D. Ranney

Muscle performance, morphology and metabolic capacity during strength training and detraining: a one leg model.

SummaryTo investigate biochemical, histochemical and contractile properties associated with strength training and detraining, six adult males were studied during and after 10 weeks of dynamic strength training for the quadriceps muscle group of one leg, as well as during and after a subsequent 12 weeks of detraining. Peak torque outputs at the velocities tested (0–270‡·s−1) were increased (p<0.05) by 39–60% and 12–37% after training for the trained and untrained legs, respectively. No significant changes in peak torques were observed in six control subjects tested at the same times. Significant decreases in strength performance of the trained leg (16–21%) and untrained leg (10–15%) were observed only after 12 weeks of detraining. Training resulted in an increase (p≪0.05) in the area of FTa (21%) and FTb (18%) fibres, while detraining was associated with a 12% decrease in FTb fibre cross-sectional area. However, fibre area changes were only noted in the trained leg. Neither training nor detaining had any significant effect on the specific activity of magnesium-activated myofibrillar ATPase or on the activities of enzymes of phosphagen, glycolytic or oxidative metabolism in serial muscle biopsy samples from both legs. In the absence of any changes in muscle enzyme activities and with only modest changes in FT fibre areas in the trained leg, the significant alterations in peak torque outputs with both legs suggest that neural adaptations play a prominent role in strength performance with training and detraining.

Regulation of fiber size, oxidative potential, and capillarization in human muscle by resistance exercise

To examine the hypothesis that increases in fiber cross-sectional area mediated by high-resistance training (HRT) would result in a decrease in fiber capillarization and oxidative potential, regardless of fiber type, we studied six untrained males (maximum oxygen consumption, 45.6 +/- 2.3 ml. kg-1. min-1; mean +/- SE) participating in a 12-wk program designed to produce a progressive hypertrophy of the quadriceps muscle. The training sessions, which were conducted 3 times/wk, consisted of three sets of three exercises, each performed for 6-8 repetitions maximum (RM). Measurements of fiber-type distribution obtained from tissue extracted from the vastus lateralis at 0, 4, 7, and 12 wk indicated reductions (P < 0.05) in type IIB fibers (15.1 +/- 2.1% vs. 7.2 +/- 1.3%) by 4 wk in the absence of changes in the other fiber types (types I, IIA, and IIAB). Training culminated in a 17% increase (P < 0.05) in cross-sectional area by 12 wk with initial increases observed at 4 wk. The increase was independent of fiber type-specific changes. The number of capillaries in contact with each fiber type increased by 12 wk, whereas capillary contacts-to-fiber area ratios remained unchanged. In a defined cross-sectional field, HRT also increased the capillaries per fiber at 12 wk. Training failed to alter cellular oxidative potential, as measured by succinic dehydrogenase (SDH) activity, regardless of fiber type and training duration. It is concluded that modest hypertrophy induced by HRT does not compromise cellular tissue capillarization and oxidative potential regardless of fiber type.To examine the hypothesis that increases in fiber cross-sectional area mediated by high-resistance training (HRT) would result in a decrease in fiber capillarization and oxidative potential, regardless of fiber type, we studied six untrained males (maximum oxygen consumption, 45.6 ± 2.3 ml ⋅ kg-1 ⋅ min-1; mean ± SE) participating in a 12-wk program designed to produce a progressive hypertrophy of the quadriceps muscle. The training sessions, which were conducted 3 times/wk, consisted of three sets of three exercises, each performed for 6-8 repetitions maximum (RM). Measurements of fiber-type distribution obtained from tissue extracted from the vastus lateralis at 0, 4, 7, and 12 wk indicated reductions ( P < 0.05) in type IIB fibers (15.1 ± 2.1% vs. 7.2 ± 1.3%) by 4 wk in the absence of changes in the other fiber types (types I, IIA, and IIAB). Training culminated in a 17% increase ( P < 0.05) in cross-sectional area by 12 wk with initial increases observed at 4 wk. The increase was independent of fiber type-specific changes. The number of capillaries in contact with each fiber type increased by 12 wk, whereas capillary contacts-to-fiber area ratios remained unchanged. In a defined cross-sectional field, HRT also increased the capillaries per fiber at 12 wk. Training failed to alter cellular oxidative potential, as measured by succinic dehydrogenase (SDH) activity, regardless of fiber type and training duration. It is concluded that modest hypertrophy induced by HRT does not compromise cellular tissue capillarization and oxidative potential regardless of fiber type.

Fiber composition, fiber size and enzyme activities in vastus lateralis of elite athletes involved in high intensity exercise.

SummaryIn order to determine the influence of an extensive history of participation in high intensity activity on muscle fiber type, fiber size, and metabolic profile, elite ice hockey players were selected for investigation from three different leagues. Biopsy samples from the vastus lateralis muscle were obtained from different groups of players prior to and following the season and compared with control subjects. No significant differences were found in the percentage (49.6 vs. 43.8%) or the size of the ST fibers between the elite athletes and the control group, nor was there any significant alteration following the season of play in these variables. For the FT fiber subgroups, a reduction in the FTb (12.2 vs. 3.9%) and an increase in FTa (38.0 to 45.2%) fiber populations occurred over the season. Similarly, increases in fiber area were observed for both FT subgroups pre to post season. Of the enzymes studied only 3-hydroxyacyl CoA dehydrogenase was elevated in the post season measures, while total phosphorylase and phosphofructokinase were significantly lower. The metabolic pattern exhibited does not appear to be substantially different from what would be expected from an untrained group of similar fiber distribution.

