Biomedical subjects

Martin J Gibala

Publications and source records attributed to Martin J Gibala.

18 recordsLinked to original sources

PubMed2026

Exercise Snacks Are Feasible to Perform in the Real World and Improve Physical Capacity for Adults Living With Non-Insulin Treated Type 2 Diabetes: A Randomised Trial.

AIMS: To investigate the feasibility and preliminary efficacy of a 12-week remotely-delivered exercise snacks (ES) intervention in adults with type 2 diabetes. MATERIAL AND METHODS: Insufficiently active adults with type 2 diabetes (N = 69; 46 females; mean age ± SD: 58 ± 11 years) were randomised to an ES or mobility/stretching comparator group (CON), which involved 4 × 1-min bouts of either vigorous or low intensity exercise, respectively, on ≥ 5 days/week. The primary outcome was feasibility based on adherence. Secondary outcomes included exercise enjoyment (1-7 scale), rating of perceived exertion (RPE; 0-10 scale), heart rate (HR), haemoglobin A1c (HbA1c), blood biomarkers of cardiometabolic health, 30-s sit-to-stand capacity, grip strength, estimated maximal oxygen uptake, and anthropometrics. RESULTS: Weekly adherence (estimated marginal mean [95% confidence interval]: 18 bouts [16-21] for both groups; p = 0.99) and total enjoyment (ES: 4.5 [4.1-4.8] vs. CON: 4.3 [4.0-4.7]; p = 0.64) were high and not different between groups. Despite higher RPE (5.7 [5.4-6.1]) and peak HR (73 [70-77] % of age-predicted HR maximum) in ES versus CON (2.0 [1.7-2.4] and 61 [58-64] % of age-predicted HR maximum, respectively) (all p < 0.001), there were no between-group differences in the change in any secondary outcome (all p > 0.05) except for greater sit-to-stand capacity in ES after training (between-group effect estimate [95% confidence interval]: 1.9 repetitions [0.3-3.4]; p = 0.02). CONCLUSIONS: Exercise snacks were feasible to perform in the real world and improved sit-to-stand capacity to a greater extent than CON in adults living with type 2 diabetes. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT06407245.

Aged↗

PubMed2006

Short-term sprint interval versus traditional endurance training: similar initial adaptations in human skeletal muscle and exercise performance.

Brief, intense exercise training may induce metabolic and performance adaptations comparable to traditional endurance training. However, no study has directly compared these diverse training strategies in a standardized manner. We therefore examined changes in exercise capacity and molecular and cellular adaptations in skeletal muscle after low volume sprint-interval training (SIT) and high volume endurance training (ET). Sixteen active men (21 +/- 1 years, ) were assigned to a SIT or ET group (n = 8 each) and performed six training sessions over 14 days. Each session consisted of either four to six repeats of 30 s 'all out' cycling at approximately 250% with 4 min recovery (SIT) or 90-120 min continuous cycling at approximately 65% (ET). Training time commitment over 2 weeks was approximately 2.5 h for SIT and approximately 10.5 h for ET, and total training volume was approximately 90% lower for SIT versus ET ( approximately 630 versus approximately 6500 kJ). Training decreased the time required to complete 50 and 750 kJ cycling time trials, with no difference between groups (main effects, P </= 0.05). Biopsy samples obtained before and after training revealed similar increases in muscle oxidative capacity, as reflected by the maximal activity of cytochrome c oxidase (COX) and COX subunits II and IV protein content (main effects, P </= 0.05), but COX II and IV mRNAs were unchanged. Training-induced increases in muscle buffering capacity and glycogen content were also similar between groups (main effects, P </= 0.05). Given the large difference in training volume, these data demonstrate that SIT is a time-efficient strategy to induce rapid adaptations in skeletal muscle and exercise performance that are comparable to ET in young active men.

Adaptation, Physiological↗

PubMed2006

Tricarboxylic acid cycle intermediates accumulate at the onset of intense exercise in man but are not essential for the increase in muscle oxygen uptake.

