Longer Periods Of Exercise Research Articles

Effect of two Exercise Training Protocols on miR-133a and Runx2 in High-Fat Diet and Streptozotocin-induced Diabetes

Background: Type 2 Diabetes (T2D) in the elderly is an epidemic that significantly impacts global health. This experimental study aimed to compare the responses of microRNA-133a (miR-133a) in different tissues and of Runt-related transcription factor 2 (Runx2) in bone marrow tissue following resistance and endurance training in old rats with High-Fat Diet and Streptozotocin (HFD/STZ)- induced type 2 diabetes. Materials and Methods: T2D was induced by HFD/low-dose STZ in 30 male Wistar rats (21-monthold, Mean±SD weight 418±43 g). The rats received HFD (55%, 31%, and 14% of energy from fat, carbohydrate, and protein, respectively; 5.2 kcal/g). The diets continued for eight weeks in both groups. Over week four, the rats in the group with HFD/STZ-induced T2D received treatment with low-dose STZ. After one week of familiarity with the laboratory environment, they were randomly divided into three groups: Diabetic Endurance Training (DET, n=10), Diabetic Resistance Training (DRT, n=10), and Diabetic Control (DC, n=10). The eight weeks of endurance training protocol comprised five sessions of moderate-intensity training (60%-75% velocity at maximal oxygen uptake (vVO2max) and low intensity (30%-30% vVO2max). In 60% Maximum Voluntary Carrying Capacity (MVCC), the resistance group climbed the ladder 14-20 times with 1-minute rest, five days a week. Results: The results of the 1-way ANOVA test showed no significant change in serum miR-133 expression (P=0.411) and muscle tissue (P=0.077) following resistance and endurance training. However, significant differences were observed in bone marrow miR-133 expression (P=0.003) and Runx2 gene expression (P=0.002) between groups. Tukey’s post hoc tests showed that the bone marrow miR-133 expression had a significant increase following eight weeks of resistance training compared to the endurance training (P=0.006) and control (P=0.002) groups, and bone marrow Runx2 gene expression in rats exposed to resistance training compared to the endurance training (P=0.044) and the control (P=0.018) groups. Conclusion: It seems that longer periods of exercise are required for cellular changes in the metabolism of these tissues after these exercise protocols. This topic should be studied in future research

It's well and truly time to stop stating that AMPK regulates glucose uptake and fat oxidation during exercise.

None for Perspective.

Comments on the dilemma in the January/February issue: Disclosing pre-existing veterinary conditions to insurance companies

In the dilemma discussed in the January/February issue of In Practice, Kathryn Henderson described a scenario where a client brings her two-year-old dog in to see you regarding his ongoing...

The effects of taurine on repeat sprint cycling after low or high cadence exhaustive exercise in females

This study investigated the effects of taurine on repeated sprint exercise, performed after fixed incremental ramp exercise to exhaustion at isokinetic high (90r/min) or low (50r/min) cadences. In a double-blind, repeated measures design, nine females completed an incremental ramp test to volitional exhaustion, followed by 2min active recovery and 6×10s sprints on a cycle ergometer, in one of four conditions: high cadence (90r/min) + taurine (50mg/kg body mass); high cadence + placebo (3mg/kg body mass maltodextrin); low cadence (50r/min) + taurine; low cadence + placebo. Heart rate (HR) and blood lactate concentration B[La] were measured before and after the ramp test and after the sprints. Taurine lowered HR vs. placebo prior to the ramp test (P = 0.004; d = 2.1). There was an effect of condition on ramp performance (P < 0.001), with higher end-test power (d = 3.7) in taurine conditions. During repeated sprints, there was a condition×time interaction (P = 0.002), with higher peak sprint power in the placebo conditions compared to taurine (sprint 2-6; P < 0.05). B[La] was higher in taurine compared to placebo post-ramp (P = 0.004; d = 4.7). Taurine-lowered pre-exercise HR and improved incremental end-test power output, with subsequent detrimental effects on sprint performance, independent of cadence. Short endurance performance can be acutely enhanced after taurine ingestion but this effect might not be maintained across longer periods of exercise or induce the need for longer recovery periods.

