156 research outputs found

    Influence of an alkalizing supplement on markers of endurance performance using a double-blind placebo-controlled design

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    <p>Abstract</p> <p>Background</p> <p>Previous research has shown that ingestion of substances that enhance the body's hydrogen ion buffering capacity during high intensity exercise can improve exercise performance. The present study aimed to determine whether the chronic ingestion of an alkalizing supplement, which purports to enhance both intracellular and extracellular buffering capacity, could impact cardiorespiratory and performance markers in trained Nordic skiers.</p> <p>Methods</p> <p>Twenty-four skiers (12 men, 12 women), matched for upper body power (UBP), were split into treatment and placebo groups. The treatment group ingested Alka-Myte<sup>®</sup>-based alkalizing tablets (1 tablet/22.7 kg body mass/day) over seven successive days while the placebo group consumed placebo tablets (i.e., no Alka-Myte<sup>®</sup>) at the same dosage. Prior to tablet ingestion (i.e., pre-testing), both groups completed a constant power UBP test, three successive 10-sec UBP tests, and then a 60-sec UBP test. Next, skiers completed the 7-day ingestion of their assigned tablets followed immediately by a repeat of the same UBP tests (i.e., post-testing). Neither the skiers nor the researchers were aware of which tablets were being consumed by either group until after all testing was complete. Dependent measures for analysis included heart rate (HR), oxygen consumption (VO<sub>2</sub>), minute ventilation (V<sub>E</sub>), blood lactate (LA), as well as 10-sec (W10, W) and 60-sec (W60, W) UBP. All data were evaluated using a two-factor multivariate repeated measures ANOVA with planned contrasts for post-hoc testing (alpha = 0.05).</p> <p>Results</p> <p>Post-testing cardiorespiratory (HR, VO<sub>2</sub>, V<sub>E</sub>) and LA measures for the treatment group tended to be significantly lower when measured for both constant power and UBP60 tests, while measures of both 10-sec (W10: 229 to 243 W) and 60-sec UBP (W60: 190 to 198 W) were significantly higher (<it>P </it>< 0.05). In contrast, there were no significant changes for the placebo group (P > 0.05).</p> <p>Conclusions</p> <p>Following the 7-day loading phase of Alka-Myte<sup>®</sup>-based alkalizing tablets, trained Nordic skiers experienced significantly lower cardiorespiratory stress, lower blood lactate responses, and higher UBP measures. Thus, the use of this supplement appeared to impart an ergogenic benefit to the skiers that may be similar to the effects expected from consuming well-studied extracellular buffering agents such as sodium bicarbonate.</p

    The kinetics of lactate production and removal during whole-body exercise

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    <p>Abstract</p> <p>Background</p> <p>Based on a literature review, the current study aimed to construct mathematical models of lactate production and removal in both muscles and blood during steady state and at varying intensities during whole-body exercise. In order to experimentally test the models in dynamic situations, a cross-country skier performed laboratory tests while treadmill roller skiing, from where work rate, aerobic power and blood lactate concentration were measured. A two-compartment simulation model for blood lactate production and removal was constructed.</p> <p>Results</p> <p>The simulated and experimental data differed less than 0.5 mmol/L both during steady state and varying sub-maximal intensities. However, the simulation model for lactate removal after high exercise intensities seems to require further examination.</p> <p>Conclusions</p> <p>Overall, the simulation models of lactate production and removal provide useful insight into the parameters that affect blood lactate response, and specifically how blood lactate concentration during practical training and testing in dynamical situations should be interpreted.</p

    Myogenin Regulates Exercise Capacity but Is Dispensable for Skeletal Muscle Regeneration in Adult mdx Mice

