The present study showed that chronic noni administration in rats induced an improved mechanical efficiency associated with higher exercise time until fatigue. In addition, noni supplementation produced an antihyperglycemic effect in diabetic rats.
Similarly, other studies have already demonstrated an ergogenic effect after noni administration (7, 19, 20). Shalan et al. (7) observed that four weeks of noni supplementation tripled the swimming effort in rats. This increase in exercise performance was attributed to the peripheral and also to central effects induced by noni.
Centrally, our results demonstrated a reduced relative effort perception in DMN compared to the DMP group (Fig. 3). This fact could be evidenced by similar oxygen consumption values between groups when analyzed at the same relative performance, which was expressed as a percentage of running time. It is worth mentioning that both the time of exercise and workload (Table 3) were higher in the DMN rats. These data suggesting a change in the central modulation that coordinates the motor drive and consequently induces delayed fatigue (21, 22).
Changes in the turnover of neuronal systems could play an important role in the peripheral adaptations associated with the development of fatigue. The Shalan et al. (7) study verified alterations to the central neurotransmitter systems, such as serotonin and dopamine receptors and transporters, associated with fatigue development in rats with noni supplementation. Furthermore, it has already been shown that peripheral signaling integrated in the central brain areas could modifies the effort perception and consequently delays the end of the running time (23). The neuronal 5-HT and DA system profile during exercise could change the running time until fatigue as a result of modifications to the lethargy, rating of perceived exertion and motivation, which interfered with central brain signaling to the active musculature (24, 25). It is important to point out that the experiment in this study was not designed to verify central fatigue. However, the observed peripheral effects could be attributed to both the drive from the central areas and feedback signaling changes.
Peripherally, the results of this study, such as increased energy efficiency in the DMN group (Fig. 4) could have been related to a direct action on central homeostasis neuromodulators, such as serotonin and dopamine, contributing to energetic control to exercise but also a feedback from different muscle and metabolic conditions after noni supplementation. In addition, the DMN group showed a reduced hyperglycemic effect compared to the DMP group (Fig. 5). This result had already been reported by Osman et al. (20) and Shalan et al. (7) during swim exercise protocols and was thought to be the cause of an observed ergogenic effect. It is interesting to note that this study is the first to relate the effects of noni supplementation in rats with diabetes during controlled-intensity exercise performed according to a running protocol until fatigue.
Wang et al. (5) reported improvements in carbohydrate and lipid metabolism via the AMPK pathway in rats supplemented with noni. With specific regard to glucose metabolism, it had already been demonstrated an improved insulin receptor sensitivity beyond an increase in glycogen stores. It has been suggested that noni improves glycogen stores either by increasing glycogen storage, delaying glycogen consumption during exercise or both (20). These data contribute to blood glucose disappear, probably through the improving the carbohydrate muscle and liver uptake.
In the present study, the improved glucose metabolism in DMN rats could have been supported by a reduction in triglyceride plasma concentrations, which could indicate higher lipid oxidation (Fig. 5). This possibility is suggested by the reduction in the relative effort perception in the DMN group associated with a change in substrate use (Fig. 4).
Some studies have associated the ergogenic and metabolic effects of noni administration to the influence antioxidant compounds such as phenols and flavonoids (e.g., epicatechin and catechin) (5, 26, 27). During exercise, there is an increase in the production of oxidative molecules, which may function as intracellular messengers in several physiological processes (28). On the other hand, evidence shows that highly oxidative molecule concentrations represent possible toxicity and damage to the cell that could interfere with the excitation–contraction muscle process and consequently performance (29, 30). The phenolic compounds and flavonoids presents in noni have antioxidant and anti-inflammatory characteristics that may contribute to reduce the oxidative status promoting the effects observed on glucose and triglycerides metabolism, beyond the performance in DM rats with noni supplementation.
Although noni supplementation has increased performance and energy efficiency beyond has lowered glycemia and triglyceridemia, it appears to have a potentially toxic effect on the kidneys as demonstrated by morphological analysis (Fig. 5). The increase in the Bowman’s space area in rats with noni supplementation (CN and DMN) suggested glomerular hyperfiltration. Our data also demonstrated an increase in Bowman’s space with the same magnitude of diabetic impair in control group that ingested noni.
Souza et al. (31) did not observe functional or histological disturbances on the kidneys or liver after nine days of noni juice consumption. Stands out that the juice dilution was lower compared to mentioned in our study (1:10 for the Sousa et al. vs. 2:1 present sudy). In addition, the period of noni juice consumption in our study was extended (60 days), which may have contributed to the effect on the kidneys.
Noni toxicity appears to be caused by its anti-inflammatory compounds. These impair the function of cycloxygenases and hydroelectrolytics, which then inhibits prostaglandin synthesis leading to chronic renal failure (32). In addition, the potassium content present in noni can negatively impact on kidney function in patients with renal failure (Mueller, 2000).