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Background: Previous studies suggested that physical activity energy expenditure (AEE) is a major determinant of dietary fat oxidation, which is a central component of fat metabolism and body weight regulation., Objective: We tested this hypothesis by investigating the effect of contrasted physical activity levels on dietary saturated and monounsaturated fatty acid oxidation in relation to insulin sensitivity while controlling energy balance., Design: Sedentary lean men (n = 10) trained for 2 mo according to the current guidelines on physical activity, and active lean men (n = 9) detrained for 1 mo by reducing structured and spontaneous activity. Dietary [d31]palmitate and [1-¹³C]oleate oxidation and incorporation into triglyceride-rich lipoproteins and nonesterified fatty acid, AEE, and muscle markers were studied before and after interventions., Results: Training increased palmitate and oleate oxidation by 27% and 20%, respectively, whereas detraining reduced them by 31% and 13%, respectively (P < 0.05 for all). Changes in AEE were positively correlated with changes in oleate (R² = 0.62, P < 0.001) and palmitate (R² = 0.66, P < 0.0001) oxidation. The d31-palmitate appearance in nonesterified fatty acid and very-low-density lipoprotein pools was negatively associated with changes in fatty acid translocase CD36 (R² = 0.30), fatty acid transport protein 1 (R² = 0.24), and AcylCoA synthetase long chain family member 1 (ACSL1) (R² = 0.25) expressions and with changes in fatty acid binding protein expression (R² = 0.33). The d31-palmitate oxidation correlated with changes in ACSL1 (R² = 0.39) and carnitine palmitoyltransferase 1 (R² = 0.30) expressions (P < 0.05 for all). Similar relations were observed with oleate. Insulin response was associated with AEE (R² = 0.34, P = 0.02) and oleate (R² = 0.52, P < 0.01) and palmitate (R² = 0.62, P < 001) oxidation., Conclusion: Training and detraining modified the oxidation of the 2 most common dietary fats, likely through a better trafficking and uptake by the muscle, which was negatively associated with whole-body insulin sensitivity.

Gain or loss of skeletal muscle mass occurs in situations of altered use such as strength training, aging, denervation, or immobilization. This review examines our current understanding of the cellular and molecular events involved in the control of muscle mass under conditions of muscle use and disuse, with particular attention to the effects of resistance exercise/training. The DNA content, which is a critical determinant of protein synthesis by providing the amount of DNA necessary to sustain gene transcription, can be either increased (activation of satellite cells) or decreased (apoptosis) depending on muscle activity and ongoing physiological processes. In addition, several transcription factors are sensitive to functional demand and may control muscle-specific protein expression to promote or repress myofiber enlargement. The control of skeletal muscle mass is also markedly mediated by the regulation of transduction pathways that promote the synthesis and/or the degradation of proteins. Insulin-like growth factor-I plays a key role in this balance by activating the Akt/tuberous sclerosis complex 2/mammalian target of rapamycin pathway. Stimulation of this pathway leads to the concomitant activation of initiation and elongation factors resulting in the elevation of protein translation and the downregulation of ubiquitin proteasome components through Forkhead-box O transcription factors.

• The physical treatment of low back pain includes a wide range of non-specific and specific physical activity. • The value of physical activity in acute or subacute low back pain has not been demonstrated. • General exercise, more specific interventions and multidisciplinary functional restoration programs reduce pain and improve physical function in patients with chronic low back pain. • The optimal delivery of physical activity in terms of modalities, quantity and intensity of the intervention, supervision, and setting is not well defined. Non-specific low back pain (LBP) is the leading cause of years lived with disability worldwide. Physical activity is an integral part of LBP treatment. To critically review available evidence regarding the efficacy of physical activity for people with LBP. Up to date critical narrative review of the efficacy of physical activity for the managment LBP. The process of article selection was unsystematic; articles were selected based on authors' expertise, self-knowledge and reflective practice. Therapeutic physical activity for LBP includes a wide range of non-specific and specific activities. The efficacy of physical activity on pain and activity limitations has been widely assessed. In acute and subacute LBP, exercise did not reduce pain compared to no exercise. In chronic low back pain (CLBP), exercise reduced pain at the earliest follow-up compared with no exercise. In a recent systematic review, exercise improved function both at the end of treatment and in the long-term compared with usual care. Exercice also reduced work disability in the long-term. We were unable to establish a clear hierarchy between different exercise modalities. Multidisciplinary functional programs consistently improved pain and function in the short- and long-term compared with usual care and physiotherapy and improved the long-term likelihood of returning to work compared to non-multidisciplinary programs. Physical activity of all types is an effective treatment for CLBP. [ABSTRACT FROM AUTHOR]