The effect of prior upper body exercise on subsequent wingate performance

It has been reported previously that the upper body musculature is continually active during high intensity cycle ergometry. The aim of this study was to examine the effects of prior upper body exercise on subsequent Wingate (WAnT) performance. Eleven recreationally active males (20.8 ± 2.2 yrs; 77.7 ± 12.0 kg;  1.79 ± 0.04 m) completed two trials in a randomised order. In one trial participants completed 2 × 30 s WAnT tests (WAnT1 and WAnT2) with a 6 min recovery period; in the other trial, this protocol was preceded with 4 sets of biceps curls to induce localised arm fatigue. Prior upper body exercise was found to have a statistically significant detrimental effect on peak power output (PPO) during WAnT1 (P < 0.05) but no effect was observed for mean power output (MPO) (P > 0.05). Handgrip (HG) strength was also found to be significantly lower following the upper body exercise. These results demonstrate that the upper body  is meaningfully involved in the generation of leg power during intense cycling

Inter-correlations between laboratory Inter-correlations between laboratory and field-based tests of muscle contractile power

International Journal of Exercise Science 9(5): 635-645, 2016. Muscle contractile properties have previously been distinguished by fiber typing muscle samples obtained from needle biopsy; however due to conflicting evidence regarding sampling bias and the related need for multiple biopsies, it is not certain if these results are a reliable reflection of whole muscle fiber type expression. Inter-correlations between laboratory and field-based measures of muscle contractile power were used to determine which assessments best discriminate between participants of varying sprint performance, and indirectly reveal potential for power vs. endurance exercise performance. Healthy active male (n=32) and female (n=17) participants were recruited from the Central West region of New South Wales. Isometric rate of force development (RFD) and isokinetic torque were assessed at different velocities. A counter movement jump (CMJ) test was implemented to assess concentric and eccentric RFD. A modified Wingate test was used to assess peak power expressed as Watts using a stationary start to the onset of decreased cadence. A 20m sprint was used as a field-based measurement of exercise performance, recording split times at 2m, 10m and 20m, and interval times from 2-10m, 2-20m, and 10-20m. Over 85% (r2=0.851) of 10-20m sprint running performance variance was significantly accounted for by a multiple regression model consisting of peak Watts per kilogram body mass during the modified Wingate (pkWkg), sex, and peak concentric rate of force development (pkcRFDkg). Results indicate a highly significant and predictive relationship between performance measures assessed by the modified Wingate test and sprint running performance in both males and females. Laboratory power tests alone seem sensitive enough to ascertain suitability for power vs. endurance performance potential

Effect of Level and Downhill Running on Breathing Efficiency

Ventilatory equivalents for oxygen and carbon dioxide are physiological measures of breathing efficiency, and are known to be affected by the intensity and mode of exercise. We examined the effect of level running (gradient 0%) and muscle-damaging downhill running (?12%), matched for oxygen uptake, on the ventilatory equivalents for oxygen () and carbon dioxide (). Nine men (27 ± 9 years, 179 ± 7 cm, 75 ± 12 kg, : 52.0 ± 7.7 mL·kg?1·min?1) completed two 40-min running bouts (5 × 8-min with 2-min inter-bout rest), one level and one downhill. Running intensity was matched at 60% of maximal metabolic equivalent. Maximal isometric force of m.quadriceps femoris was measured before and after the running bouts. Data was analyzed with 2-way ANOVA or paired samples t-tests. Running speed (downhill: 13.5 ± 3.2, level: 9.6 ± 2.2 km·h?1) and isometric force deficits (downhill: 17.2 ± 7.6%, level: 2.0 ± 6.9%) were higher for downhill running. Running bouts for level and downhill gradients had , heart rates and respiratory exchange ratio values that were not different indicating matched intensity and metabolic demands. During downhill running, the , (downhill: 29.7 ± 3.3, level: 27.2 ± 1.6) and (downhill: 33.3 ± 2.7, level: 30.4 ± 1.9) were 7.1% and 8.3% higher (p < 0.05) than level running. In conclusion, breathing efficiency appears lower during downhill running (i.e., muscle-damaging exercise) compared to level running at a similar moderate intensity

Interaction among Skeletal Muscle Metabolic Energy Systems during Intense Exercise

High-intensity exercise can result in up to a 1,000-fold increase in the rate of ATP demand compared to that at rest (Newsholme et al., 1983). To sustain muscle contraction, ATP needs to be regenerated at a rate complementary to ATP demand. Three energy systems function to replenish ATP in muscle: (1) Phosphagen, (2) Glycolytic, and (3) Mitochondrial Respiration. The three systems differ in the substrates used, products, maximal rate of ATP regeneration, capacity of ATP regeneration, and their associated contributions to fatigue. In this exercise context, fatigue is best defined as a decreasing force production during muscle contraction despite constant or increasing effort. The replenishment of ATP during intense exercise is the result of a coordinated metabolic response in which all energy systems contribute to different degrees based on an interaction between the intensity and duration of the exercise, and consequently the proportional contribution of the different skeletal muscle motor units. Such relative contributions also determine to a large extent the involvement of specific metabolic and central nervous system events that contribute to fatigue. The purpose of this paper is to provide a contemporary explanation of the muscle metabolic response to different exercise intensities and durations, with emphasis given to recent improvements in understanding and research methodology

