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C B Ebbeling

Publications and source records attributed to C B Ebbeling.

4 recordsLinked to original sources
PubMed1991

Development of a single-stage submaximal treadmill walking test.

An equation was developed to estimate maximal oxygen uptake (VO2max, ml.kg-1.min-1) based on a single submaximal stage of a treadmill walking test. Subjects (67 males, 72 females) aged 20-59 yr completed 4-min stages at 0, 5, and 10% grades walking at a constant speed (2.0-4.5 mph) and then performed a VO2max test. Heart rate and respiratory gas exchange variables were measured during the test. Multiple regression analysis (N = 117) to estimate VO2max from the 4-min stage at 5% grade yielded the following model (R2 = 0.86; SEE = 4.85 ml.kg-1.min-1): VO2max = 15.1 + 21.8*SPEED (mph) -0.327*HEART RATE (bpm) -0.263*SPEED*AGE (yr) + 0.00504*HEART RATE*AGE + 5.98*GENDER (0 = Female; 1 = Male). The constant and all coefficients were highly significant (P less than 0.01). To assess the accuracy of the model in a cross-validation group (N = 22), an estimated VO2max value was obtained using the above model. Estimated VO2max then was regressed on observed VO2max yielding the following equation (R2 = 0.92): ESTIMATED VO2max = 0.15 + 1.03*OBSERVED VO2max. The intercept and slope of this equation were not significantly different from 0 and 1, respectively. For 90.9% of the subjects in the cross-validation group, residual scores were within the range of +/- 5 ml.kg-1.min-1. In conclusion, this submaximal walking test based on a single stage of a treadmill protocol provides a valid and time-efficient method for estimating VO2max.

Adult↗
PubMed1990

Muscle adaptation prior to recovery following eccentric exercise.

The effects of performing a second eccentric exercise bout prior to and after recovery from the first bout were compared. Twenty subjects performed 70 eccentric actions with the forearm flexors. Group A (n = 9) and group B (n = 11) repeated the same exercise 5 and 14 days after the initial bout, respectively. Dependent variables included muscle soreness, elbow joint angles, isometric strength, and serum creatine kinase (SCK). Subjects were tested pre-exercise and up to day 5 following each bout. The first bout produced significant changes in all measures for both groups (P less than 0.01). Values remained significantly different from baseline on day 5 when group A repeated the exercise (P less than 0.01) but were back to normal when group B performed bout 2. For both groups an adaptation occurred; significantly smaller changes in dependent variables were produced by the second bout, and recovery time was faster whether or not muscles were fully restored (P less than 0.01). The repeated bout did not exacerbate soreness, performance decrements, and elevation of SCK when performed by affected muscles that had not fully recovered from the first bout. Thus, the results suggest that an adaptation response had taken place prior to full recovery and restoration of muscle function following the initial eccentric exercise bout.

Adaptation, Physiological↗
PubMed1989

Exercise-induced muscle damage and adaptation.

Novel, unaccustomed exercise has been shown to result in temporary, repairable skeletal muscle damage. After exhaustive endurance exercise, muscle damage can be produced by metabolic disturbances associated with ischaemia. Extensive disruption of muscle fibres also occurs after relatively short term eccentric exercise where high mechanical forces are generated. Biopsies taken after repetitive eccentric muscle actions have revealed broadening, streaming and, at times, total disruption of Z-discs. Muscles that develop active tension eccentrically also become sore, lose inherent force-producing capability, and show a marked release of muscle proteins into the circulation. Because creatine kinase (CK) is found almost exclusively in muscle tissue, it is the most common plasma marker of muscle damage. Despite the universal use of CK as a marker, several factors with regard to efflux and clearance remain unexplained. Also the large intersubject variability in response to exercise complicates its interpretation. Damage progresses in the postexercise period before tissues are repaired. However, the mechanism to explain exercise-induced muscle damage and repair is not well defined. Among the factors that may influence the damage and repair processes are calcium, lysosomes, connective tissue, free radicals, energy sources, and cytoskeletal and myofibrillar proteins. Physical conditioning results in an adaptation such that all indicators of damage are reduced following repeated bouts of exercise. Recently, investigators have suggested that the prophylactic effect of training may be due to performance of a single initial exercise bout. Following a second bout of exercise performed 1 to 6 weeks after the first bout, there is a reduction in morphological alterations and performance decrements and a profoundly reduced elevation in plasma CK levels. Several hypotheses have been presented to explain the repeated bout or rapid training effect. Stress-susceptible fibres may be eliminated or susceptible areas within a fibre may undergo necrosis and then regenerate. These regenerated fibres, along with adaptations in the connective tissue, may provide greater resistance to further insult.

Adaptation, Physiological↗