It was proposed that a contraction-induced increase in tricarboxylic acid cycle intermediates (TCAI) is obligatory for the increase in muscle oxygen uptake at the start of exercise. To test this hypothesis, we measured changes in muscle TCAI during the initial seconds of intense exercise and used dichloroacetate (DCA) in an attempt to alter the level of TCAI. Five men performed strenuous leg kicking exercise (64+/-8 W) under noninfused control (CON) and DCA-supplemented conditions; biopsies (vastus lateralis) were obtained at rest and after 5, 15, and 180 s of exercise. In CON, the total concentration of three measured TCAI (SigmaTCAI: citrate, malate, and fumarate) increased (p<0.05) by 71% during the first 15 s of exercise. The SigmaTCAI was lower (p<0.05) in DCA than in CON at rest [0.18+/-0.02 vs 0.64+/-0.09 mmol kg(-1) dry weight (d.w.)], after 5 s (0.30+/-0.07 vs 0.85+/-0.14 mmol kg(-1) d.w.), and 15 s of exercise (0.60+/-0.07 vs 1.09+/-0.16 mmol kg(-1) d.w.), but not different after 3 min (3.12+/-0.53 vs 3.23+/-0.55 mmol kg(-1) d.w.). Despite differences in the level of muscle TCAI, muscle phosphocreatine degradation was similar in DCA and CON during the first 15 s of exercise (17.5+/-3.3 vs 25.6+/-4.1 mmol kg(-1) d.w.). Taken together with our previous observation that DCA does not alter muscle oxygen uptake during the initial phase of intense leg kicking exercise (Bangsbo et al. Am J Physiol 282:R273-R280, 2002), the present data suggest that muscle TCAI accumulate during the initial seconds of exercise; however, this increase is not essential for the contraction-induced increase in mitochondrial respiration.

Adult↗

PubMed2006

Effect of short-term sprint interval training on human skeletal muscle carbohydrate metabolism during exercise and time-trial performance.

Our laboratory recently showed that six sessions of sprint interval training (SIT) over 2 wk increased muscle oxidative potential and cycle endurance capacity (Burgomaster KA, Hughes SC, Heigenhauser GJF, Bradwell SN, and Gibala MJ. J Appl Physiol 98: 1895-1900, 2005). The present study tested the hypothesis that short-term SIT would reduce skeletal muscle glycogenolysis and lactate accumulation during exercise and increase the capacity for pyruvate oxidation via pyruvate dehydrogenase (PDH). Eight men [peak oxygen uptake (VO2 peak)=3.8+/-0.2 l/min] performed six sessions of SIT (4-7x30-s "all-out" cycling with 4 min of recovery) over 2 wk. Before and after SIT, biopsies (vastus lateralis) were obtained at rest and after each stage of a two-stage cycling test that consisted of 10 min at approximately 60% followed by 10 min at approximately 90% of VO2 peak. Subjects also performed a 250-kJ time trial (TT) before and after SIT to assess changes in cycling performance. SIT increased muscle glycogen content by approximately 50% (main effect, P=0.04) and the maximal activity of citrate synthase (posttraining: 7.8+/-0.4 vs. pretraining: 7.0+/-0.4 mol.kg protein -1.h-1; P=0.04), but the maximal activity of 3-hydroxyacyl-CoA dehydrogenase was unchanged (posttraining: 5.1+/-0.7 vs. pretraining: 4.9+/-0.6 mol.kg protein -1.h-1; P=0.76). The active form of PDH was higher after training (main effect, P=0.04), and net muscle glycogenolysis (posttraining: 100+/-16 vs. pretraining: 139+/-11 mmol/kg dry wt; P=0.03) and lactate accumulation (posttraining: 55+/-2 vs. pretraining: 63+/-1 mmol/kg dry wt; P=0.03) during exercise were reduced. TT performance improved by 9.6% after training (posttraining: 15.5+/-0.5 vs. pretraining: 17.2+/-1.0 min; P=0.006), and a control group (n=8, VO2 peak=3.9+/-0.2 l/min) showed no change in performance when tested 2 wk apart without SIT (posttraining: 18.8+/-1.2 vs. pretraining: 18.9+/-1.2 min; P=0.74). We conclude that short-term SIT improved cycling TT performance and resulted in a closer matching of glycogenolytic flux and pyruvate oxidation during submaximal exercise.

Adult↗

PubMed2006

Failure of protein to improve time trial performance when added to a sports drink.

