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3.4.3.1The effect of PAD-IC on muscle pathology

PAD can adversely affect skeletal muscle strength. Further weakening of lower limb skeletal muscles occurs in claudicants due to the development of muscle metabolic myopathy (Brass and Hiatt, 2000), which is in turn due to oxidative damage to skeletal muscle structures and components (Pipinos et al., 2006). An axonal polyneuropathy also occurs (Weber and Ziegler, 2002). An abnormal ultra-structure of mitochondria in muscle has been demonstrated (Marbini et al., 1986), which involves abnormal mitochondrial respiration and adenosine triphosphate (ATP) production (Kemp, 2004, Pipinos et al., 2006), plus axonal nerve loss (Koopman et al., 1996, Weber and Ziegler, 2002). The overall effect can produce a reduction in muscle power and control especially during the propulsive phase of gait in the lower limbs. This means that subjects with IC may be responsive to orthotic interventions, which act as a surrogate to reduce the muscle power needed to ambulate (such as reducing the ankle plantarflexion power needed during propulsion).

3.4.3.2The effect of PAD-IC on gait parameters

When older subjects develop PAD - IC, a further deterioration in gait parameters occurs compared to matched control groups. The onset of IC shortens step length and slows walking velocity still further in older people (McCully et al., 1999). Whilst the type of control group has varied within papers, (age-matched controls may walk with different velocities) common conclusions have been noted. These include development of slower walking speeds, shorter step lengths (Scherer et al., 1998, Gardner et al., 2001a, McDermott et al., 2001), reduced calf muscle ability (Mockford et al., 2010, Scott-Pandorf et al., 2007,

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Crowther et al., 2009, Celis et al., 2009, Ayzin Rosoky et al., 2000) as well as decreased hip extension (Crowther et al., 2007). These gait adaptations are present even in the absence of pain in subjects with PAD, but worsen with the cramp-like calf pain associated with IC (Mockford et al., 2010, Scott-Pandorf et al., 2007).

Patients with PAD display gait patterns where the ankle takes longer to reach maximum dorsiflexion during TSt - PSw compared to controls. The ankle is also unable to generate the same amount of power as previously needed during push-off as the prolonged time to reach maximum ankle dorsiflexion means that the time available for the ankle to plantarflex for propulsion is limited (McDermott et al. 2001). The typical trace of GRFs (the Pedotti diagram) shows a flattened trace between the typical two peaks and also a reduction in peak values; showing that braking and propulsion phases of gate are not only so distinctly defined but also are less pronounced. Peak ankle plantarflexor moments and powers are reduced in subjects with PAD, and linked to reduced ground reaction force (GRF) values, this demonstrates an inability of PAD subjects to propel themselves effectively. Significant gait impairment results – even when the disease is unilateral (Celis et al., 2009, Koutakis et al., 2010). In comparison with controls, patients with PAD-IC, even whilst walking pain-free before claudicating, demonstrate a significant decrease in average maximum hip flexion (3.8 degrees) and a significantly mean increase in peak ankle plantar flexion (1.2 degrees) during early stance, plus a significantly increased peak ankle dorsiflexion (2.0 degrees) during late stance (Chen et al. 2008). In summary, PAD-IC subjects exhibit the following gait anomalies compared to controls:

 They walk slower;

 They have decreased cadence;

 They have increased stance phase durations as a percentage of gait cycle;

 They also have shorter step lengths and narrower step widths;

 They have reduced maximum hip flexion;

 They have increased maximum ankle plantarflexion during early stance;

 They have increased ankle dorsiflexion during late stance phase;

 They therefore have increased sagittal plane ankle ROM during stance phase;

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 They have reduced peak hip power absorption during mid stance;

 They have significantly reduced peak power generation at the ankle during late stance and consequently a reduced energy output;

 They have reduced hip extension power which could also lead to weaker propulsion and reduced hip flexion by the swing leg;

 They have reduced peak power absorption at the knee during late stance. However, peak joint moments are not statistically different (Wurdeman et al. 2012);

 They take longer to dorsiflex the ankle during late stance and have a shorter time frame during which they can generate ankle plantarflexion power for propulsion (McDermott et al. 2001);

 The reduced peak knee power absorption in early stance is most likely caused by the increased ankle plantarflexion found in subjects with PAD due to a relatively reclined shank;

 The reduced hip power absorption during mid stance (which is an eccentric contraction of the hip extensors to control forward motion of the trunk) signifies weak hip musculature.

Decreased ankle power generation and decreased power absorption at the knee during push-off have been demonstrated by (Wurdeman et al., 2012, Scott-Pandorf et al., 2007). This has been linked to PAD subjects having weak hip extensors and weak ankle plantarflexors. Wurdeman et al. (2012), demonstrated that PAD patients have reduced peak hip power absorption in midstance (p=0.017), reduced peak knee power absorption in early and late stance (p=0.037 and p=0.020 respectively), and reduced peak ankle power generation in late stance (p=0.021) when compared to subjects with comparable age and self-selected walking velocity. However, peak moments were not statistically altered, and indeed may not occur at the same point in the gait cycle as peak powers (as power is calculated from moments and angular velocities). Reduced knee power absorption at loading response was thought to correlate with the increased plantarflexion at the ankle; meaning shank control did not demand as much power from the knee extensors during that period.

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The decreased ankle plantarflexion power generation during late stance noted by Wurdeman et al. (2012) agreed with the findings of Scott-Pandof et al (2007) and Koutakis et al. (2010), as well as those from Chen et al. 2008 and Celis et al. (2009). However, Wurdeman et al. (2012) demonstrated this phenomenon for the first time when matching PAD subjects and controls who ambulated with similar walking velocities. This is important, since it is well known that reduced walking velocity can reduce joint powers. It was therefore confirmed that subjects with PAD- IC exhibit reduced maximal power generation at the ankle compared to accurately matched control subjects which would lead to increased metabolic cost. However, the group recommended that further research was needed to demonstrate whether peak power deficits occur as a result of reduced joint moments or angular velocities.

This led to the conclusion that there was a resultant weakness in the hip and calf muscles in subjects with PAD-IC even when not claudicating. This confirmed the hypothesis proposed by Chen et al 2008, who demonstrated that gait was altered during pain-free walking by claudicants compared to a control group, which was significantly worsened whilst claudicating. They described typical claudicant gait as being “sluggish and tired” due to the fact that the foot appeared to be in contact with the ground for a larger percentage of the gait cycle because of weak ankle plantarflexor muscles and weak propulsive muscles at the hip (the gluteal muscles). This study also confirmed previous work by Scott-Pandorf et al. (2007) and Scott-Okafor et al. (2001), who stated that the propulsion muscles of the leg were weaker than controls with reduced ankle plantarflexion strength in claudicants.