Returning an athlete to functional activity is the primary goal of the sports medicine practitioner. Eccentric exercise may be used throughout the rehabilitation program to improve muscle performance and restore normal function. The selection and progression of eccentric exercise are contingent on treatment goals and the individual's tolerance to activity. Basic concepts of eccentric muscle performance are discussed, and general treatment guidelines with an emphasis on specificity and intensity are presented, to enable the clinician to organize and implement relevant, prudent eccentric exercise within the restrictions of the clinical setting. The use of eccentric exercise in the management of tendinitis is briefly discussed.
Douglas R. Keskula
Jordan D. Philpott, Chris Donnelly, Ian H. Walshe, Elizabeth E. MacKinley, James Dick, Stuart D.R. Galloway, Kevin D. Tipton and Oliver C. Witard
Lanier, 2003 ), and various nutritional strategies ( Jackman et al., 2010 ; White et al., 2008 ) that may have application to recovery in elite soccer. The most commonly investigated nutritional strategy for promoting muscle recovery after eccentric exercise-induced muscle damage is amino acid ingestion
Peter M. Tiidus, Joel Cort, Sarah J. Woodruff and Pamela Bryden
To evaluate ultrasound’s effectiveness after eccentric-exercise-induced muscle damage.
Random assignment to ultrasound (UT) or placebo (PT). Ultrasound was applied immediately and 24, 48, and 72 h after 50 maximum eccentric contractions of the biceps.
Concentric and eccentric peak torques, resting elbow angle, and subjective muscle soreness were measured before and 24, 48, 72, and 96 h afterward.
No significant differences between UT and PT for biceps concentric or eccentric peak torque were noted. Both groups exhibited significant (P < .01) depression in eccentric and concentric peak torques with a slow return toward preexercise values over 96 h. Resting elbow angles for both groups were significantly lower than preexercise values up to 96 h (P < .01). Muscle soreness increased significantly (P < .05) at 24 and 48 h and returned to preexercise levels by 96 h.
Daily ultrasound did not influence recovery after eccentric-exercise-induced muscle damage.
Richard J. Bloomer
The purpose of this study was to determine the effects of antioxidant therapy on indirect markers of muscle damage following eccentric exercise (EE). Eighteen women were randomized to an antioxidant supplement or a placebo before a bout of EE. Plasma creatine kinase (CK) activity, muscle soreness (MS), maximal isometric force (MIF), and range of motion (ROM) were assessed before and through 14 d postexercise. Eccentric exercise resulted in an increase in CK activity and MS, and a drop in MIF and ROM during the days following EE, which returned to baseline values 14 d after EE in both groups. Antioxidants attenuated the CK activity and MS response to the EE, while little difference was noted between groups in MIF or ROM. These fndings suggest that antioxidant supplementation was helpful in reducing the elevations in plasma CK activity and MS, with little impact on MIF and ROM loss.
Kazunori Nosaka and Priscilla M. Clarkson
This study was done to determine whether eccentric exercise that causes muscle damage will produce an increase in plasma levels of zinc. Changes in total plasma zinc concentration (Zn) were examined following an eccentric and concentric exercise of the forearm flexors. Eight female subjects performed 24 maximal concentric actions (CON) with one arm and 10-14 days later performed 24 maximal eccentric actions (ECC) with the other arm. Maximal isometric force, elbow joint angles at a relaxed (RANG) and flexed position (FANG), muscle soreness, and plasma creatine kinase activity (CK) were measured as indicators of muscle damage. Zn levels were determined at the same time as CK. Maximal isometric force, RANG, FANG, and muscle soreness showed large changes after ECC but little if any change after CON. CK increased significantly after ECC but did not change after CON. Neither ECC nor CON showed significant changes in Zn following exercise. If: is concluded that exercise-induced muscle damage does not appear to produce an increase in plasma zinc levels.