INTRODUCTION: Recent studies have reported that adding approximately 2% protein to a carbohydrate sports drink increased cycle endurance capacity compared with carbohydrate alone. However, the practical implications of these studies work are hampered by the following limitations: (a) the rate of carbohydrate ingestion was less than what is considered optimal for endurance performance, and (b) the performance test (exercise time to fatigue) did not mimic the way in which athletes typically compete (i.e., a race in which a fixed distance or set amount of work is performed as quickly as possible). PURPOSE: We tested the hypothesis that adding 2% protein to a 6% carbohydrate drink (CHO-PRO) would improve 80-km cycling time trial performance, as compared with a 6% carbohydrate drink (CHO) and a nonenergetic sweetened placebo (PLAC). METHODS: Ten trained male cyclists (24 +/- 2 yr; VO2peak = 63 +/- 2 mL.kg(-1).min(-1); mean +/- SE) performed an 80-km laboratory time trial (TT) on three occasions separated by 7 d. In a double-blind crossover manner, subjects ingested CHO-PRO, CHO, or PLAC at a rate of 250 mL every 15 min with no temporal, verbal, or physiological feedback. RESULTS: Time to complete the TT was 4.4% lower (P < 0.002) during CHO (135 +/- 9 min) and CHO-PRO (135 +/- 9) compared with PLAC (141 +/- 10), with no difference between CHO and CHO-PRO (P = 0.92). CONCLUSION: Ingesting 6% carbohydrate at a rate of 1 L.h(-1) (60 g.h(-1)) improved an 80-km TT performance in trained male cyclists. However, adding 2% protein to a 6% carbohydrate drink provided no additional performance benefit during a task that closely simulated the manner in which athletes typically compete.

Adult↗

PubMed2005

An acute decrease in TCA cycle intermediates does not affect aerobic energy delivery in contracting rat skeletal muscle.

We tested the hypothesis that an acute decrease in muscle TCA cycle intermediates during contraction would compromise aerobic energy delivery. Male Wistar rats were anaesthetized and the gastrocnemius-plantaris-soleus (GPS) muscle complex from one leg was isolated and perfused with a red cell medium containing either saline (Con) or cycloserine (Cyclo; 0.05 mg g-1), an inhibitor of alanine aminotransferase (AAT). After 1 h of perfusion, the GPS muscle was either snap frozen (Con-Rest, n=11; Cyclo-Rest, n=9) or stimulated to contract for 10 min (1 Hz, 0.3 ms, 2 V) with blood flow fixed at 30 ml min-1 (100 g)-1 and then snap frozen (Con-Stim, n=10; Cyclo-Stim, n=10). Maximal AAT activity was>80% lower (P<0.001) in both Cyclo-treated groups (Rest: 0.61+/-0.02; Stim: 0.63+/-0.01 mmol (kg wet wt)-1 min-1; mean+/-s.e.m.) compared to Con (Rest: 3.56+/-0.16; Stim: 3.92+/-0.29). The sum of five measured TCAI (SigmaTCAI) was reduced by 23% in Cyclo-Rest versus Con-Rest but this was not different (P=0.08). However, after 10 min of contraction, the SigmaTCAI was 25% lower (P=0.006) in Cyclo-Stim compared to Con-Stim (1.88+/-0.15 versus 2.48+/-0.11 mmol (kg dry wt)-1). Despite the acute decrease in TCAI after Cyclo treatment, the contraction-induced changes in markers of non-oxidative energy provision (phosphocreatine, ATP and lactate) and the decline in tension after 10 min of stimulation were similar compared to Con. These data do not support the hypothesis that the total muscle concentration of TCAI is causally linked to the rate of mitochondrial respiration during contraction.

Alanine Transaminase↗

PubMed2005

Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans.