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    Duchenne muscular dystrophy (DMD) is the most prevalent inherited childhood muscle disorder in humans. mdx mice exhibit a similar pathophysiology to the human disorder allowing for an in-depth investigation of DMD. Myogenin, a myogenic regulatory factor, is best known for its role in embryonic myogenesis, but its role in adult muscle maintenance and regeneration is still poorly understood. Here, we generated an mdx:Myogflox/flox mouse harboring a tamoxifen-inducible Cre recombinase transgene, which was used to conditionally delete Myog during adult life. After tamoxifen treatment, three groups of mice were created to study the effects of Myog deletion: mdx:Myogflox/flox mice (mdx), Myogflox/flox mice (wild-type), and mdx:MyogfloxΔ/floxΔ:Cre-ER mice (mdx:Myog-deleted). mdx:Myog-deleted mice exhibited no adverse phenotype and behaved normally. When run to exhaustion, mdx:Myog-deleted mice demonstrated an enhanced capacity for exercise compared to mdx mice, running nearly as far as wild-type mice. Moreover, these mice showed the same signature characteristics of muscle regeneration as mdx mice. Unexpectedly, we found that myogenin was dispensable for muscle regeneration. Factors associated with muscle fatigue, metabolism, and proteolysis were significantly altered in mdx:Myog-deleted mice, and this might contribute to their increased exercise capacity. Our results reveal novel functions for myogenin in adult muscle and suggest that reducing Myog expression in other muscle disease models may partially restore muscle function

    Myogenin Regulates Exercise Capacity and Skeletal Muscle Metabolism in the Adult Mouse

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    Although skeletal muscle metabolism is a well-studied physiological process, little is known about how it is regulated at the transcriptional level. The myogenic transcription factor myogenin is required for skeletal muscle development during embryonic and fetal life, but myogenin's role in adult skeletal muscle is unclear. We sought to determine myogenin's function in adult muscle metabolism. A Myog conditional allele and Cre-ER transgene were used to delete Myog in adult mice. Mice were analyzed for exercise capacity by involuntary treadmill running. To assess oxidative and glycolytic metabolism, we performed indirect calorimetry, monitored blood glucose and lactate levels, and performed histochemical analyses on muscle fibers. Surprisingly, we found that Myog-deleted mice performed significantly better than controls in high- and low-intensity treadmill running. This enhanced exercise capacity was due to more efficient oxidative metabolism during low- and high-intensity exercise and more efficient glycolytic metabolism during high-intensity exercise. Furthermore, Myog-deleted mice had an enhanced response to long-term voluntary exercise training on running wheels. We identified several candidate genes whose expression was altered in exercise-stressed muscle of mice lacking myogenin. The results suggest that myogenin plays a critical role as a high-level transcriptional regulator to control the energy balance between aerobic and anaerobic metabolism in adult skeletal muscle

    Physiological and molecular responses to an acute bout of reduced-exertion high-intensity interval training (REHIT)

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    PurposeWe have previously shown that 6 weeks of reduced-exertion high-intensity interval training (REHIT) improves V˙O2V˙O2 max in sedentary men and women and insulin sensitivity in men. Here, we present two studies examining the acute physiological and molecular responses to REHIT.MethodsIn Study 1, five men and six women (age: 26 ± 7 year, BMI: 23 ± 3 kg m−2, V˙O2V˙O2 max: 51 ± 11 ml kg−1 min−1) performed a single 10-min REHIT cycling session (60 W and two 20-s ‘all-out’ sprints), with vastus lateralis biopsies taken before and 0, 30, and 180 min post-exercise for analysis of glycogen content, phosphorylation of AMPK, p38 MAPK and ACC, and gene expression of PGC1α and GLUT4. In Study 2, eight men (21 ± 2 year; 25 ± 4 kg·m−2; 39 ± 10 ml kg−1 min−1) performed three trials (REHIT, 30-min cycling at 50 % of V˙O2V˙O2 max, and a resting control condition) in a randomised cross-over design. Expired air, venous blood samples, and subjective measures of appetite and fatigue were collected before and 0, 15, 30, and 90 min post-exercise.ResultsAcutely, REHIT was associated with a decrease in muscle glycogen, increased ACC phosphorylation, and activation of PGC1α. When compared to aerobic exercise, changes in V˙O2V˙O2 , RER, plasma volume, and plasma lactate and ghrelin were significantly more pronounced with REHIT, whereas plasma glucose, NEFAs, PYY, and measures of appetite were unaffected.ConclusionsCollectively, these data demonstrate that REHIT is associated with a pronounced disturbance of physiological homeostasis and associated activation of signalling pathways, which together may help explain previously observed adaptations once considered exclusive to aerobic exercise
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