INCREASING STRENGTH OF INTRINSIC FOOT MUSCLES IN DIABETES WITH PERIPHERAL NEUROPATHY
One component of diabetic foot disease is intrinsic muscle wasting – when it is present it is often referred to as the "intrinsic minus foot". The intrinsic minus foot is often discussed as an end stage change which occurs because of, or in addition to, long standing neuropathy and peripheral arterial disease. So, in the minds of many practitioners it is viewed as an inevitable, unfortunate change which sits at the top of a number of other problems in the latter stages of diabetic foot disease.
In fact, intrinsic atrophy is one of the earliest changes in diabetic foot disease, occurs often long before peripheral neuropathy and vascular disease and is possibly one of the most important and now known to be reversible changes in the diabetic foot (Greenman et al., 2005; Höhne et al., 2012).
However, in the minds of both practitioners and patients they are often more worried about peripheral neuropathy and vascular disease than muscle and structural changes. They often believe that these are the changes that herald the major risk for diabetic ulceration.
This is not the case for majority of people with diabetes. We know that the structural changes in the foot are significant predictors of ulceration and in fact are the predominant changes which lead to ulceration for most people (Holewski et al., 1989; Mueller et al., 2003). Essentially the structural changes in the foot – stiffening and clawing of toes - predict the high pressures under the forefoot. Without these changes you are unlikely to get the high forces which crush and injure foot tissues. If this is combined with a loss of sensation so you are unable to feel the crushing, or if you have a significant reduction in blood supply you cannot repair the crushed tissues. These later problems then escalate the risk significantly.
To put it another way, if a patient does not develop stiffening and clawing of toes then they do not have the same level of crushing forces under their foot and if these forces are absent it is less of a concern when the patient develops neuropathy or a lack of blood supply.
Our biggest priorities as practitioners is to do everything in our power to educate patients to begin the process of maintaining strength and mobility, especially of the toes, so they stop or reduce their risk of developing high forefoot pressures (Sartor et al., 2014).
There is now a growing body of research which demonstrates we can indeed reverse muscle atrophy in the forefoot, improve mobility of toes and when we do so we can reduce plantar pressures which crush the tissues under the foot (Allet et al., 2010; Sartor et al., 2014; Kanchanasamut and Pensri, 2017).
An excellent example of such research was published by Höhne et al in Cologne, Germany (Höhne et al., 2012).
Fourteen diabetic patients with only 30% of normal toe flexor strength performed toe flexor training with 70% of the maximal voluntary isometric contraction on for eight weeks, 3 days per week, 4 sets per session for twelve repetitions (3s loading/ 3s relaxation). The participants were divided into groups of either those with or without neuropathy. Seven had neuropathy, seven without neuropathy.
The maximum strength of the toes was measured before and after the intervention and the volume of the intrinsic foot muscles was examined before and after the intervention using MRI.
All patients improved strength, with the average increase being a staggering 55% increase in just 8 weeks. The intervention took only 10 minutes roughly 3 times per week and could be performed at home with little difficulty. In addition, there were no instructions to utilise their strength in everyday activities. So the strength gains can only be attributed to intervention of a total of 30 minutes per subject per week. Furthermore, the MRI results showed an average increase of 5% muscle bulk in just those 8 weeks.
We can begin to understand the possible benefits if we were to perform these exercises every day, in a functional position, with functional loads (bodyweight) combined with daily use activities to create positive carry over.
Allet, L. et al. (2010) ‘An exercise intervention to improve diabetic patients’ gait in a real-life environment’, Gait and Posture. Elsevier B.V., 32(2), pp. 185–190. doi: 10.1016/j.gaitpost.2010.04.013.
Greenman, R. L. et al. (2005) ‘Foot small muscle atrophy is present before the detection of clinical neuropathy.’, Diabetes care. American Diabetes Association, 28(6), pp. 1425–30. doi: 10.2337/DIACARE.28.6.1425.
Höhne, A. et al. (2012) ‘Increased Strength of Intrinsic Foot Muscles in Diabetes and Peripheral Neuropathy’, Journal of Biomechanics. Elsevier Ltd, 45(1), p. S201. doi: 10.1016/S0021-9290(12)70202-6.
Holewski, J. J. et al. (1989) ‘Prevalence of foot pathology and lower extremity complications in a diabetic outpatient clinic.’, Journal Of Rehabilitation Research And Development, 26(3), pp. 35–44. Available at: http://www.ncbi.nlm.nih.gov/pubmed/2666642.
Kanchanasamut, W. and Pensri, P. (2017) ‘Effects of weight-bearing exercise on a mini-trampoline on foot mobility, plantar pressure and sensation of diabetic neuropathic feet; a preliminary study’, Diabetic Foot and Ankle. Taylor & Francis, 8(1). doi: 10.1080/2000625X.2017.1287239.
Mueller, M. J. et al. (2003) ‘Forefoot structural predictors of plantar pressures during walking in people with diabetes and peripheral neuropathy’, Journal of Biomechanics, 36(7), pp. 1009–1017. doi: 10.1016/S0021-9290(03)00078-2.
Sartor, C. D. et al. (2014) ‘Effects of strengthening, stretching and functional training on foot function in patients with diabetic neuropathy: Results of a randomized controlled trial’, BMC Musculoskeletal Disorders, 15(1), pp. 1–13. doi: 10.1186/1471-2474-15-137.