Effects of daytime ingestion of melatonin on heart rate response during prolonged exercise

The current study sought to investigate the effect of melatonin consumption on cardiovascular response during submaximal exercise in healthy men. For this purpose, eight students (age: 21.8 ± 0.9) were asked to run for 45 minutes at submaximal intensity after melatonin-(6 mg) or placebo-ingestion, in a randomized and counterbalanced order. Heart rate (HR) and rectal temperature (Tre) evolution during exercise were measured. Blood samples were drawn twice (before and immediately after exercise) for the determination of triglycerides, total cholesterol, high-density lipoprotein cholesterol (HDL-c), lactate, protein, and superoxide dismutase concentrations. The results showed that melatonin may disturb thermoregulatory control by exerting an effect on HR at 10 min of exercise, reducing HR by 6.6% (9 bpm; P < 0.001), and this effect decreased to 3.6% at the end of exercise (P < 0.01). Melatonin has no effect on triglycerides total cholesterol, HDL-c, lactate, and protein at rest and post-exercise. Although melatonin administration did not present a risk for cardiovascular function in healthy men, melatonin at high doses could decrease superoxide dismutase concentrations owing to the alteration of redox balance. These findings suggest that a high concentration of antioxidants does not enhance cardiovascular performance and may impair thermoregulatory control during prolonged exercise.

DECREMENTAL RESPONSE ON PROLONGED EXERCISE TEST IN A PATIENT WITH THYROTOXIC PERIODIC PARALYSIS

Paralysis of acute onset often presents a diagnostic challenge for the assessing physician because of a large number of differential diagnosis and overlap of clinical features among them. Thyrotoxic periodic paralysis is an uncommon cause of acute weakness. In addition to serological tests, electromyography findings during prolonged exercise test are very helpful in confirming the diagnosis. Only a few case reports of thyrotoxic periodic paralysis have been published from Middle East and none of them have described this specific electrophysiological data. A man in his 20s presented to us with acute onset weakness in both legs which was evaluated further and found to have hypokalemia. The work up for the etiology revealed thyrotoxic status and a final diagnosis of thyrotoxic periodic paralysis was established. The prolonged exercise test performed in this patient showed typical progressive decremental respsonse with nadir at 40 minutes after the exercise.

Meta-Analysis of Carbohydrate Solution Intake during Prolonged Exercise in Adults: From the Last 45+ Years’ Perspective

Carbohydrate (CHO) supplementation during prolonged exercise postpones fatigue. However, the optimum administration timing, dosage, type of CHO intake, and possible interaction of the ergogenic effect with athletes’ cardiorespiratory fitness (CRF) are not clear. Ninety-six studies (from relevant databases based on predefined eligibility criteria) were selected for meta-analysis to investigate the acute effect of ≤20% CHO solutions on prolonged exercise performance. The between-subject standardized mean difference [SMD = ([mean post-value treatment group–mean post-value control group]/pooled variance)] was assessed. Overall, SMD [95% CI] of 0.43 [0.35, 0.51] was significant (p < 0.001). Subgroup analysis showed that SMD was reduced as the subjects’ CRF level increased, with a 6–8% CHO solution composed of GL:FRU improving performance (exercise: 1–4 h); administration during the event led to a superior performance compared to administration before the exercise, with a 6–8% single-source CHO solution increasing performance in intermittent and ‘stop and start’ sports and an ~6% CHO solution appearing beneficial for 45–60 min exercises, but there were no significant differences between subjects’ gender and age groups, varied CHO concentrations, doses, or types in the effect measurement. The evidence found was sound enough to support the hypothesis that CHO solutions, when ingested during endurance exercise, have ergogenic action and a possible crossover interaction with the subject’s CRF.

Sport supplements and the athlete’s gut: a review.

Vigorous or prolonged exercise poses a challenge to gastrointestinal system functioning and is associated with digestive symptoms. This narrative review addresses 1) the potential of dietary supplements to enhance gut function and reduce exercise-associated gastrointestinal symptoms and 2) strategies for reducing gastrointestinal-related side effects resulting from popular sports supplements. Several supplements, including probiotics, glutamine, and bovine colostrum, have been shown to reduce markers of gastrointestinal damage and permeability with exercise. Yet, the clinical ramifications of these findings are uncertain, as improvements in symptoms have not been consistently observed. Among these supplements, probiotics modestly reduced exercise-associated gastrointestinal symptoms in a few studies, suggesting they are the most evidenced-based choice for athletes looking to manage such symptoms through supplementation. Carbohydrate, caffeine, and sodium bicarbonate are evidence-based supplements that can trigger gastrointestinal symptoms. Using glucose-fructose mixtures is beneficial when carbohydrate ingestion is high (>50 g/h) during exercise, and undertaking multiple gut training sessions prior to competition may also be helpful. Approaches for preventing caffeine-induced gastrointestinal disturbances include using low-to-moderate doses (<500 mg) and avoiding/minimizing exacerbating factors (stress, anxiety, other stimulants, fasting). Adverse gastrointestinal effects of sodium bicarbonate can be avoided by using enteric-coated formulations, low doses (0.2 g/kg), or multi-day loading protocols.

