic pain, they missed one important factor, and that is the fact that, unlike the feedback control of many superficial muscles, there is a feedforward control of the deep spinal muscles LM [24, 30] and TrA [31, 32]. In other words, the LM and TrA muscles work in anticipation of loads and movements, not in response to them, thus, providing spinal stability. Importantly, there has also been evidence that the anticipatory activation of the deep spinal muscles is impaired in people with LBP compared to non-symptomatic controls [4, 31, 33] and that this is reversible with certain exercise approaches [34]. Based on a considerable body of literature, key authors in the field [16, 35] also suggest that secondary compensatory postural mechanisms are likely to contribute further to LBP, which would go some way towards explaining chronic LBP in the face of minimal tissue abnormality. It should be noted that the studies used to have small

Astronauts returning from long-duration space missions (~6-months duration) [36] and participants following long-duration bed rest studies, which are commonly used to simulate microgravity exposure [37], have a range of muscular and postural problems. Human spaceflight results in exposure to an altered gravity state, mostly eliminating weight bearing and axial loads, resulting in physiological changes and potentially increased injury risk [36, 38, 39]. Buckey [36] grouped these changes into broad themes allowing them to be listed briefly as follows: bone loss, psychosocial, radiation biological, muscle loss, balance and postural control, cardiovascular and nutritional. These changes include decreased balance and proprioception, decreased muscle mass, force and power with increased loss of technique (specifically affecting lower limb antigravity muscles and lumbopelvic segmental control muscles) [36], decreased ability to control posture—specifically, the ability to achieve a balanced pelvic tilt

exercises, which was measured using ultrasound imaging.

sample sizes may not be strongly statistically powered.

**2.5. Lumbopelvic adaptations to microgravity**

**Figure 1.** A visual representation of the neutral zone as a flat dish with less stability (left) and a wine glass with more stability (right) (Adapted from Panjabi [29]).

#### **2.4. Theory linking low back injury with altered motor control and low back pain**

The theory of how low back injuries can cause altered motor control and lead to low back pain was summarised by Panjabi [9] as follows:


Evidence supporting these hypotheses exists from several experimental studies. Danneels et al. [11] conducted a comparison study of chronic LBP and matched non-symptomatic participants, which found reduced cross-sectional area of LM in the lower lumbar spine. In the study, 32 clinical participants were compared with 23 matched no-LBP volunteers, and the LM crosssectional area was measured using CT scans. A study in pigs by Hodges et al. [12] found that induced L4 spinal disc lesions resulted in LM cross-sectional area decreases at the same level of the injury within 3 days, compared to no change in no-LBP controls. Injury to the L3 nerve root resulted in LM cross-sectional area reduction at the affected level and down to L4, L5 and S1 levels in 15 induced injury pigs compared to six controls. The controls were, however, still subjected to a sham surgical procedure that involved all the same steps as the injured pigs apart from the inducing of the injury. A comparison study by Hides et al. [3] of 26 first episode acute unilateral low back pain patients with 51 healthy controls, found that LM asymmetry in the people with back pain, isolated to the symptomatic level compared to symmetrical LM muscles in the no-LBP controls. A comparison study by Hodges and Richardson [4] of 15 LBP patients with 15 no-LBP matched controls used electromyography to assess the activation and timing of TrA in response to upper limb movements. It was observed that TrA activation was consistently delayed in the people with back pain. A comparison study by Ferreira and Hodges [13], in which 10 low back pain patients compared with 10 healthy matched controls, found consistently reduced changes in TrA thickness in their group with back pain during lower limb exercises, which was measured using ultrasound imaging.

While Panjabi's theories were seminal to improve our understanding of lumbopelvic pain, they missed one important factor, and that is the fact that, unlike the feedback control of many superficial muscles, there is a feedforward control of the deep spinal muscles LM [24, 30] and TrA [31, 32]. In other words, the LM and TrA muscles work in anticipation of loads and movements, not in response to them, thus, providing spinal stability. Importantly, there has also been evidence that the anticipatory activation of the deep spinal muscles is impaired in people with LBP compared to non-symptomatic controls [4, 31, 33] and that this is reversible with certain exercise approaches [34]. Based on a considerable body of literature, key authors in the field [16, 35] also suggest that secondary compensatory postural mechanisms are likely to contribute further to LBP, which would go some way towards explaining chronic LBP in the face of minimal tissue abnormality. It should be noted that the studies used to have small sample sizes may not be strongly statistically powered.

