Otto F. Barak

Maximal Anaerobic Power Test in Athletes of Different Sport Disciplines

Popadic Gacesa, JZ, Barak, OF, and Grujic, NG. Maximal anaerobic power test in athletes of different sport disciplines. J Strength Cond Res 23(3): 751-755, 2009-The aim of this study was to investigate the values of anaerobic energetic capacity variables in athletes engaged in different sport disciplines and to compare them in relation to specific demands of each sport. Wingate anaerobic tests were conducted on 145 elite athletes (14 boxers, 17 wrestlers, 27 hockey players, 23 volleyball players, 20 handball players, 25 basketball players, and 19 soccer players). Three variables were measured as markers of anaerobic capacity: peak power, mean power, and explosive power. The highest values of peak power were measured in volleyball 11.71 ± 1.56 W·kg−1 and basketball players 10.69 ± 1.67 W·kg−1, and the difference was significant compared with the other athletes (p ≤ 0.05). The lowest value of peak power (8.58 ± 1.56 W·kg−1) was registered in handball players. The mean power variable showed a similar distribution as peak power among groups. The highest values of explosive power were also registered in volleyball 1.75 ± 0.33 W·s−1·kg−1 and basketball players 1.64 ± 0.35 W·s−1·kg−1, but there was no significant difference in values between volleyball players and wrestlers, between boxers and wrestlers, between boxers and basketball players, and between volleyball and hockey players (p > 0.05). The measured results show the influence of anaerobic capacity in different sports and the referral values of these variables for the elite male athletes. Explosive power presented a new dimension of anaerobic power, i.e., how fast maximal energy for power development can be obtained, and its values are high in all sports activities that demand explosiveness and fast maximal energy production. Coaches or other experts in the field could, in the future, find useful to follow and improve, through training process, one of the variables that is most informative for that sport.

Effect of Maximal Apnoea Easy-Going and Struggle Phases on Subarachnoid Width and Pial Artery Pulsation in Elite Breath-Hold Divers

Purpose The aim of the study was to assess changes in subarachnoid space width (sas-TQ), the marker of intracranial pressure (ICP), pial artery pulsation (cc-TQ) and cardiac contribution to blood pressure (BP), cerebral blood flow velocity (CBFV) and cc-TQ oscillations throughout the maximal breath hold in elite apnoea divers. Non-invasive assessment of sas-TQ and cc-TQ became possible due to recently developed method based on infrared radiation, called near-infrared transillumination/backscattering sounding (NIR-T/BSS). Methods The experimental group consisted of seven breath-hold divers (six men). During testing, each participant performed a single maximal end-inspiratory breath hold. Apnoea consisted of the easy-going and struggle phases (characterised by involuntary breathing movements (IBMs)). Heart rate (HR) was determined using a standard ECG. BP was assessed using the photoplethysmography method. SaO2 was monitored continuously with pulse oximetry. A pneumatic chest belt was used to register thoracic and abdominal movements. Cerebral blood flow velocity (CBFV) was estimated by a 2-MHz transcranial Doppler ultrasonic probe. sas-TQ and cc-TQ were measured using NIR-T/BSS. Wavelet transform analysis was performed to assess cardiac contribution to BP, CBFV and cc-TQ oscillations. Results Mean BP and CBFV increased compared to baseline at the end of the easy phase and were further augmented by IBMs. cc-TQ increased compared to baseline at the end of the easy phase and remained stable during the IBMs. HR did not change significantly throughout the apnoea, although a trend toward a decrease during the easy phase and recovery during the IBMs was visible. Amplitudes of BP, CBFV and cc-TQ were augmented. sas-TQ and SaO2 decreased at the easy phase of apnoea and further decreased during the IBMs. Conclusions Apnoea increases intracranial pressure and pial artery pulsation. Pial artery pulsation seems to be stabilised by the IBMs. Cardiac contribution to BP, CBFV and cc-TQ oscillations does not change throughout the apnoea.

Cerebral oxidative metabolism is decreased with extreme apnoea in humans; impact of hypercapnia

The present study describes the cerebral oxidative and non‐oxidative metabolism in man during a prolonged apnoea (ranging from 3 min 36 s to 7 min 26 s) that generates extremely low levels of blood oxygen and high levels of carbon dioxide. The cerebral oxidative metabolism, measured from the product of cerebral blood flow and the radial artery‐jugular venous oxygen content difference, was reduced by ∼29% at the termination of apnoea, although there was no change in the non‐oxidative metabolism. A subset study with mild and severe hypercapnic breathing at the same level of hypoxia suggests that hypercapnia can partly explain the cerebral metabolic reduction near the apnoea breakpoint. A hypercapnia‐induced oxygen‐conserving response may protect the brain against severe oxygen deprivation associated with prolonged apnoea.

