Cristiano Kalata Varela | FADERGS Laureate International (original) (raw)

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Papers by Cristiano Kalata Varela

Purpose] To compare the lumbar lordosis angle and electromyographic activities of the trunk and l... more Purpose] To compare the lumbar lordosis angle and electromyographic activities of the trunk and lower-limb muscles in the hip neutral position and external rotation during back squats. [Subjects and Methods] Ten healthy males without severe low back pain or lower-limb injury participated in this study. The lumbar lordosis angle and electromyographic activities were measured using three-dimensional motion-capture systems and surface electrodes during four back squats: parallel back squats in the hip neutral position and external rotation and full back squats in the hip neutral position and external rotation. A paired t-test was used to compare parallel and full back squats measurements in the hip neutral position and external rotation, respectively.

Accelerated trajectories of cognitive decline in older adults may increase the risk of developing... more Accelerated trajectories of cognitive decline in older adults may increase the risk of developing Alzheimer disease and related dementias (ADRD). Physical activity has potential modifying effects on these changes that could prevent and/or delay ADRD. This review explores the hypothesis that multiple, mutually complimentary and interacting factors explain the positive association between exercise and the optimization of cognition in older adults.

Sedentary behavior has a strong association with cardiovascular disease (CVD) risk, which may be ... more Sedentary behavior has a strong association with cardiovascular disease (CVD) risk, which may be independent of physical activity. To date, the mechanism(s) that mediate this relationship are poorly understood. We hypothesize that sedentary behavior modifies key hemodynamic, inflammatory, and metabolic processes resulting in impaired arterial health. Subsequently, these vascular impairments directly and indirectly contribute to the development of CVD. Key Words:

The exploits of elite athletes delight, frustrate, and confound us as they strive to reach their ... more The exploits of elite athletes delight, frustrate, and confound us as they strive to reach their physiological, psychological, and biomechanical limits. We dissect nutritional approaches to optimal performance, showcasing the contribution of modern sports science to gold medals and world titles. Despite an enduring belief in a single, superior "athletic diet," diversity in sports nutrition practices among successful athletes arises from the specificity of the metabolic demands of different sports and the periodization of training and competition goals. Pragmatic implementation of nutrition strategies in real-world scenarios and the prioritization of important strategies when nutrition themes are in conflict add to this variation. Lastly, differences in athlete practices both promote and reflect areas of controversy and disagreement among sports nutrition experts. Box 1. Move over, muscle: The brain's the boss! The brain and CNS are implicit in skilled tasks and events requiring concentration and decision-making. Only recently, however, have we recognized their role in the performance of even simple locomotor events, including strategies around pacing. A century ago, Bainbridge wrote, "There appear, however, to be two types of fatigue, one arising entirely within the central nervous system, the other in which fatigue of the muscles themselves is superadded to that of the nervous system" (71). Despite this early insight, sports nutrition has evolved with a bias toward studying peripheral mechanisms of fatigue and their role in performance, possibly because of the opportunities provided by available research tools (72). Exceptions are noted; hypoglycemia has long been recognized as a cause of fatigue during endurance sports (73), and brain astrocytes are now known to have labile glycogen stores (74). Furthermore, we now explain the ergogenic benefits of caffeine through central roles (reduced perception of effort and increased neural recruitment of muscle fibers) rather than a metabolic origin (muscle glycogen sparing because of increased availability and oxidation of plasma FFAs) (75).

Robergs, Robert A., Farzenah Ghiasvand, and Daryl Parker. Biochemistry of exercise-induced metabo... more Robergs, Robert A., Farzenah Ghiasvand, and Daryl Parker. Biochemistry of exercise-induced metabolic acidosis. Am J Physiol Regul Integr Comp Physiol The development of acidosis during intense exercise has traditionally been explained by the increased production of lactic acid, causing the release of a proton and the formation of the acid salt sodium lactate. On the basis of this explanation, if the rate of lactate production is high enough, the cellular proton buffering capacity can be exceeded, resulting in a decrease in cellular pH. These biochemical events have been termed lactic acidosis. The lactic acidosis of exercise has been a classic explanation of the biochemistry of acidosis for more than 80 years. This belief has led to the interpretation that lactate production causes acidosis and, in turn, that increased lactate production is one of the several causes of muscle fatigue during intense exercise. This review presents clear evidence that there is no biochemical support for lactate production causing acidosis. Lactate production retards, not causes, acidosis. Similarly, there is a wealth of research evidence to show that acidosis is caused by reactions other than lactate production. Every time ATP is broken down to ADP and P i, a proton is released. When the ATP demand of muscle contraction is met by mitochondrial respiration, there is no proton accumulation in the cell, as protons are used by the mitochondria for oxidative phosphorylation and to maintain the proton gradient in the intermembranous space. It is only when the exercise intensity increases beyond steady state that there is a need for greater reliance on ATP regeneration from glycolysis and the phosphagen system. The ATP that is supplied from these nonmitochondrial sources and is eventually used to fuel muscle contraction increases proton release and causes the acidosis of intense exercise. Lactate production increases under these cellular conditions to prevent pyruvate accumulation and supply the NAD ϩ needed for phase 2 of glycolysis. Thus increased lactate production coincides with cellular acidosis and remains a good indirect marker for cell metabolic conditions that induce metabolic acidosis. If muscle did not produce lactate, acidosis and muscle fatigue would occur more quickly and exercise performance would be severely impaired.

and later by Sokoloff 2 showed that glucose is the obligatory physiological energy substrate of t... more and later by Sokoloff 2 showed that glucose is the obligatory physiological energy substrate of the brain and is metabolized to CO 2 and water to yield 32-36 ATP molecules per molecule of oxidized glucose 3 . Studies over the past 20 years have added a cellular resolution to these organ stud ies, demonstrating a cellspecific metabolism of glu cose. Given the cellular heterogeneity of the brain, it is not surprising that different cell types have distinct metabolic profiles. In particular, the emerging view is that neurons are mostly oxidative, whereas glial cells -notably, astrocytes and oligodendrocytes -pre dominantly process glucose glycolytically, meaning that they produce lactate and pyruvate from glucose 4,5 . Estimates of glucose uptake from the circulation indicate that, at the most, neurons take up an amount approximately equal to that taken up by astrocytes under basal conditions 6,7 .