Download Biochemical Observations on a Non-Elite Marathon

Short communication/Kurzmitteilung
535
J. Clin. Chem. Clin. Biochem.
Vol. 22, 1984, pp. 535-537
SHORT
Biochemical Observations on a Non-Elite Marathon Runner
By /. A. Laing
Department of Child Life and Health, University of Edinburgh, Scotland
R. J. Young
Department of Metabolism and Clinical Endocrinology, Royal Infirmary of Edinburgh, Scotland and
A. Westwood
Department of Biochemistry, Royal Hospital for Sich Children, Edinburgh
(Received February 9/May 3, 1984)
Summary: Biochemical observations made on a 30 year old male
marathon runner before, during and fpllowing the race are described. The prolonged exercise appears to result in gluconeogenesis using non-essential amino acids äs Substrates while essential amino acids except lysine are spared.
Biochemische Beobachtungen an einem Nicht-Elite-Marathonläufer
Zusammenfassung: Biochemische Beobachtungen an einem
30jährigen Marathonläufer vor, während und nach dem Rennen
werden beschrieben. Die langdauernde Anstrengung scheint zu
einer Gluconeogenese aus nichtessentiellen Aminosäuren zu
führen, während essentielle, ausgenommen Lysin, verschont
bleiben.
Introduction
The newly awakehed interest in marathon running has attracted
thousands of first time competitors in the United Kingdom. Biochemical observations on exercise have previously been restricted
largely to elite athletes or to shorter periods of non-competitive
exercise; measurements have beeil recorded only before and after
a rüri, o r occasionally during episodes of collapse (1—8). In this
study specimens were collected during äs well äs before and for
one month following a marathon race, from a 30 year old man
with no recent participation in Sports who completed the run after
a 4 month training programme.
Subject and Methode
The runner was a 30 year old man, non-smoking, asthmatic but
well controlled on sodium cromoglycate and salbutamol aerosols.
The 4 month training programme consisted of a gradually in-'
creased running schedule from 12 km to 80 km per week, and was
intemipted by a minor ankle injury and an episode of mumps including bilateral orchitis.
J. Clin. Chem. Clin. Biochem. / Vol. 22,1984 / No. 8
A füll physical examination was carried out before and after the
marathon, and blood samples were collected immediately before,
during (at 8, 16 and 24 km), and after the race. Further samples
were collected on subsequent days l, 2, 7, and 28 (non-fasting,
taken between 09.00 h and 10.00 h).
On the morning of the race the maximum environmental temperature was 9.5 °C, rainfall ranged from "continuous slight" to
"continuous heavy" and an east north-east wind blew at 32 km/h.
The distance run was 42.19 km (26 miles 385 yards), and the time
taken was 3 hours 52 minutes, including 3 brief stops for venepuncture. A total of 900 ml of low electrolyte sucrose drinks were
consumed during the run at seven drinking stations.
Biochemical analyses were carried out by means of conventional
microtechniques using an IL Multistat III centrifugal analyser,
Beckman Astra 4 and Glucose Analysers, Rank Hilger Chromaspek amino acid analyser, and Wescor osmometer. Thyroxine,
cortisol and insulin were measured by radioimmunoassay.
Results
Clinical examination and electrocardiogram were normal before
and immediately after the run. Table l shows physiological and
haematological parameters at the Start and finish of the marathon.
The mpst pronounced change was a marked increase in granulocytes.
No significant changes were observed in plasma sodium or chloride, but there were small increases in mean plasma potassium,
osmolality, proteins, and creatinine during the race (tab. 2). Urine
osmolality before the race was 215 mmol/kg and rose slightly to
330 mmol/kg in the first specimen passed after its completion.
The more marked biochemical changes during the race included a
not surprising decrease in plasma glucose while lactate (and pyruvate) increased, both returning to normal within 24 h of the finish.
Plasma urea increased most markedly during the latter part of the
race, and at the same time the total amino acid concentration,
Short communication/Kurzmitteilung
536
which remained constant during the first part of the race, dropped
rapidly; both returned to pre-race concentrations within the next
2 days. Plasma triglycerides also increased during the race while
plasma cholesterol levels were maintained.
600
Changes in some individual plasma amino acid concentrations are
shown in more detail in figure l. The most pronounced alterations
were observed in alanine levels, which initially increased and then
feil dramatically during the marathon, only returning to the pre-
Tab. 1. Physiological and haematological observations before
and after the marathon run.