#### **2.5. Lumbopelvic adaptations to microgravity**

**2.4. Theory linking low back injury with altered motor control and low back pain**

was summarised by Panjabi [9] as follows:

stability (right) (Adapted from Panjabi [29]).

mechanics.

build-up of microtrauma or an acute injury.

124 Into Space - A Journey of How Humans Adapt and Live in Microgravity

zone and higher stresses on spinal structures.

**8.** If left unchecked, chronic non-specific LBP may develop.

and nociceptive pain signals produced.

response to dynamic loading to also become corrupted.

The theory of how low back injuries can cause altered motor control and lead to low back pain

**Figure 1.** A visual representation of the neutral zone as a flat dish with less stability (left) and a wine glass with more

**1.** Initial trauma occurs in spinal structures such as ligaments. This can be either a long-term

**2.** During dynamic loading of the injured spine, mechanoreceptor signals sent to the neural

**3.** The motor control area of the brain finds a mismatch between expected signals and those actually being received. This causes control unit output to the active stability system in

**4.** Corrupted output from the control unit leads to the changes in the activation of the deep muscles in response to the dynamic load. These changes lead to abnormal activation and timing of the active stabilising deep muscles—LM and TrA. This then causes altered spinal

**5.** Abnormal activation patterns of the deep muscles causes their returning feedback to also become corrupted, causing further mismatch in signals being received by the control unit.

**6.** Increased corruption of control unit output occurs in response to continued dynamic loading. This has great potential to lead to segmental instability, increased segmental neutral

**7.** Inflammation of stressed spinal tissues around unstable segments is then likely to occur

Evidence supporting these hypotheses exists from several experimental studies. Danneels et al. [11] conducted a comparison study of chronic LBP and matched non-symptomatic participants,

control system, produced by the injured tissue are now corrupted due to injury.

Astronauts returning from long-duration space missions (~6-months duration) [36] and participants following long-duration bed rest studies, which are commonly used to simulate microgravity exposure [37], have a range of muscular and postural problems. Human spaceflight results in exposure to an altered gravity state, mostly eliminating weight bearing and axial loads, resulting in physiological changes and potentially increased injury risk [36, 38, 39]. Buckey [36] grouped these changes into broad themes allowing them to be listed briefly as follows: bone loss, psychosocial, radiation biological, muscle loss, balance and postural control, cardiovascular and nutritional. These changes include decreased balance and proprioception, decreased muscle mass, force and power with increased loss of technique (specifically affecting lower limb antigravity muscles and lumbopelvic segmental control muscles) [36], decreased ability to control posture—specifically, the ability to achieve a balanced pelvic tilt and normal spinal curves in the sagittal plane, increased risk of spinal injury from poor spinal positioning during everyday activities—especially involving trunk flexion, increased chance of poor global movement patterns, and risk of injury from musculoskeletal weakness and atrophy [5, 19, 40, 41]. Those in microgravity also experience lengthening of the spine due to swelling and hyper-hydration of the intervertebral discs which, in turn, become deconditioned resulting in increased risk of disc injury [19].

Gernand [38] reported the implications of these physiological changes on subsequent safe functioning when returning to a gravity-loaded environment, highlighting the need for both countermeasure interventions during spaceflight and rapid and effective rehabilitation following spaceflight. For spaceflight of around 6 months, Gernand [38] noted significant bone and muscle loss, as well as altered postural control, leaving the body susceptible to fractures, muscle injury and the potential to develop osteoporosis. Muscle atrophy and altered motor control have been specifically observed in the lumbopelvic region [42]. A European Space Agency (ESA) report by Snijders et al. [43] reported LBP in 12 out of 20 astronauts during spaceflight. The report highlighted the importance of maintaining spinal movements, as end range flexion and extension exercises were anecdotally noted as being employed to ease pain during spaceflight. A relationship was also highlighted between LBP and atrophy of deep spinal muscles, particularly LM, during bed rest studies [44]. Wing et al. [1] reported that 53–68% of astronauts experienced moderate to severe back pain when in space. On landing after a shuttle mission, a US astronaut reported severe LBP which was later linked with a herniated nucleus pulposus at the L4-5 intervertebral (IV) disc and required surgical intervention [2]. Johnston et al. [2] also reported that astronauts had a more than fourfold increased risk of herniated disc pulposus within the first year following spaceflight, compared with controls. Sayson and Hargens [42] suggested that this back pain and disc injury could be caused by a range of factors linked to spinal lengthening and reduced loading. A review by Belavy et al. [19] supported this, suggesting the increased lumbar IV disc herniation risk in the astronaut population was most likely caused by long-term disc tissue deconditioning resulting from swelling of the discs due to unloading during spaceflight. However, the review only considered IV discs in isolation and did not refer to any potential predisposing factors such as spinal motor control. It should be noted that data from actual astronaut studies are usually from small samples, and therefore, statistical power is often low. Earth-based simulation studies, such as bed rest studies, are therefore, useful to increase the overall sample size on which to base conclusions.

