The relationship between stress and disease, in particular cardiovascular disease, has long been recognized, whereas the study of the physiological mechanisms that explain this link has only more recently received attention. The acute response to stress is generally thought to be a critically important adaptation designed to activate the system in preparation to cope with the stressor. However, prolonged stimulation of the system (acute and chronic) can lead to deleterious adaptations including the release of inflammatory cytokines (small proteins important in cell signaling) that play a critical role in the development of atherosclerosis. Scientists have therefore used a breadth of protocols and methods to identify the complexity of our fight-or-flight response and demonstrate the synergy between perception, the stress response, physical activity, and health. In addition, the critical assessment of cellular health, the gut microbiome, and genetic polymorphisms have further advanced our understanding of additional therapeutic targets against CVD.
Edmund O. Acevedo and Aaron L. Slusher
Shlomit Radom-Aizik and Dan M. Cooper
In this review, we highlight promising new discoveries that may generate useful and clinically relevant insights into the mechanisms that link exercise with growth during critical periods of development. Growth in childhood and adolescence is unique among mammals and is a dynamic process regulated by an evolution of hormonal and inflammatory mediators, age-dependent progression of gene expression, and environmentally modulated epigenetic mechanisms. Many of these same processes likely affect molecular transducers of physical activity. How the molecular signaling associated with growth is synchronized with signaling associated with exercise is poorly understood. Recent advances in “omics”—namely genomics and epigenetics, metabolomics, and proteomics—now provide exciting approaches and tools that can be used for the first time to address this gap. A biologic definition of “healthy” exercise that links the metabolic transducers of physical activity with parallel processes that regulate growth will transform health policy and guidelines that promote optimal use of physical activity.
Christopher D. Brown, Christine A. lauber and Thomas Cappaert
Iontophoresis is a method of local transfer of ionized medicated and nonmedicated substances through the skin and into the target tissues using magnetic polarization. The anti-inflammatory properties exhibited by dexamethasone sodium phosphate (DEX) combined with iontophoresis make it a potentially desirable treatment for clinicians wishing to administer a noninvasive localized drug concentration without having a large systemic concentration of that drug. Since concurrent treatments are commonly used in clinical practice, many of the published studies that included the use of DEX also used concurrent treatments. However, this may make it difficult for clinicians to determine the individual effectiveness of DEX iontophoresis in treating musculoskeletal conditions.
Focused Clinical Question:
Does DEX iontophoresis, alone, decrease pain and improve function in patients with musculoskeletal conditions when compared with placebo or control?
Lori A. Bolgla, Douglas R. Keskula and Jewell B. Duncan
Researchers have suggested that quadriceps inhibition resulting from a simulated knee effusion would lead to decreased lower extremity performance.
To investigate the relationship between a simulated knee effusion and lower extremity performance.
9 college students.
Subjects performed 3 functional-performance tests before and after a simulated knee effusion. Measurement was the average distance hopped for a single hop and crossover hop for distance and time for completion on a timed hop test.
An analysis of variance revealed significant change in average test scores after injection only for the timed hop in subjects receiving a 60-ml injection.
Nonsignificant differences might have resulted from compensation from other muscle groups, fluid movement within the knee joint, and absence of an inflammatory process. Further research on the relationship between simulated knee effusion and lower extremity performance is needed.
Dawn T. Gulick and Iris F. Kimura
Muscle soreness, a familiar phenomenon to most athletes, has been differentiated into “acute” and “delayed onset.” The etiology of acute muscle soreness has been attributed to ischemia and the accumulation of metabolic by-products. However, the etiology of delayed onset muscle soreness (DOMS) is not so clear. Six theories have been proposed: lactic acid, muscle spasm, torn tissue, connective tissue, enzyme efflux, and tissue fluid theories. The treatment of DOMS has also been investigated. Studies in which anti-inflammatory medications have been administered have yielded varying results based on the dosage and the time of administration. Submaximal concentric exercise may alleviate soreness but does not restore muscle function. Neither cryotherapy nor stretching abates the symptoms of DOMS. Transcutaneous electrical stimulation has been shown to decrease soreness and increase range of motion, but the effect on the recovery of muscle function is unknown. Therefore, the treatment of DOMS remains an enigma.
Sheri A. Hale
To review the etiology of patellar tendinopathy as it relates to clinical management of chronic patellar-tendon disease in athletes.
Information was gathered from a MEDLINE search of literature in English using the key words patellar tendinitis, patellar tendonitis, patellar tendinosis, patellar tendinopathy, and jumper’s knee.
All relevant peer-reviewed literature in English was reviewed.
The etiology of patellar tendinopathy is multifactorial, incorporating both intrinsic and extrinsic factors. Age, muscle flexibility, training program, and knee-joint dynamics have all been associated with patellar tendinopathy. The roles of gender, body morphology, and patellar mobility in patellar tendinopathy are unclear.
The pathoetiology of patellar tendinopathy is a complex process that results from both an inflammatory response and degenerative changes. There is a tremendous need for research to improve our understanding of the pathoetiology of patellar tendinopathy and its clinical management.