How does a short period of exercise effect toe pressures and toe-brachial indices? A cross-sectional exploratory study

BackgroundWhilst post exercise ankle-brachial indices (ABI) are commonly used to help identify peripheral arterial disease (PAD), the role of post exercise toe pressures (TP) or toe-brachial indices (TBI) is unclear. The aim of this study was to determine, in a population without clinical signs of PAD, the effect that 30 s of weight-bearing heel raises has on TP and TBI values. Additionally, the ability of resting TP and TBI values to predict change in post-exercise values using the heel raise method was investigated.MethodsParticipants over the age of 18 with a resting TBI of ≥0.60 and ABI between 0.90 and 1.40, without diabetes, history of cardiovascular disease and not currently smoking were included. Following ten minutes of supine rest, right TP and bilateral brachial pressures were performed in a randomized order using automated devices. Participants then performed 30 s of weight-bearing heel raises, immediately after which supine vascular measures were repeated. Data were assessed for normality using the Shapiro-Wilk test. For change in TP and TBI values the Wilcoxon Signed-Rank Test was performed. For correlations between resting and change in post exercise values, the Spearman Rank Order Correlations were performed, and where significant correlation identified, a linear regression undertaken.ResultsForty-eight participants were included. A statistically significant decrease was seen in the median TP from resting 103.00 mmHg (IQR: 89.00 to 124.75) to post exercise 98.50 mmHg (IQR: 82.00 to 119.50), z = − 2.03, p = 0.04. This difference of 4.50 mmHg represents a 4.37% change and is considered a small effect size (r = 0.21). The median TBI also demonstrated a statistically significant decrease from resting 0.79 (IQR: 0.68 to 0.94) to post exercise 0.72 (IQR: 0.60 to 0.87), z = − 2.86, p = < 0.01. This difference of 0.07 represents an 8.86% change and is considered a small effect size (r = 0.29). Linear regression demonstrated that resting TBI predicted 22.4% of the variance in post exercise TBI, p = < 0.01, coefficients beta − 0.49.ConclusionsThirty seconds of weight-bearing heel raises resulted in a similar decrease in TBI values seen in longer periods of exercise. TP values also showed a decrease post exercise; however this was contrary to previous studies.

Translating the impact of exercise on cognition: Methodological issues in animal research

Physical exercise and fitness have been proposed as potential factors that promote healthy cognitive aging. Some of the support for this hypothesis has come from animal research. Animal studies are also used to propose the physiological mechanisms underlying the cognitive performance improvement associated with exercise. In the present review and meta-analysis, we discuss several methodological problems that limit the contribution of animal studies to the understanding of the putative effects of exercise on cognitive aging. We suggest that the most likely measure to equate exercise intensity in rodent and humans may be oxygen consumption (VO2) because observed values are surprisingly similar in young and older rodents and humans. For practical reasons, several animal studies use young rodents kept in social isolation. We show that social isolation is associated with an enhanced impact of exercise on cognitive performance but not on some physiological measures thought to mediate the effect of exercise. Surprisingly, two months or more of exercise intervention appeared to be ineffective to promote cognitive performance compared to shorter durations. We argue that impact of exercise in socially isolated animals is explained by an alleviation of environmental impoverishment as much as an effect of physical exercise. It is possible that the introduction of exercise in rodents is partly mediated by environmental changes. It may explain why larger effects are observed for the shorter durations of exercise while much smaller effects are found after longer periods of exercise.

