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 in vivo and in vitro muscle performance. In vivo, 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.

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 (CAF) is widely consumed across sport and exercise for its reputed ergogenic properties, including central nervous stimulation and enhanced muscular force development. However, expectancy and the related psychological permutations that are associated with oral CAF ingestion are generally not considered in most experimental designs and these could be important in understanding if/how CAF elicits an ergogenic effect. The present paper reviews 17 intervention studies across sport, exercise, and cognitive performance. All explore CAF expectancies, in conjunction with/without CAF pharmacology. Thirteen out of 17 studies indicated expectancy effects of varying magnitudes across a range of exercise tasks and cognitive skills inclusive off but not limited to; endurance capacity, weightlifting performance, simple reaction time and memory. Factors, such as motivation, belief, and habitual CAF consumption habits influenced the response. In many instances, these effects were comparable to CAF pharmacology. Given these findings and the lack of consistency in the experimental design, future research acknowledging factors, such as habitual CAF consumption habits, habituated expectations, and the importance of subjective post-hoc analysis will help to advance knowledge within this area.

Obesity affects the major metabolic and cellular processes involved in skeletal muscle contractility. Surprisingly, the effect of obesity on isolated skeletal muscle performance remains unresolved. The present study is the first to examine the muscle-specific changes in contractility following dietary-induced obesity using an isolated muscle work-loop (WL) model that more closely represents in vivo muscle performance. Following 16-wk high-calorific feeding, soleus (SOL), extensor digitorum longus (EDL), and diaphragm (DIA) were isolated from female (CD-1) mice, and contractile performance was compared against a lean control group. Obese SOL produced greater isometric force; however, isometric stress (force per unit muscle area), absolute WL power, and normalized WL power (watts per kilogram muscle mass) were unaffected. Maximal isometric force and absolute WL power of the EDL were similar between groups. For both EDL and DIA, isometric stress and normalized WL power were reduced in the obese groups. Obesity caused a significant reduction in fatigue resistance in all cases. Our findings demonstrate a muscle-specific reduction in contractile performance and muscle quality that is likely related to in vivo mechanical role, fiber type, and metabolic profile, which may in part be related to changes in myosin heavy chain expression and AMP-activated protein kinase activity. These results infer that, beyond the additional requirement of moving a larger body mass, functional performance and quality of life may be further limited by poor muscle function in obese individuals. As such, a reduction in muscle performance may be a substantial contributor to the negative cycle of obesity.NEW & NOTEWORTHY 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.

This study examined the effect of short duration, moderate and high-intensity exercise on a Go/NoGo task. Fifteen, habitually active (9 females and 6 males aged 28 ± 5 years) agreed to participate in the study and cognitive performance was measured in three sessions lasting 10 min each, performed at three different exercise intensities: rest, moderate and high. Results indicated significant exercise intensity main effects for reaction time (RT) (p = 0.01), the omission error rate (p = 0.027) and the decision error rate (p = 0.011), with significantly longer RTs during high intensity exercise compared to moderate intensity exercise (p = 0.039) and rest (p = 0.023). Mean ± SE of RT (ms) was 395.8 ± 9.1, 396.3 ± 9.1 and 433.5 ± 16.1 for rest, moderate and high intensity exercise, respectively. This pattern was replicated for the error rate with a significantly higher omission error and decision error rate during high intensity exercise compared to moderate intensity exercise (p = 0.003) and rest (p = 0.001). Mean ± SE of omission errors (%) was 0.88 ± 0.23, 0.8 ± 0.23 and 1.8 ± 0.46% for rest, moderate and high intensity exercise, respectively. Likewise, mean ± SE of decision errors (%) was 0.73 ± 0.24, 0.73 ± 0.21 and 1.8 ± 0.31 for rest, moderate and high intensity exercise, respectively. The present study’s results suggest that 10 min workout at high intensity impairs RT performances in habitually active adults compared to rest or moderate intensity exercise.