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Hyperbaric oxygen therapy (HBOT) is a therapeutical approach based on exposure to pure oxygen in an augmented atmospheric pressure. Although it has been used for years, the exact kinetics of the reactive oxygen species (ROS) between different pressures of hyperbaric oxygen exposure are still not clearly evidenced. In this study, the metabolic responses of hyperbaric hyperoxia exposures for 1 h at 1.4 and 2.5 ATA were investigated. Fourteen healthy non-smoking subjects (2 females and 12 males, age: 37.3 ± 12.7 years old (mean ± SD), height: 176.3 ± 9.9 cm, and weight: 75.8 ± 17.7 kg) volunteered for this study. Blood samples were taken before and at 30 min, 2 h, 24 h, and 48 h after a 1 h hyperbaric hyperoxic exposure. The level of oxidation was evaluated by the rate of ROS production, nitric oxide metabolites (NOx), and the levels of isoprostane. Antioxidant reactions were assessed through measuring superoxide dismutase (SOD), catalase (CAT), cysteinylglycine, and glutathione (GSH). The inflammatory response was measured using interleukine-6, neopterin, and creatinine. A short (60 min) period of mild (1.4 ATA) and high (2.5 ATA) hyperbaric hyperoxia leads to a similar significant increase in the production of ROS and antioxidant reactions. Immunomodulation and inflammatory responses, on the contrary, respond proportionally to the hyperbaric oxygen dose. Further research is warranted on the dose and the inter-dose recovery time to optimize the potential therapeutic benefits of this promising intervention.

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In this study, the metabolic responses of hypoxic breathing for 1 h to inspired fractions of 10% and 15% oxygen were investigated. To this end, 14 healthy nonsmoking subjects (6 females and 8 males, age: 32.2 ± 13.3 years old (mean ± SD), height: 169.1 ± 9.9 cm, and weight: 61.6 ± 16.2 kg) volunteered for the study. Blood samples were taken before, and at 30 min, 2 h, 8 h, 24 h, and 48 h after a 1 h hypoxic exposure. The level of oxidative stress was evaluated by considering reactive oxygen species (ROS), nitric oxide metabolites (NOx), lipid peroxidation, and immune-inflammation by interleukin-6 (IL-6) and neopterin, while antioxidant systems were observed in terms of the total antioxidant capacity (TAC) and urates. Hypoxia abruptly and rapidly increased ROS, while TAC showed a U-shape pattern, with a nadir between 30 min and 2 h. The regulation of ROS and NOx could be explained by the antioxidant action of uric acid and creatinine. The kinetics of ROS allowed for the stimulation of the immune system translated by an increase in neopterin, IL-6, and NOx. This study provides insights into the mechanisms through which acute hypoxia affects various bodily functions and how the body sets up the protective mechanisms to maintain redox homeostasis in response to oxidative stress.

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We investigated the effects of intermittent long-term stretch training (5 weeks) on the architectural and mechanical properties of the muscle-tendon unit (MTU) in healthy humans. MTU's viscoelastic and architectural properties in the human medial gastrocnemius (MG) muscle and the contribution of muscle and tendon structures to the MTU lengthening were analyzed. Ten healthy volunteers participated in the study (four females and six males). The passive stretch of the plantar flexor muscles was achieved from 0° (neutral ankle position) to 25° of dorsiflexion. Measurements were obtained during a single passive stretch before and after the completion of the stretching protocol. During the stretch, the architectural parameters of the MG muscle were measured via ultrasonography, and the passive torque was recorded by means of a strain-gauge transducer. Repeated-measure ANOVA was applied for all parameters. When expressed as a percentage for all dorsiflexion angles, the relative torque values decreased (p < 0.001). In the same way, architectural parameters (pennation angle and fascicle length) were compared for covariance and showed a significant difference between the slopes (ANCOVA p < 0.0001 and p < 0.001, respectively) suggesting a modification in the mechanical behavior after stretch training. Furthermore, the values for passive stiffness decreased (p < 0.05). The maximum ankle range of motion (ROM) (p < 0.01) and the maximum passive torque (p < 0.05) increased. Lastly, the contribution of the free tendon increased more than fascicle elongation to the total lengthening of the MTU (ANCOVA p < 0.001). Our results suggest that five weeks of intermittent static stretch training significantly change the behavior of the MTU. Specifically, it can increase flexibility and increase tendon contribution during MTU lengthening.

