Claude H. Côté

Therapeutic exercise and orthopedic manual therapy for impingement syndrome: a systematic review.

ObjectiveTo review randomized controlled trials evaluating the effectiveness of therapeutic exercise and orthopedic manual therapy for the treatment of impingement syndrome. Data SourceReports up to October 2002 were located from MEDLINE, the Cochrane Database of Systematic Reviews, the Physiotherapy Evidence Database (PEDro), the TRIP database, and the Cumulative Index to Nursing & Allied Health Literature (CINAHL) using “shoulder” and “clinical trial”/“randomized controlled trial” as search terms. Study SelectionStudies were included if (1) they were a randomized controlled trial; (2) they were related to impingement syndrome, rotator cuff tendinitis, or bursitis; (3) one of the treatments included therapeutic exercise or manual therapy. Data ExtractionTwo independent observers reviewed the methodological quality of the studies using an assessment tool developed by the Cochrane Musculoskeletal Injuries Group. Differences were resolved by consensus. Data SynthesisSeven trials met our inclusion criteria. After consensus, the mean methodological score for all studies was 13.9 ± 2.4 (of 24). Four studies of 7, including the 3 trials with the best methodological score (67%), suggested some benefit of therapeutic exercise or manual therapy compared with other treatments such as acromioplasty, placebo, or no intervention. ConclusionsThere is limited evidence to support the efficacy of therapeutic exercise and manual therapy to treat impingement syndrome. More methodologically sound studies are needed to further evaluate these interventions.

Acromio-humeral distance variation measured by ultrasonography and its association with the outcome of rehabilitation for shoulder impingement syndrome.

Objective:First, to validate an ultrasonographic measure of the acromio-humeral distance (AHD); second, to compare the AHD variation during active abduction in patients with shoulder impingement syndrome (SIS) and healthy subjects; and third, to evaluate the relationship between functional status and AHD variations before and after rehabilitation in SIS subjects. Design:This study has 3 components: (1) a reliability study, (2) a case-control study, and (3) a preliminary pretreatment/posttreatment clinical trial. Setting:Primary care hospital setting. Participants:Seven SIS patients and 13 healthy subjects. Interventions:For the clinical trial, the SIS subjects participated in 12 sessions of a rehabilitation program over 4 weeks. Main Outcome Measures:First, intraclass correlation coefficient for interobserver reliability; second, AHD measured at 0°, 45°, and 60° of active abduction; and third, Western Ontario Rotator Cuff Index. Results:Intraclass correlation coefficient for interobserver reliability ranged from 0.86 to 0.92 for the 3 shoulder positions. A significant reduction of the AHD was found within groups between rest and active abduction (P < 0.05). Comparison of AHD between groups was not statistically different (P = 0.06; β< 0.80). In pre-post rehabilitation analysis, improvement of the Western Ontario Rotator Cuff Index score was positively correlated to the reduction of the AHD narrowing as the arm was abducted (r = 0.86; P = 0.01). Conclusions:The ultrasound measure of AHD is reliable and sensitive. Although a distinct pattern of AHD variation in SIS patients could not be confirmed, a strong positive relationship was found between the reduction of AHD narrowing and functional improvement following rehabilitation. Ultrasound measurement of AHD might help identify SIS patients who will benefit from rehabilitation.

Nonsteroidal Anti-Inflammatory Drug Reduces Neutrophil and Macrophage Accumulation but Does Not Improve Tendon Regeneration

Whether nonsteroidal anti-inflammatory drugs have a beneficial effect on tendon regeneration is still a matter of debate. Given that inflammatory cells are thought to induce nonspecific damage following an injury, we tested the hypothesis that a 3-day treatment with diclofenac would protect tendons from inflammatory cell injury and would promote healing. Neutrophil and ED1+ macrophage concentrations were determined in the paratenon and the core of the rat Achilles tendon following collagenase-induced injury. Hydroxyproline content, edema, and mechanical properties were also evaluated at 1, 3, 7, 14, and 28 days post-trauma. Collagenase injections induced a 70% decrease in the ultimate rupture point at Day 3. Diclofenac treatments (1 mg/kg bid) selectively decreased the accumulation of neutrophils and ED1+ macrophages by 59% and 35%, respectively, in the paratenon, where blood vessels are numerous, but did not reduce the accumulation of neutrophils and ED1+ macrophages in the core of the tendon. Edema was significantly reduced on Day 3 but persisted during the remodeling phase in the diclofenac-treated group only. The inhibition of leukocyte accumulation by diclofenac did not translate into a reduction of tissue damage or a promotion of tissue healing, because the mechanical properties of injured Achilles tendons were identical in placebo and diclofenac-treated groups. These results indicate that diclofenac reduced both edema and the accumulation of inflammatory cells within the paratenon but provided no biochemical or functional benefits for the Achilles tendon.

