Purpose: This study aimed to determine whether a series of repeated maximal voluntary apnoeas is effective in improving subsequent time trial performance in competitive level track and field athletes.

Methods: Seventeen competitive runners volunteered for this study and based on their preferred competitive distance they were placed either in the 200 m (5 male, 4 female) or 1000 m group (3 male, 5 female). On two separate occasions (≤ 7 days apart), the participants performed a running time-trial that was preceded either by: (i) a standardised warm up (WO) or (ii) a standardised warm up succeeded by five repeated maximal dry static apnoeas (WA). Splenic volume, haematology and cardiovascular parameters were monitor at rest, before and after each time-trial.

Results: WA resulted in a significantly faster performance (27.51 ± 3.49 s; P = 0.009) compared with WO (27.96 ± 3.34 s) in the 200 m group, whereas no differences were observed in the 1000 m group (WA, 211.10 ± 26.18 s; WO, 215.82 ± 25.13 s, P = 0.120). No differences were noted in splenic volume between WO and WA in either group (P ≥ 0.081). Haemoglobin was significantly elevated after breath-holding in the 200 m (+ 7 g/dL, P = 0.041) but not 1000 m group.

Conclusion: This study demonstrates that five repeated maximal apnoeas are capable of significantly improving a 200 m but not a 1000 m time-trial performance in competitive track and field athletes.

Previous studies have suggested that, during prolonged cold exposure, shivering thermogenesis may gradually be attenuated, supposedly reflecting a state of central fatigue (aka ‘thermoregulatory fatigue’) provoked by extended shivering activity, that precipitates hypothermia. The purpose of this study was to revisit the validity of this notion. Twelve noncold-acclimatized men participated in three ∼10-h sessions, during which they performed repeatedly three 120-min cold-water immersions. To induce discrete amounts of heat-producing thermoeffector output, presumptively leading to distinct levels of fatigue during each session, subjects were submersed, within each session, in either severely (15°C), moderately (20°C), or slightly (28°C) cold water. The cold-induced elevation in thermogenic rate was similar across the three repeated immersions performed within the 15°C (∼130 W·m2) and 20°C (∼100 W·m2) sessions (P ≥ 0.43). In the 28°C-session, the metabolic heat production was augmented by ∼7% in the second and third immersions compared with the first immersion (P = 0.01). No intrasession differences were noted with regards to the body-core cooling rate, the cold-induced drop in skin temperature and forearm cutaneous vascular conductance, or the stress-hormone (salivary α-amylase and cortisol concentrations) and thermoperceptual responses (P > 0.05). The present findings, therefore, demonstrate that the ability to generate heat remains intact during prolonged iterative exposure to a high-heat loss environment in a single day, regardless of the severity of cold stressor. The intermittent application of slight cold stress (i.e., 28°C water) appears to mediate metabolic sensitization, reflecting either the circadian rhythmicity of heat-producing thermoeffector activity, or perhaps the rapid induction of metabolic adaptation.

We examined whether finger vasomotor and thermoperceptual responses to local cooling would be modulated by sustained cognitive loading. Finger temperature, circulatory [i.e., cutaneous vascular conductance (CVC)] and perceptual responses were monitored, in 12 healthy men, during and after a 30-min hand-immersion in 8°C-water, performed either immediately after a 60-min continual execution of a cognitive task (cognitive→cold trial), or during the simultaneous performance of the cognitive task (cognitive + cold trial). Subjects’ responses were compared with those obtained in a control cold-provocation trial, wherein they watched an emotionally neutral documentary. The cognitive task temporarily enhanced the perceived levels of mental effort and fatigue in both intervention trials. During cooling in the cognitive→cold trial, the area under the curve (AUC) for finger CVC was enhanced [49 (23) PU·mmHg −1 ·min vs. control: 36 (22) PU·mmHg −1 ·min], the cold-induced increase in mean arterial pressure was blunted [2 (4) mmHg vs. control: 8 (4) mmHg] ( P < 0.01), and the thermal discomfort was alleviated [2.2 (0.5) vs. control: 2.5 (0.7); P = 0.05]. In the cognitive + cold trial, no intertrial differences were noted during the cold-water immersion ( P ≥ 0.28), but AUC for finger CVC was augmented during the last part of the rewarming [29 (12) PU·mmHg −1 ·min vs. control: 24 (11) PU·mmHg −1 ·min; P = 0.05]. Present findings demonstrate that 1) in moderately mentally fatigued individuals, finger cold-induced vasoconstriction is transiently attenuated, and thermal discomfort is mitigated, and 2) superimposition of cognitive loading on cold stress does not alter finger vasoreactivity or thermosensitivity during cooling, but facilitates reperfusion following cooling.