Parra et al. (Acta Physiol. Scand 169: 157-165, 2000) showed that 2 wk of daily sprint interval training (SIT) increased citrate synthase (CS) maximal activity but did not change "anaerobic" work capacity, possibly because of chronic fatigue induced by daily training. The effect of fewer SIT sessions on muscle oxidative potential is unknown, and aside from changes in peak oxygen uptake (Vo(2 peak)), no study has examined the effect of SIT on "aerobic" exercise capacity. We tested the hypothesis that six sessions of SIT, performed over 2 wk with 1-2 days rest between sessions to promote recovery, would increase CS maximal activity and endurance capacity during cycling at approximately 80% Vo(2 peak). Eight recreationally active subjects [age = 22 +/- 1 yr; Vo(2 peak) = 45 +/- 3 ml.kg(-1).min(-1) (mean +/- SE)] were studied before and 3 days after SIT. Each training session consisted of four to seven "all-out" 30-s Wingate tests with 4 min of recovery. After SIT, CS maximal activity increased by 38% (5.5 +/- 1.0 vs. 4.0 +/- 0.7 mmol.kg protein(-1).h(-1)) and resting muscle glycogen content increased by 26% (614 +/- 39 vs. 489 +/- 57 mmol/kg dry wt) (both P < 0.05). Most strikingly, cycle endurance capacity increased by 100% after SIT (51 +/- 11 vs. 26 +/- 5 min; P < 0.05), despite no change in Vo(2 peak). The coefficient of variation for the cycle test was 12.0%, and a control group (n = 8) showed no change in performance when tested approximately 2 wk apart without SIT. We conclude that short sprint interval training (approximately 15 min of intense exercise over 2 wk) increased muscle oxidative potential and doubled endurance capacity during intense aerobic cycling in recreationally active individuals.

Adaptation, Physiological↗

PubMed2004

Effects of 7 wk of endurance training on human skeletal muscle metabolism during submaximal exercise.

This is the first study to examine the effects of endurance training on the activation state of glycogen phosphorylase (Phos) and pyruvate dehydrogenase (PDH) in human skeletal muscle during exercise. We hypothesized that 7 wk of endurance training (Tr) would result in a posttransformationally regulated decrease in flux through Phos and an attenuated activation of PDH during exercise due to alterations in key allosteric modulators of these important enzymes. Eight healthy men (22 +/- 1 yr) cycled to exhaustion at the same absolute workload (206 +/- 5 W; approximately 80% of initial maximal oxygen uptake) before and after Tr. Muscle biopsies (vastus lateralis) were obtained at rest and after 5 and 15 min of exercise. Fifteen minutes of exercise post-Tr resulted in an attenuated activation of PDH (pre-Tr: 3.75 +/- 0.48 vs. post-Tr: 2.65 +/- 0.38 mmol.min(-1).kg wet wt(-1)), possibly due in part to lower pyruvate content (pre-Tr: 0.94 +/- 0.14 vs. post-Tr: 0.46 +/- 0.03 mmol/kg dry wt). The decreased pyruvate availability during exercise post-Tr may be due to a decreased muscle glycogenolytic rate (pre-Tr: 13.22 +/- 1.01 vs. post-Tr: 7.36 +/- 1.26 mmol.min(-1).kg dry wt(-1)). Decreased glycogenolysis was likely mediated, in part, by posttransformational regulation of Phos, as evidenced by smaller net increases in calculated muscle free ADP (pre-Tr: 111 +/- 16 vs. post-Tr: 84 +/- 10 micromol/kg dry wt) and P(i) (pre-Tr: 57.1 +/- 7.9 vs. post-Tr: 28.6 +/- 5.6 mmol/kg dry wt). We have demonstrated for the first time that several signals act to coordinately regulate Phos and PDH, and thus carbohydrate metabolism, in human skeletal muscle after 7 wk of endurance training.

Acetylcarnitine↗

PubMed2004

Effect of endurance training on muscle TCA cycle metabolism during exercise in humans.

