Hangovers

Hangovers are a set of unpleasant physiological and psychological reactions from drinking to intoxication. The severity of the hangover is related to the amount and type of alcohol consumed. There is a range of symptoms (Table 1.2) that are commonly experienced, although the combination and intensity of symptoms vary widely between people. The symptoms of a hangover begin to occur as the blood alcohol concentration starts to fall, with the most intense symptoms experienced as the blood alcohol concentration falls to zero (Swift and Davidson, 1998).

Table 1.2: Hangover symptoms. Collated from Harburg, et al., (1981) and Roehers and Roth (2001).

Physical symptoms Mental symptoms

Diarrhoea Anxiety Fatigue Depression Gastritis Dizziness Headache Irritability Increased blood pressure Memory loss (partial or total)

Increased sensitivity to light and sound Vertigo Loss of appetite

Muscular aches and tremor Nausea and vomiting

Rapid heartbeat (tachycardia) Redness of the eyes

Sweating Thirst

The headache experienced during a hangover can be a result of vasodilatation combined with the increased release of substances such as serotonin, histamines and prostaglandins (Swift and Davidson, 1998).

There is continuing debate about whether a hangover is merely mild alcohol withdrawal, although hangovers do not include symptoms such as seizures or hallucinations, and the period of negative symptoms is much shorter (Swift and Davidson, 1998). Alcohol is not the only contributing factor to the appearance of a hangover, as drinking behaviour is often associated with disrupted sleep patterns. In addition, a person’s mental attitude towards drinking can increase or decrease the severity of the hangover experienced (Harburg et al., 1981). Also, biologically active

metabolites of alcohol and components of alcoholic drinks (congeners) can contribute to the severity of a hangover (Swift and Davidson, 1998). Alcoholic beverages such as wine can also cause the release of other substances that can contribute to the hangover experience, such as serotonin and histamine (Swift and Davidson, 1998).

Metabolites

As mentioned earlier, acetaldehyde is the primary product of alcohol metabolism, and it can affect the body independently of alcohol. Acetaldehyde has the ability to bind to proteins and other biological compounds, and can induce the following symptoms at

toxic levels: rapid pulse, sweating, skin flushing, nausea and vomiting. The effects are short-lived, as the enzyme aldehyde dehydrogenase metabolises acetaldehyde to acetate (Swift and Davidson, 1998).

Congeners

Congeners are substances that are added to alcoholic drinks to alter their taste, appearance and smell. Such substances can include methanol, propanol, butanol, ketones, aldehydes, esters and other compounds (Jones, 1989). There are different stages during the process of producing alcoholic beverages that congeners can be added, however their presence is thought to contribute both to intoxication and hangovers (Swift and Davidson, 1998). Methanol is a congener that also exhibits toxic effects at high concentrations, and is found in beverages such as brandies and whiskeys (Swift and Davidson, 1998).

1.5.6.1 Alcohol, Hangovers and Performance

Athletes in general participate in more ‘risky behaviour’ such as binge drinking than their non-athletic peers (O'Brien and Lyons, 2000). In addition, the type of sport one participates in appears to be a determinant of alcohol consumption, with heavier drinkers playing rugby, cricket, soccer and Gaelic football. This trend appears to be related to the social aspects of sporting clubs rather than related to behaviour during intense training or competition (Economos et al., 1993; O'Brien, 1993).

When alcohol is consumed prior to exercise, the effects produced are different from those experienced the morning after a drinking session, although the result of a poorer performance may be the same. The acute effects on performance while intoxicated include a decrease in psychomotor skill capacity and impaired temperature regulation, which may negatively affect performance. In contrast, indices of performance such as VO2max, cardiac function, muscular work capacity and respiratory dynamics are

apparently not affected (O’Brien and Lyons, 2000). Measures related to performance such as time to exhaustion, aerobic performance and the pumping force of the heart are decreased, while performance time in a 5-mile run is increased following alcohol consumption (Bond et al., 1983).