and return to a g-loaded environment, which have the potential to be at least as demanding as those undertaken in normal Earth gravity [38]. It is necessary, therefore, to know what physiological changes occur, which could lead to increased injury risk, and which interventions, both preventative and rehabilitative, can be used to minimise and effectively rehabilitate physiological compromise. The current evidence also suggests that interventions to address lumbopelvic physiological adaptations are likely to be a required element of any rehabilitation programme following exposure to microgravity. While Evetts et al. [47] indicated that European post-flight rehabilitation includes specific training for lumbopelvic posture and spinal muscles involved in intersegmental control of the lumbar spine, they highlighted a need to compare the effectiveness of interventions to advance the treatments given to astronauts. Such improvements are also likely to aid terrestrial healthcare with more effective interventions for people with LBP

**Figure 2.** Postural adaptation to microgravity, showing loss of normal spinal curvature and increased flexion of the

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**3. Management of low back pain on Earth using the motor control** 

Management of segmental instability using specific motor control exercises aimed at normalising the recruitment patterns of the deep muscles was first summarised by O'Sullivan [48]. The first stage of training is learning to isolate and correctly voluntarily contract the deep muscle system. The voluntary contractions are intended to be low level and at 30–40%

**approach to improve spinal stability and control**

and post-bed rest rehabilitation [47].

spinal column.

Lumbopelvic adaptations to microgravity include adoption of a flexed posture (**Figure 2**) [36], spinal lengthening, increased intervertebral disc height and disc deconditioning, altered spinal curvatures [42] and atrophy of the lumbopelvic musculature. Selective atrophy of spinal extensors without corresponding atrophy of the psoas muscle was also seen in terrestrial individuals with LBP compared to no-LBP controls by Danneels et al. [11]. Atrophy and motor control changes in the LM muscle have been linked with LBP [3, 10] and development of poor intersegmental control of the lumbar spine [15, 21, 27, 45], which can potentially cause increased stress on spinal structures, resulting in pain [25, 29, 46].

Humans exposed to sustained microgravity develop a risk of significant spinal injury as a result of microgravity-induced poor intersegmental control of the lumbar spine combined with loaded activities, such as extra-vehicular activity, physically demanding medical procedures, landing

and normal spinal curves in the sagittal plane, increased risk of spinal injury from poor spinal positioning during everyday activities—especially involving trunk flexion, increased chance of poor global movement patterns, and risk of injury from musculoskeletal weakness and atrophy [5, 19, 40, 41]. Those in microgravity also experience lengthening of the spine due to swelling and hyper-hydration of the intervertebral discs which, in turn, become decondi-

