The effect of obesity on isolated muscle function is surprisingly underresearched. The present study is the first to examine the effects of obesity on isolated muscle performance using a method that more closely represents real-world muscle function. This work uniquely establishes a muscle-specific profile of mechanical changes in relation to underpinning mechanisms. These findings may be important to understanding the negative cycle of obesity and in designing interventions for improving weight status.

Obesity can cause a decline in contractile function of skeletal muscle, thereby reducing mobility and promoting obesity-associated health risks. We reviewed the literature to establish the current state-of-knowledge of how obesity affects skeletal muscle contraction and relaxation. At a cellular level, the dominant effects of obesity are disrupted calcium signalling and 5'-adenosine monophosphate-activated protein kinase (AMPK) activity. As a result, there is a shift from slow to fast muscle fibre types. Decreased AMPK activity promotes the class II histone deacetylase (HDAC)-mediated inhibition of the myocyte enhancer factor 2 (MEF2). MEF2 promotes slow fibre type expression, and its activity is stimulated by the calcium-dependent phosphatase calcineurin. Obesity-induced attenuation of calcium signalling via its effects on calcineurin, as well as on adiponectin and actinin affects excitation-contraction coupling and excitation-transcription coupling in the myocyte. These molecular changes affect muscle contractile function and phenotype, and thereby and muscle performance. , obesity can increase the absolute force and power produced by increasing the demand on weight-supporting muscle. However, when normalised to body mass, muscle performance of obese individuals is reduced. Isolated muscle preparations show that obesity often leads to a decrease in force produced per muscle cross-sectional area, and power produced per muscle mass. Obesity and ageing have similar physiological consequences. The synergistic effects of obesity and ageing on muscle function may exacerbate morbidity and mortality. Important future research directions include determining: the relationship between time course of weight gain and changes in muscle function; the relative effects of weight gain and high-fat diet feeding per se; the effects of obesity on muscle function during ageing; and if the effects of obesity on muscle function are reversible.

Previous isolated muscle studies examining the effects of ageing on contractility have used isometric protocols, which have been shown to have poor relevance to dynamic muscle performance in vivo. The present study uniquely uses the work-loop technique for a more realistic estimation of in vivo muscle function to examine changes in mammalian skeletal muscle mechanical properties with age. Measurements of maximal isometric stress, activation and relaxation time, maximal power output, and sustained power output during repetitive activation and recovery are compared in locomotory extensor digitorum longus (EDL) and core diaphragm muscle isolated from 3-, 10-, 30-, and 50-wk-old female mice to examine the early onset of ageing. A progressive age-related reduction in maximal isometric stress that was of greater magnitude than the decrease in maximal power output occurred in both muscles. Maximal force and power developed earlier in diaphragm than EDL muscle but demonstrated a greater age-related decline. The present study indicates that ability to sustain skeletal muscle power output through repetitive contraction is age- and muscle-dependent, which may help rationalize previously reported equivocal results from examination of the effect of age on muscular endurance. The age-related decline in EDL muscle performance is prevalent without a significant reduction in muscle mass, and biochemical analysis of key marker enzymes suggests that although there is some evidence of a more oxidative fiber type, this is not the primary contributor to the early age-related reduction in muscle contractility.