Matthew David Cook, Stephen David Myers, John Stephen Michael Kelly and Mark Elisabeth Theodorus Willems
Impaired glucose tolerance was shown to be present 48 hr following muscle-damaging eccentric exercise. We examined the acute effect of concentric and muscle-damaging eccentric exercise, matched for intensity, on the responses to a 2-hr 75-g oral glucose tolerance test (OGTT). Ten men (27 ± 9 years, 178 ± 7 cm, 75 ± 11 kg, VO2max: 52.3 ± 7.3 ml·kg-1·min-1) underwent three OGTTs after an overnight 12 hr fast: rest (control), 40-min (5 × 8-min with 2-min interbout rest) of concentric (level running, 0%, CON) or eccentric exercise (downhill running, –12%, ECC). Running intensity was matched at 60% of maximal metabolic equivalent. Maximal isometric force of m. quadriceps femoris of both legs was measured before and after the running protocols. Downhill running speed was higher (level: 9.7 ± 2.1, downhill: 13.8 ± 3.2 km·hr-1, p < .01). Running protocols had similar VO2max (p = .59), heart rates (p = .20) and respiratory exchange ratio values (p = .74) indicating matched intensity and metabolic demands. Downhill running resulted in higher isometric force deficits (level: 3.0 ± 6.7, downhill: 17.1 ± 7.3%, p < .01). During OGTTs, area-under-the-curve for plasma glucose (control: 724 ± 97, CON: 710 ± 77, ECC: 726 ± 72 mmol·L-1·120 min, p = .86) and insulin (control: 24995 ± 11229, CON: 23319 ± 10417, ECC: 21842 ± 10171 pmol·L-1·120 min, p = .48), peak glucose (control: 8.1 ± 1.3, CON: 7.7 ± 1.2, ECC: 7.7 ± 1.1 mmol·L-1, p = .63) and peak insulin levels (control: 361 ± 188, CON: 322 ± 179, ECC: 299 ± 152 pmol·L-1, p = .30) were similar. It was concluded that glucose tolerance and the insulin response to an OGTT were not changed immediately by muscle-damaging eccentric exercise.
Javier T. Gonzalez, Martin J. Barwood, Stuart Goodall, Kevin Thomas and Glyn Howatson
Unaccustomed eccentric exercise using large muscle groups elicits soreness, decrements in physical function and impairs markers of whole-body insulin sensitivity; although these effects are attenuated with a repeated exposure. Eccentric exercise of a small muscle group (elbow flexors) displays similar soreness and damage profiles in response to repeated exposure. However, it is unknown whether damage to small muscle groups impacts upon whole-body insulin sensitivity. This pilot investigation aimed to characterize whole-body insulin sensitivity in response to repeated bouts of eccentric exercise of the elbow flexors. Nine healthy males completed two bouts of eccentric exercise separated by 2 weeks. Insulin resistance (updated homeostasis model of insulin resistance, HOMA2-IR) and muscle damage profiles (soreness and physical function) were assessed before, and 48 h after exercise. Matsuda insulin sensitivity indices (ISIMatsuda) were also determined in 6 participants at the same time points as HOMA2-IR. Soreness was elevated, and physical function impaired, by both bouts of exercise (both p < .05) but to a lesser extent following bout 2 (time x bout interaction, p < .05). Eccentric exercise decreased ISIMatsuda after the first but not the second bout of eccentric exercise (time x bout interaction p < .05). Eccentric exercise performed with an isolated upper limb impairs whole-body insulin sensitivity after the first, but not the second, bout.
Che-Hsiu Chen, Trevor C. Chen, Mei-Hwa Jan and Jiu-Jenq Lin
To examine whether an acute bout of active or dynamic hamstring-stretching exercises would reduce the amount of muscle damage observed after a strenuous eccentric task and to determine whether the stretching protocols elicit similar responses.
A randomized controlled clinical trial.
Thirty-six young male students performed 5 min of jogging as a warm-up and were allocated to 1 of 3 groups: 3 min of static active stretching (SAS), 3 min of dynamic active stretching (DAS), or control (CON). All subjects performed eccentric exercise immediately after stretching. Heart rate, core temperature, maximal voluntary isometric contraction, passive hip flexion, passive hamstring stiffness (PHS), plasma creatine kinase activity, and myoglobin were recorded at prestretching, at poststretching, and every day after the eccentric exercises for 5 d.