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Impaired flow mediated dilation (FMD), an index of vascular stress, is known after SCUBA diving. This is related to a dysfunction of nitric oxide (NO) availability and a disturbance of the redox status, possibly induced by hyperoxic/hyperbaric gas breathing. SCUBA diving is usually performed with a mask only covering "half face" (HF) and therefore forcing oral breathing. Nasal NO production is involved in vascular homeostasis and, as consequence, can significantly reduce NO possibly promoting vascular dysfunction. More recently, the utilization of "full-face" (FF) mask, allowing nasal breathing, became more frequent, but no reports are available describing their effects on vascular functions in comparison with HF masks. In this study we assessed and compared the effects of a standard shallow dive (20 min at 10 m) wearing either FF or a HF mask on different markers of vascular function (FMD), oxidative stress (ROS, 8-iso-PGF2α) and NO availability and metabolism (NO2, NOx and 3-NT and iNOS expression). Data from a dive breathing a hypoxic (16% O2 at depth) gas mixture with HF mask are shown allowing hyperoxic/hypoxic exposure. Our data suggest that nasal breathing might significantly reduce the occurrence of vascular dysfunction possibly due to better maintenance of NO production and bioavailability, resulting in a better ability to counter reactive oxygen and nitrogen species. Besides the obvious outcomes in terms of SCUBA diving safety, our data permit a better understanding of the effects of oxygen concentrations, either in normal conditions or as a strategy to induce selected responses in health and disease.

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Inflammation is an adaptive response to both external and internal stimuli including infection, trauma, surgery, ischemia-reperfusion, or malignancy. A number of studies indicate that physical activity is an effective means of reducing acute systemic and low-level inflammation occurring in different pathological conditions and in the recovery phase after disease. As a proof-of-principle, we hypothesized that low-intensity workout performed under modified oxygen supply would elicit a "metabolic exercise" inducing a hormetic response, increasing the metabolic load and oxidative stress with the same overall effect expected after a higher intensity or charge exercise. Herein, we report the effect of a 5-week low-intensity, non-training, exercise program in a group of young healthy subjects in combination with the exposure to hyperoxia (30% and 100% pO2, respectively) or light hypoxia (15% pO2) during workout sessions on several inflammation and oxidative stress parameters, namely hemoglobin (Hb), redox state, nitric oxide metabolite (NOx), inducible nitric oxide synthase (iNOS), inflammatory cytokine expression (TNF-α, interleukin (IL)-6, IL-10), and renal functional biomarkers (creatinine, neopterin, and urates). We confirmed our previous reports demonstrating that intermittent hyperoxia induces the normobaric oxygen paradox (NOP), a response overlapping the exposure to hypoxia. Our data also suggest that the administration of modified air composition is an expedient complement to a light physical exercise program to achieve a significant modulation of inflammatory and immune parameters, including cytokines expression, iNOS activity, and oxidative stress parameters. This strategy can be of pivotal interest in all those conditions characterized by the inability to achieve a sufficient workload intensity, such as severe cardiovascular alterations and articular injuries failing to effectively gain a significant improvement of physical capacity.

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PURPOSE: Prolonged exhaustive exercise induces a failure of the nervous system to activate the involved muscles maximally (i.e., central fatigue). Part of central fatigue may reflect insufficient output from the motor cortex (i.e., supraspinal fatigue), but the cause is unresolved. To investigate the potential link between supraspinal fatigue and changes in brain concentration of dopamine and noradrenaline in temperate environment, we combined neurophysiological methods and pharmacological manipulation of these two neurotransmitters. METHODS: Changes in performance of a cycling exercise (time trial [TT]) were tested after oral administration of placebo (Pla), dopamine, or noradrenaline reuptake inhibitors (methylphenidate and reboxetine [Rebox], respectively) in well-trained male subjects. Changes in voluntary activation, corticospinal excitability, and muscle contractile properties were tested in the knee extensors using transcranial magnetic stimulation and motor nerve electrical stimulation before and after exercise. A psychomotor vigilance task (PVT) was also performed. RESULTS: Compared with Pla, methylphenidate did not affect exercise performance (P = 0.19), but more time was needed to complete the TT after administration of Rebox (approximately 9%, P < 0.05). For the latter condition, the reduced performance was accompanied by a central/supraspinal fatigue (5%-6%, P < 0.05) and worsened PVT performance (7%, P < 0.05). For the three conditions, corticospinal excitability was unchanged, and peripheral fatigue was similar. Because the ingestion of Rebox induced a greater decrease in voluntary activation and PVT performance after the TT than Pla, with no modification in corticospinal excitability, the noradrenaline reuptake inhibitor likely affected supraspinal circuits located before the motor cortex. CONCLUSION: These results suggest that noradrenaline, but not dopamine reuptake inhibition, contributes to the development of central/supraspinal fatigue after a prolonged cycling exercise performed in temperate conditions.