Gernand [38] reported the implications of these physiological changes on subsequent safe functioning when returning to a gravity-loaded environment, highlighting the need for both countermeasure interventions during spaceflight and rapid and effective rehabilitation following spaceflight. For spaceflight of around 6 months, Gernand [38] noted significant bone and muscle loss, as well as altered postural control, leaving the body susceptible to fractures, muscle injury and the potential to develop osteoporosis. Muscle atrophy and altered motor control have been specifically observed in the lumbopelvic region [42]. A European Space Agency (ESA) report by Snijders et al. [43] reported LBP in 12 out of 20 astronauts during spaceflight. The report highlighted the importance of maintaining spinal movements, as end range flexion and extension exercises were anecdotally noted as being employed to ease pain during spaceflight. A relationship was also highlighted between LBP and atrophy of deep spinal muscles, particularly LM, during bed rest studies [44]. Wing et al. [1] reported that 53–68% of astronauts experienced moderate to severe back pain when in space. On landing after a shuttle mission, a US astronaut reported severe LBP which was later linked with a herniated nucleus pulposus at the L4-5 intervertebral (IV) disc and required surgical intervention [2]. Johnston et al. [2] also reported that astronauts had a more than fourfold increased risk of herniated disc pulposus within the first year following spaceflight, compared with controls. Sayson and Hargens [42] suggested that this back pain and disc injury could be caused by a range of factors linked to spinal lengthening and reduced loading. A review by Belavy et al. [19] supported this, suggesting the increased lumbar IV disc herniation risk in the astronaut population was most likely caused by long-term disc tissue deconditioning resulting from swelling of the discs due to unloading during spaceflight. However, the review only considered IV discs in isolation and did not refer to any potential predisposing factors such as spinal motor control. It should be noted that data from actual astronaut studies are usually from small samples, and therefore, statistical power is often low. Earth-based simulation studies, such as bed rest studies, are

therefore, useful to increase the overall sample size on which to base conclusions.

increased stress on spinal structures, resulting in pain [25, 29, 46].

Lumbopelvic adaptations to microgravity include adoption of a flexed posture (**Figure 2**) [36], spinal lengthening, increased intervertebral disc height and disc deconditioning, altered spinal curvatures [42] and atrophy of the lumbopelvic musculature. Selective atrophy of spinal extensors without corresponding atrophy of the psoas muscle was also seen in terrestrial individuals with LBP compared to no-LBP controls by Danneels et al. [11]. Atrophy and motor control changes in the LM muscle have been linked with LBP [3, 10] and development of poor intersegmental control of the lumbar spine [15, 21, 27, 45], which can potentially cause

Humans exposed to sustained microgravity develop a risk of significant spinal injury as a result of microgravity-induced poor intersegmental control of the lumbar spine combined with loaded activities, such as extra-vehicular activity, physically demanding medical procedures, landing

tioned resulting in increased risk of disc injury [19].

126 Into Space - A Journey of How Humans Adapt and Live in Microgravity

**Figure 2.** Postural adaptation to microgravity, showing loss of normal spinal curvature and increased flexion of the spinal column.

and return to a g-loaded environment, which have the potential to be at least as demanding as those undertaken in normal Earth gravity [38]. It is necessary, therefore, to know what physiological changes occur, which could lead to increased injury risk, and which interventions, both preventative and rehabilitative, can be used to minimise and effectively rehabilitate physiological compromise. The current evidence also suggests that interventions to address lumbopelvic physiological adaptations are likely to be a required element of any rehabilitation programme following exposure to microgravity. While Evetts et al. [47] indicated that European post-flight rehabilitation includes specific training for lumbopelvic posture and spinal muscles involved in intersegmental control of the lumbar spine, they highlighted a need to compare the effectiveness of interventions to advance the treatments given to astronauts. Such improvements are also likely to aid terrestrial healthcare with more effective interventions for people with LBP and post-bed rest rehabilitation [47].

### **3. Management of low back pain on Earth using the motor control approach to improve spinal stability and control**

Management of segmental instability using specific motor control exercises aimed at normalising the recruitment patterns of the deep muscles was first summarised by O'Sullivan [48]. The first stage of training is learning to isolate and correctly voluntarily contract the deep muscle system. The voluntary contractions are intended to be low level and at 30–40% maximal voluntary contraction. Contractions are taught in postures such as supine, prone and four-point-kneeling while patients are asked to perform abdominal drawing in using TrA while maintaining a neutral lumbar lordosis. In addition to this, patients are taught: differentiation of lumbar, pelvic and hip movements and diaphragmatic breathing and maintenance of neutral lordosis in different postural sets such as sitting and standing.

