The effect of additional dead space on respiratory exchange ratio and carbon dioxide production due to training.

Author:Smolka, Lukasz
Position::Research article - Report
 
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Introduction

Breathing through additional dead space has been a widely used intervention strategy in varying areas of physiology. For example, it has been used in studies to determine the effects of hypercapnia on long term modulation of pulmonary ventilation (Cathcart et al., 2005; Sumners and Turner, 2003), as well as the effects of respiratory muscle training on muscle endurance (Koppers et al., 2006), effectiveness of interventions for sleep disorders (Khayat et al., 2003) and alterations in blood morphology following training in professional cyclists (Zaton et al., 2010). Rebreathing one's own air, referred to as additional dead space, is a known way to increase blood carbon dioxide pressure (pC[O.sub.2]) without the need for using complex devices (Khayat et al., 2003; Koppers et al., 2006; McParland et al., 1991; Smejkal et al., 1989; Toklu et al. 2003). The additional dead space volume determines the level of increase in pC[O.sub.2] and accompanying respiratory acidosis. Enhanced pC[O.sub.2] and the respiratory acidosis have been studied to examine their influence on changes in respiratory function (Cathcart et al., 2005, Maruyama et al., 1988; Poon 1989), blood flow distribution (Howden et al., 2004; Ogoh et al., 2009,), muscle contractility (Mador et al., 1997; Vianna et al., 1990) and metabolic pathways of energy production (Graham et al., 1980; 1982; 1986; Graham and Wilson 1983; Kato et al., 2005; McLellan, 1991; Ostergard et al., 2012).

Under most conditions enhanced pC[O.sub.2] with the accompanying respiratory acidosis will cause a decrease in plasma lactate concentration (LA) during and after a bout of exercise. During an incremental test (Graham et al., 1980; McLellan, 1991) or a constant work test (Ehrsam et al., 1982; Graham et al., 1982; Graham and Wilson 1983, Ishida et al., 1988; Ostergard et al., 2012) breathing air with enhanced C[O.sub.2] content is accompanied by significant blood pH reduction and decrease in lactate plasma concentration. In the above cited studies, a decrease in plasma lactate concentration occurred despite no significant changes in performance time in an incremental test or workload in a constant work test. The decrease in lactate plasma concentration is mainly associated with enhanced blood hydrogen ion concentration. Likewise, metabolic acidosis (with no changes in carbon dioxide pressure) has been shown to lower lactate concentration (Hollidge-Horvat et al., 1999; Jones et al., 1977; Zoladz et al. 1998). The decrease of lactate concentration might be caused by an impaired lactate transport out of the muscle, increased lactate oxidation (Graham et al., 1986) or decreased lactate production due to the inhibition of glycogenolysis and glycolysis (Graham et al., 1986; HollidgeHorvat et al., 1999). Glycogenolysis and glycolysis inhibition have been confirmed directly in a study with respiratory acidosis on animals (Graham et al., 1986) and with metabolic acidosis in humans (Hollidge-Horvat et al., 1999). Hollidge-Horvat and colleagues induced metabolic acidosis and reported a significant decrease in glycogen utilization, suppression of phosphofructokinase and pyruvate dehydrogenase activity and decrease in pyruvate production (Hollidge-Horvat et al., 1999).

Decreased respiratory exchange ratio (RER) (Ehrsam et al., 1982; Graham and Wilson, 1983; Graham et al., 1982; Graham et al. 1980; Ostergard et al., 2012) or carbon dioxide production (VC[O.sub.2]) (McLellan, 1991; Ostergard et al., 2012) have been reported in studies on respiratory acidosis. These changes in RER were recently confirmed using more sophisticated instrumentation. Ostergard and colleagues have shown that RER decreased from 0.98 [+ or -] 0.04 to 0.85 [+ or -] 0.04, recorded during the last minute of a 6-minute exercise test, performed with the intensity of 80% V[O.sub.2]max (Ostergard et al., 2012). Likewise, metabolic acidosis has been shown to lower RER significantly (Hollidge-Horvat et al., 1999). The decrease of plasma lactate concentration and the decrease in respiratory exchange ratio, provoked by respiratory acidosis, may suggest a substrate shift towards increased lipid utilization (Graham et al., 1980; 1982; Graham and Wilson, 1983; McLellan, 1991; Kato et al., 2005; Ostergard et al., 2012). If the respiratory acidosis inhibits glycolysis even in a single session it would be reasonable to expect that a similar or enhanced adaptation would be observed due to multiple training sessions and that the aerobic effects would be accelerated. No studies so far have examined the additive effects of multiple training sessions on respiratory acidosis. Hence, the purpose of this study was to investigate the effects of implementing an additional 1200ml of dead space volume on respiratory exchange ratio and carbon dioxide production following 12, 30-minute sessions of aerobic training using cycle ergometry. We hypothesized that the addition of dead space volume during moderate intensity aerobic training will result in decreased RER and VC[O.sub.2] measurements in comparison to sessions without adding dead space.

Methods

Subjects

Thirty healthy males were recruited for this study. Subjects led active lifestyles (70 [+ or -] 13 minutes per week) but were not competing in any sports. Written consent was obtained from each subject upon explaining the purpose and associated risks of the study protocol. The experiment was approved by Ethics Committee at University School of Physical Education in Wroclaw (Poland).

Experimental protocol

An a-priori randomization was established. Based on that scheme, subjects were assigned to two groups: experimental (Exp, n = 15) and control (Con, n = 15). Participants were ranked from 1 to 30 on the basis of time performance in pre-training test. Men with odd number rankings were assigned to Con and men with even number rankings were assigned to Exp.

Each test and training session was performed in an air conditioned chamber at a temperature of 24[degrees]C, relative humidity of 50% and barometric pressure at 762.75 mmHg. Subjects were instructed to refrain from caffeine, alcohol, and any exercise for 24 hours prior to the testing and training sessions.

Pre-training test

An incremental exercise test until exhaustion constituted the pre-training test. The test was conducted on an electrically braked cycle ergometer (Excalibur, Lode, Netherlands). Exhaustion was defined as the subject refusing to continue the test due to fatigue. The workload, starting from 50 Watt (W), was incrementally increased by 50W every three minutes. The subjects were instructed to keep a constant pedaling rate between 60 and 90rpm. To assure constant workload, pedaling rate was coupled with resistance, i.e., when the rate of pedaling increased the resistance decreased. Gas-exchange (Quark Gas Analyzer, Cosmed, Italy) was recorded continuously beginning three minutes prior to the test, throughout the test and five minutes following completion of the test. Breath-by-breath gas-exchange was averaged every 15 seconds and saved for further analyses.

Training sessions

One week following completion of the Pre-test, all participants began the training period. The training period consisted of twelve cycloergometric (Ergomedic 874E, Monark, Sweden) training sessions. Each training session was carried out at the same time of day, twice a week, three days apart, for six weeks. A single training bout consisted of continuous, constant-rate exercise on a cycle ergometer at 60% of V[O.sub.2]max and maintained for 30 minutes. Subjects in Exp group starting from the third minute before exercise until the fifth minute after exercise were breathing through...

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