Short Duration Small Sided Football and to a Lesser Extent Whole Body Vibration Exercise Induce Acute Changes in Markers of Bone Turnover.

We aimed to study whether short-duration vibration exercise or football sessions of two different durations acutely changed plasma markers of bone turnover and muscle strain. Inactive premenopausal women (n = 56) were randomized to complete a single bout of short (FG15) or long duration (FG60) small sided football or low magnitude whole body vibration training (VIB). Procollagen type 1 amino-terminal propeptide (P1NP) was increased during exercise for FG15 (51.6 ± 23.0 to 56.5 ± 22.5 µg·L-1, mean ± SD, P < 0.05) and FG60 (42.6 ± 11.8 to 50.2 ± 12.8 µg·L-1, P < 0.05) but not for VIB (38.8 ± 15.1 to 36.6 ± 14.7 µg·L-1, P > 0.05). An increase in osteocalcin was observed 48 h after exercise (P < 0.05), which did not differ between exercise groups. C-terminal telopeptide of type 1 collagen was not affected by exercise. Blood lactate concentration increased during exercise for FG15 (0.6 ± 0.2 to 3.4 ± 1.2 mM) and FG60 (0.6 ± 0.2 to 3.3 ± 2.0 mM), but not for VIB (0.6 ± 0.2 to 0.8 ± 0.4 mM) (P < 0.05). Plasma creatine kinase increased by 55 ± 63% and 137 ± 119% 48 h after FG15 and FG60 (P < 0.05), but not after VIB (26 ± 54%, NS). In contrast to the minor elevation in osteocalcin in response to a single session of vibration exercise, both short and longer durations of small sided football acutely increased plasma P1NP, osteocalcin, and creatine kinase. This may contribute to favorable effects of chronic training on musculoskeletal health.

Decline in voluntary activation contributes to reduced maximal performance of fatigued human lower limb muscles.

In upper limb muscles, altered corticospinal excitability and reduction in neural drive are observed in parallel with peripheral fatigue during prolonged and/or repeated contractions. However, the fatigue-induced adaptations of central and peripheral elements and their relative contribution to lower limb muscle performance are yet to be fully explored. In the present study, corticospinal excitability and peripheral contractility of ankle flexor muscles were quantified before, during and after repeated brief unilateral maximal dorsiflexions to fatigue in eleven healthy volunteers. Transcranial magnetic stimulation of the motor cortex area related to lower limb muscles was performed, and the evoked twitch and EMG responses in tibialis anterior (TA) and soleus (SOL) were measured. The motor evoked potentials (MEPs) in fatigued TA during post-exercise maximal dorsiflexions were smaller (-20 ± 6 %, p = 0.026) and remained depressed for at least 5 min. Post-exercise MEPs in fatigued SOL and silent periods in TA and SOL were not different compared to pre-exercise. These changes were accompanied by lower voluntary torque (-8 ± 3 %, p = 0.013), estimated resting twitch (-36 ± 5 %, p = 0.003) and voluntary activation (-17 ± 9 %, p = 0.021) versus pre-exercise. During last versus first maximal contraction in the fatiguing protocol lower voluntary torque (-40 ± 4 %, p = 0.003), higher MEP amplitudes (>+49 %, p < 0.021) and longer silent periods (>+24 %, p < 0.004) were recorded in both muscles. Decreased corticospinal excitability contributes significantly to the reduced maximal performance of fatigued lower limb muscles. During prolonged intermittent maximal dorsiflexions the performance of ankle muscles declines despite enhanced corticospinal excitability presumably due to deficient descending drive and/or spinal motoneuron responsiveness to the cortical drive.

Interaction between glutamine availability and metabolism of glycogen, tricarboxylic acid cycle intermediates and glutathione.