After stretching, the change in hip flexion was significantly higher in the SAS (5°) and DAS (10.8°) groups than in the CON (–4.1°) group. The change in PHS was significantly higher in the DAS (5.6%) group than in the CON (–5.7%) and SAS (–6.7%) groups. Furthermore, changes in muscle-damage markers were smaller in the SAS group than in the DAS and CON groups.
Prior active stretching could be useful for attenuating the symptoms of muscle damage after eccentric exercise. SAS is recommended over DAS as a stretching protocol in terms of strength, hamstring range of motion, and damage markers.
Michael S. Green, J. Andrew Doyle, Christopher P. Ingalls, Dan Benardot, Jeffrey C. Rupp and Benjamin T. Corona
This study determined whether disrupted glucose and insulin responses to an oral glucose-tolerance test (OGTT) induced by eccentric exercise were attenuated after a repeated bout. Female participants (n = 10, age 24.7 ± 3.0 yr, body mass 64.9 ± 7.4 kg, height 1.67 ± 0.02 m, body fat 29% ± 2%) performed 2 bouts of downhill running (DTR 1 and DTR 2) separated by 14 d. OGTTs were administered at baseline and 48 hr after DTR 1 and DTR 2. Maximum voluntary isometric quadriceps torque (MVC), subjective soreness (100-mm visual analog scale), and serum creatine kinase (CK) were assessed pre-, post-, and 48 hr post-DTR 1 and DTR 2. Insulin and glucose area under the curve (38% ± 8% and 21% ± 5% increase, respectively) and peak insulin (44.1 ± 5.1 vs. 31.6 ± 4.0 μU/ml) and glucose (6.5 ± 0.4 vs. 5.5 ± 0.4 mmol/L) were elevated after DTR 1, with no increase above baseline 48 hr after DTR 2. MVC remained reduced by 9% ± 3% 48 hr after DTR 1, recovering back to baseline 48 hr after DTR 2. Soreness was elevated to a greater degree 48 hr after DTR 1 (48 ± 6 vs. 13 ± 3 mm), with a tendency for greater CK responses 48 hr after DTR 1 (813 ± 365 vs. 163 ± 43 U/L, p = .08). A novel bout of eccentric exercise confers protective effects, with subsequent bouts failing to elicit disruptions in glucose and insulin homeostasis.
Kevin S. O’Fallon, Diksha Kaushik, Bozena Michniak-Kohn, C. Patrick Dunne, Edward J. Zambraski and Priscilla M. Clarkson
The flavonoid quercetin is purported to have potent antioxidant and anti-inflammatory properties. This study examined if quercetin supplementation attenuates indicators of exercise-induced muscle damage in a doubleblind laboratory study. Thirty healthy subjects were randomized to quercetin (QU) or placebo (PL) supplementation and performed 2 separate sessions of 24 eccentric contractions of the elbow flexors. Muscle strength, soreness, resting arm angle, upper arm swelling, serum creatine kinase (CK) activity, plasma quercetin (PQ), interleukin-6 (IL-6), and C-reactive protein (CRP) were assessed before and for 5 d after exercise. Subjects then ingested nutrition bars containing 1,000 mg/d QU or PL for 7 d before and 5 d after the second exercise session, using the opposite arm. PQ reached 202 ± 52 ng/ml after 7 d of supplementation and remained elevated during the 5-d postexercise recovery period (p < .05). Subjects experienced strength loss (peak = 47%), muscle soreness (peak = 39 ± 6 mm), reduced arm angle (–7° ± 1°), CK elevations (peak = 3,307 ± 1,481 U/L), and arm swelling (peak = 11 ± 2 mm; p < .0001), indicating muscle damage and inflammation; however, differences between treatments were not detected. Eccentric exercise did not alter plasma IL-6 (peak = 1.9 pg/ml) or CRP (peak = 1.6 mg/L) relative to baseline or by treatment. QU supplementation had no effect on markers of muscle damage or inflammation after eccentric exercise of the elbow flexors.