NEW & NOTEWORTHY The study examined whether finger vasoreactivity and thermosensitivity to local cooling would be modulated by two different paradigms of enhanced cognitive strain evoked by the prolonged execution of a mentally demanding task. When localized cold stress was applied in moderately mentally fatigued individuals, finger cold-induced vasoconstriction was temporarily attenuated, and thermal discomfort was mitigated. The simultaneous application of cognitive loading and local cooling did not potentiate finger vasoconstriction during cooling but facilitated digit reperfusion following cooling.

Purpose: There is a scarcity of information regarding the effect of upper-body eccentric exercise on biomarkers of muscle damage. This study sought to investigate the effect of eccentric arm cycling on muscle damage [exercise-induced muscle damage (EIMD)].

Method: Ten subjects performed a 15 min eccentric arm cycling protocol (cadence 49 ± 7 rpm, power absorbed 248 ± 34 W). Maximal voluntary contraction (MVC) of the elbow flexors was evaluated at rest and at 5 min, 24 h, and 48 h post-exercise. In addition, blood samples were drawn at rest and thereafter at 30 min, 24 h, and 48 h intervals after exercise for quantification of creatine kinase (CK), myoglobin, lactate dehydrogenase (LDH) and endothelin (ET-1) concentrations. Delayed onset muscle soreness (DOMS) was assessed using a category ratio scale (0-10).

Results: Myoglobin was increased from baseline at 30 min post-exercise (+114%, 46.08 ± 22.17 µg/L, p = 0.018). Individual peak values were higher than baseline values for CK (+72.8%, 204 ± 138 U/L, p = 0.046) and LDH (+17%, 3.3 ± 0.88 nmole/min/mL, p = 0.017), but not for ET-1 (+9%, 1.4 ± 0.48 pg/mL, p = 0.45). DOMS was reported at 24 h (median 4) and 48 h (median 4) post-exercise and MVC of the elbow flexors were reduced from baseline (216 ± 44 N) at 5 min (-34%, 147 ± 61 N, p < 0.001), 24 h (-17%, 181 ± 56 N, p = 0.005) and 48 h (-9%, 191 ± 54 N, p = 0.003).

Conclusion: Eccentric arm cycling incites EIMD with reduced MVC and elevation of myoglobin, CK and LDH.

Divers are at enhanced risk of suffering from acute cognitive deteriorations, due to the low ambient temperatures, and the narcotic action of inert gases inspired at high pressures. Yet, the behavioral effects of cold and inert-gas narcosis have commonly been assessed in isolation, and during short-term provocations. We, therefore, evaluated the interactive influence of mild hypothermia and narcosis engendered by a subanaesthetic dose of nitrous oxide (N2O; a normobaric intervention analogue of hyperbaric nitrogen) on cognitive function during prolonged iterative exposure. Fourteen men partook in two ~12-h sessions (separated by ≥4 days), wherein they performed sequentially three 120-min cold (20°C) water immersions (CWIs), while inhaling, in a single-blinded manner, either normal air, or a normoxic gas mixture containing 30% N2O. CWIs were separated by 120-min rewarming in room-air breathing conditions. Prior to the first CWI and during each CWI, subjects performed a finger dexterity test, and the Spaceflight Cognitive Assessment Tool for Windows (WinSCAT) test assessing aspects of attention, memory, learning and visuo-spatial ability. Rectal and skin temperatures were, on average, reduced by ~1.2°C and ~8°C, respectively (P<0.001). Cooling per se impaired (P≤0.01) only short-term memory (~37%) and learning (~18%); the impairments were limited to the first CWI. N2O also attenuated (P≤0.02) short-term memory (~37%) and learning (~35%), but the reductions occurred in all CWIs. Further, N2O invariably compromised finger dexterity, attention, concentration, working memory and spatial processing (P<0.05). Present results demonstrate that inert-gas narcosis aggravates, in a persistent manner, basic and higher-order cognitive abilities during protracted cold exposure.

