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Jet lag can impair a variety of physical and mental functions. The impact of jet lag on athletic performance has been assumed but difficult to prove methodologically. The challenges have involved eliminating the impact of the quality of the opponent and the difficulties determining when an athlete actually traveled across time zones. Analyzing free throw (FT) shooting in the National Basketball Association allowed these challenges to be overcome. 48,309 games across 19 consecutive seasons were examined of which 675 games involved a team that met our definition of jet lag. In these games, players on the jet lagged teams made 12,154 of 16,286 (74.6%) FTs that were attempted while in the remaining games of that season, the same players on these teams made 993,962 of 1,318,188 (75.4%) FTs attempted, X2 (1, N = 1,334,474) = 5.21, p =.02. There was no significant impact of jet lag on the players who took the most number of FTs in these jet lagged games. However, the remaining players on the team made 7,394 of 10,016 (73.8%) FTs attempted in jet lagged games while the same players made 794,009 of 1,056,587 (75.1%) FTs in other games that season, X2 (1, N = 1,066,603) = 9.35, p =.002. When subcategorized further, the impact on the players on jet lagged teams was only seen when they traveled from east to west but not when travel was from west to east. Our analysis reveals that jet lag does negatively influence athletic performance, primarily through circadian rhythm disruption. However, elite athletes appear to be able to overcome this impact if they are given enough opportunities to do so. [ABSTRACT FROM AUTHOR]

As obesity becomes more common worldwide, the prevalence of obstructive sleep apnoea (OSA) continues to rise. Obstructive sleep apnoea is a well-known disorder that causes chronic intermittent hypoxia (CIH), which is considered a risk factor for atherosclerosis directly and indirectly. Ischaemic heart disease remains the leading cause of death. Most risk factors for atherosclerosis are well understood. However, other factors such as CIH are less well understood. Several studies have investigated the pathophysiology of CIH, attempting to uncover its link to atherosclerosis and to determine whether OSA treatment can be a therapeutic modality to modify the risk for atherosclerosis. In this article, we will review the pathophysiology of OSA as an independent risk factor for cardiovascular disease and discuss the most common markers that have been studied. We will also examine the potential impact of OSA management as a risk factor modifier on the reversibility of atherosclerosis. [ABSTRACT FROM AUTHOR]