MAPK signaling in the quadriceps of patients with chronic obstructive pulmonary disease.

Muscle atrophy in chronic obstructive pulmonary disease (COPD) is associated with reduced exercise tolerance, muscle strength, and survival. The molecular mechanisms leading to muscle atrophy in COPD remain elusive. The mitogen-activated protein kinases (MAPKs) such as p38 MAPK and ERK 1/2 can increase levels of MAFbx/Atrogin and MuRF1, which are specifically involved in muscle protein degradation and atrophy. Our aim was to investigate the level of activation of p38 MAPK, ERK 1/2, and JNK in the quadriceps of patients with COPD. A biopsy of the quadriceps was obtained in 18 patients with COPD as well as in 9 healthy controls. We evaluated the phosphorylated as well as total protein levels of p38 MAPK, ERK 1/2, and JNK as well as MAFbx/Atrogin and MuRF1 in these muscle samples. The corresponding mRNA expression was also assessed by RT-PCR. Ratios of phosphorylated to total level of p38 MAPK (P = 0.02) and ERK 1/2 (P = 0.01) were significantly elevated in patients with COPD compared with controls. Moreover, protein levels of MAFbx/Atrogin showed a tendency to be greater in patients with COPD (P = 0.08). mRNA expression of p38 MAPK (P = 0.03), ERK 1/2 (P = 0.02), and MAFbx/Atrogin (P = 0.04) were significantly elevated in patients with COPD. In addition, phosphorylated-to-total p38 MAPK ratio (Pearsons r = -0.45; P < 0.05) and phosphorylated-to-total ERK 1/2 ratio (Pearsons r = -0.47; P < 0.05) were negatively associated with the mid-thigh muscle cross-sectional area. These data support the hypothesis that the MAPKs might play a role in the development of muscle atrophy in COPD.

Quadriceps metabolism during constant workrate cycling exercise in chronic obstructive pulmonary disease

Impaired resting metabolism in peripheral muscles potentially contributes to exercise intolerance in chronic obstructive pulmonary disease (COPD). This study investigated the cytosolic energy metabolism of the quadriceps, from glycogen degradation to lactate accumulation, in exercising patients with COPD, in comparison to healthy controls. We measured, in 12 patients with COPD and 10 control subjects, resting and post-cycling exercise quadriceps levels of 1) energy substrates and end products of glycolysis (glycogen, glucose, pyruvate, and lactate) and intermediate markers of glycolysis (glucose-6-phosphate, glucose-1-phosphate, fructose-6-phosphate) and 2) the activity of key enzymes involved in the regulation of glycolysis (phosphofructokinase, lactate dehydrogenase). Exercise intensity (P < 0.01), duration (P = 0.049), and total work (P < 0.01) were reduced in patients with COPD. The variations in energy substrates and end products of glycolysis after cycling exercise were of similar magnitude in patients with COPD and controls. Glucose-6-phosphate (P = 0.036) and fructose-6-phosphate (P = 0.042) were significantly elevated in patients with COPD after exercise. Phosphofructokinase (P < 0.01) and lactate dehydrogenase (P = 0.02) activities were greater in COPD. Muscle glycogen utilization (P = 0.022) and lactate accumulation (P = 0.025) per unit of work were greater in COPD. We conclude that cycling exercise induced changes in quadriceps metabolism in patients with COPD that were of similar magnitude to those of healthy controls. These intramuscular events required a much lower exercise work load and time to occur in COPD. Our data suggest a greater reliance on glycolysis during exercise in COPD, which may contribute to exercise intolerance in COPD.

Ubiquitination and Proteolysis in Limb and Respiratory Muscles of Patients with Chronic Obstructive Pulmonary Disease

Peripheral muscle dysfunction associated with chronic diseases is undeniably a growing problem as one of its main causes, chronic obstructive pulmonary disease (COPD), progresses. Among others, muscle atrophy is one component building the concept of muscle dysfunction. Muscle atrophy has a significant impact on patient clinical status, independent of the impairment in lung function. A lot of effort has been devoted lately to increasing our understanding of the relationship between COPD and the initiation and the development of muscle atrophy. A growing body of evidence is showing that the ubiquitin-proteasome system, an ATP-dependent proteolytic pathway, is playing a crucial role in the cascade leading to degradation of contractile proteins, thus promoting the development of muscle atrophy. Interestingly, this system is also involved in essential cellular processes such as response to hypoxemia and muscle tissue regeneration. In this review, existing evidence linking the activity of the ubiquitin-proteasome system and the cellular events taking place in respiratory and peripheral muscles of patients with COPD are reported. Based on this information, the reader should be able to understand the essential role of this pathway in the context of muscle homeostasis and to picture the coming research in this area.

