Neither Beetroot Juice Supplementation nor Increased Carbohydrate Oxidation Enhance Economy of Prolonged Exercise in Elite Race Walkers.

Given the importance of exercise economy to endurance performance, we implemented two strategies purported to reduce the oxygen cost of exercise within a 4 week training camp in 21 elite male race walkers. Fourteen athletes undertook a crossover investigation with beetroot juice (BRJ) or placebo (PLA) [2 d preload, 2 h pre-exercise + 35 min during exercise] during a 26 km race walking at speeds simulating competitive events. Separately, 19 athletes undertook a parallel group investigation of a multi-pronged strategy (MAX; n = 9) involving chronic (2 w high carbohydrate [CHO] diet + gut training) and acute (CHO loading + 90 g/h CHO during exercise) strategies to promote endogenous and exogenous CHO availability, compared with strategies reflecting lower ranges of current guidelines (CON; n = 10). There were no differences between BRJ and PLA trials for rates of CHO (p = 0.203) or fat (p = 0.818) oxidation or oxygen consumption (p = 0.090). Compared with CON, MAX was associated with higher rates of CHO oxidation during exercise, with increased exogenous CHO use (CON; peak = ~0.45 g/min; MAX: peak = ~1.45 g/min, p < 0.001). High rates of exogenous CHO use were achieved prior to gut training, without further improvement, suggesting that elite athletes already optimise intestinal CHO absorption via habitual practices. No differences in exercise economy were detected despite small differences in substrate use. Future studies should investigate the impact of these strategies on sub-elite athletes' economy as well as the performance effects in elite groups.

Chronic pantothenic acid supplementation does not affect muscle coenzyme A content or cycling performance.

This study determined if supplementation with pantothenic acid (PA) for 16 weeks could increase skeletal muscle coenzyme A (CoASH) content and exercise performance. Trained male cyclists (n = 14) were matched into control or PA (6 g·day-1) groups. At 0, 4, 8, and 16 weeks, subjects performed an incremental time to exhaustion cycle with muscle biopsies taken prior to and following exercise. Prolonged PA supplementation did not change skeletal muscle CoASH and acetyl-CoA contents or exercise performance. Novelty: Supplementation with pantothenic acid for 16 weeks had no effect on skeletal muscle CoASH and acetyl-CoA content or exercise performance in trained male cyclists.

Acute Ketogenic Diet and Ketone Ester Supplementation Impairs Race Walk Performance.

PURPOSE: This study aimed to determine if LCHF and ketone ester (KE) supplementation can synergistically alter exercise metabolism and improve performance. METHODS: Elite race walkers (n = 18, 15 males and 3 females; V˙O2peak, 62 ± 6 mL·min-1·kg-1) undertook a four-stage exercise economy test and real-life 10,000-m race before and after a 5-d isoenergetic high-CHO (HCHO, ~60%-65% fat; CHO, 20% fat; n = 9) or LCHF (75%-80% fat, <50 g·d-1 CHO, n = 9) diet. The LCHF group performed additional economy tests before and after diet after supplementation with 573 mg·kg-1 body mass KE (HVMN; HVMN Inc., San Francisco, CA), which was also consumed for race 2. RESULTS: The oxygen cost of exercise (relative V˙O2, mL·min-1·kg-1) increased across all four stages after LCHF (P < 0.005). This occurred in association with increased fat oxidation rates, with a reciprocal decrease in CHO oxidation (P < 0.001). Substrate utilization in the HCHO group remained unaltered. The consumption of KE before the LCHF diet increased circulating KB (P < 0.05), peaking at 3.2 ± 0.6 mM, but did not alter V˙O2 or RER. LCHF diet elevated resting circulating KB (0.3 ± 0.1 vs 0.1 ± 0.1 mM), but concentrations after supplementation did not differ from the earlier ketone trial. Critically, race performance was impaired by ~6% (P < 0.0001) relative to baseline in the LCHF group but was unaltered in HCHO. CONCLUSION: Despite elevating endogenous KB production, an LCHF diet does not augment the metabolic responses to KE supplementation and negatively affects race performance.

Beetroot Juice Increases Human Muscle Force without Changing Ca2+-Handling Proteins.