Performance in flight simulators under the influence of alcohol or during hangovers has been extensively studied. Pilots’ performance using Link GAT-1 stimulator was significantly impaired during a hangover condition (Yesavage and Leirer, 1986). Although different phases of the menstrual cycle can affect alcohol pharmacokinetics, alcohol-impaired performance in a flight simulator, (both acutely and after 8 hours following the last alcoholic drink) is similar in each phase of the menstrual cycle (Mumenthaler et al., 1999; Mumenthaler et al., 2001).

It is a logical assumption that the presence of a hangover would negatively affect indices of psychological and physical performance, due to its negative effects upon the functioning of synaptic transmission within the central nervous system (Ekman et al.,

1996). There is a wide range of literature on the deleterious effects of alcohol on different indices of mental performance [for more information see Seppala, et al.,

(1976), Misawa et al., (1983), Lemon et al., (1983)].

Heart rate (HR) at rest and following exercise during a hangover was shown to be significantly higher than at rest and following exercise when sober (Karvinen et al.,

1962). Aerobic (but not anaerobic) performance also suffers as a result of a hangover, with decrements in performance noted at quantities ranging from between 1 and 38 units of alcohol (O’Brien, 1993). The decrease in aerobic performance can be explained by describing the metabolic and psychological changes induced by alcohol, some of which are mentioned earlier. When alcohol is metabolised (described above) there is a change in the ratio of NADH to NAD. More specifically, the increase in NAD (an electron carrier) causes the citric acid cycle (part of the aerobic metabolic pathway) to slow down, decreasing the maximal rate at which aerobic metabolism can occur (O’Brien and Lyons, 2000). Combined with the slowing of the citric acid cycle, increased NAD concentrations also result in hyperlactacidemia and hypoglycaemia, both of which can have a negative effect on aerobic performance (O’Brien and Lyons, 2000).

Aside from the acute and delayed effects of alcohol, there is a significant difference in the injury rates between drinkers and non-drinkers. This trend was apparent in an athletic population, when in 1993 the injury rate for drinkers was about 55% compared to about 24% in the non-drinking athletic population (O’Brien and Lyons, 2000).

Outline of thesis

The following chapters outline the steps taken to answer the research questions described below. The second chapter outlines the experimental design of the study and the materials and methods used, the third chapter reports the results obtained during the study, and the fourth and final chapter consists of a discussion of the findings of the study and their implications, a general discussion of the lessons learnt during the study and some wider implications of the findings.

Research Objectives

The first research objective was to assess whether changes in aerobic fitness occurred between the first and sixth weeks of the study in a group of sedentary participants as a result of little or no activity, and in a group of training participants after six weeks of rugby training. Changes in fitness were assessed by references to changes in heart rate, rating of perceived exertion and oxygen consumption (VO2) during treadmill fitness

tests. A comparison of VO2 results between the sedentary control participants and the

training participants was conducted in the first and final weeks of the experiment.

The second research objective was to investigate effects of variables such as sleep quality, sleep duration, stage of the menstrual cycle, oral contraceptive use and alcohol consumption on VO2 in both sedentary and training participants.

The third objective was to investigate acute or chronic changes in the plasma concentrations of cortisol, testosterone and growth hormone during the six-week training period in training participants. In addition, any relationships between either oral contraceptive use or alcohol consumption on the plasma concentrations of the three hormones were to be examined.

The fourth objective was to determine the accuracy of the electrosonophoretic method in predicting plasma concentrations of cortisol, testosterone and growth hormone, by using correlation analysis. In addition, the derivation of equation that would allow the concentrations of these three hormones in plasma to be estimated from those in

interstitial fluid obtained by electrosonophoresis was investigated. The relationships between concentrations of cortisol and testosterone in plasma or saliva and those in interstitial fluid were also to be evaluated.