Concurrent strength and endurance training appears to inhibit strength development when compared with strength training alone. Our understanding of the nature of this inhibition and the mechanisms responsible for it is limited at present. This is due to the difficulties associated with comparing results of studies which differ markedly in a number of design factors, including the mode, frequency, duration and intensity of training, training history of participants, scheduling of training sessions and dependent variable selection. Despite these difficulties, both chronic and acute hypotheses have been proposed to explain the phenomenon of strength inhibition during concurrent training. The chronic hypothesis contends that skeletal muscle cannot adapt metabolically or morphologically to both strength and endurance training simultaneously. This is because many adaptations at the muscle level observed in response to strength training are different from those observed after endurance training. The observation that changes in muscle fibre type and size after concurrent training are different from those observed after strength training provide some support for the chronic hypothesis. The acute hypothesis contends that residual fatigue from the endurance component of concurrent training compromises the ability to develop tension during the strength element of concurrent training. It is proposed that repeated acute reductions in the quality of strength training sessions then lead to a reduction in strength development over time. Peripheral fatigue factors such as muscle damage and glycogen depletion have been implicated as possible fatigue mechanisms associated with the acute hypothesis. Further systematic research is necessary to quantify the inhibitory effects of concurrent training on strength development and to identify different training approaches that may overcome any negative effects of concurrent training.
This investigation evaluated the effects of oral beta-hydroxy-beta-methylbutyrate (HMB) supplementation on training responses in resistance-trained male athletes who were randomly administered HMB in standard encapsulation (SH), HMB in time release capsule (TRH), or placebo (P) in a double-blind fashion. Subjects ingested 3 g x day(-1) of HMB or placebo for 6 weeks. Tests were conducted pre-supplementation and following 3 and 6 weeks of supplementation. The testing battery assessed body mass, body composition (using dual energy x-ray absorptiometry), and 3-repetition maximum isoinertial strength, plus biochemical parameters, including markers of muscle damage and muscle protein turnover. While the training and dietary intervention of the investigation resulted in significant strength gains (p < .001) and an increase in total lean mass (p = .01), HMB administration had no influence on these variables. Likewise, biochemical markers of muscle protein turnover and muscle damage were also unaffected by HMB supplementation. The data indicate that 6 weeks of HMB supplementation in either SH or TRH form does not influence changes in strength and body composition in response to resistance training in strength-trained athletes.
Athletic strength and power refer to the forces or torques generated during sporting activity. Their assessment can be used for strength diagnosis or talent identification, to monitor the effects of training interventions and to estimate the relative significance of strength and power to particular athletic pursuits. However, strength and power assessment is a difficult task. Reasons for this include: the fledgling status of research within the area, our limited understanding of the mechanisms underpinning strength and power performance and development, and limitations associated with various forms of dynamometry. This article describes a frame work for the collection of data which may ultimately lead to recommendations for the assessment of strength and power in sporting contexts. Such a framework will be evolutionary and depends upon synergistic improvements in our understanding of: the physiological mechanisms underpinning strength and power development; the effect that various training regimens have upon the development of strength and power; and factors influencing the validity and reliability of dynamometry. Currently, isometric, isoinertial and isokinetic dynamometry are employed in assessment. Each form has its supporters and detractors. Basically, proponents and critics of isokinetic and isometric dynamometry emphasis their apparently high internal and apparently low external [corrected] validity respectively. While the converse applies for isoinertial dynamometry. It appears that all 3 modalities can have acceptable reliability, however this should be established rather than assumed, as the reliability of each can be threatened by a number of considerations (e.g. instruction for isometric tasks, the impact of weight used during weighted jumping tasks, and the effects of gravity and feedback on isokinetic performance). While reliability is a seminal issue in assessment, it is not the only critical issue. Specifically, there has been little research into the correlation between strength and power measures and athletic performance. This work is central to the use of such indices in talent identification. To date, this work has generally been limited to heterogeneous rather than homogeneous groups. More work is required in this area. Furthermore, not all modes of assessment are sensitive or similarly sensitive to various training interventions. This suggests that these modalities are measuring different neuromuscular qualities. How these qualities relate to performance requires more work, and will determine the contexts in which various strength and power assessment modalities and protocols are used.(ABSTRACT TRUNCATED AT 400 WORDS)
Skeletal muscle tissue is sensitive to the acute and chronic stresses associated with resistance training. These responses are influenced by the structure of resistance activity (i.e. frequency, load and recovery) as well as the training history of the individuals involved. There are histochemical and biochemical data which suggest that resistance training alters the expression of myosin heavy chains (MHCs). Specifically, chronic exposure to bodybuilding and power lifting type activity produces shifts towards the MHC I and IIb isoforms, respectively. However, it is not yet clear which training parameters trigger these differential expressions of MHC isoforms. Interestingly, many programmes undertaken by athletes appear to cause a shift towards the MHC I isoform. Increments in the cross-sectional area of muscle after resistance training can be primarily attributed to fibre hypertrophy. However, there may be an upper limit to this hypertrophy. Furthermore, significant fibre hypertrophy appears to follow the sequence of fast twitch fibre hypertrophy preceding slow twitch fibre hypertrophy. Whilst some indirect measures of fibre number in living humans suggest that there is no interindividual variation, postmortem evidence suggests that there is. There are also animal data arising from investigations using resistance training protocols which suggest that chronic exercise can increase fibre number. Furthermore, satellite cell activity has been linked to myotube formation in the human. However, other animal models (i.e. compensatory hypertrophy) do not support the notion of fibre hyperplasia. Even if hyperplasia does occur, its effect on the cross-sectional area of muscle appears to be small. Phosphagen and glycogen metabolism, whilst important during resistance activity appear not to normally limit the performance of resistance activity. Phosphagen and related enzyme adaptations are affected by the type, structure and duration of resistance training. Whilst endogenous glycogen reserves may be increased with prolonged training, typical isotonic training for less than 6 months does not seem to increase glycolytic enzyme activity. Lipid metabolism may be of some significance in bodybuilding type activity. Thus, not surprisingly, oxidative enzyme adaptations appear to be affected by the structure and perhaps the modality of resistance training. The dilution of mitochondrial volume and endogenous lipid densities appears mainly because of fibre hypertrophy.
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