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INTRODUCTION: The main limiting factors determining apnea time are generally considered to be related to blood and cerebrospinal fluid chemistry. Several physiological (adaptive) mechanisms and some psychologic parameters, such as motivation, are also known to increase apnea time. AIM: We wished to study the link between peripheral muscle fatigue, the concomitant alteration of long latency (transcortical) reflexes and respiratory control. METHODS: Fatigue was induced in a small hand muscle (abductor pollicis brevis) (n = 11). This muscle is sufficiently small that its fatigue and the resulting production of metabolites are unlikely to alter whole-blood biochemistry. The Hoffmann reflex, an involuntary reaction to electrical stimulation of muscle afferent sensory fibreswas studied, as was the long latency reflex (LLR) using the Dueschl method in which electrical stimulation is superimposed on a slight voluntary contraction, Different fatiguing protocols were performed, and respiratory rate continuously recorded. RESULTS: The 'muscular metabolites increasing protocol' (at 50% maximum voluntary contraction, MVC) showed a significant dissociation between the decreases in the H-reflex and the LLR, compared to contraction at 25% MVC. This was associated with an increase in the respiratory rate to 148.25 (SD 11.37)% of control at 3 min (the maximum time the contraction could be sustained), whereas at 25% MVC, respiratory rate did not change during the contraction. CONCLUSIONS: This suggests a peripherally mediated, central input to the respiratory centres, triggering a powerful stimulus when metabolites accumulate in muscles. We believe this to be a possible mechanism terminating extreme breath holds.

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This study investigated the influence of different initial conditions on a subsequent fast (ballistic) isometric contraction of the ankle dorsiflexor muscles. Surface electromyograms (EMGs) of dorsiflexor and plantarflexor muscles were recorded during ballistic contractions performed without any pre-activation (BAL) and in ballistic contractions preceded by a sustained submaximal contraction (20% MVC) that was followed either by a rapid voluntary relaxation of the agonist muscle (VRBAL) or by a rapid antagonist (reversal) contraction (ARBAL). In the latter condition, three different antagonist torque levels were compared (25, 50 and 75% MVC). The results showed that the mean average rate of torque development was significantly (P < 0.001) greater for the ARBAL condition (968.5 ± 183.9% MVC/s) compared with the VRBAL (509.3 ± 78.7% MVC/s) and BAL (461.8 ± 79.9% MVC/s) conditions. Furthermore, the mean value recorded for VRBAL was significantly (P < 0.05) greater than for BAL condition. The faster increases in torque during the VRBAL and ARBAL conditions were associated with a greater agonist EMG activity. Compared with VRBAL, performance during the ARBAL condition was improved by a greater level of antagonist coactivation and, in some trials, by the presence of a silent EMG period between the end of the antagonist activation and the onset of the agonist ballistic contraction. Together, these results indicate that the initial conditions can have a substantial influence on the rate of torque development during ballistic contractions performed in isometric conditions.

