Vitamin C maintains endurance athletes

testosterone levels
Performing endurance sports reduces testosterone levels. [Eur J Appl Physiol. 2003
Apr;89(2):198-201.] This happens, for example, if you run for longer than 45 minutes. [Eur J
Appl Physiol. 2005 Aug;94(5-6):505-13.] Pharmacologists at the BJ Govt Medical College in
India did an animal study which seems to have uncovered a surprisingly simple way for
endurance athletes to limit the reduction in their testosterone level: supplementation with
vitamin C.

Vitamin C and testosterone

Ten years ago researchers from Firat University published an animal study in which a
megadose of vitamin C boosted testosterone levels. [Theriogenology. 2005 Apr
15;63(7):2063-72.] Converting the figures, an adult human would need 3 to 7 g vitamin C a
day to induce a modest rise in testosterone level.
In the animal study that the Indian researchers published in the Journal of Clinical and
Diagnostic Research male rats were given less extreme doses. The human equivalent of these
would be about 140, 280 and 420 mg per day.

Study
The researchers got rats to swim to the point of exhaustion on 15 consecutive days [Exercise;
Stress]. Some of the lab animals did not swim [Normal].
Testosterone level
The fortnight of physical exertion lowered the rats testosterone level, as the figure below
shows. When the rats were given vitamin C 30 minutes before they started swimming,
however, the decrease in testosterone was less.

Vitamine C
The physical exercise reduced the rats fertility, probably because of the release of free
radicals during their exertions, which damaged the testes. Supplementation only partially
negated the reduction in sperm quality, the table above shows.

Sexual effects
The physical exertion reduced the percentage of pairings the researchers discovered when
they placed sexually mature females in a cage with the lab rats. Administration of vitamin C
limited the decline in sexual interest. Copulatory index = an indicator of the animals interest
in sex.

Conclusion

Vitamin C supplementation improves the stress induced reproductive infertility possibly

mediated through an increase in testosterone and an antioxidant effect, the researchers write.
Effect of vitamin C on male fertility in rats subjected to forced swimming stress.
Abstract

INTRODUCTION:
Stress is defined as a general body response to initially threatening external or internal
demands, involving the mobilization of physiological and psychological resources to deal
with them. Recently, oxidative stress has become the focus of interest as a potential cause of
male infertility. Normally, equilibrium exists between reactive oxygen species (ROS)
production and antioxidant scavenging activities in the male reproductive organs. The
ascorbic acid is a known antioxidant present in the testis with the precise role of protecting
the latter from the oxidative damage. It also contributes to the support of spermatogensis at
least in part through its capacity to maintain antioxidant in an active state.

MATERIALS AND METHODS:

Group1: Normal Control animal received Distilled water, Group 2: Positive control (Only
Stress), Group 3: Normal rats received an intermediate dose of Vitamin C (20mg/kg/day),
Group 4: Stress + Low dose Vitamin C (10mg/kg/day), Group 5: Stress+ Intermediate dose
Vitamin C (20mg/kg/day), Group 6: High dose Vitamin C (30mg/kg/day). On 16(th) day
effect of stress on body weight, Reproductive organ weight, sperm parameters, and hormonal
assay was studied.

RESULTS:
In the present context, in stress group the sperm count, motility, testicular weight declined
significantly. The intermediate dose and high dose of vitamin C showed significantly
increased effect on the sperm count and motility.

CONCLUSION:
Various physiological changes produced force swimming indicates that swimming is an
effective model for producing stress in albino rats. The results suggest that Vitamin C
supplementation improves the stress induced reproductive infertility due to both their
testosterone increase effect and their antioxidant effect.

PMID: 25177581 PMCID: PMC4149087 DOI: 10.7860/JCDR/2014/8432.4622

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