A Study of Effect of the Compound Physical Activity Therapy on Muscular Strength in Obese Women

[Purpose] The aim of this study was to determine how compound physical activity affects muscular strength of middle-aged obese women. [Subjects] The research subjects were 40–50 year-old middle-aged women with excess body fat (30%). [Methods] The subjects were randomly assigned to two group, the experimental group and the control group. The experimental group performed two types of exercise programs for 16 weeks. Aerobic physical activity was performed 5 times per week, and anaerobic physical activity was performed every two days, and the exercise program each day was composed of a warm-up, the main exercise, and cooldown. The type of exercise focused on walking at a quick pace, and the intensity of the exercise focused on long periods of exercise at low intensity with the level of HRmax being 40–60%. The weight training, which was useful for beginners, as a type of kinetic load exercise, was applied with a composition recommended by the ACSM for muscle fitness (intensity of 40–60% of 1 RM and 10–15 repetitions). SPSS version 16.0 was used to analyze the data by ANCOVA and the t-test. [Results] The chest, leg, and abdominal strengths were significantly increased in the experimental group, and this indicates that compound physical activity is effective for improvement of muscular strength. [Conclusion] In conclusion, there were significant differences between groups in terms of muscular strength.

EFFECTS OF CHANGES IN PHYSIQUE AND LIFESTYLE ON BONE MINERAL DENSITY IN THE EARLY TEENS

1) Abstract The purpose of this longitudinal study was to reveal the effects of physique, body composition, and lifestyles on bone mineral density (BMD) in the early teens. Subjects of the current study were 73 boys and 73 girls. Osteo-sono assessment index (OSI) , body mass index (BMI) , body fat percentage and fat-free mass index (FFMI) were measures. All subjects were measured at two points; 5th grade and 8th grade. The association between changes in these values and the OSI at 8th grade were evaluated with multiple regression analysis. Positive correlations were observed between the OSI and exercise time/FFMI in both sexes. Furthermore, this trend was also observed between the OSI and BMI in boys. The results suggested that an increase in exercise time and FFMI are factors that may enhance BMD in both sexes. However, the increase in BMI was found to increase BMD only in boys. Such gender difference was suggested to be the result of what BMI represents for each group. For boys, increased BMI reflects the increasing amount of muscle mass, whereas for girls, it mainly reflects an increase in body fat. Therefore, muscle mass needs to be increased by long periods of exercise in order to increase BMD, especially in girls.

