The Assessment, Management and Prevention of Calf Muscle Strain Injuries: A Qualitative Study of the Practices and Perspectives of 20 Expert Sports Clinicians

Background Despite calf muscle strain injuries (CMSI) being problematic in many sports, there is a dearth of research to guide clinicians dealing with these injuries. The aim of this study was to evaluate the current practices and perspectives of a select group of international experts regarding the assessment, management and prevention of CMSI using in-depth semi-structured interviews. Results Twenty expert clinicians working in elite sport and/or clinician-researchers specialising in the field completed interviews. A number of key points emerged from the interviews. Characteristics of CMSI were considered unique compared to other muscle strains. Rigor in the clinical approach clarifies the diagnosis, whereas ongoing monitoring of calf capacity and responses to loading exposure provides the most accurate estimate of prognosis. Athlete intrinsic characteristics, injury factors and sport demands shaped rehabilitation across six management phases, which were guided by key principles to optimise performance at return to play (RTP) while avoiding subsequent injury or recurrence. To prevent CMSI, periodic monitoring is common, but practices vary and data are collected to inform load-management and exercise selection rather than predict future CMSI. A universal injury prevention program for CMSI may not exist. Instead, individualised strategies should reflect athlete intrinsic characteristics and sport demands. Conclusions Information provided by experts enabled a recommended approach to clinically evaluate CMSI to be outlined, highlighting the injury characteristics considered most important for diagnosis and prognosis. Principles for optimal management after CMSI were also identified, which involved a systematic approach to rehabilitation and the RTP decision. Although CMSI were reportedly difficult to prevent, on- and off-field strategies were implemented by experts to mitigate risk, particularly in susceptible athletes.

Reactivate Your Second Heart

Sitting or standing without moving the leg muscles puts additional stress on your heart, as blood and lymph pool in the legs. Tightening and relaxing the calf muscles can prevent the pooling of the blood. The inactivity of the calf muscles does not allow the blood to flow upward and may result in “sitting disease,” contributing to the development of diabetes and cardiovascular disease. Activating the calf muscles as well as other leg muscles are strategies to support cardiovascular health. Thus, the calf muscles are sometimes called “our second heart.” The important function of our “second heart” is to act as a pump to return venous blood and lymph fluids upward, which can occur only when we interrupt sitting with many brief exercises by frequently standing up during the day. Suggestions regarding how to implement short breaks are included. Note that, medically, the term second heart refers to the cisterna chyli, which brings the lymphatic fluids up from the abdomen; however, in this article, second heart is used in a common popular sense of the term as the description of the calf muscle to pump the venous blood toward the heart.

Exercise Training Increases Resting Calf Muscle Oxygen Metabolism in Patients with Peripheral Artery Disease

Exercise training can mitigate symptoms of claudication (walking-induced muscle pain) in patients with peripheral artery disease (PAD). One adaptive response enabling this improvement is enhanced muscle oxygen metabolism. To explore this issue, we used arterial-occlusion diffuse optical spectroscopy (AO-DOS) to measure the effects of exercise training on the metabolic rate of oxygen (MRO2) in resting calf muscle. Additionally, venous-occlusion DOS (VO-DOS) and frequency-domain DOS (FD-DOS) were used to measure muscle blood flow (F) and tissue oxygen saturation (StO2), and resting calf muscle oxygen extraction fraction (OEF) was calculated from MRO2, F, and blood hemoglobin. Lastly, the venous/arterial ratio (γ) of blood monitored by FD-DOS was calculated from OEF and StO2. PAD patients who experience claudication (n = 28) were randomly assigned to exercise and control groups. Patients in the exercise group received 3 months of supervised exercise training. Optical measurements were obtained at baseline and at 3 months in both groups. Resting MRO2, OEF, and F, respectively, increased by 30% (12%, 44%) (p < 0.001), 17% (6%, 45%) (p = 0.003), and 7% (0%, 16%) (p = 0.11), after exercise training (median (interquartile range)). The pre-exercise γ was 0.76 (0.61, 0.89); it decreased by 12% (35%, 6%) after exercise training (p = 0.011). Improvement in exercise performance was associated with a correlative increase in resting OEF (R = 0.45, p = 0.02).

Functional assessment of stretch hyperreflexia in children with cerebral palsy using treadmill perturbations

Background As hyperactive muscle stretch reflexes hinder movement in patients with central nervous system disorders, they are a common target of treatment. To improve treatment evaluation, hyperactive reflexes should be assessed during activities as walking rather than passively. This study systematically explores the feasibility, reliability and validity of sudden treadmill perturbations to evoke and quantify calf muscle stretch reflexes during walking in children with neurological disorders. Methods We performed an observational cross-sectional study including 24 children with cerebral palsy (CP; 6–16 years) and 14 typically developing children (TD; 6–15 years). Short belt accelerations were applied at three different intensities while children walked at comfortable speed. Lower leg kinematics, musculo-tendon lengthening and velocity, muscle activity and spatiotemporal parameters were measured to analyze perturbation responses. Results We first demonstrated protocol feasibility: the protocol was completed by all but three children who ceased participation due to fatigue. All remaining children were able to maintain their gait pattern during perturbation trials without anticipatory adaptations in ankle kinematics, spatiotemporal parameters and muscle activity. Second, we showed the protocol’s reliability: there was no systematic change in muscle response over time (P = 0.21–0.54) and a bootstrapping procedure indicated sufficient number of perturbations, as the last perturbation repetition only reduced variability by ~ 2%. Third, we evaluated construct validity by showing that responses comply with neurophysiological criteria for stretch reflexes: perturbations superimposed calf muscle lengthening (P < 0.001 for both CP and TD) in all but one participant. This elicited increased calf muscle activity (359 ± 190% for CP and 231 ± 68% for TD, both P < 0.001) in the gastrocnemius medialis muscle, which increased with perturbation intensity (P < 0.001), according to the velocity-dependent nature of stretch reflexes. Finally, construct validity was shown from a clinical perspective: stretch reflexes were 1.7 times higher for CP than TD for the gastrocnemius medialis muscle (P = 0.017). Conclusions The feasibility and reliability of the protocol, as well as the construct validity—shown by the exaggerated velocity-dependent nature of the measured responses—strongly support the use of treadmill perturbations to quantify stretch hyperreflexia during gait. We therefore provided a framework which can be used to inform clinical decision making and treatment evaluation.