Pre-exercise dietary manipulation effect on substrate utilisation during rest and exercise periods.

Introduction

Nowadays sport nutrition has become one of the most important elements for athletic performance optimization. The type and quantity of food that athletes eat during training periods and prior to competitions influence how well they perform. Based on that, several nutritional studies have been done in order to identify the most appropriate manner in which athletes should meet their ongoing energy needs.

Sherman et al (1989) showed that consumption of 312 g of carbohydrate 4 h before moderately intense prolonged exercise can improve performance, perhaps via an enhancement of carbohydrate oxidation. Conversely, none of the research supported that high fat diet can enhance performance (Whitley et al 1989). Some researches suggested that a greater availability of fat during exercise could improve performance via the carbohydrate-sparing effect of "fat loading." But until this time this is a plausible hypothesis (Sherman et al 1995).  However, in a resent study Whitley et al (1998) examined the effects of fat and carbohydrate pre-exercise meals on performance.  They found that substrate oxidation during the 90-min exercise period was similar and that there were not any differences in performance on the time trial.

The aim of the experiment was to examine the alterations of substrate utilisation following two different pre-exercise feeding methods. The comparison was between CHO pre-exercise feeding and FAT pre-exercise feeding during 30min running exercise (20min at 50% HRR and 10min at 70% HRR). Experimental output was focused on: i) CHO and Fat oxidation rates at rest, 50% and 70% HRR; RER ii)  Errors in measurement of VO₂ & VCO₂; the effects on energy expenditure and substrate utilisation on selected steady states exercise periods. iii) Blood glucose, iv) substrate contribution, and v) metabolic rate.    

Method

Subjects

Four young, fit, healthy male subjects participated in this experiment. Subjects were fully informed about the experimental investigation before they gave written informed consent to participate (appendix 1, 2).

Protocol

Exercise group:

First subject (75kg) consumed a fat cream drink (48% fat). Subject consumed a single bolus (1.3 g^-1 body mass) 50 min prior to exercise (calculated fat drink quantity: 203ml).

Second subject (98kg) consumed 20 g l^-1 sucrose and flavoured with lemon squash in 1 litre of water. Subject consumed a single bolus (15% conc: 7.14 ml kg^-1 body mass) 20 min prior to exercise (calculated CHO drink quantity 699 ml).

Both subjects performed 30 min exercise on a treadmill ergometer, the first 20 min of exercise at 50% HRR, and the following 10 min of exercise at 70% HRR.

Ø      Target HR estimation was based on the equation 1 (appendix 3)

Control croup:

First subject (79kg) consumed a fat cream drink (48% fat).  Subject consumed a single bolus (1.3 g^-1 body mass). (Calculated fat drink quantity: 213 ml).

Second subject (106kg) consumed 20 g l^-1 sucrose and flavoured with lemon squash in 1 litre of water. Subject consumed a single bolus (15% conc: 7.14 ml kg^-1 body mass). (Calculated CHO drink quantity: 756ml).

Both subjects stayed rest, without performing any kind of physical activity throughout the experimental period.

Measures

Exercise group

Resting period:

i) Ventilation values (VO₂, VCO₂, RER) for 5 min period

ii) Blood glucose concentration

ii) Resting heart rate for the calculation of HRR (HRR=MaxHR-RHR)

Exercise period (30min):

i) Continuously measurement of ventilation values (VO₂, VCO₂, RER) using the online system

ii) Blood glucose concentration every 5 min

Control group

i) Ventilation values (VO₂, VCO₂, RER) for 5 min period

ii) Blood glucose concentration every 5 min for 30 min

v        The beginning of measurements for both groups took place under specific period of time. Measurements for FAT group started 50min after fat drink consumption and for CHO group took place 20 min after CHO drink consumption.     

 Results section...

Discussion

According to the experimental procedure, subjects divided into two groups. One group performed exercise and one group stayed rest. One subject from each group consumed a fat drink cream and one subject from each group consumed a CHO drink. The discussion will be focused on the exercise group. More specific, on the effect or pre exercise fat and CHO manipulation during different intensity exercise periods.