the operational countermeasures currently in use on the ISS [50]. Tested countermeasures included lower body negative pressure treadmill running, resistance exercises with external vibration, resistance exercise alone, rowing like exercises using a flywheel device and selfperformed exercises designed to mobilise the spine. In a recent systematic review of these bed rest studies, Winnard et al. [50] identified that no single potential countermeasure can successfully prevent all lumbopelvic musculoskeletal adaptations to simulated microgravity. For example, resistive vibration exercise was the only countermeasure, which is able to protect against lumbopelvic muscle adaptations, but it did not prevent spinal morphology changes such as loss of lumbar lordosis. No other countermeasure tested was able to do more than partially prevent (at best) the lumbopelvic muscle adaptations. This demonstrates a need for further research into new interventions to better protect the spine during microgravity exposure. It might be possible to translate ground-based interventions into new countermeasures or develop new ones based on the current lumbopelvic deconditioning rehabilitation theory. Any new interventions will need testing in ground-based microgravity simulations before incurring costs associated with actual spaceflight testing. Lower body negative pressure treadmill was the most effective currently researched countermeasure against lumbopelvic deconditioning. As this countermeasure is not yet used in operational spaceflight and no

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countermeasure is fully effective, there remains a need for rehabilitation.

**5. Rehabilitation following actual and simulated spaceflight**

correct postural alignment and control [54, 55].

Due to the lack of effective in-flight countermeasures targeted at preventing lumbopelvic musculoskeletal adaptations, astronauts require significant rehabilitation to reduce injury risk on their return to Earth. During spaceflight, a general pattern of selective extensor muscle atrophy has been seen throughout the body [51]. Decrease in spinal extensor volume has been reported as being greater than hip flexor (psoas muscle) decline in astronauts [52]. Anecdotal accounts also appear to show selective atrophy of trunk extensor muscles concomitant with improved flexor muscle performance immediately post mission [53]. This muscle imbalance results in temporary loss of lumbopelvic posture, flexion of thoracic spine and hyperextension of cervical spine, the centre of gravity is moved anteriorly and increases the risk of musculoskeletal injury [47]. Hides et al. [40] suggested that deep spinal muscle changes such as atrophy of LM and TrA muscles, along with selective hypertrophy of spinal flexors over extensors [5], may impact on the ability of the spine to distribute loads appropriately shortly after spaceflight simulation via bed rest. The European approach to post-space mission rehabilitation addresses the muscle imbalance and uses motor control training in a way very similar to that described for people with LBP on Earth and based mostly on the existing terrestrial evidence transferred to a post-spaceflight setting. Initially, postural control, muscle control and muscle balance are restored, followed by the use of strategies to normalise muscle recruitment. Astronauts are then supported to redevelop postural alignment in line with the centre of gravity and to develop adequate motor control before they start to exercise with elements of loading and strength training. The latter is only started after the astronauts have regained

Live biofeedback with use of palpation, ultrasound imaging or possibly electromyography can be included to help isolate TrA and LM activation [49]. Treatment is then progressed to the second stage where the deep muscle recruitment learned in stage one is incorporated into functional movement, and compensatory muscle strategies are discouraged. Patients are taught movements such as sit to stand, walking, bending and twisting while maintaining activation of deep muscles. The third and final stage of training is for patients to carry the newly learned and stable functional movements into their activities of daily life.

The 'bare bones' have evolved since 2000 into an evidence-based and integrated approach which is summarised by Hodges et al. [28] and too complex to discuss here. However, it is based on a considerable amount of good evidence, one of which will be summarised in the following paragraph.

Hides et al. [49] assessed LM size in athletes with LBP and determined the effectiveness of a motor control intervention. Ten participants with back pain underwent a 6-week intervention programme of learning to correctly activate TrA and LM. Live biofeedback using ultrasound imaging was used during muscle activation teaching. Abdominal drawing in exercises were used to teach recruitment of TrA while maintaining a normal, relaxed, breathing pattern, followed by participants attempting to swell the LM muscle while holding a breath out and keeping the spine still with a neutral lumbar lordosis. Initially, activation was taught in lying and then progressed to upright sitting and standing, all the while maintaining a neutral lumbar lordosis. Further progression to functional movements was then performed. By the end of the programme, pain scores had dropped from an average of 4.3–2.3 (p < 0.05). Before treatment, asymmetry had been observed in LM cross-sectional area, which also significantly decreased, while overall muscle size increased. This is just one study that provides evidence that motor control exercises including recruitment of deep muscles can improve clinical outcomes.