Initial aerobic power does not alter muscle metabolic adaptations to short-term training

To investigate the hypothesis that training-induced increases in muscle mitochondrial potential are not obligatory to metabolic adaptations observed during submaximal exercise, regardless of peak aerobic power (V˙o 2 peak) of the subjects, a short-term training study was utilized. Two groups of untrained male subjects ( n = 7/group), one with a high (HI) and the other with a low (LO)V˙o 2 peak(means ± SE; 51.4 ± 0.90 vs. 41.0 ± 1.3 ml ⋅ kg-1 ⋅ min-1; P< 0.05), cycled for 2 h/day at 66-69% ofV˙o 2 peak for 6 days. Muscle tissue was extracted from vastus lateralis at 0, 3, and 30 min of standardized cycle exercise before training (0 days) and after 3 and 6 days of training and analyzed for metabolic and enzymatic changes. During exercise after 3 days of training in the combined HI + LO group, higher ( P < 0.05) concentrations (mmol/kg dry wt) of phosphocreatine (40.5 ± 3.4 vs. 52.2 ± 4.2) and lower ( P < 0.05) concentrations of Pi (61.5 ± 4.4 vs. 53.3 ± 4.4), inosine monophosphate (0.520 ± 0.19 vs. 0.151 ± 0.05), and lactate (37.9 ± 5.5 vs. 22.8 ± 4.8) were observed. These changes were also accompanied by reduced levels of calculated free ADP, AMP, and Pi. All adaptations were fully expressed by 3 min of exercise and by 3 days of training and were independent of initialV˙o 2 peak levels. Moreover, maximal activity of citrate synthase, a measure of mitochondrial capacity, was only increased with 6 days of training (5.71 ± 0.29 vs. 7.18 ± 0.37 mol ⋅ kg protein-1 ⋅ h-1; P < 0.05). These results demonstrate that metabolic adaptations to prolonged exercise occur within the first 3 days of training and during the non-steady-state period. Moreover, neither time course nor magnitude of metabolic adaptations appears to depend on increases in mitochondrial potential or on initial aerobic power.

Thoracic outlet: An anatomical redefinition that makes clinical sense

The diagnosis of thoracic outlet syndrome (TOS) is intrinsically difficult, and the literature about it is full of confusing terminology. Symptoms may arise due to compression of neural and/or vascular elements in one or more of three different locations. A number of tests were developed during the early part of this century, and a variety of syndromes have been described that relate to these tests, all of which are now considered to be subtypes of the thoracic outlet syndrome. Yet anatomists and clinicians fail to agree on even the definition of the thoracic outlet. It is proposed that anatomists not use the term thoracic inlet as a synonym for the superior thoracic aperture, nor thoracic outlet for the inferior thoracic aperture. What many clinicians call the thoracic outlet should be called the scalene triangle by both anatomists and clinicians, divisible into a lower portion to be called the thoracic outlet (for subclavian vessels and nerve roots C.8 and T.1) and an upper portion, the cervical outlet (for nerve roots C.5, C.6, and normally C.7). What is currently called thoracic outlet syndrome should be renamed the cervico‐axillary syndrome (CAS), divisible into three subtypes: thoracic outlet, costoclavicular, and pectoralis minor syndromes. Compression of the upper roots of the brachial plexus between the anterior and middle scalene muscles should be recognized as cervical outlet syndrome, and all terms containing the word scalenus should be discarded.

Work-related chronic injuries of the forearm and hand: their specific diagnosis and management

Work-related chronic injuries occur in muscles, tendons, and nerves. Epidemiological, histological, and physiological data confirm their often disputed physical basis. Terms such as repetitive strain injury and cumulative trauma disorder, when used as a diagnosis, have obscured the issue for they are really statements of causation. Definitive diagnosis is required both to treat and prevent such injuries. Precise terminology that identifies the tissue and its pathology is required. A detailed assessment methodology is described that allows a precise diagnosis. A clear relationship to work stress is necessary both to establish the cause and formulate prevention strategies. Treatment must begin early and be appropriate to the tissue and the nature of the injury. Examples are presented and discussed. Early treatment begins before too much damage has been done and yields better results.

Physiological and muscle enzyme adaptations to two different intensities of swim training

SummaryTo test the hypothesis that a smaller quantity of high intensity (HI) as opposed to a larger quantity of moderate intensity (MI) swim training would result in adaptations more specific to the short performance times of swimming competitions, two groups of elite university swimmers were tested before and after 6.5 weeks of specific HI or MI intermittent swim training. In training, swimming times were faster and blood lactate concentrations were higher (10.2 vs. 7.5 mM) during HI compared to MI training. No significant differences were observed between the two groups for any of the variables measured, before or after training. However, significant increases with training were observed for the activities of hexokinase, phosphorylase, phosphofructokinase, succinate dehydrogenase, and 3-hydroxyacyl CoA dehydrogenase in the deltoid, but not the gastrocnemius muscles. Training resulted in significant increases in

Muscle metabolism and acid-base status during exercise in forearm work-related myalgia measured with 31P-MRS

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