Capsiate supplementation reduces oxidative cost of contraction in exercising mouse skeletal muscle in vivo.

Chronic administration of capsiate is known to accelerate whole-body basal energy metabolism, but the consequences in exercising skeletal muscle remain very poorly documented. In order to clarify this issue, the effect of 2-week daily administration of either vehicle (control) or purified capsiate (at 10- or 100-mg/kg body weight) on skeletal muscle function and energetics were investigated throughout a multidisciplinary approach combining in vivo and in vitro measurements in mice. Mechanical performance and energy metabolism were assessed strictly non-invasively in contracting gastrocnemius muscle using magnetic resonance (MR) imaging and 31-phosphorus MR spectroscopy (31P-MRS). Regardless of the dose, capsiate treatments markedly disturbed basal bioenergetics in vivo including intracellular pH alkalosis and decreased phosphocreatine content. Besides, capsiate administration did affect neither mitochondrial uncoupling protein-3 gene expression nor both basal and maximal oxygen consumption in isolated saponin-permeabilized fibers, but decreased by about twofold the Km of mitochondrial respiration for ADP. During a standardized in vivo fatiguing protocol (6-min of repeated maximal isometric contractions electrically induced at a frequency of 1.7 Hz), both capsiate treatments reduced oxidative cost of contraction by 30-40%, whereas force-generating capacity and fatigability were not changed. Moreover, the rate of phosphocreatine resynthesis during the post-electrostimulation recovery period remained unaffected by capsiate. Both capsiate treatments further promoted muscle mass gain, and the higher dose also reduced body weight gain and abdominal fat content. These findings demonstrate that, in addition to its anti-obesity effect, capsiate supplementation improves oxidative metabolism in exercising muscle, which strengthen this compound as a natural compound for improving health.

Effects of exercise-induced intracellular acidosis on the phosphocreatine recovery kinetics: a 31P MRS study in three muscle groups in humans.

Little is known about the metabolic differences that exist among different muscle groups within the same subjects. Therefore, we used (31)P-magnetic resonance spectroscopy ((31)P-MRS) to investigate muscle oxidative capacity and the potential effects of pH on PCr recovery kinetics between muscles of different phenotypes (quadriceps (Q), finger (FF) and plantar flexors (PF)) in the same cohort of 16 untrained adults. The estimated muscle oxidative capacity was lower in Q (29 ± 12 mM min(-1), CV(inter-subject) = 42%) as compared with PF (46 ± 20 mM min(-1), CV(inter-subject) = 44%) and tended to be higher in FF (43 ± 35 mM min(-1), CV(inter-subject) = 80%). The coefficient of variation (CV) of oxidative capacity between muscles within the group was 59 ± 24%. PCr recovery time constant was correlated with end-exercise pH in Q (p < 0.01), FF (p < 0.05) and PF (p < 0.05) as well as proton efflux rate in FF (p < 0.01), PF (p < 0.01) and Q (p = 0.12). We also observed a steeper slope of the relationship between end-exercise acidosis and PCr recovery kinetics in FF compared with either PF or Q muscles. Overall, this study supports the concept of skeletal muscle heterogeneity by revealing a comparable inter- and intra-individual variability in oxidative capacity across three skeletal muscles in untrained individuals. These findings also indicate that the sensitivity of mitochondrial respiration to the inhibition associated with cytosolic acidosis is greater in the finger flexor muscles compared with locomotor muscles, which might be related to differences in permeability in the mitochondrial membrane and, to some extent, to proton efflux rates.

The slow components of phosphocreatine and pulmonary oxygen uptake can be dissociated during heavy exercise according to training status.