After exhaustive exercise, intravenous or oral glutamine promoted skeletal muscle glycogen storage. However, when glutamine was ingested with glucose polymer, whole-body carbohydrate storage was elevated, the most likely site being liver and not muscle, possibly due to increased glucosamine formation. The rate of tricarboxylic acid (TCA) cycle flux and hence oxidative metabolism may be limited by the availability of TCA intermediates. There is some evidence that intramuscular glutamate normally provides alpha-ketoglutarate to the mitochondrion. We hypothesized that glutamine might be a more efficient anaplerotic precursor than endogenous glutamate alone. Indeed, a greater expansion of the sum of muscle citrate, malate, fumarate and succinate concentrations was observed at the start of exercise (70% VO2(max)) after oral glutamine than when placebo or ornithine alpha-ketoglutarate was given. However, neither endurance time nor the extent of phosphocreatine depletion or lactate accumulation during the exercise was altered, suggesting either that TCA intermediates were not limiting for energy production or that the severity of exercise was insufficient for the limitation to be operational. We have also shown that in the perfused working rat heart, there is a substantial fall in intramuscular glutamine and alpha-ketoglutarate, especially after ischemia. Glutamine (but not glutamate, alpha-ketoglutarate or aspartate) was able to rescue the performance of the postischemic heart. This ability appears to be connected to the ability to sustain intracardiac ATP, phosphocreatine and glutathione.

Glutamine supplementation promotes anaplerosis but not oxidative energy delivery in human skeletal muscle.

The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity exercise in human skeletal muscle could be enhanced independently of pyruvate availability by ingestion of glutamine or ornithine alpha-ketoglutarate, and second, if it was, whether this modification of TCAI pool expansion had any effect on oxidative energy status during subsequent exercise. Seven males cycled for 10 min at approximately 70% maximal O2) uptake 1 h after consuming either an artificially sweetened placebo (5 ml/kg body wt solution, CON), 0.125 g/kg body wt L-(+)-ornithine alpha-ketoglutarate dissolved in 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt L-glutamine dissolved in 5 ml/kg body wt solution (GLN). Vastus lateralis muscle was biopsied 1 h postsupplement and after 10 min of exercise. The sum of four measured TCAI (SigmaTCAI; citrate, malate, fumarate, and succinate, approximately 85% of total TCAI pool) was not different between conditions 1 h postsupplement. However, after 10 min of exercise, SigmaTCAI (mmol/kg dry muscle) was greater in the GLN condition (4.90 +/- 0.61) than in the CON condition (3.74 +/- 0.38, P < 0.05) and the OKG condition (3.85 +/- 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduced (P < 0.05) in all conditions, but there was no significant difference between conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of glutamine carbon at the level of alpha-ketoglutarate. However, this increased expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise.

Effect of different carbohydrate drinks on whole body carbohydrate storage after exhaustive exercise.

Seven untrained male subjects participated in a double-blind, crossover study conducted to determine the efficacy of different carbohydrate drinks in promoting carbohydrate storage in the whole body and skeletal muscle during recovery from exhaustive exercise. The postabsorptive subjects first completed an exercise protocol designed to deplete muscle fibers of glycogen, then consumed 330 ml of one of three carbohydrate drinks (18.5% glucose polymer, 18.5% sucrose, or 12% sucrose; wt/vol) and also received a primed constant infusion of [1-(13)C]glucose for 2 h. Nonoxidative glucose disposal (3.51 +/- 0.28, 18.5% glucose polymer; 2.96 +/- 0.32, 18.5% sucrose; 2.97 +/- 0.16, 12% sucrose; all mmol. kg(-1). h(-1)) and storage of muscle glycogen (5.31 +/- 1.11, 18.5% glucose polymer; 4.07 +/- 1.05, 18.5% sucrose; 3.45 +/- 0.85, 12% sucrose; all mmol. kg wet wt(-1). h(-1); P < 0.05) were greater after consumption of the glucose polymer drink than after either sucrose drink. The results suggest that the consumption of a glucose polymer drink (containing 61 g carbohydrate) promotes a more rapid storage of carbohydrate in the whole body, skeletal muscle in particular, than an isoenergetic sucrose drink.