Before
marathon
Ό
O
l 200
After
marathon
σ
σ
E
61.3
60.8
36.8
37.6
58 (resting) 75
125/65
110/65
660
600
157
159
0.47
0.49
7.6
29.6
0.66
0.90
Weight(kg)
Sublingual temperature (°C)
Pulse (min"1)
Blood pressure (mm Hg)
Forced expiratory volume (min""1)
Blood haemoglobin (g/l)
haematocrit
whitecellcount(109/l)
neutrophils', fraction
•r
οc
l 400
l
ι
l
8
16
2
Distance run
[km]
7
l
l
1
2
Time fter race
IdJ
/
Fig. 1. Plasma alanine (B), valine (0), and lysine (φ) in samples
collected prior to (0 km), during (8, 16, 24 km), at the
finish of (42 km), and following (1,2 days) the marathon.
Tab. 2. Biochemical observations before, during, and following the marathon run.
Before
race
Sodium (mmol/1)
Potassium (mmol/1)
Chloride (mmol/1)
Hydrogencarbonate (mmol/1)
Urea (mmol/1)
Creatinine (μιηοΐ/ΐ)
Osmolality (mmol/kg)
Albumin (g/l)
Total protein (g/l)
Bilirubin (μιηοΙ/1)
Alkaline phosphatase (U/l)
Alanine aminotransferase (U/l)
γ-Glutamyltransferase (U/l)
Creatine kinase (U/l)
Cholesterol (mmol/1)
Triglycerides (mmol/1)
Cortisol (nmol/1)
Thyroxine (nmol/1)
Triiodothyronine (nmol/1)
Insulin (mU/1)
Glucose (mmol/1)
Lactate (mmol/1)
Pyruvate (μmol/l)
Total amino acids (mmol/1)
Alanine (μηιοΐ/ΐ)
Glutamine (μηιοΐ/ΐ)
Glycine (μπιοΐ/ΐ)
Histidine (μιηοΐ/ΐ)
Isoleucine (μιηοΐ/ΐ)
Leucine (μιηοΐ/l)
Lysine (μιηοΐ/ΐ)
Phenylalanine (μιηοΐ/l)
Serine (μπιοΐ/ΐ)
Tyrosine (μηιοΐ/ΐ)
Valine (μmol/l)
137
4.2
105
21
5.3
97
287
48
75
10
126
25
13
83
5.7
0.6
647
106
1.8
31.2
6.0
2.2
145
2.01
320
433
205
125
60
128
164
64
113
74
192
During race
(km)
8
16
137
4.7
105
19
5.1
110
297
50
79
8
132
29
15
111
6.0
0.5
644
106
2.1
3.1
4.5
4.6
176
2.16
545
441
229
125
49
104
140
59
98
61
216
24
140
4.4
104
23
5.4
104
294
50
79
9
142
27
16
133
5.7
0.6
564
111
2.2
1.1
3.8
4.4
139
2.29
527
474
218
125
59
121
132
66
93
71
209
After race
(days)
1
2
Finish
140
4.5
102
25
6.7
107
298
49
78
10
146
27
16
480
5.5
1-1
139
4.6
104
22
5.9
111
292
49
80
10
139
28
16
168
5.8
0.8
709
112
2.2
< 0.5
3.4
4.5
153
2.29
509
483
228
105
59
128
89
70
92
86
224
1142
123
1.9
<
0.5
2.8
3.9
156
1.52
232
312
135
94
54
112
85
56
51
60
207
28
7
140
140
138
4.4
4.2
4.2
104
106
105
27
27
29
5.2
4.9
6.1
.v 91- r
97
96
280
297
278
50
46
48
73
73
69
14
13
< 5
134
122
126
50
30
48
12
16
15
1965
136
3410
4.6
5.5
4.6
0.5
0.4
0.5
272
211
279
92
95
96
1.6
1.5
1.9
«.
1.3
—
4.8
4.2
—
1.7
1.4
0.9
119
120
109
1.67
256
388
153
123
50
103
112
68
69
47
167
1.94
416
403
201
102
43
96
171
54
94
59 *
22l·»
1.91
291
389
215.
101
43
100
174
54
90
51
211
137
4.1
105
25
4.9
90
287
48
71
8
108
18
< 10
63
4.6
1.1
196
90
1.4
—
4.8
1.1
99
1.88
290
365
180
85
57
99
149
55
90
54
180
J. Clin. Cheiii. Clin. Biochem. / Vol. 22,1984 / No. 8
537
Short communication/Kurzmitteilung
race concentration about 48h later. Similar, but less marked
changes, were seen in other non-essential amino acids (glycine,
glutamine, serine). In contrast, the plasma concentration of valine
(and other branched chain amino acids) was maintained during
the whole period of running, and there were no substantial
changes in other essential amino acids with the notable exception
of lysine. The lysine concentration feil steadily during the race to
about half the pre-race level, returning to normal about 2 days later.
The maximum increase in plasma creatine kinase occurred on the
day after completion of the run, returning to normal within the
next week (tab. 2). The increase in alanine aminotransferase was
much less marked and reached a peak on the second day after the
race, while there was no significant change in alkaline phosphatase nor -glutamyltransferase during the period of study.