We tested the theory that links the capacity to perform prolonged exercise with the size of the muscle tricarboxylic acid (TCA) cycle intermediate (TCAI) pool. We hypothesized that endurance training would attenuate the exercise-induced increase in TCAI concentration ([TCAI]); however, the lower [TCAI] would not compromise cycle endurance capacity. Eight men (22 +/- 1 yr) cycled at approximately 80% of initial peak oxygen uptake before and after 7 wk of training (1 h/day, 5 days/wk). Biopsies (vastus lateralis) were obtained during both trials at rest, after 5 min, and at the point of exhaustion during the pretraining trial (42 +/- 6 min). A biopsy was also obtained at the end of exercise during the posttraining trial (91 +/- 6 min). In addition to improved performance, training increased (P < 0.05) peak oxygen uptake and citrate synthase maximal activity. The sum of four measured TCAI was similar between trials at rest but lower after 5 min of exercise posttraining [2.7 +/- 0.2 vs. 4.3 +/- 0.2 mmol/kg dry wt (P < 0.05)]. There was a clear dissociation between [TCAI] and endurance capacity because the [TCAI] at the point of exhaustion during the pretraining trial was not different between trials (posttraining: 2.9 +/- 0.2 vs. pretraining: 3.5 +/- 0.2 mmol/kg dry wt), and yet cycle endurance time more than doubled in the posttraining trial. Training also attenuated the exercise-induced decrease in glutamate concentration (posttraining: 4.5 +/- 0.7 vs. pretraining: 7.7 +/- 0.6 mmol/kg dry wt) and increase in alanine concentration (posttraining: 3.3 +/- 0.2 vs. pretraining: 5.6 +/- 0.3 mmol/kg dry wt; P < 0.05), which is consistent with reduced carbon flux through alanine aminotransferase. We conclude that, after aerobic training, cycle endurance capacity is not limited by a decrease in muscle [TCAI].

Adult↗

PubMed2004

Neuromuscular adaptations in human muscle following low intensity resistance training with vascular occlusion.

Low-intensity (approximately 50% of a single repetition maximum-1 RM) resistance training combined with vascular occlusion results in increases in muscle strength and cross-sectional area [Takarada et al. (2002) Eur J Appl Physiol 86:308-331]. The mechanisms responsible for this hypertrophy and strength gain remain elusive and no study has assessed the contribution of neuromuscular adaptations to these strength gains. We examined the effect of low-intensity training (8 weeks of unilateral elbow flexion at 50% 1 RM) both with (OCC) and without vascular occlusion (CON) on neuromuscular changes in the elbow flexors of eight previously untrained men [19.5 (0.4) years]. Following training, maximal voluntary dynamic strength increased (P<0.05) in OCC (22%) and CON (23%); however, isometric maximal voluntary contraction (MVC) strength increased in OCC only (8.3%, P<0.05). Motor unit activation, assessed by interpolated twitch, was high (approximately 98%) in OCC and CON both pre- and post-training. Evoked resting twitch torque decreased 21% in OCC (P<0.05) but was not altered in CON. Training resulted in a reduction in the twitch:MVC ratio in OCC only (29%, P<0.01). Post-activation potentiation (PAP) significantly increased by 51% in OCC (P<0.05) and was not changed in CON. We conclude that low-intensity resistance training in combination with vascular occlusion produces an adequate stimulus for increasing muscle strength and causes changes in indices of neuromuscular function, such as depressed resting twitch torque and enhanced PAP.

Adaptation, Physiological↗

PubMed2004

Nutritional strategies to influence adaptations to training.

This article highlights new nutritional concerns or practices that may influence the adaptation to training. The discussion is based on the assumption that the adaptation to repeated bouts of training occurs during recovery periods and that if one can train harder, the adaptation will be greater. The goal is to maximize with nutrition the recovery/adaptation that occurs in all rest periods, such that recovery before the next training session is complete. Four issues have been identified where recent scientific information will force sports nutritionists to embrace new issues and reassess old issues and, ultimately, alter the nutritional recommendations they give to athletes. These are: (1) caffeine ingestion; (2) creatine ingestion; (3) the use of intramuscular triacylglycerol (IMTG) as a fuel during exercise and the nutritional effects on IMTG repletion following exercise; and (4) the role nutrition may play in regulating the expression of genes during and after exercise training sessions. Recent findings suggest that low doses of caffeine exert significant ergogenic effects by directly affecting the central nervous system during exercise. Caffeine can cross the blood-brain barrier and antagonize the effects of adenosine, resulting in higher concentrations of stimulatory neurotransmitters. These new data strengthen the case for using low doses of caffeine during training. On the other hand, the data on the role that supplemental creatine ingestion plays in augmenting the increase in skeletal muscle mass and strength during resistance training remain equivocal. Some studies are able to demonstrate increases in muscle fibre size with creatine ingestion and some are not. The final two nutritional topics are new and have not progressed to the point that we can specifically identify strategies to enhance the adaptation to training. However, it is likely that nutritional strategies will be needed to replenish the IMTG that is used during endurance exercise. It is not presently clear whether the IMTG store is chronically reduced when engaging in daily sessions of endurance training or if this impacts negatively on the ability to train. It is also likely that the increased interest in gene and protein expression measurements will lead to nutritional strategies to optimize the adaptations that occur in skeletal muscle during and after exercise training sessions. Research in these areas in the coming years will lead to strategies designed to improve the adaptive response to training.