At rest and during low intensity exercise, a relative high percentage of the energy production is derived from Fat oxidation (Romijn et al 1993). RER value of 0.70 would indicate that only fats are metabolized, and an RER of 1.00 would mean only CHO. During rest period and after CHO feeding, energy production was delivered mostly from carbohydrate oxidation. In five minutes rest period, total fat oxidation was 0.51 grams, where total carbohydrate oxidation was 2.57 grams; with average RER: 0.88 (table 1). Conversely, after fat feeding, energy production was based on fat metabolism, since total fat oxidation was 1.1grams, and total carbohydrate oxidation was 1.04grams; with average RER: 0.77 (table 1). During rest period, blood glucose for CHO pre-exercise feeding subject remained significant higher (average: 6.5mmol.l^-1), comparing to fat pre-exercise feeding subject blood glucose (average: 4.5mmol.l^-1), (table 5). 

Based on the literature review, energy production for exercise at 50% VO₂ max derived from fat oxidation. However, pre-exercise carbohydrate feeding altered the primary source for energy production. Total fat oxidation for 20min exercise at 50% HRR was 2.24 grams, and total carbohydrate oxidation was 50.44 grams; average RER 0.98 (table 1). Carbohydrate feeding before exercise suppressed plasma nonesterified fatty acid (NEFA) concentration and decreased the rate of fat oxidation. This was associated with an elevation in the concentration of plasma insulin before exercise and an increase in the rate of carbohydrate oxidation during exercise (Coyle et al 1985). Insulin plays a key role in fuel partitioning, since insulin tends to increase the metabolism of carbohydrate and reduce fat use. As a result of this faster rate of carbohydrate oxidation, blood glucose levels may actually fall (a condition known as hypoglycemia) shortly after exercise begins (Whitley et al 1998). Blood glucose was decreased during the first 15 min of exercise and then remained almost constant for the next 15 min (figure 3). Additionally, substrate contribution was 86.1% glucose and 13.09% fatty acids; with average metabolic rate at 44.1 kJ min^-1 (table 4).

When exercise intensity increases above 70% to 80% maximal oxygen uptake (VO₂ max), there is a progressive shift from fat to CHO oxidation (Romijn et al 1993). For 10min exercise at 70% HRR, total CHO oxidation was 32.44grams, and total fat oxidation was 0.63grams; average RER 0.99 (table 1). Additionally, substrate contribution was 94.8% glucose and 5.2% fatty acids; with average metabolic rate at 58.8 kJ min^-1 (table 4). At that stage, shifting from fat oxidation to CHO oxidation was not only based on pre-exercise CHO feeding. Several explanations for this shift from fat to CHO have been proposed, including the increase blood lactate formation which occurs when glycogen breakdown and glycolytic flux are increase and suppress lipolysis (Mcdemott et al 1987; Mazzeo and Marshall 1989). At the end of the two exercise periods, total CHO oxidation was 88.84grams, and total fat oxidation was 3.38grams, indicating that pre-exercise CHO feeding can shift metabolism from fat oxidation to CHO oxidation. In the seventieths, it has been suggested that many athletes avoid high-carbohydrate meals prior to the performance, since elevated blood insulin at the onset of the exercise could lead to a lowering of blood glucose during exercise (Costill et al 1977). However, a research from Coyle et al (1985) showed that these responses are transient and probably will not reduce performance.   

Fat feeding before exercise will increase the plasma triacylglycerol (TAG) concentration at rest and during exercise (Whitley et al 1998) and will increase fatty acid availability (Hawley et al 2000).  Any dietary intervention that elevates fatty acid concentration in plasma could have a positive effect on exercise performance by slowing the rate of glycogen depletion. Costill et al (1977) showed that elevation of plasma Fatty acid could decrease the rate of muscle glycogen depletion by 40%. After fat feeding, fat oxidation predominated to the CHO oxidation only for the first 2min of exercise. After that point CHO oxidation was higher throughout the exercise period (Table 1). At 50% HRR, and during 20min of exercise at that intensity, total fat oxidation was 14.67grams, and total CHO oxidation was 34.28grams; average RER 0.83 (table 1). Substrate contribution was 42.3%% glucose and 57.7% fatty acids; with average metabolic rate at 57.7 kJ min^-1 (table 4). RER values and substrate contribution verified that during low intensity exercise, a relative high percentage of energy production is delivered from FAT oxidation (Romijn et al 1993). When exercise intensity increased to 70% HRR, fat oxidation remained constant, but CHO oxidation rose significantly. During 10min exercise at 70% HRR, total fat oxidation was 7.3grams and CHO oxidation was 23.03grams; with average RER at 0.86 (table 1). Substrate contribution was 50.3% glucose and 49.7% fatty acids; with average metabolic rate at 57.7 kJ min^-1 (table 4). At that stage of the exercise, CHO oxidation started slightly to predominate to the FAT oxidation. Blood glucose remained constant, at 4.3 mmol.l^-1 throughout the exercise period. That supported the Costill et al (1977) findings that the aim of fat pre-exercise feeding is not to increase the blood glucose concentration, but to reduce the rate of glycogen depletion.            