Remaining plasma was assayed for the concentration of four hörmones (attempts to measure more were curtailed äs a result of
insufficient sample volumes). The most marked changes were apparent in insulin and Cortisol levels, but there were also small increases in both thyroxine and triiodothyronine (tab. 2).
Discossion
The weight loss of 0.5 kg during the marathon was probably
caused largely by energy Output, since the haematocrit and urine
and plasma osmolalities indicated well-maintained hydration.
This is in keeping with the Suggestion that the energy cost of a
marathon is 12.6 MJ (3000 kcal) and that 0.5 kg of true weight
loss may occur (9), although elite runners taking in little fluid and
in warmer conditions may lose over 3 kg largely due to dehydration (3). In this study the runner's sublingual temperature rose by
0.8 °C, but elite marathon runners may have racing core temperatures of 39-41 °C (2).
The steady fall in plasma glucose during the race was accompanied by a more rapid initial increase in lactate (and to a lesser extent pyruvate) which then reached a plateau and began to fall
again before its completion. These observations are consistent
with reports for both athletes and non-athletes exercising for
shorter periods (6, 8). Free fatty acids and ketone bodies also increase in plasma concentration during exercise, especially in untrained individuals (6, 8), presumably äs a result of increased mobilisation of fat. There was only a small increase in plasma potassium during the race, and the late rise in urea, seen only in the
longer events (8), is consistent with the increased use of amino
acids äs energy Substrates in the second half of the race (tab. 2,
fig. 1). The tissue source of plasma enzymes after exercise is unclear (10) but the changes observed in this study confirm other
reports (11).
The hormonal response to prolonged exercise is known to include
a decrease in plasma insulin and increases in catecholamines, glucagon, growth hormone, and cortisol, although the magnitude of
the changes is not necessarily consistent between trained and untrained individuals (8, 12). Cortisol stimulates gluconeogenesis,
and the increase observed later in the race is consistent with the
sharp decrease in plasma amino acids at this time.
Alanine is known to be released from muscle during shorter periods of exercise and in proportion to its intensity (13), and the
initial rise in plasma concentration observed in the present study is
consistent with previous reports (7, 8). In prolonged exercise,
however, increased demand for this amino acid äs a hepatic substrate for gluconeogenesis (13) results in a fall in blood concentration; in this study it was found that the plasma alanine concentration increased and was maintained until the second half of the
race, when it feil rapidly (fig. 1). Other non-essential amino acids
also decreased in concentration later in the race but no significant
changes were observed in any of the essential amino acids except
lysine. The latter feil steadily from the Start of the race, then rose
to the pre-race level over the next two days. It is not clear why
lysine should so markedly differ in this respect, and this observation is being further investigated.
Acknowledgements
We are grateful to Drs. J. Seth and G. /. Becken of the Department of Clinical Chemistry, Royal Infirmary of Edinburgh, who
undertook the hormone assays, and to Mrs. 5. M. McCormick and
Mrs. 7. M. Lowther, who typed the manuscript.
References
1. Milvy, P. (1977) Ann. NY. Acad. Sei. 301, 620-626.
2. Leader (1978) Lancet //, 718-719.
3. Muir, A. L., Percy.Robb, I. W., Davidson, . ., Walsh, E. G.
& Passmore, R. (1970) Lancet //, 1125-1128.
4. Ledingham, I. M., MacVicar, S., Watt, L, Weston, G. A.
(1982) Lancet //, 1096-1097.
5. Waller, B. F. & Roberts, C. (1980) Am. J. Cardiol. 45,
1292-1300.
6. Johnson, R. H., Walton, J. L., Krebs, H. A. & Williamson, D.
H. (1969) Lancet 77, 452-455;
7. Rettenmeier, A., Weicker, H. & Frank, H. (1982) Dtsch.
Zeitschr. Sportmed. 33, 37-45.
8. Weicker, H. (1982) In: „Sport: Leistung und Gesundheit",
Kongreßband Dtsch. Sportärztekongreß in Köln 1982, pp.
177-192.
9. Feiig, P. (1977) Ann. NY. Acad. Sei. 307, 56-63.
10. Tunstall-Pedoe, D. S. (1982) Lancet 77, 154.
11. Stansbie, D., Aston, J. P., Powell, N. H. & Willis, N. (1982)
Lancet 7, 1413-1414.
12. Galbo, H., Richter, E. A., Hilsted, J., Holst, J. J., Christensen, N. J. & Henrikson, J. (1977) Ann. NY. Acad. Sei.
307, 72-80.
13. Pugh, L. G. C. E., Corbett, J. L. & Johnson, R. H. (1967) J.
Appl. Physiol. 23, 347-352.
Dr. I. Laing
Department of Child Life and Health
University of Edinburgh
Hatton Place
Edinburgh
Scotland, U.K.
J. Clin. Chem. Clin. Biochem. / Vol. 22,1984 / No. 8