A fisherman who could not row

In July, 2007, a 28-year-old man came to our institute. Until recently, he had worked as a fi sherman, off the coast of Kerala—where boats traditionally carry 4–5 fi sher men, who must row against strong currents and waves. He had had to leave his job, because, when rowing, he could not keep to the same rhythm as his fellows: he could not extend his elbows rapidly after fl exion. After 5 min, this problem disappeared. Additionally, he could not release his grip quickly, after holding things tightly. His problems had gradually increased over 5 years; he had had to leave his job, and was now working as an assistant in a roadside shop. He had no other medical history of note. General examination showed nothing of note. Neurological examination showed no abnormality of cognitive function, cranial nerves, the somatosensory system, or cerebellum; power and refl exes were normal, and the patient had no muscle atrophy or fasciculations. However, repeated gripping and releasing of the examiner’s fi ngers, tapping over the extensor digitorum communis, and tapping the tongue revealed grip myotonia, percussion myotonia, and tongue myotonia respectively. Blood tests revealed a high concentration of creatine kinase (CK) (2960 IU/L; normal range 21–232 IU/L). Needle electromyography (EMG) showed diff use myotonic discharges (fi gure), but no evidence of myopathy. On cooling of muscle to 20°C, by wrapping the limb in a plastic bag and immersing it in iced water, and after short and long periods of exercise (voluntary contraction of the muscle tested, for 5–10 s and 3–5 min with brief rest breaks), we found no decrease in compound muscle action-potential amplitude. These fi ndings were consistent with true myotonia. But of what cause? The age of onset, high concentration of CK, and normal EMG after exercise were atypical for myotonia congenita. The persistence of symptoms indicated that the patient probably did not have potassium-aggravated myotonia (also known as myotonia fl uctuans). Slit-lamp examin ation showed no cataract, which, together with the absence of muscle weakness, made type 1 myotonic dystrophy unlikely; moreover, genetic testing for this disease gave a negative result. However, routine echo cardiography revealed mode rate pericardial eff usion without tamponade, so we requested thyroid function tests. The thyrotropin con cen tration was very high (>60 mIU/L; normal range 0∙25–5 mIU/L); tri-iodothyronine and thyroxine concentrations were low, at <0∙4 nmol/L (normal 0∙92–2∙33 nmol/L) and 8∙01 nmol/L (normal 60–120 nmol/L) respect ively. We prescribed thyroxine. The pa tient’s symp toms subsided rapidly. At 3-month and 6-month follow-up, we found no clinical or electro physiological evidence of myotonia; concentrations of CK and thyroid hormones were normal. When last seen, in June, 2008, the patient was well, on a thyroxine dose of 200 μg daily, and had returned to work as a fi sher man. Myotonia is the slow relaxation of muscle, after voluntary contraction or percussion. It is painless, but patients often describe muscle stiff ness that improves with repeated use of muscle, the so-called “warm-up phenomenon”. On examination, myotonia may be evident from a delayed release of the hand, in the introductory handshake. EMG shows spontaneous, repetitive discharges with waxing and waning of amplitude and frequency, producing a characteristic “dive-bomber” like sound. Myotonia can be a presenting sign of myotonic dystrophy; non-dystrophic myotonias, in which mytonia is caused by dysfunction of channels for chloride (in myotonia congenita) or sodium (in paramyotonia congenita, potassium-aggravated myotonia, and hyperkalaemic periodic paralysis with myotonia); myopathies (acid maltase defi ciency, polymyositis, myotubular myopathy); or, rarely, denervation of any cause. Syndromes causing myotonia are distinguished by associated clinical features, and by EMG after cooling and exercise. Pseudomyotonia is slow relaxation without myotonic discharge on EMG, and is found in hypothyroidism, when it is characteristically revealed by testing of tendon refl exes. However, hypothyroidism can also cause true myotonia, and can unmask type 2 myotonic dystrophy. Patients with myotonia caused by hypo thyroidism should be given thyroxine; patients in whom myotonic dystrophy is unmasked may benefi t symptom atically from thyroxine, despite persistent myotonic dis charges on EMG. We suspect, on clinical grounds, that our patient had myotonia caused by hypothyroidism; he declined genetic testing for type 2 myotonic dystrophy.