Adaptation, Physiological↗

PubMed2003

Short-term training attenuates muscle TCA cycle expansion during exercise in women.

Muscle glycogenolytic flux and lactate accumulation during exercise are lower after 3-7 days of "short-term" aerobic training (STT) in men (e.g., Green HJ, Helyar R, Ball-Burnett M, Kowalchuk N, Symon S, and Farrance B. J Appl Physiol 72: 484-491, 1992). We hypothesized that 5 days of STT would attenuate pyruvate production and the increase in muscle tricarboxylic acid cycle intermediates (TCAI) during exercise, because of reduced flux through the reaction catalyzed by alanine aminotransferase (AAT; pyruvate + glutamate <--> 2-oxoglutarate + alanine). Eight women [22 +/- 1 yr, peak oxygen uptake (Vo2 peak) = 40.3 +/- 4.6 ml. kg-1. min-1] performed seven 45-min bouts of cycle exercise at 70% Vo2 peak over 9 days (1 bout/day; rest only on days 2 and 8). During the first and last bouts, biopsies (vastus lateralis) were obtained at rest and after 5 and 45 min of exercise. Muscle glycogen concentration was approximately 50% higher at rest after STT (493 +/- 38 vs. 330 +/- 20 mmol/kg dry wt; P <or= 0.05), and net glycogenolysis and lactate accumulation were reduced after 5 min of exercise by 59 and 49%, respectively (P <or= 0.05). The net increase in four measured TCAI was approximately 40% lower (P <or= 0.05) during exercise after training (1.68 +/- 0.60 vs. 2.71 +/- 0.44 mmol/kg dry wt), and the net decrease in glutamate concentration was attenuated (P <or= 0.05). We conclude that 1). the contraction-induced increase in flux through AAT is reduced after 5 days of aerobic training and 2). the muscle glycogenolytic response during exercise after STT in women is similar to that in men.

Adult↗

PubMed2003

Anaplerosis of the muscle tricarboxylic acid cycle pool during contraction: does size matter?

Explore the source record for details and available documents.

Animals↗

PubMed2003

Resistance training with vascular occlusion: metabolic adaptations in human muscle.

UNLABELLED: Two recent studies have reported increases in strength and whole muscle cross-sectional area after low-intensity resistance training (LIT) with vascular occlusion (OCC) that are greater than LIT alone (e.g., 22, 25). The OCC stress might be expected to induce metabolic alterations that are consistent with compromised oxygen delivery rather than an increase in strength per se, but this has not been studied. PURPOSE: We examined the effect of LIT and LIT+OCC on resting metabolites in m. biceps brachii and elbow flexor strength. METHODS: Eight men (19.5 +/- 0.4 yr) performed 8 wk of LIT at approximately 50% of one-repetition maximum (2 sessions per week; 3-6 sets, 8-10 repetitions, final set to failure); one arm trained with OCC and the other without (CON). :Biopsies obtained before and 72 h after the final training bout revealed that resting [glycogen] was higher (P <or= 0.05) in both arms after LIT (CON: 452 +/- 20 vs 325 +/- 28, OCC: 501 +/- 12 vs 332 +/- 28 mmol.kg-1 dry weight) and the increase was larger in the OCC arm (P <or= 0.05). Resting [ATP] was lower (P <or= 0.05) after LIT in both arms (CON: 20.5 +/- 0.5 vs 22.8 +/- 0.7, OCC: 18.2 +/- 0.6 vs 23.1 +/- 0.5 mmol.kg-1 dry weight), and the decrease was larger in the OCC arm (P <or= 0.05). Maximal isotonic and isokinetic elbow flexor strength increased (P <or= 0.05) after training to a similar extent in both arms. CONCLUSION: We conclude that [glycogen] was increased and [ATP] was decreased in resting human muscle, 72 h after an 8-wk LIT protocol. OCC potentiated the metabolic changes, perhaps by inducing an ischemic stimulus that enhanced muscle glucose transport and adenine nucleotide catabolism after LIT, but did not augment the increases in strength.