Dietary inorganic nitrate (NO3) supplementation improves skeletal muscle (SkM) contractile efficiency, and although rodent literature has suggested improvements in calcium handling or redox modifications as likely explanations, the direct mechanism of action in humans remains unknown. PURPOSE: This study aimed to examine the effects of 7 d of beetroot juice (BRJ) supplementation on SkM contractile characteristics and function. METHODS: Recreationally active males (n = 8) underwent transcutaneous electrical muscle stimulation of the vastus lateralis for the evaluation of contractile characteristics before and after 7 d of BRJ supplementation (280 mL·d, ~26 mmol NO3). An additional group of individuals (n = 8) followed the same supplementation protocol but underwent SkM biopsies pre- and post-supplementation for the determination of proteins associated with calcium handling via Western blotting, and the ratio of reduced/oxidized glutathione (GSH:GSSG), an indicator of cellular redox state, via high-performance liquid chromatography (HPLC). RESULTS: After supplementation, there was no change in maximal voluntary force production (602 ± 50 vs 596 ± 56 N) or electrically induced tetanic contractions. By contrast, force production was increased at 10 Hz electrical stimulation (41.1% ± 2.3% vs 37.6% ± 2.4% of peak force, P < 0.05), as was peak twitch tension (164.0 ± 12.5 vs 136.5 ± 7.2 N, P < 0.01) and maximal rates of force development and relaxation (3582.8 ± 382.3 vs 2575.7 ± 196.2 and -2752.4 ± 423.9 vs -2104.4 ± 249.0 N·s, respectively, P < 0.05). Despite these measurements implicating a change in calcium handling, the content of associated proteins (SERCA1a, SERCA2a, dihydropyradine receptor, ryanodine receptor, and calsequestrin) and the GSH:GSSG ratio were unaltered by BRJ. CONCLUSION: BRJ supplementation increases force production at low-stimulation frequencies; however, in human SkM, this is independent of changes in redox stress or the expression of protein targets associated with calcium handling.

α-Linolenic acid and exercise training independently, and additively, decrease blood pressure and prevent diastolic dysfunction in obese Zucker rats.

KEY POINTS: α-linolenic acid (ALA) and exercise training both attenuate hyperlipidaemia-related cardiovascular derangements, however, there is a paucity of information pertaining to their mechanisms of action when combined. We investigated both the independent and combined effects of exercise training and ALA consumption in obese Zucker rats, aiming to determine the potential for additive improvements in cardiovascular function. ALA and exercise training independently improved cardiac output, end-diastolic volume, left ventricular fibrosis and mean blood pressure following a 4 week intervention. Combining ALA and endurance exercise yielded greater improvements in these parameters, independent of changes in markers of oxidative stress or endogenous anti-oxidants. We postulate that divergent mechanisms of action may explain these changes: ALA increases peripheral vasodilation, and exercise training stimulates angiogenesis. ABSTRACT: Although α-linolenic acid (ALA) and endurance exercise training independently attenuate hyperlipidaemia-related cardiovascular derangements, there is a paucity of information pertaining to their mechanisms of action and efficacy when combined as a preventative therapeutic approach. Therefore, we used obese Zucker rats to investigate the independent and combined effects of these interventions on cardiovascular disease. Specifically, animals were randomly assigned to one of the following groups: control diet-sedentary, ALA supplemented-sedentary, control diet-exercise trained or ALA supplemented-exercise trained. Following a 4 week intervention, although the independent and combined effects of ALA and exercise reduced (P < 0.05) the serum free/esterified cholesterol ratio, only the ALA supplemented-exercise trained animals displayed a reduction in the content of both serum free and esterified cholesterol. Moreover, although ALA and endurance training individually increased cardiac output, stroke volume and end-diastolic volume, as well as reduced left ventricle fibrosis, mean blood pressure and total peripheral resistance, these responses were all greater following the combined intervention (ALA supplemented-exercise trained). These effects occurred independent of changes in oxidative phosphorylation proteins, markers of oxidative stress or endogenous anti-oxidant capacity. We propose that the beneficial effects of a combined intervention occur as a result of divergent mechanisms of action elicited by ALA and endurance exercise because only exercise training increased the capillary content in the left ventricle and skeletal muscle, and tended to decrease protein carbonylation in the left ventricle (P = 0.06). Taken together, our data indicate that combining ALA and endurance exercise provides additional improvements in cardiovascular disease risk reduction compared to singular interventions in the obese Zucker rat.

Taurine and skeletal muscle function.