Carbohydrate utilization in rat soleus muscle is influenced by carbonic anhydrase III activity

Inhibition of carbonic anhydrase III (CA III; EC 4.2.1.1) activity in type I muscle can influence resistance to fatigue and glycogen utilization. Our aim was to determine if CA III inhibition could influence muscle pH and glycolytic rate. Muscle pH, hexosemonophosphates (HMP), glycolytic intermediates, ATP, and creatine phosphate (CP) were measured at rest and during a fatigue protocol in rat soleus muscles in vitro with or without CA inhibitors (CAI). In resting muscles, CAI resulted in a significant drop in pH (7.11 vs. 7.06, P < 0.05) and in a two- to threefold increase in HMP content compared with control muscles. Measurements of HMP and glycolytic intermediates during the fatigue protocol suggested, however, that the glycolytic flux was not influenced. Globally, muscles incubated with CAI showed larger perturbations of their CP and ATP content than control muscles. The accumulation of HMP induced by the CAI was found to be totally dependent on the combined presence of external glucose and contractile activity, suggesting that inhibiting CA III may augment the responsitivity of the contraction-induced glucose uptake process.Inhibition of carbonic anhydrase III (CA III; EC 4.2.1.1 ) activity in type I muscle can influence resistance to fatigue and glycogen utilization. Our aim was to determine if CA III inhibition could influence muscle pH and glycolytic rate. Muscle pH, hexosemonophosphates (HMP), glycolytic intermediates, ATP, and creatine phosphate (CP) were measured at rest and during a fatigue protocol in rat soleus muscles in vitro with or without CA inhibitors (CAI). In resting muscles, CAI resulted in a significant drop in pH (7.11 vs. 7.06, P < 0.05) and in a two- to threefold increase in HMP content compared with control muscles. Measurements of HMP and glycolytic intermediates during the fatigue protocol suggested, however, that the glycolytic flux was not influenced. Globally, muscles incubated with CAI showed larger perturbations of their CP and ATP content than control muscles. The accumulation of HMP induced by the CAI was found to be totally dependent on the combined presence of external glucose and contractile activity, suggesting that inhibiting CA III may augment the responsitivity of the contraction-induced glucose uptake process.

Motor unit function in skeletal muscle autografts of rats

Standard and nerve-intact grafts of the extensor digitorum longus (EDL) muscles of rats do not fully recover control values for maximum tetanic tension (Po). We compared the physiologic properties of motor units from standard and nerve-intact EDL grafts of rats with those of control EDL muscles. Standard grafts were completely removed and replaced in their original site. For nerve-intact grafts all physical connections were severed except for the nerve. Isometric contractile properties of whole muscles and single motor units were measured in situ 75 and 50 days after surgery for standard and nerve-intact grafts, respectively. Motor units from both types of grafts showed a mean and distribution for time-to-peak twitch tension (TPT) not different from control motor units. The absolute Po of nerve-intact grafts showed a greater recovery than the standard grafts, but was still significantly lower than the control value. The average decrease in the Po of motor units from nerve-intact grafts of 16% was not different from the decrease in the Po of the total EDL graft which suggests no loss of motor units in nerve-intact grafts. In standard grafts, the 57% decrease in Po for the whole muscle was attributable to a 20% decrease in the average tension development per motor unit and a 45% decrease in the number of motor units. These differences suggest a more complete reinnervation of the nerve-intact grafts than standard grafts.

Transplantation and transposition of skeletal muscles into the faces of monkeys

Restoration of normal facial movement after long-term facial paralysis with muscle atrophy has not yet been achieved reliably by either free grafts, in which fibers degenerate and regenerate, or by grafts made with microneurovascular repair, in which most fibers survive. Our purpose was to compare the structural and functional properties of free muscle grafts and continuously perfused muscle flaps transplanted into the faces of monkeys. In adult monkeys, the facial muscles were replaced by either a free graft of a donor muscle from the lower limb or a denervated flap of ipsilateral temporalis muscle. Each graft or flap was reinnervated with the preserved buccal branch of the facial nerve. The control muscles, grafts, and flaps were examined 90 days later for gross appearance, contractile properties, and fiber areas. Compared with muscle flaps, free grafts showed greater adaptability to the new location and innervation and a closer approximation to the structural and functional properties of the original facial musculature.

Studies on the turnover of proteins of the rat erythrocyte membrane

The membrane proteins of erythrocytes were labeled by injecting L-[14C]-leucine and later L-[3H]leucine into rats, the two injections being 31 days apart. Control animals received the two isotopic forms of L-leucine simultaneously. Deviations in labeling ratio from control patterns were found on sodium dodecyl sulfate-polyacrylamide gel electrophorograms in restricted regions suggestive of turnover or loss of a few small proteins from the membrane between the 31 days. Most of the ghost proteins show no turnover.