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This study compared the mechanisms that limit the time to failure of a sustained submaximal contraction at 20% of maximum when the elbow flexors either supported an inertial load (position task) or exerted an equivalent constant torque against a rigid restraint (force task). The surface electromyogram (EMG), the motor-evoked potential (MEP) in response to transcranial magnetic stimulation (TMS) of the motor cortex, and the Hoffmann reflex (H-reflex) and maximal M-wave (Mmax) elicited by electrical stimulation of the brachial plexus were recorded in biceps brachii during the two tasks. Although the time to failure for the position task was only 44% of that for the force task, the rate of increase of the average EMG (aEMG; % initial MVC) and MEP area (% Mmax) did not differ significantly during the two tasks. At task failure, however, the increases in normalized aEMG and MEP area were significantly (P < 0.05) greater for the force task (36.4 and 219.9%) than for the position task (22.4 and 141.7%). Furthermore, the superimposed mechanical twitch (% initial MVC), evoked by TMS during a brief MVC of the elbow flexors immediately after task failure, was increased similarly in both tasks. Although the normalized H-reflex area (% Mmax) decreased during the two fatiguing contractions, the reduction was more rapid and greater during the position task (59.8%) compared with the force task (34.7%). Taken together, the results suggest that spinal mechanisms were a major determinant of the briefer time to failure for the position task.

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This study investigates the control mechanisms at the cortical and spinal levels of antagonist coactivation during a submaximal fatiguing contraction of the elbow flexors at 50% of maximal voluntary contraction (MVC). We recorded motor-evoked potentials in the biceps brachii and triceps brachii muscles in response to magnetic stimulation of the motor cortex (MEP) and corticospinal tract (cervicomedullary motor-evoked potentials--CMEPs), as well as the Hoffmann reflex (H-reflex) and maximal M-wave (Mmax) elicited by electrical stimulation of the brachial plexus, before, during, and after the fatigue task. The results showed that although the coactivation ratio did not change at task failure, the MVC torque produced by the elbow flexors declined by 48% (P < 0.01) with no change in MVC torque for the elbow extensors. While the MEP and CMEP areas (normalized to Mmax) of the biceps brachii increased ( approximately 50%) over the first 40% of the time to task failure and then plateaued, both responses in the triceps brachii increased ( approximately 150-180%) gradually throughout the fatigue task. In contrast to the monotonic increase in the MEP and CMEP of the antagonist muscles, the H-reflex of the triceps brachii exhibited a biphasic modulation, increasing during the first part of the contraction before declining subsequently to 65% of its initial value. Collectively, these results suggest that the level of coactivation during a fatiguing contraction is mediated by supraspinal rather than spinal mechanisms and involves differential control of agonist and antagonist muscles.

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This study examined the involvement of spinal mechanisms in the control of coactivation during a sustained contraction of the ankle dorsiflexors at 50% of maximal voluntary contraction. Changes in the surface electromyogram (EMG) of the tibialis anterior and of two antagonist muscles, the soleus and lateral gastrocnemius, were investigated during and after the fatigue task. Concurrently, the compound action potential (M-wave) and the Hoffmann reflex of the soleus and lateral gastrocnemius were recorded. The results showed that the torque of the ankle dorsiflexors and the average EMG of the tibialis anterior during maximal voluntary contraction declined by 40.9 +/- 17.7% (mean +/- SD; P < 0.01) and 37.0 +/- 19.9% (P < 0.01), respectively, at task failure. During the submaximal fatiguing contraction, the average EMG of both the agonist and antagonist muscles increased, leading to a nearly constant ratio at the end of the contraction when normalized to postfatigue values. In contrast to the monotonic increase in average EMG of the antagonist muscles, the excitability of their spinal reflex pathways exhibited a biphasic modulation. The amplitude of the Hoffman reflexes in the soleus and lateral gastrocnemius increased to 147.5 +/- 52.9% (P < 0.05) and 166.7 +/- 74.9% (P < 0.01), respectively, during the first 20% of the contraction and then subsequently declined to 66.3 +/- 44.8 and 74.4 +/- 44.2% of their initial values. In conclusion, the results show that antagonist coactivation did not contribute to task failure. The different changes in voluntary EMG activity and spinal reflex excitability in the antagonist muscles during the fatiguing contraction support the concept that the level of coactivation is controlled by supraspinal rather than spinal mechanisms. The findings indicate, however, that antagonist coactivation cannot simply be mediated by a central descending "common drive" to the motor neuron pools of the agonist-antagonist muscle pairs. Rather, they suggest a more subtle regulation of the drive, possibly through presynaptic mechanisms, to the motoneurons that innervate the antagonist muscles.

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