Eccentric upper-body exercise performed 24 h prior to high-altitude decompression has previously been shown to aggravate venous gas emboli (VGE) load. Yet, it is unclear whether increasing the muscle mass recruited (i.e., upper vs. whole-body) during eccentric exercise would exacerbate the decompression strain. Accordingly, this study aimed to investigate whether the total muscle mass recruited during eccentric exercise influences the decompression strain. Eleven male participants were exposed to a simulated altitude of 24,000 ft for 90 min on three separate occasions. Twenty-four hours before each exposure, participants performed one of the following protocols: (i) eccentric whole-body exercise (ECCw; squats and arm-cycling exercise), (ii) eccentric upper-body exercise (ECCu; arm-cycling), or (iii) no exercise (control). Delayed onset muscle soreness (DOMS) and isometric strength were evaluated before and after each exercise intervention. VGE load was evaluated at rest and after knee- and arm-flex provocations using the 6-graded Eftedal-Brubakk scale. Knee extensor (-20 ± 14%, P = 0.001) but not elbow flexor (-12 ± 18%, P = 0.152) isometric strength was reduced 24 h after ECCw. ECCu reduced elbow flexor isometric strength at 24 h post-exercise (-18 ± 10%, P < 0.001). Elbow flexor DOMS was higher in the ECCu (median 6) compared with ECCw (5, P = 0.035). VGE scores were higher following arm-flex provocations in the ECCu (median (range), 3 (0-4)) compared with ECCw (2 (0-3), P = 0.039) and control (0 (0-2), P = 0.011), and in ECCw compared with control (P = 0.023). VGE were detected earlier in ECCu (13 ± 20 min) compared with control (60 ± 38 min, P = 0.021), while no differences were noted between ECCw (18 ± 30 min) and control or ECCu. Eccentric exercise increased the decompression strain compared with control. The VGE load varied depending on the body region but not the total muscle mass recruited.

HIGHLIGHTS: What is the central question of this study? Does exercise-induced muscle damage (EIMD) resulting from eccentric exercise influence the presence of venous gas emboli (VGE) during a 90 min continuous exposure at 24,000 ft? What is the main finding and its importance? EIMD led to an earlier manifestation and greater VGE load compared with control. However, the decompression strain was dependent on the body region but not the total muscle mass recruited.

This study aimed to investigate the effect of eccentric exercise on exercise-induced muscle damage (EIMD) and inflammation on high-altitude-induced venous gas emboli (VGE). Subjects were exposed to an altitude of 24,000 ft. for 90 min, with either prior eccentric exercise (ECC) or no exercise (Control) 24 h before. Blood samples were collected at baseline (T0), before (T1), and after (T2) altitude exposures. VGE load was evaluated using the Eftedal-Brubakk (ΕΒ) scale. Creatine kinase (CK) and myoglobin were used to assess muscle damage, while interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), C-reactive protein (CRP), and fibrinogen were used to evaluate inflammation. ECC showed higher EB-scores during altitude exposures [median(range), 3(0–5)] than Control [1(0–4), p = 0.019]. Increases in myoglobin (+35%, p = 0.012), CK (+130%, p < 0.001), IL-6 (+72%, p = 0.02), and CRP (+63%, p = 0.004) were observed from T0 to T1 in ECC, but not Control. Significantly higher levels of myoglobin (p = 0.033), CK (p < 0.001), IL-6 (p = 0.016), and CRP (p = 0.002) were noted in the ECC compared to Control at T1. IL-6 increased from T1 to T2 in ECC (p = 0.005), with higher levels than Control at T2 (p = 0.046). A correlation was found between EB-scores and T1 myoglobin levels (rs = 0.450; p = 0.004), and to T1-T2 IL-6 changes (rs = 0.396; p = 0.037). Eccentric EIMD followed by inflammation is associated with a higher decompression strain, with VGE load aggravating systemic inflammation.