Daniela JS Mattos, Susana Cristina Domenech, Noé Gomes Borges Junior and Marcio José Santos
Eight subjects with carpal tunnel syndrome (CTS) (47.13 ± 7.83 years) and 8 matched controls (46.29 ± 7.27 years) manipulated a test object fitted with an accelerometer and force sensor, both before and after hand muscle fatigue. Grip force and object acceleration were recorded and used to calculate grip force control variables that included Grip Force Peak, Safety Margin, and Time to Grip Force Peak. Individuals with CTS exhibited a higher Safety Margin (p = .010) and longer Time to Peak of Grip Force (p = .012) than healthy controls during object manipulation. Once fatigued, both groups significantly decreased their grip force to perform the task (Grip Force Peak; p = .017 and Safety Margin; p < .001). Nevertheless, individuals with CTS maintained an unnecessarily high safety margin. Our results suggest that CTS can adversely affect how the central nervous system regulates grip force, which might aggravate the inflammatory process and exacerbate the symptoms of this disease.
Tiaki B. Smith, Will G. Hopkins and Tim E. Lowe
There is a need for markers that would help determine when an athlete’s training load is either insufficient or excessive. In this study we examined the relationship between changes in performance and changes in physiological and psychological markers during and following a period of overload training in 10 female and 10 male elite rowers. Change in performance during a 4-wk overload was determined with a weekly 30-min time-trial on a rowing ergometer, whereas an incremental test provided change in lactate-threshold power between the beginning of the study and following a 1-wk taper after the overload. Various psychometric, steroid-hormone, muscle-damage, and inflammatory markers were assayed throughout the overload. Plots of change in performance versus the 4-wk change in each marker were examined for evidence of an inverted-U relationship that would characterize undertraining and excessive training. Linear modeling was also used to estimate the effect of changes in the marker on changes in performance. There was a suggestion of an inverted U only for performance in the incremental test versus some inflammatory markers, due to the relative underperformance of one rower. There were some clear linear relationships between changes in markers and changes in performance, but relationships were inconsistent within classes of markers. For some markers, changes considered to predict excessive training (eg, creatine kinase, several proinflammatory cytokines) had small to large positive linear relationships with performance. In conclusion, some of the markers investigated in this study may be useful for adjusting the training load in individual elite rowers.
Regina M. Lewis, Maja Redzic and D. Travis Thomas
The purpose of this 6-month randomized, placebo-controlled trial was to determine the effect of season-long (September–March) vitamin D supplementation on changes in vitamin D status, which is measured as 25(OH) D, body composition, inflammation, and frequency of illness and injury. Forty-five male and female athletes were randomized to 4,000 IU vitamin D (n = 23) or placebo (n = 22). Bone turnover markers (NTx and BSAP), 25(OH)D, and inflammatory cytokines (TNF-alpha, IL-6, and IL1-β) were measured at baseline, midpoint, and endpoint. Body composition was assessed by DXA and injury and illness data were collected. All athletes had sufficient 25(OH)D (> 32 ng/ml) at baseline (mean: 57 ng/ml). At midpoint and endpoint, 13% and 16% of the total sample had 25(OH)D < 32 ng/ml, respectively. 25(OH)D was not positively correlated with bone mineral density (BMD) in the total body, proximal dual femur, or lumbar spine. In men, total body (p = .04) and trunk (p = .04) mineral-free lean mass (MFL) were positively correlated with 25(OH)D. In women, right femoral neck BMD (p = .02) was positively correlated with 25(OH)D. 25(OH)D did not correlate with changes in bone turnover markers or inflammatory cytokines. Illness (n = 1) and injury (n = 13) were not related to 25(OH)D; however, 77% of injuries coincided with decreases in 25(OH)D. Our data suggests that 4,000 IU vitamin D supplementation is an inexpensive intervention that effectively increased 25(OH)D, which was positively correlated to bone measures in the proximal dual femur and MFL. Future studies with larger sample sizes and improved supplement compliance are needed to expand our understanding of the effects of vitamin D supplementation in athletes.
Elizabeth L. Abbey and Janet Walberg Rankin
Maintenance of repeated-sprint performance is a goal during team-sport competition such as soccer. Quercetin has been shown to be an adenosine-receptor antagonist and may reduce oxidative stress via inhibition of the enzyme xanthine oxidase (XO). The purpose of the study was to determine the effect of quercetin consumption on performance of repeated sprints and, secondarily, the XO and inflammatory-marker response induced by repeated-sprint exercise. Fifteen recreationally active, young adult men completed 2 repeated-sprint tests (RST), 12 × 30-m maximal-effort sprints (S1–S12), each after 1 wk supplementation with a placebo, a 6% carbohydrate commercial sports drink, or that drink with 500 mg of quercetin-3-glucoside, consumed twice a day (1,000 mg/d). Blood samples were collected before supplementation (B0), at baseline before each RST (B1), immediately after RST (B2), and 1 hr after RST (B3). Mean sprint time increased progressively and was significantly higher by S9 for both treatments (5.9%); however, there were no significant differences between treatments. Percent fatigue decrement (%FD) for placebo (3.8% ± 2.3%) was significantly less than with quercetin (5.1% ± 2.7%). Changes in blood XO, IL-6, and uric acid from B1 to B2 were +47%, +77%, and +25%, respectively, with no difference by treatment. In conclusion, repeated-sprint performance was not improved by quercetin supplementation and was worse than with placebo when expressed as %FD. Quercetin did not attenuate indicators of XO activity or IL-6, a marker of the inflammatory response after sprint exercise.