Cerebral, cardiac and skeletal muscle stress associated with a series of static and dynamic apnoeas.

Abstract

This study sought to explore, for the first time, the effects of repeated maximal static and dynamic apnoeic attempts on the physiological milieu by assessing cerebral, cardiac and striatal muscle stress-related biomarkers in a group of elite breath-hold divers (EBHD). Sixteen healthy males were recruited (EBHD=8; controls=8). On two separate occasions, EBHD performed two sets of five repeated maximal static apnoeas (STA) or five repeated maximal dynamic apnoeas (DYN). Controls performed a static eupnoeic protocol to negate any effects of water immersion and diurnal variation on haematology (CTL). Venous blood samples were drawn at 30, 90, and 180min after each protocol to determine S100β, neuron-specific enolase (NSE), myoglobin, and high sensitivity cardiac troponin T (hscTNT) concentrations. S100β and myoglobin concentrations were elevated following both apnoeic interventions (p<0.001; p≤0.028, respectively) but not after CTL (p≥0.348). S100β increased from baseline (0.024±0.005µg/L) at 30 (STA, +149%, p<0.001; DYN, +166%, p<0.001) and 90min (STA, +129%, p<0.001; DYN, +132%, p=0.008) following the last apnoeic repetition. Myoglobin was higher than baseline (22.3±2.7ng/ml) at 30 (+42%, p=0.04), 90 (+64%, p<0.001) and 180min (+49%, p=0.013) post-STA and at 90min (+63%, p=0.016) post-DYN. Post-apnoeic S100β and myoglobin concentrations were higher than CTL (STA, p<0.001; DYN, p≤0.004). NSE and hscTNT did not change from basal concentrations after the apnoeic (p≥0.146) nor following the eupnoeic (p≥0.553) intervention. This study suggests that a series of repeated maximal static and dynamic apnoeas transiently disrupt the blood-brain barrier and instigate muscle injury but do not induce neuronal-parenchymal damage or myocardial damage.