Nutrition and exercise determinants of postexercise glycogen synthesis

During the initial hours of recovery from prolonged exhaustive lower body exercise, muscle glycogen synthesis occurs at rates approximating 1-2 mmol.kg-1 wet wt.hr-1 if no carbohydrate is consumed. When carbohydrate is consumed during the recovery, the maximal rate of glycogen synthesis approximates 7-10 mmol.kg-1 wet wt.hr-1. The rate of post-exercise glycogen synthesis is lower if the magnitude of glycogen degradation is small, if less than 0.7 gm glucose.kg-1 body wt.hr-1 is ingested, when the recovery is active, and when the carbohydrate feeding is delayed. The rate of postexercise glycogen synthesis is not reduced during the initial hours (< 4) after eccentric exercise. For studies evaluating muscle glycogen synthesis in excess of 12 hours of recovery, average rates of glycogen synthesis are below 4 mmol.kg-1 wet wt.hr-1. Glycogen synthesis is known to be impaired for time periods in excess of 24 hours following exercise causing eccentric muscle damage. Following intense exercise resulting in high concentrations of muscle lactate, muscle glycogen synthesis occurs at between 15-25 mmol.kg-1 wet wt.hr-1. These synthesis rates occur without ingested carbohydrate during the recovery period and are maintained when a low intensity active recovery is performed

Intra-Arterial Blood Pressure Characteristics during Submaximal Cycling and Recovery

The purpose of this study was to measure intra-arterial (IA) blood pressure from rest to steady-state submaximal exercise and immediately post-exercise. Beat-to-beat blood pressure was compared to breath-by-breath VO2 during steady-state and maximal exercise. Fourteen normotensive subjects volunteered. Systolic (SBP), diastolic (DBP) and mean (mBP) blood pressure was measured from rest to steady state during cycling at 45, 60, and 75% maximal power output (POmax). BP was assessed during recovery from VO2peak through 2 min of cycling at 50 W. During the rest to exercise transition, mBP decreased from 103.41 ± 9.4 to 90.1 ± 8.9 mmHg after 11.6 ± 6.2 s (

Exercise physiologists should not recommend the use of ephedrine and related compounds as ergogenic aids or stimulants for increased weight loss

Ephedra, or ma huang, refers to the above ground portion of the plants that comprise the genus ephedra. Although the species of ephedra differ in their chemical composition, the content of biologically active compounds in these plants is mainly due to ephedrine (other compounds being pseudoephedrine, norpseudoephedrine cathine, and norephedrine phenylpropanolamine). Ephedrine is similar in chemical structure and biological function to amphetamine, although having a 25-fold lower biological potency. Nonetheless, ephedrine is a potent central and peripheral nervous system stimulant, causing the stimulation of both α and β adrenergic receptors, and the release of dopamine within the brain and norepinephrine (noradrenaline) from sympathetic nerves within and external to the CNS. These mechanisms of action cause bronchial smooth muscle relaxation, increases in heart rate and blood pressure, variable peripheral vasculature constriction and dilation, general feelings of emotional and/or psychological arousal and increased alertness, and an accelerated metabolic rate. The biological responses to ephedrine have lead to its use as a stimulant in efforts to improve exercise performance, and assist in weight loss. It has been estimated that at least 3 billion doses of over-the-counter ephedrine or extracts from ephedra were ingested in the U.S. in 2000 for the purpose of stimulating increased weight loss. In addition, compounds high in ephedrine, such as over-the-counter medications to treat sinus congestion or symptoms of the common cold, can be and are used to synthesize the illegal drug metamphetamine. Intake of ephedrine exposes the user to unacceptable negative side effects, including mood disturbances, abnormal heart function, hypertension, gastrointestinal dysfunction and headache, while providing small amounts of added weight loss and/or central nervous system stimulation. Furthermore, individuals with underlying cardiovascular disease or other illnesses may be at more serious health risk when taking ephedrine. Individuals who need to lose weight (body fat) should rely on modifications to diet and increased daily physical activity and exercise. The need for body fat loss rather than gross weight loss should also be recommended and understood. Where additional assistance is needed in body fat reduction, individuals should consult a registered dietitian or their physician

Drug-induced metabolic acidosis

Summary: Drug causes of metabolic acidosis are numerous and their mechanisms are diverse. Broadly, they can cause metabolic acidosis with either a normal anion gap (e.g. drug-induced renal tubular acidosis) or an elevated anion gap (e.g. drug-induced lactic acidosis or pyroglutamic acidosis). This review describes the drugs that can cause or contribute to metabolic acidosis during therapeutic use, the mechanisms by which this occurs, and how they may be identified in practice

Lactate Regulates Metabolic and Proinflammatory Circuits in Control of T Cell Migration and Effector Functions

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