PURPOSE OF REVIEW: To discuss the recent work examining the importance of taurine in skeletal muscle and outline the discrepancy that exists between research findings in rodent vs. human skeletal muscle. RECENT FINDINGS: There is clear evidence that a normal taurine level is important for the normal functioning of skeletal muscle. Taurine is believed to be involved in many cellular functions, but in skeletal muscle its main roles are to facilitate Ca2+ dependent excitation-contraction processes, contribute to the regulation of cellular volume, and aid in antioxidant defense from stress responses. Most research has studied the importance of taurine in rodent skeletal muscle by downregulating and upregulating the muscle taurine content and examining the effects on the functioning of skeletal muscle at rest and during the stress of contractions (exercise). One successful research approach is to supplement the diet with taurine, which leads to increases in muscle taurine content and contractile function in rodents. However, this approach does not work in human skeletal muscle as the processes involved in the transport of taurine into the muscle are resistant to large and prolonged increases in plasma taurine following oral taurine supplementation. At present, attempts to influence muscle function with taurine supplementation can only occur through interactions outside the muscle cell in humans. SUMMARY: Future research should target the mechanisms responsible for the transport of taurine into human skeletal muscle and determine why the muscle defends the normal taurine content in the face of elevated plasma taurine levels, as opposed to the results in rodent muscle. This may lead to more fruitful usage of taurine as a skeletal muscle enhancing nutrient in athletic and clinical populations.

Variable effects of 12 weeks of omega-3 supplementation on resting skeletal muscle metabolism.

Omega-3 supplementation has been purported to improve the function of several organs in the body, including reports of increased resting metabolic rate (RMR) and reliance on fat oxidation. However, the potential for omega-3s to modulate human skeletal muscle metabolism has received little attention. This study examined the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) supplementation on whole-body RMR and the content of proteins involved in fat metabolism in human skeletal muscle. Recreationally active males supplemented with 3.0 g/day of EPA and DHA (n = 21) or olive oil (n = 9) for 12 weeks. Resting muscle biopsies were sampled in a subset of 10 subjects before (pre) and after (post) omega-3 supplementation. RMR significantly increased (5.3%, p = 0.040) following omega-3 supplementation (Pre, 1.33 ±0.05; Post, 1.40 ±0.04 kcal/min) with variable individual responses. When normalizing for body mass, this effect was lost (5.2%, p = 0.058). Omega-3s did not affect whole-body fat oxidation, and olive oil did not alter any parameter assessed. Omega-3 supplementation did not affect whole muscle, sarcolemmal, or mitochondrial FAT/CD36, FABPpm, FATP1 or FATP4 contents or mitochondrial electron chain and PDH proteins, but did increase the long form of UCP3 by 11%. In conclusion, supplementation with a high dose of omega-3s for 12 weeks increased RMR in a small and variable manner in a group of healthy young men. Omega-3 supplementation also had no effect on several proteins involved in skeletal muscle fat metabolism and did not cause mitochondrial biogenesis.

Beetroot juice supplementation does not improve performance of elite 1500-m runners.

PURPOSE: Dietary nitrate supplementation with beetroot juice (BR) has received widespread attention as an ergogenic aid. However, recent evidence in well-trained cyclists has not consistently reported improved cycling economy or performance. The present study examined the effects of acute and chronic BR supplementation on V˙O2 during submaximal running and 1500-m time trial (TT) performance of elite distance runners. METHODS: Eight male 1500-m runners (V˙O2peak, 80 ± 5 mL·kg·min; 1500-m personal best, 3:56 ± 9 s) participated in this study. In a randomized, double-blind, crossover design, subjects supplemented with BR or a nitrate-free BR placebo (PL) for 8 d separated by at least 1 wk. On days 1 (acute) and 8 (chronic), subjects ingested 210 mL of BR (19.5-mmol nitrate) or PL and completed a submaximal treadmill run and 1500-m TT on an indoor 200-m track. RESULTS: Plasma nitrate increased from 37 ± 15 to 615 ± 151 µM (acute) and 870 ± 259 µM (chronic) after BR supplementation. There were no V˙O2 differences between conditions at 50%, 65%, and 80% V˙O2peak (acute PL, 4194 ± 90 mL·min; chronic PL, 4216 ± 95 mL·min; acute BR, 4192 ± 113 mL·min; chronic BR, 4299 ± 92 mL·min). The 1500-m TT was unaffected by acute or chronic BR supplementation (acute PL, 4:10.4 min:s ± 2.5 s; chronic PL, 4:11.4 min:s ± 2.7 s; acute BR, 4:10.7 min:s ± 1.5 s; chronic BR, 4:10.5 min:s ± 2.2 s). However, two subjects improved their TT performance after acute (5.8 and 5.0 s) and chronic BR supplementation (7.0 and 0.5 s). CONCLUSIONS: Acute and chronic BR supplementation did not reduce running V˙O2 or improve 1500-m TT performance of a group of elite distance runners, but two responders to BR were identified.