Motivation and motoric tests in sports

Motivation in sport performance has been an interesting topic for many investigators during the past decade. This area can be considered from different viewpoints: motivation for participation in sport activity, achievement motivation, competitiveness etc. Motivation plays an important role in all out tests, as well as in sport activities and at all levels of competition. Motivation climate, or positive social environment may influence and modulate motivation of individuals involved in sports. Experience has shown that conventional encouragement and feedback during the test may affect its outcome. According to Wingate research team recommendations, verbal encouragement, as a motivation factor, was given to all examined subjects during Wingate anaerobic test, which is considered the most reliable test for assessing anaerobic capacity. The investigated group consisted of 30 young men--medical students, who were not actively involved in any programmed sport activity. The investigated group included second-year students of the Faculty of Medicine in Novi Sad chosen by random sampling. The Wingate anaerobic test was performed in all subjects, and changes of parameters when test was performed with verbal encouragement, were recorded The results show statistically significant increase of Wingate test parameters when conducted with verbal encouragement: anaerobic power (622/669 W); relative anaerobic power (7.70/8.27 W/kg); slope of the power (95.5/114 W/s); relative slope of the power (1.18/1.40 W/s/kg); anaerobic capacity (12.7/13.2 kJ) and relative anaerobic capacity (158/164 J/kg).

Cerebral oxidative metabolism is decreased with extreme apnea in humans; impact of acidosis

The present study describes the cerebral oxidative and non‐oxidative metabolism in man during a prolonged apnoea (ranging from 3 min 36 s to 7 min 26 s) that generates extremely low levels of blood oxygen and high levels of carbon dioxide. The cerebral oxidative metabolism, measured from the product of cerebral blood flow and the radial artery‐jugular venous oxygen content difference, was reduced by ∼29% at the termination of apnoea, although there was no change in the non‐oxidative metabolism. A subset study with mild and severe hypercapnic breathing at the same level of hypoxia suggests that hypercapnia can partly explain the cerebral metabolic reduction near the apnoea breakpoint. A hypercapnia‐induced oxygen‐conserving response may protect the brain against severe oxygen deprivation associated with prolonged apnoea.

Hypercapnia is essential to reduce the cerebral oxidative metabolism during extreme apnea in humans

The cerebral metabolic rate of oxygen (CMRO2) is reduced during apnea that yields profound hypoxia and hypercapnia. In this study, to dissociate the impact of hypoxia and hypercapnia on the reduction in CMRO2, 11 breath-hold competitors completed three apneas under: (a) normal conditions (NM), yielding severe hypercapnia and hypoxemia, (b) with prior hyperventilation (HV), yielding severe hypoxemia only, and (c) with prior 100% oxygen breathing (HX), yielding the greatest level of hypercapnia, but in the absence of hypoxemia. The CMRO2 was calculated from the product of cerebral blood flow (ultrasound) and the radial artery-jugular venous oxygen content difference (cannulation). Secondary measures included net-cerebral glucose/lactate exchange and nonoxidative metabolism. Reductions in CMRO2 were largest in the HX condition (−44 ± 15%, p < 0.05), with the most severe hypercapnia (PaCO2 = 58 ± 5 mmHg) but maintained oxygen saturation. The CMRO2 was reduced by 24 ± 27% in NM (p = 0.05), but unchanged in the HV apnea where hypercapnia was absent. A net-cerebral lactate release was observed at the end of apnea in the HV and NM condition, but not in the HX apnea (main effect p < 0.05). These novel data support hypercapnia/pH as a key mechanism mediating reductions in CMRO2 during apnea, and show that severe hypoxemia stimulates lactate release from the brain.

Very Few Exercise-Induced Arterialized Gas Bubbles Reach the Cerebral Vasculature.

INTRODUCTION Arterialization of venous gas emboli (VGE) formed after surfacing from SCUBA diving can become arterial gas emboli (AGE) through intrapulmonary arterial-venous anastomoses that open with exercise. METHODS We recruited twenty patent foramen ovale-negative SCUBA divers and conducted a field and a laboratory study with the aim of investigating the appearance of AGE in intracranial vessels. At the field, they performed a single dive to a depth of 18-m sea water with a 47-min bottom time and a direct ascent to the surface. Transthoracic echocardiography was used to score VGE and AGE, and transcranial Doppler was used to visualize middle and posterior cerebral arteries with automated objective bubble detection. Observations were conducted for 45-min after dive at rest and at the laboratory after agitated saline injection at rest and throughout an incremental cycle supine exercise test until exhaustion and for 10 min of recovery. RESULTS After resurfacing, all divers presented endogenous VGE and arterialization was present in three divers. Saline contrast injection led to AGE in nine of 19 subjects at rest. AGE that reached the cerebral arteries after dive were recorded in two divers at 60 W, three at 90 W, five at 120 W, six at 150 W, and four at 180 W and in three, four, five, nine, and nine, respectively, after saline contrast injection in the laboratory. All divers had AGE grades of 1 or 2, and only single AGE reached the cerebral vasculature. CONCLUSIONS These data suggest that few emboli of venous origin reach the brain through exercise-induced intrapulmonary arterial-venous anastomoses but cerebral embolization is not high risk in the studied population.