To better understand the mechanisms underlying the pulmonary O(2) uptake (V(O(2P))) slow component during high-intensity exercise, we used (31)P magnetic resonance spectroscopy, gas exchange, surface electromyography and near-infrared spectroscopy measurements to examine the potential relationship between the slow components of V(O(2P)) and phosphocreatine (PCr), muscle recruitment and tissue oxygenation in endurance-trained athletes and sedentary subjects. Specifically, six endurance-trained and seven sedentary subjects performed a dynamic high-intensity exercise protocol during 6 min at an exercise intensity corresponding to 35-40% of knee-extensor maximal voluntary contraction. The slow component of V(O(2P))(117 ± 60 ml min(-1), i.e. 20 ± 10% of the total response) was associated with a paradoxical PCr resynthesis in endurance-trained athletes (-0.90 ± 1.27 mm, i.e. -12 ± 16% of the total response). Meanwhile, oxygenated haemoglobin increased throughout the second part of exercise and was significantly higher at the end of exercise compared with the value at 120 s (P < 0.05), whereas the integrated EMG was not significantly changed throughout exercise. In sedentary subjects, a slow component was simultaneously observed for V(O(2P)) and [PCr] time-dependent changes (208 ± 14 ml min(-1), i.e. 38 ± 18% of the total V(O(2P))response, and 1.82 ± 1.39 mm, i.e. 16 ± 13% of the total [PCr] response), but the corresponding absolute or relative amplitudes were not correlated. The integrated EMG was significantly increased throughout exercise in sedentary subjects. Taken together, our results challenge the hypothesis of a mechanistic link between [PCr] and V(O(2P)) slow components and demonstrate that, as a result of a tighter metabolic control and increased O(2) availability, the [PCr] slow component can be minimized in endurance-trained athletes while the V(O(2P)) slow component occurs.

Muscle cross-sectional areas and performance power of limbs and trunk in the rowing motion.

Although it is clear that rowers have a large muscle mass, their distribution of muscle mass and which of the main motions in rowing mediates muscle hypertrophy in each body part are unclear. We examine the relationships between partial motion power in rowing and muscle cross-sectional area of the thigh, lower back, and upper arms. Sixty young rowers (39 males and 21 females) participated in the study. Joint positions and forces were measured by video cameras and rowing ergometer software, respectively. One-dimensional motion analysis was performed to calculate the power of leg drive, trunk swing, and arm pull motions. Muscle cross-sectional areas were measured using magnetic resonance imaging. Multiple regression analyses were carried out to determine the association of different muscle cross-sectional areas with partial motion power. The anterior thigh best explained the power demonstrated by leg drive (r2 = 0.508), the posterior thigh and lower back combined best explained the power demonstrated by the trunk swing (r2 = 0.493), and the elbow extensors best explained the power demonstrated by the arm pull (r2 = 0.195). Other correlations, such as arm muscles with leg drive power (r2 = 0.424) and anterior thigh with trunk swing power (r2 = 0.33 5), were also significant. All muscle cross-sectional areas were associated with rowing performance either through the production of power or by transmitting work. The results imply that rowing motion requires a well-balanced distribution of muscle mass throughout the body.

Deterioration of muscle function after 21-day forearm immobilization.

PURPOSE: Although it is well known that immobilization causes muscle atrophy, most immobilization models have examined lower limbs, and little is known about the forearm. The purpose of this study was to determine whether forearm immobilization produces changes in muscle morphology and function. METHODS: Six healthy males (age: 21.5 +/- 1.4, mean +/- SD) participated in this study. The nondominant arm was immobilized with a cast (CAST) for 21 d, and the dominant arm was measured as the control (CONT). The forearm cross-sectional area (CSA) and circumference were measured as muscle morphology. Maximum grip strength, forearm muscle oxidative capacity, and dynamic grip endurance were measured as muscle function. Magnetic resonance (MR) imaging was used to measure CSA, and 31phosphorus MR spectroscopy was used to measure time constant (Tc) for phosphocreatine (PCr) recovery after submaximal exercise (PCr-Tc). Grip endurance was expressed by the number of handgrip contractions at 30% maximum grip strength load. All measurements were taken before and after the immobilization. RESULTS: After the 21-d forearm immobilization, no changes were seen for each measurement in CONT. CSA and the circumference showed no significant changes in CAST. However, maximum grip strength decreased by 18% (P < 0.05), PCr-Tc was prolonged by 45% (P < 0.05), and the grip endurance at the absolute load was reduced by 19% (P < 0.05) for CAST. CONCLUSION: In this model, 21-d forearm immobilization caused no significant changes in forearm muscle morphology, but the muscle function showed remarkable deterioration ranging from 18 to 45%.