Acute Strength Loss Induced By Concurrent Exercise Is Associated With Alterations In Metabolic, But Not Inflammatory Response

Por: B. M. M. Antunes, D. S. I. Yoshimura, E. Franchini, F. E. Rossi, F. S. Lira, J. Gerosa Neto, L. A. Gobbo, P. A. Monteiro e V. L. G. Panissa.

IX Congresso Internacional de Educação Física e Motricidade Humana XV Simpósio Paulista de Educação Física

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Resumo

Strength loss induced by concurrent exercise may be promoted by a residual fatigue due to insufficient recovery between the aerobic and strength activity although the mechanisms remain unclear. Causes not so well defined of muscle fatigue include inflammatory interleukin 6 (IL-6) cytokine. In addition, IL-6 and tumor necrosis factor alpha (TNF-α) have been considered an energetic sensor able to signalize a hormone-like manner to mobilize extracellular glucose and free fatty acids during exercise. The objective of this study was to evaluate the effect of high-intensity running on acute strength performance, metabolic and inflammatory response related to fatigue (lactate, free fatty acid, glucose, interleukin 6, interleukin 10 and tumor necrosis factor alpha). Participated in this study ten physically active male subjects who underwent three randomized session: 1) four sets of half-squat strength exercise until exhaustion at 80% 1MR (S), 2) 5-kilometer run high-intensity intermittent aerobic exercise at maximal intensity - Vmax (A), 3) 5- kilometer run high-intensity intermittent aerobic exercise at maximal intensity - Vmax before the strength exercise (AS). The blood samples were collected at rest and immediately after the S, A or AS conditions and fatigue markers were analyzed. The appropriated statistical methods were applied. The S condition presented higher number of repetitions and total volume than AS condition (p = 0.001). The Uglucose (p = 0.006), and Ulactate (p < 0.001) were superior in S compared to AS condition. There were no differences in UIL-6, IL-10, TNF-α and UNEFA. Our data demonstrated that acute strength loss induced by concurrent exercise was associated with alterations in metabolic, but not inflammatory response, possibly because a fail in the skeletal muscle contraction occurred. Studies that explore strategies aiming the reduction of this failure in skeletal muscle contraction in concurrent exercise, such as nutritional supplementation, can help for performance improvement. We suggest that the concurrent exercise, in which the interference phenomena is observed, can leads disturbance in the intracellular signaling pathways that regulates contractile of skeletal muscle during exercise, prejudicing all apparatus related with muscle work during exercise, and impairing glucose uptake and/or oxidation and IL-6 production. However, more studies are needed to better understand the mechanisms involved in the condition.

Endereço: http://www.periodicos.rc.biblioteca.unesp.br/index.php/motriz/article/view/10060/10060

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