Aim: The purpose of this study was to evaluate hydration status, fluid intake, sweat rate, and sweat sodium concentration in recreational tropical native runners. Methods: A total of 102 males and 64 females participated in this study. Participants ran at their self-selected pace for 30–100 min. Age, environmental conditions, running profiles, sweat rates, and sweat sodium data were recorded. Differences in age, running duration, distance and pace, and physiological changes between sexes were analysed. A p-value cut-off of 0.05 depicted statistical significance. Results: Males had lower relative fluid intake (6 ± 6 vs. 8 ± 7 mL·kg⁻¹·h⁻¹, p < 0.05) and greater relative fluid balance deficit (−13 ± 8 mL·kg⁻¹·h⁻¹ vs. −8 ± 7 mL·kg⁻¹·h⁻¹, p < 0.05) than females. Males had higher whole-body sweat rates (1.3 ± 0.5 L·h⁻¹ vs. 0.9 ± 0.3 L·h⁻¹, p < 0.05) than females. Mean rates of sweat sodium loss (54 ± 27 vs. 39 ± 22 mmol·h⁻¹) were higher in males than females (p < 0.05). Conclusions: The sweat profile and composition in tropical native runners are similar to reported values in the literature. The current fluid replacement guidelines pertaining to volume and electrolyte replacement are applicable to tropical native runners.

Rosmarinic acid (RA) is a natural pure compound from herbs belonging to the Lamiaceae family, such as rosemary, sage, basil, and mint. The antioxidant, angiotensin-converting enzyme inhibitory, and vasodilatory effects of RA have been revealed. Angiotensin II (ANG II) is a potent agent that generates hypertension and oxidative stress. Hypertension and skeletal muscle insulin resistance are strongly related. The aim of this study was to evaluate the effects of acute and chronic RA treatment on blood pressure and skeletal muscle glucose transport in ANG II-induced hypertensive rats. Eight-week-old male Sprague Dawley rats were separated into SHAM and ANG II-infused (250 ng/kg/min) groups. ANG II rats were treated with or without acute or chronic RA at 10, 20, or 40 mg/kg. At the end of the experiment, body weight, liver and heart weights, oral glucose tolerance, skeletal muscle glucose transport activity, and signaling proteins were evaluated. Both acute and chronic RA treatment decreased systolic, diastolic, and mean arterial blood pressure. Only acute RA at 40 mg/kg resulted in a reduction of fasting plasma glucose levels and an induction of skeletal muscle glucose transport activity. These effects might involve increased ERK activity in skeletal muscle. Meanwhile, chronic RA treatment with 10, 20, and 40 mg/kg prevented ANG II-induced hyperglycemia. Both acute and chronic RA treatment attenuated ANG II-induced cardiometabolic abnormalities in rats. Therefore, RA would be an alternative strategy for improving skeletal muscle glucose transport and protecting against ANG II-induced hypertension and hyperglycemia.