Breath-holding preceded by either an overnight fast or hyperventilation has been shown to potentiate the risk of a hypoxic blackout. However, no study has explored the combined effects of fasting and hyperventilation on apneic performance and associated physiological responses. Nine nondivers (8 males) attended the laboratory on two separate occasions (≥48 h apart), both after a 12-h overnight fast. During each visit, a hyperoxic rebreathing trial was performed followed by three repeated maximal static apneas preceded by either normal breathing (NORM) or a 30-s hyperventilation (HYPER). Splenic volume, hematology, cardiovascular, and respiratory variables were monitored. There were no interprotocol differences at rest or during hyperoxic rebreathing for any variable (P ≥ 0.09). On nine occasions (8 in HYPER), the subjects reached our safety threshold (oxygen saturation 65%) and were asked to abort their apneas, with the preponderance of these incidents (6 of 9) occurring during the third repetition. Across the sequential attempts, longer apneas were recorded in HYPER [median(range), 220(123–324) s vs. 185(78–296) s, P ≤ 0.001], with involuntary breathing movements occurring later [134(65–234) s vs. 97(42–200) s, P ≤ 0.001] and end-apneic partial end-tidal pressures of oxygen (PETO2) being lower (P ≤ 0.02). During the final repetition, partial end-tidal pressure of carbon dioxide [(PETCO2), 6.53 ± 0.46 kPa vs. 6.01 ± 0.45 kPa, P = 0.005] was lower in HYPER. Over the serial attempts, preapneic tidal volume was gradually elevated [from apnea 1 to 3, by 0.26 ± 0.24 L (HYPER) and 0.28 ± 0.30 L (NORM), P ≤ 0.025], with a correlation noted with preapneic PETCO2 (r = −0.57, P < 0.001) and PETO2 (r = 0.76, P < 0.001), respectively. In a fasted state, preapnea hyperventilation compared with normal breathing leads to longer apneas but may increase the susceptibility to a hypoxic blackout.

Purpose

We evaluated the hypothesis that repetitive gravitoinertial stress would augment the arterial-pressure response to peripheral sympathetic stimulation.

Methods

Before and after a 5-weeks G-training regimen conducted in a human-use centrifuge, twenty healthy men performed a hand cold-pressor test, and nine of them also a foot cold-pressor test (4 min; 4 °C water). Arterial pressures and total peripheral resistance were monitored.

Results

The cold-induced elevation (P ≤ 0.002) in arterial pressures and total peripheral resistance did not vary between testing periods, either in the hand [mean arterial pressure: Before =  + 16% vs. After =  + 17% and total peripheral resistance: Before =  + 13% vs. After =  + 15%], or in the foot [mean arterial pressure: Before =  + 19% vs. After =  + 21% and total peripheral resistance: Before =  + 16% vs. After =  + 16%] cold-pressor tests (P > 0.05).

Conclusion

Present results demonstrate that 5 weeks of prolonged iterative exposure to hypergravity does not alter the responsiveness of sympathetically mediated circulatory reflexes.

Purpose: This study examined the magnitude of physiological strain imposed by repeated maximal static and dynamic apneas through assessing a panel of stress-related biomarkers. Methods: Eleven healthy men performed on three separate occasions (≥72-h apart): a series of five repeated maximal (i) static (STA) or (ii) dynamic apneas (DYN) or (iii) a static eupneic protocol (CTL). Venous blood samples were drawn at 30, 90, and 180-min after each protocol to determine ischaemia modified albumin (IMA), neuron-specific enolase (NSE), myoglobin, and high sensitivity cardiac troponin T (hscTnT) concentrations. Results: IMA was elevated after the apnoeic interventions (STA,+86%;DYN,+332%,p ≤ 0.047) but not CTL (p = 0.385). Myoglobin was higher than baseline (23.6 ± 3.9 ng/mL) 30-min post DYN (+70%,38.8 ± 13.3 ng/mL,p = 0.030). A greater myoglobin release was recorded in DYN compared with STA and CTL (p ≤ 0.035). No changes were observed in NSE (p = 0.207) or hscTnT (p = 0.274). Conclusions: Five repeated maximal DYN led to a greater muscle injury compared with STA but neither elicited myocardial injury or neuronal-parenchymal damage.