A botanical extract blend of Mangifera indica and Sphaeranthus indicus combined with resistance exercise training improves muscle strength and endurance over exercise alone in young men: a randomized, blinded, placebo-controlled trial.

Resistance exercise training (RET) is used to improve muscular strength and function. This study tested the hypothesis that RET alongside daily supplementation of a Sphaeranthus indicus and Mangifera indica extract blend (SMI) would augment bench press (BP) and leg extension (LE) strength and repetitions to failure (RTF) compared to RET alone. Ninety-nine men (age 22 ± 3) completed the trial after randomization into one of four groups: (A1) 425 mg SMI plus one RET set; (A2) 850 mg SMI plus one RET set; (P1) placebo plus one RET set; and (P2) placebo plus two RET sets. RET sets were 6-8 BP and LE repetitions at 80% of a progressive one repetition maximum (1-RM), performed 3x/week for 8 weeks. Strength and RTF were evaluated at baseline and days 14, 28, and 56 while serum values of total testosterone (TT), free testosterone (FT), and cortisol (C) values were evaluated at baseline and day 56. RET significantly (p < 0.05) increased 1-RM, RTF, and T measures above baselines regardless of group assignment, but the increases were greater in the supplemented groups. At week 8, A1 bench pressed more than P1 (71.5.5 ± 17.5 kg vs. 62.0 ± 15.3 kg, p = 0.003), while A2 pressed 13.8 ± 3.0 kg more (95% CI 5.7-21.8, p < 0.001) than P1 and 9.9 ± 13.0 kg more (95% CI 1.7-18.2, p = 0.01) than P2. Also at week 8, the mean LE 1-RM of A1 (159.4 ± 22.6 kg) and A2 (162.2 ± 22.9 kg) was greater (p < 0.05) than that of P1 (142.2 ± 25.6 kg) and P2 (146.5 ± 19.7 kg). Supplementation improved RTF, TT, and FT values over those measured in exercise alone (p < 0.05), while C levels in A2 (9.3 ± 3.8 µg/dL) were lower than P2 (11.7 ± 3.8 µg/dL, p < 0.05). Daily supplementation with SMI was well tolerated and may help optimize muscle adaptive responses to RET in men.

Neural network interactions and ingestive behavior control during anorexia.

Many models have been proposed over the years to explain how motivated feeding behavior is controlled. One of the most compelling is based on the original concepts of Eliot Stellar whereby sets of interosensory and exterosensory inputs converge on a hypothalamic control network that can either stimulate or inhibit feeding. These inputs arise from information originating in the blood, the viscera, and the telencephalon. In this manner the relative strengths of the hypothalamic stimulatory and inhibitory networks at a particular time dictates how an animal feeds. Anorexia occurs when the balance within the networks consistently favors the restraint of feeding. This article discusses experimental evidence supporting a model whereby the increases in plasma osmolality that result from drinking hypertonic saline activate pathways projecting to neurons in the paraventricular nucleus of the hypothalamus (PVH) and lateral hypothalamic area (LHA). These neurons constitute the hypothalamic controller for ingestive behavior, and receive a set of afferent inputs from regions of the brain that process sensory information that is critical for different aspects of feeding. Important sets of inputs arise in the arcuate nucleus, the hindbrain, and in the telencephalon. Anorexia is generated in dehydrated animals by way of osmosensitive projections to the behavior control neurons in the PVH and LHA, rather than by actions on their afferent inputs.

Activation in neural networks controlling ingestive behaviors: what does it mean, and how do we map and measure it?

Over the past thirty years many of different methods have been developed that use markers to track or image the activity of the neurons within the central networks that control ingestive behaviors. The ultimate goal of these experiments is to identify the location of neurons that participate in the response to an identified stimulus, and more widely to define the structure and function of the networks that control specific aspects of ingestive behavior. Some of these markers depend upon the rapid accumulation of proteins, while others reflect altered energy metabolism as neurons change their firing rates. These methods are widely used in behavioral neuroscience, but the way results are interpreted within the context of defining neural networks is constrained by how we answer the following questions. How well can the structure of the behavior be documented? What do we know about the processes that lead to the accumulation of the marker? What is the function of the marker within the neuron? How closely in time does the marker accumulation track the stimulus? How long does the marker persist after the stimulus is removed? We will review how these questions can be addressed with regard to ingestive and related behaviors. We will also discuss the importance of plotting the location of labeled cells using standardized atlases to facilitate the presentation and comparison of data between experiments and laboratories. Finally, we emphasize the importance of comprehensive and accurate mapping for using newly emerging technologies in neuroinfomatics.

Differential suppression of hyperglycemic, feeding, and neuroendocrine responses in anorexia.

We have used the anorexia shown by rats given hypertonic saline to drink to investigate central mechanisms that can inhibit feeding. Rats dehydrated in this manner for 3 or 5 days showed a severe attenuation of the compensatory feeding observed after an overnight fast compared with control euhydrated rats or rats whose food was restricted to match the intake of anorexic rats. Food intake after injections of 2-deoxy-d-glucose (2-DG) was also significantly decreased in dehydrated animals compared with that after a 2-DG injection given before dehydration. However, all the dehydrated animals demonstrated a robust eating response after water was returned whether they had received injection of 2-DG or vehicle. Despite a profound reduction in 2-DG-induced feeding, other glucoregulatory responses to 2-DG remained intact in dehydrated animals. After 2-DG injection, corticosterone secretion and blood glucose were significantly elevated from preinjection values whether or not animals were dehydrated. Thus the mechanisms responsible for anorexia in dehydrated animals specifically target stimulatory feeding pathways but leave intact other counterregulatory glucometabolic motor events.