Adaptation, Physiological↗

PubMed2002

Dissociation between muscle tricarboxylic acid cycle pool size and aerobic energy provision during prolonged exercise in humans.

It has been suggested that a decrease in the total concentration of tricarboxylic acid cycle intermediates (TCAIs)--secondary to a reduction in glycogen availability--compromises oxidative energy provision in skeletal muscle during prolonged exercise. However, no study has directly tested this hypothesis. We therefore studied six men (28 +/- 2 years) during 90 min of leg kicking exercise at an intensity equivalent to 70 % of maximum. Biopsies (vastus lateralis) were obtained at rest and after 5, 10, 15, 30, 60 and 90 min of exercise, and thigh oxygen uptake (V(O(2),thigh)) was calculated according to the Fick principle. The sum of six measured TCAIs (approximately 95 % of total pool size) was 1.30 +/- 0.15 mmol (kg dry wt)(-1) at rest and increased (P < or = 0.05) rapidly during exercise to a peak value of 3.15 +/- 0.23 mmol (kg dry wt)(-1) after 10 min. Thereafter, the [TCAI] declined to 2.14 +/- 0.23, 1.73 +/- 0.32 and 1.62 +/- 0.10 mmol (kg dry wt)(-1) after 30, 60 and 90 min, respectively (P < or = 0.05 vs.10 min). Despite the 50 % decrease in [TCAI], aerobic energy provision was not compromised, as evidenced by stable V(O(2),thigh) values throughout the entire exercise bout and little change in muscle [phosphocreatine] after 10 min. The largest decrease in [TCAI] (delta = 1.00 +/- 0.24 mmol (kg dry wt)(-1)) occurred from 10 to 30 min of exercise despite the fact that muscle [glycogen] remained relatively high at this point in exercise (approximately 274 +/- 24 mmol (kg dry wt)(-1) after 30 min; approximately 65 % of rest value). Conversely, there was little change in [TCAI] during the final 30 min of exercise (delta = 0.11 +/- 0.29 mmol (kg dry wt)(-1)) despite a decrease in [glycogen] to approximately 72 +/- 3 mmol (kg dry wt)(-1) after 90 min (approximately 13 % of rest value). We conclude that there is a progressive decrease in muscle [TCAI] during prolonged exercise in humans; however this decrease does not compromise aerobic energy provision and is not attributable to the depletion of muscle [glycogen].

Adult↗

PubMed2002

Glycogen availability does not affect the TCA cycle or TAN pools during prolonged, fatiguing exercise.

The hypothesis that fatigue during prolonged exercise arises from insufficient intramuscular glycogen, which limits tricarboxylic acid cycle (TCA) activity due to reduced TCA cycle intermediates (TCAI), was tested in this experiment. Seven endurance-trained men cycled at approximately 70% of peak O(2) uptake (Vo(2 peak)) until exhaustion with low (LG) or high (HG) preexercise intramuscular glycogen content. Muscle glycogen content was lower (P < 0.05) at fatigue than at rest in both trials. However, the increase in the sum of four measured TCAI (>70% of the total TCAI pool) from rest to 15 min of exercise was not different between trials, and TCAI content was similar after 103 +/- 15 min of exercise (2.62 +/- 0.31 and 2.59 +/- 0.28 mmol/kg dry wt for LG and HG, respectively), which was the point of volitional fatigue during LG. Subjects cycled for an additional 52 +/- 9 min during HG, and although glycogen was markedly reduced (P < 0.05) during this period, no further change in the TCAI pool was observed, thus demonstrating a clear dissociation between exercise duration and the size of the TCAI pool. Neither the total adenine nucleotide pool (TAN = ATP + ADP + AMP) nor IMP was altered compared with rest in either trial, whereas creatine phosphate levels were not different when values measured at fatigue were compared with those measured after 15 min of exercise. These data demonstrate that altered glycogen availability neither compromises TCAI pool expansion nor affects the TAN pool or creatine phosphate or IMP content during prolonged exercise to fatigue. Therefore, our data do not support the concept that a decrease in muscle TCAI during prolonged exercise in humans compromises aerobic energy provision or is the cause of fatigue.

