Does type 1 diabetes mellitus affect Achilles tendon response to a 10 km run? A case control study
- Wong, Andrea, Docking, Sean, Cook, Jill, Gaida, Jamie
- Authors: Wong, Andrea , Docking, Sean , Cook, Jill , Gaida, Jamie
- Date: 2015
- Type: Text , Journal article
- Relation: Bmc Musculoskeletal Disorders Vol. 16, no. (2015), p. 1-7
- Full Text:
- Reviewed:
- Description: Background: Achilles tendon structure deteriorates 2-days after maximal loading in elite athletes. The load-response behaviour of tendons may be altered in type 1 diabetes mellitus (T1DM) as hyperglycaemia accelerates collagen cross-linking. This study compared Achilles tendon load-response in participants with T1DM and controls. Methods: Achilles tendon structure was quantified at day-0, day-2 and day-4 after a 10 km run. Ultrasound tissue characterisation (UTC) measures tendon structural integrity by classifying pixels as echo-type I, II, III or IV. Echo-type I has the most aligned collagen fibrils and IV has the least. Results: Participants were 7 individuals with T1DM and 10 controls. All regularly ran distances greater than 5 km and VISA-A scores indicated good tendon function (T1DM = 94 +/- 11, control = 94 +/- 10). There were no diabetic complications and HbA1c was 8.7 +/- 2.6 mmol/mol for T1DM and 5.3 +/- 0.4 mmol/mol for control groups. Baseline tendon structure was similar in T1DM and control groups -UTC echo-types (I-IV) and anterior-posterior thickness were all p > 0.05. No response to load was seen in either T1DM or control group over the 4-days post exercise. Conclusion: Active individuals with T1DM do not have a heightened Achilles tendon response to load, which suggests no increased risk of tendon injury. We cannot extrapolate these findings to sedentary individuals with T1DM.
- Authors: Wong, Andrea , Docking, Sean , Cook, Jill , Gaida, Jamie
- Date: 2015
- Type: Text , Journal article
- Relation: Bmc Musculoskeletal Disorders Vol. 16, no. (2015), p. 1-7
- Full Text:
- Reviewed:
- Description: Background: Achilles tendon structure deteriorates 2-days after maximal loading in elite athletes. The load-response behaviour of tendons may be altered in type 1 diabetes mellitus (T1DM) as hyperglycaemia accelerates collagen cross-linking. This study compared Achilles tendon load-response in participants with T1DM and controls. Methods: Achilles tendon structure was quantified at day-0, day-2 and day-4 after a 10 km run. Ultrasound tissue characterisation (UTC) measures tendon structural integrity by classifying pixels as echo-type I, II, III or IV. Echo-type I has the most aligned collagen fibrils and IV has the least. Results: Participants were 7 individuals with T1DM and 10 controls. All regularly ran distances greater than 5 km and VISA-A scores indicated good tendon function (T1DM = 94 +/- 11, control = 94 +/- 10). There were no diabetic complications and HbA1c was 8.7 +/- 2.6 mmol/mol for T1DM and 5.3 +/- 0.4 mmol/mol for control groups. Baseline tendon structure was similar in T1DM and control groups -UTC echo-types (I-IV) and anterior-posterior thickness were all p > 0.05. No response to load was seen in either T1DM or control group over the 4-days post exercise. Conclusion: Active individuals with T1DM do not have a heightened Achilles tendon response to load, which suggests no increased risk of tendon injury. We cannot extrapolate these findings to sedentary individuals with T1DM.
Tendon neuroplastic training : Changing the way we think about tendon rehabilitation : A narrative review
- Rio, Ebonie, Kidgell, Dawson, Lorimer Moseley, Graham, Gaida, Jamie, Docking, Sean, Purdam, Craig, Cook, Jill
- Authors: Rio, Ebonie , Kidgell, Dawson , Lorimer Moseley, Graham , Gaida, Jamie , Docking, Sean , Purdam, Craig , Cook, Jill
- Date: 2016
- Type: Text , Journal article
- Relation: British Journal of Sports Medicine Vol. 50, no. 4 (2016), p. 209-215
- Full Text:
- Reviewed:
- Description: Tendinopathy can be resistant to treatment and often recurs, implying that current treatment approaches are suboptimal. Rehabilitation programmes that have been successful in terms of pain reduction and return to sport outcomes usually include strength training. Muscle activation can induce analgesia, improving self-efficacy associated with reducing one's own pain. Furthermore, strength training is beneficial for tendon matrix structure, muscle properties and limb biomechanics. However, current tendon rehabilitation may not adequately address the corticospinal control of the muscle, which may result in altered control of muscle recruitment and the consequent tendon load, and this may contribute to recalcitrance or symptom recurrence. Outcomes of interest include the effect of strength training on tendon pain, corticospinal excitability and short interval cortical inhibition. The aims of this concept paper are to: (1) review what is known about changes to the primary motor cortex and motor control in tendinopathy, (2) identify the parameters shown to induce neuroplasticity in strength training and (3) align these principles with tendon rehabilitation loading protocols to introduce a combination approach termed as tendon neuroplastic training. Strength training is a powerful modulator of the central nervous system. In particular, corticospinal inputs are essential for motor unit recruitment and activation; however, specific strength training parameters are important for neuroplasticity. Strength training that is externally paced and akin to a skilled movement task has been shown to not only reduce tendon pain, but modulate excitatory and inhibitory control of the muscle and therefore, potentially tendon load. An improved understanding of the methods that maximise the opportunity for neuroplasticity may be an important progression in how we prescribe exercise-based rehabilitation in tendinopathy for pain modulation and potentially restoration of the corticospinal control of the muscle-tendon complex.
- Authors: Rio, Ebonie , Kidgell, Dawson , Lorimer Moseley, Graham , Gaida, Jamie , Docking, Sean , Purdam, Craig , Cook, Jill
- Date: 2016
- Type: Text , Journal article
- Relation: British Journal of Sports Medicine Vol. 50, no. 4 (2016), p. 209-215
- Full Text:
- Reviewed:
- Description: Tendinopathy can be resistant to treatment and often recurs, implying that current treatment approaches are suboptimal. Rehabilitation programmes that have been successful in terms of pain reduction and return to sport outcomes usually include strength training. Muscle activation can induce analgesia, improving self-efficacy associated with reducing one's own pain. Furthermore, strength training is beneficial for tendon matrix structure, muscle properties and limb biomechanics. However, current tendon rehabilitation may not adequately address the corticospinal control of the muscle, which may result in altered control of muscle recruitment and the consequent tendon load, and this may contribute to recalcitrance or symptom recurrence. Outcomes of interest include the effect of strength training on tendon pain, corticospinal excitability and short interval cortical inhibition. The aims of this concept paper are to: (1) review what is known about changes to the primary motor cortex and motor control in tendinopathy, (2) identify the parameters shown to induce neuroplasticity in strength training and (3) align these principles with tendon rehabilitation loading protocols to introduce a combination approach termed as tendon neuroplastic training. Strength training is a powerful modulator of the central nervous system. In particular, corticospinal inputs are essential for motor unit recruitment and activation; however, specific strength training parameters are important for neuroplasticity. Strength training that is externally paced and akin to a skilled movement task has been shown to not only reduce tendon pain, but modulate excitatory and inhibitory control of the muscle and therefore, potentially tendon load. An improved understanding of the methods that maximise the opportunity for neuroplasticity may be an important progression in how we prescribe exercise-based rehabilitation in tendinopathy for pain modulation and potentially restoration of the corticospinal control of the muscle-tendon complex.
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