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Musculação: Crenças vs. Evidências
Abstract
Strength training is a common form of physical exercise in gyms and a scientific fields that has evolved over the past decades. However, the practice of strength training in gyms is still surrounded by myths, cultural beliefs and the practical application of scientific evidence in the training prescription seems to be far from the reality. Thus, it is necessary to confront common practices with the most relevant scientific findings in order to endorse this behavior if they are converging, or redirect them, in case of disagreement. The aim of this
study is do a critical essay on some beliefs adopted in strength training routines, based on relevant theoretical and scientific references.
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Exercise-induced muscle damage (EIMD) is commonly experienced following either a bout of unaccustomed physical activity or following physical activity of greater than normal duration or intensity. The mechanistic factor responsible for the initiation of EIMD is not known; however, it is hypothesised to be either mechanical or metabolic in nature. The mechanical stress hypothesis states that EIMD is the result of physical stress upon the muscle fibre. In contrast, the metabolic stress model predicts that EIMD is the result of metabolic deficiencies, possibly through the decreased action of Ca(2+)-adenosine triphosphatase. Irrespective of the cause of the damage, EIMD has a number of profound metabolic effects. The most notable metabolic effects of EIMD are decreased insulin sensitivity, prolonged glycogen depletion and an increase in metabolic rate both at rest and during exercise. Based on current knowledge regarding the effects that various types of damaging exercise have on muscle metabolism, a new model for the initiation of EIMD is proposed. This model states that damage initiation may be either metabolic or mechanical, or a combination of both, depending on the mode, intensity and duration of exercise and the training status of the individual.
The objective of this study was to investigate the acute effects of performing paired set (PS) vs. traditional set (TS) training over 3 consecutive sets on volume load (VL) and electromyographic (EMG) activity of the pectoralis major, anterior deltoid, latissimus dorsi, and trapezius muscles. Following a familiarization session 16 trained males performed 2 testing protocols using 4 repetition maximum loads: TS (3 sets of bench pull [Bpull] followed by 3 sets of bench press [Bpress] performed in approximately 20 minutes) or PS (3 sets of Bpull and 3 sets of Bpress performed in an alternating manner in approximately 10 minutes). Bpull and Bpress VL decreased significantly from set 1 to set 2 and from set 2 to set 3 under both conditions. There was no difference between VL per set, or over the sessions, between the 2 conditions. PS was determined to be more efficient (VL/time) as compared to TS. EMG activity of the 4 monitored muscles was not different for the 2 conditions or within each condition over the 3 sets. However, there was a significant within-set response in EMG activity in the Bpress exercise. The data suggest that a 4-minute rest interval between sets may not be adequate to maintain VL using either protocol. The data further suggest that PS training may be as effective as TS training in terms of VL maintenance and more effective in terms of efficiency. The comparison of EMG activity between the PS and TS protocols suggests that the level of neuromuscular fatigue does not differ under the 2 conditions. PS training would appear to be an effective method of exercise with respect to VL maintenance and efficiency.
This placebo-controlled, double-blind crossover study assessed whether exclusive activation of peripheral opioid receptors results in significant pain reduction. To achieve opioid activity restricted to the periphery, we used a short-term (2 h) low dose infusion of morphine-6-beta-glucuronide (M6G) because M6G does not pass the blood-brain barrier during this time in amounts sufficient to induce CNS effects. The lack of central opioid effects of M6G was confirmed by a lack of change of the pupil size and absence of other opioid-related CNS effects. As a positive control, morphine was infused at a dosage that definitely produced CNS effects. This was evident by a rapid decrease of the pupil size and by other typical opioid-related side effects including nausea, vomiting, itchiness, hiccup and sedation. Three different pain models were employed to evaluate the analgesic effects: (i) cutaneous inflammatory hyperalgesia induced by briefly freezing a small skin area to -30 degrees C ('freeze lesion'); (ii) muscle hyperalgesia induced by a series of concentric and eccentric muscle contractions (DOMS model; delayed onset of muscle soreness); and (iii) pain induced by electrical current (5 Hz sinus stimuli of 0-10 mA). M6G significantly reduced cutaneous hyperalgesia in the 'freeze lesion' model as assessed with von Frey hairs. It also reduced muscle hyperalgesia in the DOMS model. Electrical pain, however, was not affected by M6G. Morphine was significantly more active in the 'freeze lesion' and DOMS model, and also significantly increased the electrical pain threshold and tolerance. Subcutaneous tissue concentrations of M6G and morphine as assessed with microdialysis were about half those of the respective plasma concentrations. The results of the study indicate that M6G has antihyperalgesic effects in inflammatory pain through activation of peripheral opioid receptors. Since this occurs at concentrations that do not cause central opioid effects, M6G might be useful as a peripheral opioid analgesic.
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