Peripheral chemoreflex inhibition with low-dose dopamine; new insight into mechanisms of extreme apnea

The purpose of this study was to determine the impact of peripheral chemoreflex inhibition with low-dose dopamine on maximal apnea time, and the related hemodynamic and cerebrovascular responses in elite apnea divers. In a randomized order, participants performed a maximal apnea while receiving either intravenous 2 μg·kg(-1)·min(-1) dopamine or volume-matched saline (placebo). The chemoreflex and hemodynamic response to dopamine was also assessed during hypoxia [arterial O2 tension, (PaO2 ) ∼35 mmHg] and mild hypercapnia [arterial CO2 tension (PaCO2 ) ∼46 mmHg] that mimicked the latter parts of apnea. Outcome measures included apnea duration, arterial blood gases (radial), heart rate (HR, ECG), mean arterial pressure (MAP, intra-arterial), middle (MCAv) and posterior (PCAv) cerebral artery blood velocity (transcranial ultrasound), internal carotid (ICA) and vertebral (VA) artery blood flow (ultrasound), and the chemoreflex responses. Although dopamine depressed the ventilatory response by 27 ± 41% (vs. placebo; P = 0.01), the maximal apnea duration was increased by only 5 ± 8% (P = 0.02). The PaCO2 and PaO2 at apnea breakpoint were similar (P > 0.05). When compared with placebo, dopamine increased HR and decreased MAP during both apnea and chemoreflex test (P all <0.05). At rest, dopamine compared with placebo dilated the ICA (3.0 ± 4.1%, P = 0.05) and VA (6.6 ± 5.0%, P < 0.01). During apnea and chemoreflex test, conductance of the cerebral vessels (ICA, VA, MCAv, PCAv) was increased with dopamine; however, flow (ICA and VA) was similar. At least in elite apnea divers, the small increase in apnea time and similar PaO2 at breakpoint (∼31 mmHg) suggest the apnea breakpoint is more related to PaO2 , rather than peripheral chemoreflex drive to breathe.

Ascorbic acid supplementation diminishes microparticle elevations and neutrophil activation following SCUBA diving

Predicated on evidence that diving-related microparticle generation is an oxidative stress response, this study investigated the role that oxygen plays in augmenting production of annexin V-positive microparticles associated with open-water SCUBA diving and whether elevations can be abrogated by ascorbic acid. Following a cross-over study design, 14 male subjects ingested placebo and 2-3 wk later ascorbic acid (2 g) daily for 6 days prior to performing either a 47-min dive to 18 m of sea water while breathing air (∼222 kPa N2/59 kPa O2) or breathing a mixture of 60% O2/balance N2 from a tight-fitting face mask at atmospheric pressure for 47 min (∼40 kPa N2/59 kPa O2). Within 30 min after the 18-m dive in the placebo group, neutrophil activation, and platelet-neutrophil interactions occurred, and the total number of microparticles, as well as subgroups bearing CD66b, CD41, CD31, CD142 proteins or nitrotyrosine, increased approximately twofold. No significant elevations occurred among divers after ingesting ascorbic acid, nor were elevations identified in either group after breathing 60% O2. Ascorbic acid had no significant effect on post-dive intravascular bubble production quantified by transthoracic echocardiography. We conclude that high-pressure nitrogen plays a key role in neutrophil and microparticle-associated changes with diving and that responses can be abrogated by dietary ascorbic acid supplementation.

Cardiac power output and its response to exercise in athletes and non-athletes

Cardiac power output (CPO) is an integrative measure of overall cardiac function as it accounts for both, flow‐ and pressure‐generating capacities of the heart. The purpose of the present study was twofold: (i) to assess cardiac power output and its response to exercise in athletes and non‐athletes and (ii) to determine the relationship between cardiac power output and reserve and selected measures of cardiac function and structure. Twenty male athletes and 32 age‐ and gender‐matched healthy sedentary controls participated in this study. CPO was calculated as the product of cardiac output and mean arterial pressure, expressed in watts. Measures of hemodynamic status, cardiac structure and pumping capability were assessed by echocardiography. CPO was assessed at rest and after peak bicycle exercise. At rest, the two groups had similar values of cardiac power output (1·08 ± 0·2 W versus 1·1 ± 0·24 W, P>0·05), but the athletes demonstrated lower systolic blood pressure (109·5 ± 6·2 mmHg versus 117·2 ± 8·2 mmHg, P<0·05) and thicker posterior wall of the left ventricle (9·8 ± 1 mm versus 9 ± 1·1 mm, P<0·05). Peak CPO was higher in athletes (5·87 ± 0·75 W versus 5·4 ± 0·69 W, P<0·05) as was cardiac reserve (4·92 ± 0·66 W versus 4·26 ± 0·61 W, P<0·05), respectively. Peak exercise CPO and reserve were only moderately correlated with end‐diastolic volume (r = 0·54; r = 0·46, P<0·05) and end‐diastolic left ventricular internal diameter (r = 0·48; r = 0·42, P<0·05), respectively. Athletes demonstrated greater maximal cardiac pumping capability and reserve than non‐athletes. The study provides new evidence that resting measures of cardiac structure and function need to be considered with caution in interpretation of maximal cardiac performance.