GENES FOR THE LONG RUN

Can the same genes both improve your aptitude for endurance exercise and lower your life expectancy? A recent study of mitochondrial DNA (mtDNA) in track athletes suggests that the answer may be `yes'.The mitochondrial genome is a small (17-kb), circular chromosome that encodes 13 components of the electron transport chain, which generate the proton gradient necessary for aerobic ATP production. Mitochondrial DNA might therefore be expected to influence an individual's ability to sustain long periods of exercise. To determine whether the mitochondrial genes of track athletes differ systematically from those of the population at large, Niemi and Majamaa analyzed the mtDNA sequences of 141 elite Finnish long-distance runners and sprinters as well as 1060 Finnish control subjects. They found that certain groups of mtDNA sequences (called haplogroups, since there is only one copy of the chromosome per mitochondrion) occurred less frequently in the distance runners than in the sprinters and control subjects. In particular, no distance runner belonged to haplogroup K or subhaplogroup J2,whose combined frequency is at least 4.5% among control subjects and is even higher among sprinters.Since distance runners are heavily dependent on aerobic ATP production by their mitochondria, it isn't surprising that their mtDNA differs from that of people with different exercise habits. For example, genes for protein isoforms that mildly impair ATP synthesis should presumably be rare among endurance athletes. What's interesting, however, is that the haplogroups underrepresented among the distance runners are overrepresented among very old people. Previous work by the Niemi/Majamaa group and others has shown that members of haplogroup K and subhaplogroup J2 tend to live longer than people of other haplogroups.Is it plausible that the mitochondrial genes of haplogroup K and subhaplogroup J2 limit endurance performance but improve life expectancy?Niemi and Majamaa offer an intriguing hypothesis to explain this potential paradox: perhaps J2 and K are `uncoupling genomes' that increase proton leak across the mitochondrial membrane. An elevated proton leak could certainly limit aerobic ATP production, and thus endurance performance. But it could also prevent the mitochondrial membrane potential from rising into the range(&gt;140 mV) where production of reactive oxygen species (ROS) becomes high. ROS have been implicated in ageing, so limiting ROS production could contribute to a longer life. Although the link between ROS and ageing is still under investigation, several mouse studies have suggested that relatively`leaky' mitochondria could promote longevity by minimizing the generation of ROS. Thus, if members of J2 and K haplotypes limit their ROS production, this could explain why they live longer than other people.If the rareness of J2 and K among endurance athletes is confirmed by additional work, the `uncoupling genome' hypothesis should be tested with biochemical measurements of mitochondria isolated from representatives of different haplogroups. If the hypothesis is correct, mitochondria of haplogroup K and subhaplogroup J2 should have lower membrane potentials, lower ROS production rates and lower ATP production rates (relative to O2consumption rates) than other mitochondria. Such studies would represent the completion of another lap in our race to understand the genetic basis of differences in athletic performance.

Painful piezogenic pedal papules: response to local etectro-acupuncture

We report the case of a woman who had pain in both heels which was exacerbated by long periods of exercise. On examination, there were small flesh-coloured papules which appeared over the medial and lateral aspects of the heels only on weight bearing. Coincidentally, she was noted to have larger flesh-coloured papules over the anterior surface of the shins. The diagnoses of painful piezogenic pedal papules and bilateral tibialis anterior muscle herniation, respectively, were made. After many attempts to control the pain, a course of electro-acupuncture was commenced. A good subjective clinical response was achieved which has been maintained by fortnightly treatments. We discuss the prevalence, pathogenesis and treatment of painful piezogenic pedal papules. We believe that our patient is the first to have 'herniations' at both heel and shin sites and the first to have successful sustained pain relief for painful piezogenic pedal papules.

The effects of sustained exercise on gluconeogenesis, glycogenolysis and glycogen synthesis in Merino sheep

The ability of sheep to maintain an elevated rate of glucose metabolism in the splanchnic tissues and skeletal muscle during long-term exercise was studied using isotope dilution and arteriovenous difference techniques. Comparisons were made between Merino ewes at rest or walking at 4.5 km h-1 on a 0' incline (30% VO2max) for 4 h or 9� incline (60% VO2max.) for 2 h. Sheep were close to exhaustion at the completion of the later rate of exercise. Exercise elicited an initial hyperglycemia with a return to euglycemia at the end of exercise. The entry rate of glucose increased 2-6 and 3.4 times during exercise at 30 and 60% VO2max respectively. Similar increases in the rate of glucose release by the liver, were seen; the increases were maintained throughout the exercise period. Assuming complete conversion of gluconeogenic substrates extracted by the liver gluconeogenesis could have accounted for 90% and 60% of the glucose release during exercise at 30% and 60% VO2max. Hepatic glycogenolysis was also substantial, and when summed with gluconeogenesis 120-150% of the glucose release was accounted for. The ability of sheep to replace glycogen depleted owing to exercise was significant in liver and type IIA muscle (m. semimembranosis) and represented rates 3-6 times those previously reported in sheep and cattle. Providing sheep do not suffer hyperthermia, they are well equipped to endure long periods of exercise owing to an ability to maintain carbohydrate balance.