Local Vibration Reduces Muscle Damage after Prolonged Exercise in Men

Prolonged exercise can lead to muscle damage, with soreness, swelling, and ultimately reduced strength as a consequence. It has been shown that whole-body vibration (WBV) improves recovery by reducing the levels of stress hormones and the activities of creatine kinase (CK) and lactate dehydrogenase (LDH). The aim of the study was to demonstrate the effect of local vibration treatment applied after exercise on the level of selected markers of muscle fiber damage. The study involved 12 untrained men, aged 21.7 ± 1.05 years, with a VO2peak of 46.12 ± 3.67 mL·kg−1·min−1. A maximal intensity test to volitional exhaustion was performed to determine VO2peak and individual exercise loads for prolonged exercise. The subjects were to perform 180 min of physical effort with an intensity of 50 ± 2% VO2peak. After exercise, they underwent a 60 min vibration treatment or placebo therapy using a mattress. Blood samples were taken before, immediately after the recovery procedure, and 24 h after the end of the exercise test. Myoglobin (Mb) levels as well as the activities of CK and LDH were recorded. Immediately after the hour-long recovery procedure (vibration or placebo), the mean concentrations of the determined indices were significantly different from baseline values. In the vibration group, significantly lower values of Mb (p = 0.005), CK (p = 0.030), and LDH (p = 0.005) were seen. Differences were also present 24 h after the end of the exercise test. The results of the vibration group compared to the control group differed in respect to Mb (p = 0.002), CK (p = 0.029), and LDH (p = 0.014). After prolonged physical effort, topical vibration improved post-workout recovery manifested by lower CK and LDH activity and lower Mb concentration compared to a control group.

Exercise-activated Ca2+ entry and enhanced risk of heat stroke

Exertional/environmental heat strokes (EHSs) are hyperthermic crises triggered by strenuous physical exercise and/or exposure to environmental heat, and are caused by an altered intracellular Ca2+ homeostasis in muscle. We recently demonstrated that a single bout of exercise on treadmill leads to formation of calcium entry units (CEUs), intracellular junctions that promote interaction between STIM1 and Orai1, the two proteins that mediate store-operated Ca2+ entry (SOCE). SOCE is a mechanism that is activated during muscle fatigue and that allows for recovery of extracellular Ca2+ during prolonged activity. The hypothesis underlying this work is that assembly of CEUs during prolonged exercise may predispose to EHSs when exercise is performed in challenging environmental conditions. To test this hypothesis, 4-mo-old mice were (1) divided into three experimental groups: control, trained-1m (1 mo of voluntary running in wheel cages), and exercised-1h (1 h of incremental treadmill run); and (2) subjected to an exertional stress (ES) protocol consisting of an incremental 45-min treadmill run at 34°C and 40% humidity. We then (a) measured the internal temperature of mice, which was higher in the two pre-exercised groups (trained-1m: 38.9°C ± 0.33; exercised-1h: 38.7°C ± 0.40) compared with control animals (37.9°C ± 0.17); (b) applied an ex vivo ES protocol to isolated EDL muscles (tetanic stimulation performed at 30°C) and verified that samples from trained-1m and exercised-1h mice generated a tension significantly greater than control samples; and (c) analyzed CEUs by electron microscopy (EM) and verified that EDL muscles of trained-1m and exercised-1h mice contained a greater number of membranes elements forming CEUs. The data collected indicates that the presence of CEUs correlates with a greater increase in body temperature and could, in principle, predispose to EHS when exercise is performed in challenging environmental conditions.

