Background Few interventions reduce patellar tendinopathy (PT) pain in the short term. Eccentric exercises are painful and have limited effectiveness during the competitive season. Isometric and isotonic muscle contractions may have an immediate effect on PT pain. Methods This single-blinded, randomised cross-over study compared immediate and 45 min effects following a bout of isometric and isotonic muscle contractions. Outcome measures were PT pain during the single-leg decline squat (SLDS, 0-10), quadriceps strength on maximal voluntary isometric contraction (MVIC), and measures of corticospinal excitability and inhibition. Data were analysed using a split-plot in time-repeated measures analysis of variance (ANOVA). Results 6 volleyball players with PT participated. Condition effects were detected with greater pain relief immediately from isometric contractions: isometric contractions reduced SLDS (mean±SD) from 7.0±2.04 to 0.17±0.41, and isotonic contractions reduced SLDS (mean±SD) from 6.33±2.80 to 3.75±3.28 ( p<0.001). Isometric contractions released cortical inhibition (ratio mean±SD) from 27.53%±8.30 to 54.95%±5.47, but isotonic contractions had no significant effect on inhibition ( pre 30.26±3.89, post 31.92±4.67; p=0.004). Condition by time analysis showed pain reduction was sustained at 45 min postisometric but not isotonic condition ( p<0.001). The mean reduction in pain scores postisometric was 6.8/10 compared with 2.6/10 postisotonic. MVIC increased significantly following the isometric condition by 18.7±7.8%, and was significantly higher than baseline ( p<0.001) and isotonic condition ( p<0.001), and at 45 min ( p<0.001). Conclusions A single resistance training bout of isometric contractions reduced tendon pain immediately for at least 45 min postintervention and increased MVIC. The reduction in pain was paralleled by a reduction in cortical inhibition, providing insight into potential mechanisms. Isometric contractions can be completed without pain for people with PT. The clinical implications are that isometric muscle contractions may be used to reduce pain in people with PT without a reduction in muscle strength.

Tendon pain remains an enigma. Many clinical features are consistent with tissue disruption-the pain is localised, persistent and specifically associated with tendon loading, whereas others are not-investigations do not always match symptoms and painless tendons can be catastrophically degenerated. As such, the question 'what causes a tendon to be painful?' remains unanswered. Without a proper understanding of the mechanism behind tendon pain, it is no surprise that treatments are often ineffective. Tendon pain certainly serves to protect the area-this is a defining characteristic of pain-and there is often a plausible nociceptive contributor. However, the problem of tendon pain is that the relation between pain and evidence of tissue disruption is variable. The investigation into mechanisms for tendon pain should extend beyond local tissue changes and include peripheral and central mechanisms of nociception modulation. This review integrates recent discoveries in diverse fields such as histology, physiology and neuroscience with clinical insight to present a current state of the art in tendon pain. New hypotheses for this condition are proposed, which focus on the potential role of tenocytes, mechanosensitive and chemosensitive receptors, the role of ion channels in nociception and pain and central mechanisms associated with load and threat monitoring.

Repeated high force voluntary muscle activation in the form of short-term strength training reduces short-interval intracortical inhibition. This is consistent with studies involving skilled/complex tasks or novel movement patterns and acute studies investigating acute voluntary contractions.

Light-load exercise training with blood flow restriction (BFR) increases muscle strength and size. However, the hemodynamics of BFR exercise appear elevated compared with non-BFR exercise. This questions the suitability of BFR in special/clinical populations. Nevertheless, hemodynamics of standard prescription protocols for BFR and traditional heavy-load exercise have not been compared. We investigated the hemodynamics of two common BFR exercise methods and two traditional resistance exercises. Twelve young males completed four unilateral elbow flexion exercise trials in a balanced, randomized crossover design: (a) heavy load [HL; 80% one-repetition maximum (1-RM)]; (b) light load (LL; 20% 1-RM); and two other light-load trials with BFR applied (c) continuously at 80% resting systolic blood pressure (BFR-C) or (d) intermittently at 130% resting systolic blood pressure (BFR-I). Hemodynamics were measured at baseline, during exercise, and for 60-min post-exercise. Exercising heart rate, blood pressure, cardiac output, and rate-pressure product were significantly greater for HL and BFR-I compared with LL. The magnitude of hemodynamic stress for BFR-C was between that of HL and LL. These data show reduced hemodynamics for continuous low-pressure BFR exercise compared with intermittent high-pressure BFR in young healthy populations. BFR remains a potentially viable method to improve muscle mass and strength in special/clinical populations.

Evidence suggests that the cross-transfer of strength following unilateral training may be modulated by increased corticospinal excitability of the ipsilateral primary motor cortex, due to cross-activation. Anodal-tDCS (a-tDCS) has been shown to acutely increase corticospinal excitability and motor performance, which may enhance this process. Therefore, we sought to examine changes in neural activation and strength of the untrained limb following the application of a-tDCS during a single unilateral strength training session. Ten participants underwent three conditions in a randomized, double-blinded crossover design: (1) strength training + a-tDCS, (2) strength training + sham-tDCS and (3) a-tDCS alone. a-tDCS was applied for 20 min at 2 mA over the right motor cortex. Unilateral strength training of the right wrist involved 4 × 6 wrist extensions at 70 % of maximum. Outcome measures included maximal voluntary strength, corticospinal excitability, short-interval intracortical inhibition, and cross-activation. We observed a significant increase in strength of the untrained wrist (5.27 %), a decrease in short-interval intracortical inhibition (-13.49 %), and an increase in cross-activation (15.71 %) when strength training was performed with a-tDCS, but not following strength training with sham-tDCS, or tDCS alone. Corticospinal excitability of the untrained wrist increased significantly following both strength training with a-tDCS (17.29 %), and a-tDCS alone (15.15 %), but not following strength training with sham-tDCS. These findings suggest that a single session of a-tDCS combined with unilateral strength training of the right limb increases maximal strength and cross-activation to the contralateral untrained limb.

The findings provide evidence for corticomotor adaptation for unilateral leg strength training within the iM1 that is modulated by changes in interhemispheric inhibition.

Both protocols appear efficacious for in-season athletes to reduce pain, however, isometric contractions demonstrated significantly greater immediate analgesia throughout the 4-week trial. Greater analgesia may increase the ability to load or perform.

The results show that eccentric training uniquely modulates corticospinal excitability and inhibition of the untrained limb to a greater extent than concentric training. These findings suggest that unilateral eccentric contractions provide a greater stimulus in cross-education paradigms and should be an integral part of the rehabilitative process following unilateral injury to maximize the response.