Effect of oral glucose on leucine turnover in human subjects at rest and during exercise at two levels of dietary protein.

The aim of this study was to determine the effect of glucose supplementation on leucine turnover during and after exercise and whether variation in the previous dietary protein content modulated this effect. Postabsorptive subjects received a primed constant [1-13C, 15N]leucine infusion for 6 h, after previous consumption of a high (1.8 g kg-1 day-1, HP, n = 16) or low (0.7 g kg-1 day-1, LP, n = 16) protein diet for 7 days. The subjects were studied at rest; during 2 h of exercise, during which half of the subjects from each dietary protocol received 0.75 g kg-1 h-1 glucose (HP + G, LP + G) and the other half received water (HP + W, LP + W); then again for 2 h of rest. Glucose supplementation suppressed leucine oxidation (P < 0.01) by 20% in subjects consuming the high protein diet (58.2 +/- 2.8 micromol kg-1 h-1, HP + G; 72.4 +/- 3.9 micromol kg-1 h-1, HP + W) but not the low protein diet (51.1 +/- 5.9 micromol kg-1 h-1, LP + G; 51.7 +/- 5.5 micromol kg-1 h-1, LP + W), with no difference in skeletal muscle branched-chain 2-oxo acid dehydrogenase (BCOADH) activity between groups. Glucose supplementation did not alter the rate of whole-body protein synthesis or breakdown. The sparing effect of glucose on leucine oxidation appears only to occur if previous protein intake was high. It was not mediated by a suppression of BCOADH fractional activity but may be due to reduced substrate availability.

Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise.

The purpose of this study was to determine the efficacy of glutamine in promoting whole body carbohydrate storage and muscle glycogen resynthesis during recovery from exhaustive exercise. Postabsorptive subjects completed a glycogen-depleting exercise protocol, then consumed 330 ml of one of three drinks, 18.5% (wt/vol) glucose polymer solution, 8 g glutamine in 330 ml glucose polymer solution, or 8 g glutamine in 330 ml placebo, and also received a primed constant infusion of [1-13C]glucose for 2 h. Plasma glutamine concentration was increased after consumption of the glutamine drinks (0.7-1.1 mM, P < 0.05). In the second hour of recovery, whole body nonoxidative glucose disposal was increased by 25% after consumption of glutamine in addition to the glucose polymer (4.48 +/- 0.61 vs. 3.59 +/- 0.18 mmol/kg, P < 0.05). Oral glutamine alone promoted storage of muscle glycogen to an extent similar to oral glucose polymer. Ingestion of glutamine and glucose polymer together promoted the storage of carbohydrate outside of skeletal muscle, the most feasible site being the liver.

Modulation of whole body protein metabolism, during and after exercise, by variation of dietary protein.

The aim of this study was to investigate dietary protein-induced changes in whole body leucine turnover and oxidation and in skeletal muscle branched chain 2-oxo acid dehydrogenase (BCOADH) activity, at rest and during exercise. Postabsorptive subjects received a primed constant infusion of L-[1-13C,15N]leucine for 6 h, after previous consumption of a high- (HP; 1.8 g . kg-1 . day-1, n = 8) or a low-protein diet (LP; 0.7 g . kg-1 . day-1, n = 8) for 7 days. The subjects were studied at rest for 2 h, during 2-h exercise at 60% maximum oxygen consumption, then again for 2 h at rest. Exercise induced a doubling of both leucine oxidation from 20 micromol . kg-1 . h-1 and BCOADH percent activation from 7% in all subjects. Leucine oxidation was greater before (+46%) and during (+40%, P < 0.05) the first hour of exercise in subjects consuming the HP rather than the LP diet, but there was no additional change in muscle BCOADH activity. The results suggest that leucine oxidation was increased by previous ingestion of an HP diet, attributable to an increase in leucine availability rather than to a stimulation of the skeletal muscle BCOADH activity.