Possible mechanisms underlying the dynamic assembly of calcium entry units: The role of temperature and pH

Skeletal muscle function is regulated by intracellular Ca2+ levels. Two main mechanisms control movements of Ca2+ ions from intracellular stores (i.e., the sarcoplasmic reticulum; SR) and from extracellular space: (1) excitation–contraction (EC) coupling and (2) store-operated Ca2+ entry (SOCE). SOCE allows recovery of extracellular Ca2+ during prolonged muscle activity, when the SR undergoes depletion. We recently discovered that prolonged exercise leads to formation of calcium entry units (CEUs), intracellular junctions located at the I band that are formed by two distinct elements: SR stacks and transverse tubules (TTs). Assembly of CEUs during exercise promotes the interaction between STIM1 and Orai1, the two main proteins that mediate SOCE, and increases muscle resistance to fatigue in the presence of extracellular Ca2+. The molecular mechanisms underlying the exercise-dependent remodeling of SR and TT leading to CEU assembly remain to be fully elucidated. Here, we first verified whether CEUs can assemble ex vivo (in the absence of blood supply and innervation), subjecting excised EDL muscles from mice to an ex vivo incremental fatigue protocol (80 Hz tetanus stimulation lasting 45 min): the data collected demonstrate that CEUs can assemble ex vivo in isolated EDL muscles. We then evaluated if intracellular parameters that are affected by exercise, such as temperature and pH, may influence the assembly of CEUs. We found that higher temperature (36°C versus 25°C) and lower pH (7.2 versus 7.4) promotes formation of CEUs increasing the percentage of fibers containing SR stacks, the number of SR stacks/area, and the elongation of TTs at the I band. Importantly, increased assembly of CEUs at higher temperature (36°C) or at lower pH (7.2) correlated with increased fatigue resistance of EDL muscles in the presence of extracellular Ca2+, suggesting that CEUs assembled ex vivo are functional.

Exogenous ketosis increases blood and muscle oxygenation but not performance during exercise in hypoxia

Available evidence indicates that elevated blood ketones are associated with improved hypoxic tolerance in rodents. From this perspective, we hypothesized that exogenous ketosis by oral intake of the ketone ester (R)-3-hydroxybutyl (R)-3-hydroxybutyrate (KE) may induce beneficial physiological effects during prolonged exercise in acute hypoxia. As we recently demonstrated KE to deplete blood bicarbonate, which per se may alter the physiological response to hypoxia, we evaluated the effect of KE both in the presence and absence of bicarbonate intake (BIC). Fourteen highly trained male cyclists performed a simulated cycling race (RACE) consisting of 3h intermittent cycling (IMT180') followed by a 15-min time-trial (TT15') and an all-out sprint at 175% of lactate threshold (SPRINT). During RACE, fraction of inspired oxygen (FiO2) was gradually decreased from 18.6 to 14.5%. Before and during RACE, participants received either i) 75g ketone ester (KE), ii) 300 mg/kg body mass bicarbonate (BIC), iii) KE+BIC or iv) a control drink in addition to 60g carbohydrates per h in a randomized, crossover design. KE counteracted the hypoxia-induced drop in blood (SpO2) and muscle oxygenation by ~3%. In contrast, BIC decreased SpO2 by ~2% without impacting muscle oxygenation. Performance during TT15' and SPRINT were similar between all conditions. In conclusion, KE slightly elevated the degree of blood and muscle oxygenation during prolonged exercise in moderate hypoxia without impacting exercise performance. Our data warrant to further investigate the potential of exogenous ketosis to improve muscular and cerebral oxygenation status, and exercise tolerance in extreme hypoxia.

Sodium bicarbonate ingestion mitigates the heat-induced hyperventilation and reduction in cerebral blood velocity during exercise in the heat

Hyperthermia during exercise in the heat causes minute ventilation (VE) to increase, which leads to reductions in arterial CO2 partial pressure (PaCO2) and cerebral blood flow. On the other hand, sodium bicarbonate ingestion reportedly results in metabolic alkalosis, leading to decreased and increased PaCO2 during prolonged exercise in a thermoneutral environment. Here, we investigated whether sodium bicarbonate ingestion suppresses heat-induced hyperventilation and the resultant hypocapnia and cerebral hypoperfusion during prolonged exercise in the heat. Eleven healthy men ingested a solution of sodium bicarbonate (0.3 g/kg body weight) (NaHCO3 trial) or sodium chloride (0.208 g/kg) (NaCl trial). Ninety minutes after the ingestion, the subjects performed a cycle exercise for 60 min at 50% of peak oxygen uptake in the heat (35°C and 40% relative humidity). Esophageal temperature did not differ between the trials throughout (P = 0.56, main effect of trial). VE gradually increased with exercise duration in the NaCl trial, but the increases in VE were attenuated in the NaHCO3 trial (P = 0.01, main effect of trial). Correspondingly, estimated PaCO2 and middle cerebral artery blood velocity (an index of anterior cerebral blood flow) were higher in the NaHCO3 than the NaCl trial (P = 0.002 and 0.04, main effects of trial). Ratings of perceived exertion were lower in the NaHCO3 than the NaCl trial (P = 0.02, main effect of trial). These results indicate that sodium bicarbonate ingestion mitigates heat-induced hyperventilation and reductions in PaCO2 and cerebral blood velocity during prolonged exercise in the heat.