The aim of this study was exploratory and sought to examine the effect on blood pressure (BP), heart rate (HR) and mood state responses in primary school children of moderate intensity cycling whilst viewing a green environment compared to exercise alone. Following ethics approval and parental informed consent, 14 children (seven boys, seven girls, Mean age ± SD = 10 ± 1 years) undertook two, 15 min bouts of cycling at a moderate exercise intensity in a counterbalanced order. In one bout they cycled whilst viewing a film of cycling in a forest setting. In the other condition participants cycled with no visual stimulus. Pre-, immediately post-exercise and 15 min post-exercise, BP, HR and Mood state were assessed. Analysis of variance, indicated significant condition X time interaction for SBP (p = 0.04). Bonferroni post-hoc pairwise comparisons indicated that systolic blood pressure (SBP) 15 min post exercise was significantly lower following green exercise compared to the control condition (p = 0.01). There were no significant differences in diastolic blood pressure (DBP) (all p > 0.05). HR immediately post exercise was significantly higher than HR pre exercise irrespective of green exercise or control condition (p = 0.001). Mood scores for fatigue were significantly higher and scores for vigor lower 15 min post exercise irrespective of green exercise or control condition (both p = 0.0001). Gender was not significant in any analyses (p > 0.05). Thus, the present study identifies an augmented post exercise hypotensive effect for children following green exercise compared to exercise alone.

Caffeine is an increasingly popular nutritional supplement due to the legal, significant improvements in sporting performance that it has been documented to elicit, with minimal side effects. Therefore, the effects of caffeine on human performance continue to be a popular area of research as we strive to improve our understanding of this drug and make more precise recommendations for its use in sport. Although variations in exercise intensity seems to affect its ergogenic benefits, it is largely thought that caffeine can induce significant improvements in endurance, power and strength-based activities. There are a number of limitations to testing caffeine-induced effects on human performance that can be better controlled when investigating its effects on isolated muscles under in vitro conditions. The hydrophobic nature of caffeine results in a post-digestion distribution to all tissues of the body making it difficult to accurately quantify its key mechanism of action. This review considers the contribution of evidence from isolated muscle studies to our understating of the direct effects of caffeine on muscle during human performance. The body of in vitro evidence presented suggests that caffeine can directly potentiate skeletal muscle force, work and power, which may be important contributors to the performance-enhancing effects seen in humans. Abbreviations

Tallis J, James RS, Cox VM, Duncan MJ. The effect of physiological concentrations of caffeine on the power output of maximally and submaximally stimulated mouse EDL (fast) and soleus (slow) muscle. J Appl Physiol 112: 64 -71, 2012. First published October 6, 2011 doi:10.1152/japplphysiol.00801.2011The ergogenic effects of caffeine in human exercise have been shown to improve endurance and anaerobic exercise performance. Previous work has demonstrated that 70 M caffeine (physiological maximum) can directly increase mouse extensor digitorum longus (EDL) muscle power output (PO) in sprintlike activity by 3%. Our study used the work loop technique on isolated mouse muscles to investigate whether the direct effect of 70 M caffeine on PO differed between 1) maximally and submaximally activated muscle; 2) relatively fast (EDL) and relatively slow (soleus) muscles; and 3) caffeine concentrations. Caffeine treatment of 70 M resulted in significant improvements in PO in maximally and submaximally activated EDL and soleus (P Ͻ 0.03 in all cases). For EDL, the effects of caffeine were greatest when the lowest, submaximal stimulation frequency was used (P Ͻ 0.001). Caffeine treatments of 140, 70, and 50 M resulted in significant improvements in acute PO for both maximally activated EDL (3%) and soleus (6%) (P Ͻ 0.023 in all cases); however, there was no significant difference in effect between these concentrations (P Ͼ 0.420 in all cases). Therefore, the ergogenic effects of caffeine on PO were higher in muscles with a slower fiber type (P Ͻ 0.001). Treatment with 35 M caffeine failed to elicit any improvement in PO in either muscle (P Ͼ 0.72 in both cases). Caffeine concentrations below the physiological maximum can directly potentiate skeletal muscle PO. This caffeine-induced increase in force could provide similar benefit across a range of exercise intensities, with greater gains likely in activities powered by slower muscle fiber type.

Caffeine caused an improvement in some aspects of muscle strength, but there was no additional effect of expectancy. Performance was poorer in participants who believed caffeine would have the greatest benefit, which highlights a link between expected ergogenicity, motivation, and personality characteristics. Muscle Nerve 54: 479-486, 2016.

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