Adenine Nucleotides↗

PubMed2002

Exercise with low muscle glycogen augments TCA cycle anaplerosis but impairs oxidative energy provision in humans.

We tested the hypotheses that: (i) exercise with low muscle glycogen would reduce pyruvate flux through the alanine aminotransferase (AAT) reaction and attenuate the increase in tricarboxylic acid (TCA) cycle intermediates, and (ii) attenuation of tricarboxylic acid cycle intermediate (TCAI) pool expansion would limit TCA cycle flux, thereby accelerating phosphocreatine (PCr) degradation. Eight men cycled for 10 min at 70 % of their (VO(2,max) on two occasions: (i) following their normal diet (CON) and (ii) after cycling to exhaustion and consuming a low carbohydrate diet for approximately 2 days (LG). Biopsies (m. vastus lateralis) confirmed that [glycogen] was lower in LG vs. CON at rest (257 +/- 18 vs. 611 +/- 54 mmol (kg dry mass)(-1); P 0.05); however, net glycogenolysis was not different after 1 or 10 min of exercise. PCr degradation from rest to 1 min was approximately 26 % higher in LG vs. CON (38 +/- 4 vs. 28 +/- 4 mmol (kg dry mass)(-1); P< or =0.05). The sum of five measured TCAIs (approximately 90 % of total pool) was not different between trials at rest and after 1 min, but was higher after 10 min in LG vs. CON (5.51 +/- 0.43 vs. 4.45 +/- 0.49 mmol (kg dry mass)(-1); P 0.05). Pyruvate dehydrogenase complex (PDC) activity was lower during exercise in LG vs. CON (2.2 +/- 0.2 vs. 1.4 +/- 0.2 mmol min(-1) (kg wet weight)(-1) after 10 min; P< or =0.05), and acetylcarnitine was approximately threefold less, implying increased pyruvate availability for flux through AAT. Resting muscle [glutamate] was higher in LG vs. CON (16.1 +/- 0.8 vs. 11.8 +/- 0.4 mmol (kg dry mass)(-1); P< or =0.05) and the net decrease in [glutamate] during exercise was approximately 30 % greater in LG vs. CON. These findings suggest that: (i) contrary to our hypotheses, LG increased anaplerosis by decreasing PDC flux and/or increasing the conversion of glutamate carbon to TCAIs, and (ii) accelerating the rate of muscle TCAI expansion did not affect oxidative energy provision during the initial phase of contraction, since changes in [TCAI] were not temporally related to PCr degradation.

Adult↗

PubMed2002

Enhanced pyruvate dehydrogenase activity does not affect muscle O2 uptake at onset of intense exercise in humans.

It has been proposed that the activation state of pyruvate dehydrogenase (PDH) may influence the rate of skeletal muscle O2 uptake during the initial phase of exercise; however, this has not been directly tested in humans. To remedy this, we used dichloroacetate (DCA) infusion to increase the active form of PDH (PDH(a)) and, subsequently, measured leg O2 uptake and markers of anaerobic ATP provision during conditions of intense dynamic exercise, when the rate of muscle O2 uptake would be very high. Six subjects performed brief bouts of one-legged knee-extensor exercise at approximately 110% of thigh peak O2 uptake (65.3 +/- 3.7 W) on several occasions: under noninfused control (Con) and DCA-supplemented conditions. Needle biopsy samples from the vastus lateralis muscle were obtained at rest and after 5 s, 15 s, and 3 min of exercise during both experimental conditions. In addition, thigh blood flow and femoral arteriovenous differences for O2 and lactate were measured repeatedly during the 3-min work bouts (Con and DCA) to calculate thigh O2 uptake and lactate release. After DCA administration, PDH(a) was four- to eightfold higher (P < 0.05) than Con at rest, and PDH(a) remained approximately 130% and 100% higher (P < 0.05) after 5 and 15 s of exercise, respectively. There was no difference between trials after 3 min. Despite the marked difference in PDH(a) between trials at rest and during the initial phase of exercise, thigh O2 uptake was the same. In addition, muscle phosphocreatine utilization and lactate production were similar after 5 s, 15 s, and 3 min of exercise in DCA and Con. The present findings demonstrate that increasing PDH(a) does not alter muscle O2 uptake and anaerobic ATP provision during the initial phase of intense dynamic knee-extensor exercise in humans.

Adult↗