ABSTRACT
OBJECTIVE: To identify the characteristics of physical activity that are the most correlated to total and truncal fatness and to physiological parameters involved in fat oxidation in elderly men. DESIGN: Cross-sectional study. SUBJECTS: A total of 25 healthy elderly men selected with a wide range of physical activity behavior (65.9 +/- 3.4 years). MEASUREMENTS: Total and truncal fat masses (by dual-energy X-ray absorptiometry), time spent and energy expended (EE(day)) at specific activity intensities (<40, 40-60, >60% VO2max) during 1 week in free living conditions (using heart rate recording and individual calibrated equations), sport-exercising volume (V(sport), using Baecke questionnaire), maximal oxygen uptake (VO2max), muscle fat oxidative capacity (OX(FA), using muscle biopsy), lipid oxidation and respiratory exchange ratio during exercise at 50% VO2max (using indirect calorimetry). RESULTS: V(sport) was the main determinant of total and truncal fatness, VO2max and OX(FA) (r = -0.69, P < 0.0001; r = -0.80, P < 0.0001; r = 0.70, P < 0.0001; r = 0.66, P<0.001, respectively). Among physical activity parameters measured over a week, total EE(day) was the main determinant of total fat mass. Furthermore, EE(day) at % VO2max > 60 was closely correlated to truncal fat mass, VO2max and OX(FA) (r = -0.58, P > 0.01; r = 0.55, P < 0.01; r = 0.49, P < 0.05, respectively). Finally, VO2max and OX(FA) were positively correlated to absolute fat oxidation and to the contribution of fat to energy production during moderate exercise. CONCLUSION: Sport-exercising volume is the main factor regulating total and truncal fat masses and physiological parameters involved in fat oxidation. With regard to the characteristics of physical activity, overall energy expended during the alert period plays a major role in the regulation of total body fatness. In addition, vigorous exercises may be beneficial for the regulation of abdominal fat depot partly through the stimulation of muscle fat oxidation during the effort.
Subject(s)
Body Composition/physiology , Intra-Abdominal Fat/physiology , Motor Activity/physiology , Absorptiometry, Photon , Aged , Calorimetry, Indirect , Cross-Sectional Studies , Energy Metabolism , Humans , Linear Models , Lipid Metabolism , Male , Middle Aged , Muscle, Skeletal/metabolism , Oxidation-Reduction , Oxygen Consumption , SportsABSTRACT
Age-related changes in mitochondrial H2O2 release (MHR) could be responsible for an increase in oxidative stress in skeletal muscle and participate in the development of sarcopenia. We compared MHR in vastus lateralis biopsies obtained from young (23.5+/-2.0 year, n=6) and elderly (67.3+/-1.5 year, n=6) healthy sedentary men. Isolated mitochondria were incubated in the presence of glutamate/malate/succinate, with or without rotenone. Muscle fat oxidative capacity, citrate synthase, complex II, complex III, and cytochrome c oxidase activities were also measured. In parallel, we analyzed in gastrocnemius of young male Wistar rats (n=6), the impact of lidocaine (local anesthetic used in humans) on mitochondrial respiration and MHR. In humans, muscle oxidative capacity was preserved with age but muscle MHR was markedly enhanced in elderly subjects compared to young adults (+175%, P<0.05). Rotenone abolished this increase, demonstrating that it was due to a free radical release during reverse electron transfer from complex II towards complex I. Lidocaine can interfere with MHR measurements (intra-muscular injection in rats) but it can be avoided by minimizing contact with muscle (small multiple subcutaneous injections in humans). Physiologic consequences of the observed increase in muscle MHR with aging remain to be determined.