Making a comparison between the two trials, the following can be highlighted: The respiratory exchange ratio (RER) was greater before exercise in CHO pre-exercise feeding trial compared with the fat pre-exercise feeding trial, reflecting an increase in the proportion of carbohydrate oxidized. During the exercise periods RER gradually rose above pre-exercise values for CHO pre-exercise feeding trial, whereas RER for fat pre-exercise feeding trial rose over the first 5 min, and then remained relatively constant throughout the exercise period. Additionally, before exercise, the rate of carbohydrate oxidation was also greatest after CHO pre-exercise feeding, but carbohydrate oxidation rose noticeably, for both trials, during the 30min exercise period. In contrast, fat oxidation was greater before exercise for fat pre-exercise feeding trial compared with CHO pre-exercise feeding trial.  During exercise period, fat oxidation remained constant for both trials; However at lower levels for CHO pre-exercise feeding trial, than the fat pre-exercise feeding trial (table 1). At the beginning of exercise blood glucose for CHO pre-exercise feeding trial was higher than fat pre-exercise feeding trial. For CHO pre-exercise feeding trial; blood glucose concentration decreased during the first 15 min of exercise and then remained almost constant for the next 15 min. For fat pre-exercise feeding trial; blood glucose concentration was slightly increased throughout the 30 min of exercise period (figure 3). 

According to the results and the literature review, fat or CHO feeding prior to exercise can alter substrate utilisation during rest and exercise periods (Whitley et al

1998; Coyle et al 1985). Indirect calorimetry was used for the estimation of fat and CHO oxidation throughout the experimental period. Indirect calorimetry is based on the concept of heat production assessed by gas exchange, and it was first described by Lovoisier 200 years ago (Schutz 1995). An accurate collection of gases (VO₂ VCO₂) is needed in order to maximize the reliability of the method. A 5% error in the VO₂ or VCO₂ data collection could have a significant impact on substrate utilisation calculations. Tables 2 and 3 represent the impact on substrate utilization, when 5% errors of VO₂ or VCO₂ values occur. For both conditions, 5% errors in measurements of VO₂ and VCO₂ showed almost ±30% overestimation of substrate utilisation (table 2 and 3). The impact for metabolic rate estimation and RER values were lower, with overestimation of +1, +4 and ±5, ±4 respectively (table 2 and 3).

Errors in substrate utilisation calculations depend on absolute VO₂, VCO₂ and the ratio between those two (RER). A selection of steady state exercise period (figures 1 and 2) and the longer the duration of measurement, will lead to more reliable calculations of substrate oxidation. The physiological sources of errors could be based on: a) Hyperventilation, which may be voluntary or may sometimes occur under psychological stress, b) Hyperventilation during the first minute of submaximal exercise, resulting on the increase of CO₂ blow off than O₂ consumed, c) Continues challenges to acid-base balance. Lactate and ketone bodies will increase the bicarbonate loss through urinary excretion (Burnier et al 1993), and d) Buffering of lactic acid, which cause large quantities of CO₂ to be released. However, despite the numerous physiological sources of errors, indirect calorimetry remains one of the most reliable methods for measuring substrate utilisation.

Conclusion     

In summary, fat or CHO feeding prior to exercise can alter substrate utilisation during rest and exercise period. Additionally, several researches showed that CHO loading or pre exercise feeding can enhance performance (Sherman et al 1989; Hawley et al 1997, Jeukendrup et al 1996; Wilber et al 1992: and Laurie et al 1995). On the other hand, there are no scientific proofs to suggest that FAT loading or pre-exercise feeding can improve performance (Whitley et al 1998). There are some suggestions, but according to Sherman (1995), performance enchantment through fat pre-exercise feeding or loading is a plausible hypothesis. Indirect calorimetry is a valid and acceptable method for substrate oxidation calculations; however several physiological factors, like hyperventilation and elevated blood lactate levels could lead to inaccurate calculation of substrate oxidation rates.